Step Up To Medicine Not Own

Front 1

Most common cause of endocarditis in a native valve

Back 1

Strep viridans

Front 2

most common cause of early (within 60 days of surgery) endocarditis on a prosthetic valve? late (>60 days after surgery) endocarditis?

Back 2

early––> staphylococci (e.g. staph epidermidis– skin bact)
late––> streptococci

Front 3

Atrial fibrillation

Back 3

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Hint 3

irregularly irregular rhythm with absent p waves

Front 4

most common cause of right sided endocarditis

Back 4

S. aureus (often seen in IV drug users)

Front 5

complications of endocarditis

Back 5

1. cardiac failure
2. myocardial abscess
3. various solid organ damage from showered emboli
4. glomerulonephritis

Front 6

What should you always suspect in a patient with fever and new onset murmur?

Back 6

endocarditis

Front 7

Janeway lesions vs oslers nodes

Back 7

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Hint 7

Janeway lesions– painless erythematous lesions on palms and soles–– symptom of endocarditis
Osler's nodes– painful raised lesions on fingers, toes and feet

Front 8

Roth spots

Back 8

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Hint 8

oval, retinal hemorrhages with clear, pale center seen in endocarditis

Front 9

Is TEE or TTE better in the diagnosis of endocarditis?

Back 9

Transesophageal Echo (TEE)

Front 10

What should be given to any patient with cardiac valve disease undergoing GI/GU/dental procedures?

Back 10

amoxicillin as endocarditis prophylaxis

Front 11

Diagnosis of endocarditis (Duke's Criteria)

Back 11

Need 2 Major, 1 major + 3 minor or 5 minor

Major = sustained bacteremia, endocardial involvement (vegetation, abscess, valve perforation) or New onset valve regurgitation

Minor = predisposing condition (abnormal valve), fever, vascular phenomena (septic arterial or pulmonary emboli, mycotic aneurysms, Janeway lesions), immune mediate phenomena (glomerulonephritis, oslers nodes, roth spots), positive blood cultures, positive echo

Front 12

Tx for endocarditis

Back 12

IV (parenteral) antibiotics based on culture results for extended periods (4–6 weeks)

If culture negative, but high clinical suspicion, treat empirically with penicillin or vancomycin plus an aminoglycoside (e.g. gentamycin, neomycin etc) until organism can be isolated.

Front 13

4 parts to Tetralogy of Fallot

Back 13

1. Pulmonary Stenosis
2. Right Ventricular Hypertrophy (secondary pulm stenosis)
3. Overriding Aorta
4. Ventricular Septal Defect (VSD)

Hint 13

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Front 14

Non–bacterial thrombotic endocarditis (Marantic endocarditis)

Back 14

associated with debilitating disease such as metastatic cancer
– sterile deposits of fibrin and platelets form along the closure line of cardiac valve leaflets
– vegetation can embolize to brain or periphery
– heparin may be used but NOT proven effective

Front 15

Nonbacterial Verrucous Endocarditis (Libman Sacks Endocarditis)
1. associations
2. what is it?
3. treatment

Back 15

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Hint 15

– typically involves the AV valves in individuals with SLE
– characterized by formation of small warty vegetations on BOTH sides of valve leaflets +/– regurgitation murmurs
– rarely gives rise to infective endocarditis but can be a source of systemic emboli
– Tx: treat underlying SLE + anticoagulation

Front 16

5 congenital cyanotic Heart Diseases

Back 16

early cyanosis– Terrible Ts
1. Truncus Arteriosus– one trunk arising from RV and LV
2. Transposition of Great Vessels– Pulmonary artery and aorta arise from wrong sides of the heart
3. Tricuspid Atresia
4. Tetralogy of Fallot
5. Total Anomalous Pulmonary Venous Connection

Front 17

Atrial Septal Defect
1. most common type
2. pathophysiology

Back 17

1. ostium secundum– central portion of the septum
2. oxygenated blood from the LA goes thru ASD into RA which leads to increased pulm. blood flow and inc work of right side of heart. As the shunt size inc, RA and RV dilatation occur. Pulm HTN is a serious sequelae, but RARE in ASD

Hint 17

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Front 18

Clinical course of ASD

Back 18

Patients are usually asymptomatic until middle age (age 40). thereafter sx may begin–– exercise intolerance, dysnpea on exertion, and fatigue
– if mild patients may have a normal life span

Front 19

Luetic Heart
1. Cause
2. demographic
3. features
4. treatment

Back 19

1. complication of syphilitic aortitis–– usually affecting men in the 4th to 5th decade of life.
3. aneurysm of aortic arch with retrograde extension that causes Aortic Regurg plus stenosis of aortic branches
4. IV penicillin and surgical repair

Front 20

Mycotic aneurysm
1. definition
2. Blood Cultures
3. Treatment

Back 20

1. aneurysm resulting from damage to the vessel wall secondary to infection
2. Blood cx are positive in most cases
3. IV abx plus surgical excision

Front 21

Acute Arterial Occlusion
1. Pathophysiology
2. Most common site

Back 21

1. Acute occlusion is usually caused by an embolus, although rarely from an in situ thrombosis
2. most common site = common femoral artery

Front 22

most common sources of emboli in acute arterial occlusion

Back 22

1. Heart – 85% (Afib is the most common cause, post–MI stasis, endocarditis, myxoma)
2. Aneurysms
3. Atheromatous plaque

Front 23

Clinical Features of Acute Arterial Occlusion

Back 23

6 Ps
1. Pain
2. Pallor
3. Polar
4. Pulselessness (use doppler US to assess)
5. Paresthesia
6. Paralysis

Front 24

Diagnosis of Acute arterial Occlusion

Back 24

1. Arteriogram to define site
2. ECG to look for MI or Afib (sources)
3. Echo to evaluate heart valves, clots, MI

Front 25

Compartment Syndrome
1. definition
2. treatment

Back 25

Compression of nerves, blood vessels, muscle etc inside an enclosed space/compartment within the body

tx: fasciotomy to relieve pressure

Front 26

Treatment of Acute Arterial Occlusion
1. main goal
2. how long can skeletal muscle survive without perfusion?
3. What if there is paralysis or paresthesia?

Back 26

Immediate anticoagulation with IV Heparin and emergent embolectomy via cutdown or fogarty balloon–– if this fails then bypass. Treat compartment syndrome as necessary
1. main goal it to assess viability of tissues and salvage the limb
2. skeletal muscle can tolerate 6 hours of ischemia– perfusion should be re–established within this time
3. if paralysis or paresthesia are present then amputation is probably necessary

Hint 26

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Front 27

Treatment of Rheumatic Fever
1. prevention
2. acute treatment
3. pts with h/o RF
4. rheumatic heart dz

Back 27

1. Treat strep pharyngitis with penicillin or erythromycin (if pen allergy) to prevent it
2. Acute Rheumatic Fever = NSAIDs
3. pts with h/o RF should get abx before all GI/GU/dental procedures–– amoxicillin or erythromycin
4. treat valvular disease as indicated

Front 28

Diagnosis of Acute Rheumatic Fever

Back 28

Jones criteria: 2 major, 1 major and 2 minor

Major
1. Migratory polyarthritis
2. Eyrthema marginatum– pink rings on the trunk that come and go
3. cardiac involvement– pericarditis, CHF, valve disease
4. subQ nodules– Aschoff nodules
5. chorea

Minor
1. fever
2. inc ESR
3. polyarthralgias
4. h/o s. pyogenes infection (positive ASO titer –antistreptolysin O antibodies)
5. h/o rheumatic fever
6. prolonged PR

Hint 28

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Front 29

Causes of hypertensive emergency

Back 29

1. Medication non–compliance
2. cocaine, LSD, methamphetamine
3. Alcohol withdrawal
4. hyperaldosteronism– inc aldo ––> inc reabsorption of sodium and water, inc secretion of K+
5. Cushings syndrome– inc cortisol secretion
6. eclampsia– seizure in pre–eclampsia
7. vasculitis
8. pheochromocytoma
9. Non–compliance with dialysis

Front 30

Treatment of aortic dissection
1. Medical for all
2. Type A vs Type B

Back 30

Initiate medical treatment– IV Beta blockers to decrease HR and force of LV Ejection, Nitropusside or Nitroglycerin to decrease blood pressure to below 120 mmHg

2. For Type A (proximal aorta dissections) – surgery is indicated as cardiac tamponade may develop
For Type B (distal dissections)– medical management only unless pt is unstable

Front 31

Best Tests for Aortic Dissection
1. stable pt
2. unstable pt

Back 31

1. TEE and CT
2. TEE at the bedside

Front 32

Aortic Dissection
1. definition
2. types–– Stanford

Back 32

1. tear in the inner wall of the aorta causes blood to flow between vessel/intimal wall layers, forcing them apart
2. Type A– involves ascending aorta +/– arch– may spread retrograde into heart––> tamponade
Type B– involves descending aorta or arch

Hint 32

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Front 33

Hypertensive Emergency Treatment
1. over 1st 1–2 hours
2. if severe? (how do you define severe?)
3. if less immediate danger?

Back 33

1. reduce MAP by 25% in the 1st 1–2 hours. The goal is NOT immediately to achieve normal BP, but to get the patient out of danger and then gradually reduce it
2. if SEVERE (DBP > 130 mmHg) or hypertensive encephalopathy ––> IV agents such as nitroglycerin, nitroprusside, or labetalol (alpha and beta antagonist) are appropriate
3. If in less immediate danger – oral agents such as captopril, clonidine, labetalol, or diazoxide

Front 34

Clinical features of Patent Ductus Arteriosus (PDA)

Back 34

1. Maybe asx
2. signs of HF
3. loud P2– sign of pulm HTN
4. LVH ( L––> R shunt)––> Left heart has to pump against increased PVR
5. continuous machinery murmur at 2nd ICS (both systolic and diastolic)
6. Wide Pulse pressure (SBP–DBP)
7. Differential cyanosis– lower extremity clubbing– toes are more likely to be cyanotic than fingers

Hint 34

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Front 35

Complications of VSD

Back 35

1. Heart Failure
2. Endocarditis
3. Progressive Aortic Regurgitation
4. pulm HTN and shunt reversal (R––>L) = Eisenmenger's syndrome

Front 36

Symptoms of hypertensive emergency

Back 36

severe headache, visual disturbances, and altered mental status (AMS)

Front 37

Complications of aortic coarctation

Back 37

1. Severe HTN
2. rupture of cerebral aneurysms (inc flow/pressure above coarctation)
3. infective endocarditis
4. aortic dissection

Front 38

Treatment of PDA
1. if pulm HTN absent
2. if PHTN present or R––> L shunt

Back 38

1. surgical ligation if there is NO PHTN
2. if severe PHTN or R––>L shunt do not correct PDA–– this is a contraindication

Front 39

What are the leading causes of death in adults with a PDA (2)?

Back 39

Heart failure and infective endocarditis

Front 40

What is PDA associated with (3)?

Back 40

Congenital rubella syndrome
High altitude
Premature births

Front 41

Treatment of VSD
1. when indicated
2. what needs to be given as ppx
3. for asx pts with a small defect?

Back 41

1. surgical repair when pulmonary to systemic blood flow ratio is greater than 1.5:1 or 2:1 (same as with ASD)
2. endocarditis prophylaxis (amoxicillin, or erythromycin if allergy)
3. surgery is not indicated

Front 42

Non–cyanotic congenital heart diseases (4)

Back 42

1. ASD
2. VSD
3. PDA
4. Coarctation of the Aorta – narrowing of the aorta

Front 43

Signs of VSD
1. type of murmur
2. what happens to murmur with valsalva
3. other sx
4. what happens to pulm component of S2 as Pulmonary Vascular Resistance inc?
5. What causes AR when a VSD is present?

Back 43

1. harsh, blowing holosystolic murmur with thrill (blood crossing VSD)–– the smaller the defect, the louder the murmur
2. murmur decreases with valsalva and handgrip (decreased return of blood to heart– decreased preload)
3. sternal lift from RV enlargement
4. As PVR increases the pulm component of s2 increases in intensity
5. Aortic Regurgitation– flow through VSD creates low pressure zone leading to AV prolapse by venturi effect

Front 44

Clinical features of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 44

superficial thrombophlebitis– local tenderness and erythema along course of superficial vein

CVI– aching of lower extremities worse at end of day, relieved by elevation of the lefts and worsened by recumbency. May see edema, pigmentation and ulcers

DVT– usually asymptomatic, but may calf pain, and unilateral swelling

Front 45

Diagnosis of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 45

superficial thrombophlebitis– clinical dx

CVI– clinical dx

DVT– duplex US, D–Dimer to r/o

Front 46

Treatment of superficial thrombophlebitis vs chronic venous insufficiency vs DVT

Back 46

superficial thrombophlebitis– analgesics, monitor for spread or cellulitis

CVI– leg elevation, avoid long periods of standing, elastic stockings, and if ulcers present then Unna boot and wet to dry dressings

DVT– anticoagulation

Front 47

Systemic Inflammatory Response Syndrome (SIRS)
1. criteria
2. sepsis
3. septic shock
4. multi–organ dysfunction syndrome (MODS)

Back 47

Characterized by 2 or more of the following
Temperature >38 or <36 C (fever or hypothermia)
HR >100 or <60 bpm
hyperventilation (rate >20 bpm or PaCO2 > 32 mmHg)
tachycardia (HR >90 bpm)
inc WBC count (>12,000 cell/hpf) or dec WBC count (<4,000 cell/hpf) or >10% band form (immature cells)

Sepsis– when blood cultures are positive + SIRS (two sets of blood cultures must be taken from two sites before abx are given)

Septic shock– decreased blood pressure due to sepsis despite fluid resuscitation

Multiorgan dysfunction syndrome– usually leads to death

Front 48

What is the most common primary cardiac neoplasm?

Back 48

atrial myxoma

Front 49

Atrial myxoma
1. definition
2. benign or malignant?
3. complications
4. causes
5. protypical presentation
6. tx

Back 49

1. benign gelatinous growth that is usually pedunculated and usually arising from the interatrial septum in the region of the fossa ovalis
2. benign
3. can embolize leading to metastatic disease or can cause relative valvular dynfunction
4. most are sporadic put some autosomal dominant cases have been reported
5. fatigue, fever, syncope, palpitations, malaise, low pitched diastolic murmur that changes with body position (diastolic plop)
6. tx– surgical excision

Hint 49

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Front 50

patient presents with fatigue, fever, syncope, palpitations, and malaise. On exam you hear a low pitched diastolic murmur that changes with body position. What do they most likely have?

Back 50

Atrial myxoma– benign primary cardiac tumor

Hint 50

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Front 51

General characteristics of cardiac neoplasms
1. primary vs metastatic more likely?
2. if metastatic where are the most likely primaries?

Back 51

1. primary cardiac neoplasms are rare, 75% are from mets
2. sites of primaries = lungs, breast, skin, kidney, lymphomas, kaposi's sarcoma (HHV–8) in AIDS pts

Front 52

Treatment of neurogenic shock

Back 52

1. judicious use of IV Fluids = mainstay
2. vasoconstrictors but be cautious
3. put patient supine or in trendelenburg position (head down)
4. maintain body temp

Hint 52

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Front 53

Clinical features of neurogenic shock
– skin
– Urine output
– HR and BP?
– CO, SVR and PCWP

Back 53

– warm, well perfused skin (vasodilation)
– decrease urine output or nl
– decreased HR and BP (but can be tachy)
– C.O. is nl to decreased, dec SVR, PCWP is nl to decreased

Front 54

Neurogenic shock– general characteristics
1. mechanism
2. causes

Back 54

failure of the sympathetic nervous system to maintain adequate vascular tone (sympathetic denervation leading to decreased epi and norepi)
– causes include spinal cord injury, severe head injury, spinal anesthesia, pharmacologic sympathetic blockade
– characterized by peripheral vasodilation with dec SVR
– dec CO, SVR, and PCWP

Front 55

Definition of cardiogenic shock
1. SBP and Urine output criteria

Back 55

SBP <90mmHg and urine output <20 cc/hr with adequate LV filling pressure

Front 56

What is the most common cause of death in the ICU?

Back 56

septic shock

Front 57

1. diagnosis of septic shock
2. treatment of septic shock

Back 57

1. clinical diagnosis, confirmed by blood culture but blood cultures are commonly negative
2. IV antibiotics broad spectrum at max doses, surgical drainage if necessary (depending on source of infection), fluids to inc BP, pressors if BP remains low despite aggressive fluid fluids (1st dopamine, 2nd norepi)

Front 58

Clinical features of septic shock
1. skin

Back 58

– manifestations related to the cause of sepsis (pneumonia, UTI, peritonitis etc)
– signs of SIRS
– dec BP, oliguria, lactic acidosis
– fever or hypothermia
– hypothermia is more common in the very young, elderly or debilitated or ICH– don't have immune response that leads to the fever

Front 59

Septic shock
1. definition
2. causes
3. progression
4. presentation
5. complications

Back 59

1. decreased BP induced by sepsis that persists despite adequate fluid resuscitation
2. causes– pneumonia, pyelonephritis, meninigitis, abscess, cholangitis, cellulitis, peritonitis
3. Progression– SIRS ––> sepsis––> septic shock ––> multiorgan dysfunction
4. Severe decrease in SVR secondary to peripheral vasodilation, nl to increased C.O. (due to inc HR and maintained SV), warm extremities, dec EF secondary to decreased contractility
5. complications– ARDS, acute tubular necrosis (ATN), Disseminated Intravascular Coagulopathy (DIC)––form a bunch of clots then start hemorrhaging because you have used up all your clotting factors, multi–organ failure, death

Front 60

Treatment of hypovolemic shock

Back 60

1. Airway and Breathing– pts in severe shock and circulatory collapse generally require intubation and mechanical ventilation
2. Circulation– if hemorrhage– apply direct pressure +/– transfusion. IV hydration – pts with class I usually do not require IV fluids, class II benefits, and class III and IV require fluid resuscitation. Give fluid bolus and continuous infusion and then reassess
3. For non–hemorrhagic shock– do not transfuse. Crystalloids with electrolyte replacement is adequate

Front 61

What is the only type of shock where PCWP/LA filling pressure is increased?

Back 61

cardiogenic shock

Front 62

Clinical features of cardiogenic shock

Back 62

1. Altered mental status (AMS)
2. dec BP
3. inc HR
4. engorged neck veins (JVD) – inc venous pressure
5. pulmonary congestion (LVF)

Front 63

Cardiogenic shock
1. general characteristics
2. causes

Back 63

1. occurs when the heart is unable to generate enough C.O. to maintain tissue perfusion. Defined as SBP< 90 mmHg with urine output <20 cc/hr + adequate PCWP/LA filling pressure
2. After acute MI – most common cause
– cardiac tamponade (compression of the heart)
– tension pneumothorax (compression of the heart)
– arrhythmias
– massive PE ––> RVF
– myocardial disease (cardiomyopathies, myocarditis)

Front 64

What is the most effective method of monitoring response to treatment in hypovolemic shock?

Back 64

measuring urinary output (UOP)

– also helpful are pulmonary catheter +/– central line

Front 65

Hypovolemic shock
1. general characteristics
2. causes

Back 65

1. Primary pathophysiology– dec effective circulatory volume (ECV) leads to dec preload and dec CO
2. Rate of volume loss is important– the slower the loss then the greater the compensatory mechanisms
3. patients with signs of medical commorbidities (esp cardiac) may be unable to compensate physiologically
4. there are 4 classes depending on the severity of the volume loss
5. causes
– hemorrhage– trauma, GI bleed, retroperitoneal
– non–hemorrhagic– lots of vomiting, severe dehydration, severe diarrhea, burns, 3rd spacing in bowel obstruction

Front 66

Treatment of the cardiogenic shock

Back 66

1. ABCs– airway, breathing and circulation
2. Identify and treat underlying cause
a. Acute MI– MONAH (standard), Aggressive revascularization with PTCA or CABG
b. tamponade– periocardiocentesis/surgery
c. surgery for valve issues
d. treat arrythmias
3. Vasopressors – dopamine = 1st, dopamine and dobutamine = 2nd, Norepi and epi if severe
4. Afterload reduction – Nitroglycerin or Nitroprusside– not usually indicated because they exacerbate hypotension but may be used later with vasopressor
5. IV fluids are likely harmful because of elevated LV pressures. Patients may actually need diuretics
6. Intra–aortic balloon pump (IABP) – dec afterload, inc CO, dec myocardial demand

Front 67

Diagnosis of cardiogenic shock

Back 67

1. ECG– ST elevation or arrythmia
2. Echo– mechanical compression of heart, valve disease, estimate EF, pericardial effusion
3. Hemodynamic monitoring–– Swan Ganz catheter (pulm artery catheter) to measure PCWP, PA pressure, CO, Cardiac Index, SVR, keep CO > 4 L/min (nl = 5 L/min), Cardiac Index > 2.2, and PCWP < 18 mmHg

Front 68

Surgical Treatment for peripheral vascular disease (PVD)
1. indications
2. methods

Back 68

1. rest pain, ischemic ulcerations (tissue necrosis), severe symptoms refractory to conservative treatment
2. options = surgical bypass graft is most common and has a 5 yr patency of 70% or angioplasty

Front 69

Causes of Abdominal Aortic Aneursym

Back 69

MULTIFACTORIAL– most cases = atherosclerotic weakening of the aortic wall

– Predisposing factors = trauma, HTN, vasculitis, smoking, and a positive family history
– syphilis + connective tissue abnormalities (E.g. Marfans, Ehler's Danlos) are associated with thoracic aneurysms but they may involve the lower aorta as well

Front 70

Rupture of AAA
1. triad of findings
2. Other symptoms

Back 70

1. Abdominal pain, hypotension, palpable pulsatile mass – ruptured AAA ––> emergent laporotomy with further diagnostic tests
2. circulatory collapse, syncope, pre–syncope secondary to sudden hemorrhage, n/v

Front 71

Treatment of unruptured AAA vs ruptured AAA

– what is the normal size/diameter of the infrarenal Aorta?

Back 71

1. unruptured AAA– depends on the size. If the diameter > 5 cm or symptomatic then operate (synthetic graft). If asymptomatic and <5 cm diameter, treatment is controversial, but periodic imaging is recommended to F/U growth (NO SAFE SIZE EXISTS)
– consider life expectancy of patients vs risk of surgery and lengthy recovery
2. ruptured–– emergery laporotomy
3. nl = 2 cm

Front 72

Peripheral Vascular Disease (PVD)
1. definition
2. typical patients
3. sites of occlusion/stenosis

Back 72

1. PVD = atherosclerotic disease of the lower extremities
2. patients with PVD usually have co–existing CAD (with CHF, or h/o MI etc) plus other chronic medical problems like diabetes or lung disease
3. most common site is the superficial femoral artery (in Hunter's canal), popliteal artery, aortoiliac occlusive disease

Front 73

Prognosis of peripheral vascular disease (PVD)

Back 73

1. If the patient has intermittent claudication– good prognosis
2. patients with rest pain or ischemic ulcers have the worst prognosis (especially if they are diabetic or are smokers)

Front 74

Treatment of Peripheral Vascular Disease (PVD)

Back 74

– Diabetics have an amputation rate 4x higher than others
– Conservative management for intermittent claudication includes: 1) smoking cessation– cannot be over–emphasized), 2) graduated exercise program (walk to point of claudication, rest then continue), 3) foot care (especially in diabetics), 4) Atherosclerotic RF reduction (dec HLP, HTN, weight, and improve glycemic control), 5) avoid extremes of temperature (esp extreme cold), 6) aspirin, 7) Trental (pentoxyfylline)– lowers blood viscosity

Front 75

Diagnosis of Peripheral Vascular Disease
1. most common
2. other
3. gold standard

Back 75

1. Ankle–Brachial Index (ABI) – ratio of SBP at ankle vs arm (nl >/= 1.0, claudication ABI < 0.7, Rest pain ABI < 0.4)
2. pulse volume recordings – excellent assessment of segmental perfusion/non–invasive using pressure cuffs
3. gold standard – arteriography – contrast in vessels + radiographs– helps locate PVD– only needed if surgery/revascularization is being considered

Front 76

1. What is a normal ABI?
2. when does claudication begin (what ABI)?
3. When does rest pain begin (what ABI)?

Back 76

1. > 1.0 mmHg
2. <0.7 mmHg
3. < 0.4 mmHg

ABI = ankle–branchial index = SBP in ankle/SBP in arm (brachial artery)

Front 77

Signs of peripheral vascular disease (PVD) on physical exam

Back 77

1. dec or absent pulses
2. muscular atrophy
3. dec hair growth
4. thick toenails
5. dec skin temp
6. ischemic ulceration (usually on toes)– localized skin necrosis secondary to trauma that does NOT heal
7. tissue infarction/gangrene (end stage disease)
8. pallor of elevation and rubor of dependency

Front 78

Diagnosis of Atrial Septal Defect

Back 78

1. Transesophageal Echo is diagnostic (better than TTE)
2. CXR – may show large pulmonary arteries (secondary to inc blood flow) – inc pulmonary vascular markings
3. ECG– RBBB, right axis deviation, atrial abnormalities such as AFib or Aflutter

Front 79

Complications of ASD

Back 79

1. pulmonary HTN– common in > 40 yo
2. Eisenmenger's disease – irreversible pulmonary HTN leads to shunt reversal (R––> L shunt), HF and cyanosis
3. Right sided HF
4. atrial arrhythmias–– esp Afib
5. Stroke secondary to paradoxical emboli or afib

Front 80

Clinical features of ASD

Back 80

1. Mild Systolic Ejection murmur at pulmonary area secondary to inc blood flow
2. wide fixed splitting of S2 due to inc pulm blood flow and delayed closure of the Pulm Valve
3. diastolic flow "rumble" murmur – inc blood flow across the tricuspid valve
4. if advanced – signs of RVF – ascites, hepatomegaly, JVD etc

Front 81

What does fixed splitting of S2 indicate?

Back 81

ASD

Front 82

Treatment of ASD

Back 82

1. surgical repair when pulm to systemic blood flow ratio > 1.5 : 1 or 2.0 : 1 OR if the patient is symptomatic

Front 83

What is the most common congenital cardiac malformation?

Back 83

VSD

Front 84

What is a paradoxical embolus?

Back 84

DVT forms and instead of traveling to the lungs and causing a PE is transverses the ASD to the brain causing stroke

Front 85

Symptoms of Peripheral Vascular Disease (PVD)

Back 85

1. Intermittent claudication– cramping leg pain that is reliably reproduced by the same walking distance (relieved by rest or dangling legs over the bed)
2. Rest pain (continuous) – usually felt over distal metatarsals, often prominent at night–– awakens patient from sleep. Hanging foot over the bed or standing relieves the pain due to extra perfusion to ischemic areas – using gravity. This suggests severe ischemia such that frank gangrene may occur without intervention

Front 86

Peripheral Vascular Disease (PVD) Risk Factors

Back 86

1. Diabetes Mellitus – prevalence markedly increased
2. smoking
3. CAD
4. HLP
5. HTN
6. hyperhomocystinemia

Front 87

Diagnosis of AAA

Back 87

1. US = test of choice to evaluation both location and size of aneurysm – 100% sensitive
2. CT Scan – 100% sensitive, but is more expensive and more time consuming– should only be used if patient is hemodynamically stable
3. Abd Xray – may show calcification of dilated segment –– allowing measurement of aortic diameter. Quick method of diagnosis but a negative study is not helpful–– cannot r/o

Hint 87

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Front 88

Grey–Turner's sign vs Cullen's sign

Back 88

Both are signs of acute pancreatitis or retroperitoneal bleed

Grey Turner's sign – ecchymosis on back or flanks

Cullen's sign – ecchymosis around the umbilicus (U in cullens and umbilicus)

Hint 88

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Front 89

Clinical features of AAA

Back 89

– Usually asymptomatic and discovered incidentally on exam or radiologic study for another reason
– may have a sense of abd fullness
– +/– pain, usually in hypogastrium (below umbilicus) + lower back– throbbing
– pulsatile mass of exam
– symptoms suggest expansion or impending rupture
– sudden onset of severe pain in back or lower abd with radiation to groin or buttocks/legs ––> rupture (may see grey turner's or cullen's signs)

Hint 89

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Front 90

Abdominal Aortic Aneurysm
1. definition
2. where is it most common?
3. average age of diagnosis
4. women or men most likely afflicted?

Back 90

1. abnormal localized dilatation of the aorta
2. between the renal arteries and iliac bifurcation (infrarenal aorta)
3. incidence increase with age. They are rare before 50. Average age at the time of diagnosis is 65–70 yo
4. much more common in men

Front 91

Right–sided vs left–sided endocarditis

Back 91

Right–sided is more likely in IV drug users (s. aureus)– due to injection into the venous system–– then infection goes back to the Right heart

Left–sided is more commonly due to infection of a damaged or prosthetic valve–– usually caused by s. viridans, a less virulent organism than s. aureus

Front 92

Infective Endocarditis
1. definition
2. acute vs subacute

Back 92

1. infection of heart valves that can be acute or subacute
2. acute– usually caused by s. aureus (virulent), on a normal heart valve, if no treatment then death occurs in < 6 weeks
subacute– less virulent organisms (s. viridans or enterococcus), usually on damaged valves. If untreated then death may occur in > 6 weeks

Hint 92

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Front 93

Rheumatic heart disease

Back 93

Complication of untreated S. pyogenes pharyngitis – acute RF is immunologically mediated process that may progress to rheumatic heart disease with chronic valvular abnormalities

The most common valve problem = mitral stenosis, but there may be AV or TV issues as well

Front 94

Hemodynamic changes in hypovolemic shock by class (% blood lost, pulse inc, SBP dec, pulse pressure (SBP– DBP) dec, cap refill dec, RR inc, CNS sx, UOP)
1. Class I
2. Class II
3. Class III
4. Class IV

Back 94

1. Class I – 10–15% blood lost, normal pulse, normal SBP, normal pulse pressure, normal cap refill, normal RR, no CNS sx, UOP is normal
2. Class II – 20–30% of blood lost, pulse > 100, normal SBP, dec PP, delayed cap refill, mild inc in RR, anxious, UOP = 20–30 cc/hr
3. Class III – 30–40% blood lost, pulse > 120 bpm and weak, dec SBP, dec PP, delayed cap refill, marked tachypnea, confusion, UOP = 20 cc/hr
4. Class IV – > 40% blood lost, pulse > 140 bpm or non–palpable, marked decrease in SBP and PP, absent cap refill, marked tachypnea, lethargy/ coma, and negligible UOP

Front 95

Hypertensive Emergency
1. definition
2. vs urgency

Back 95

1. SBP > 220 +/– DBP > 120 mmHg in addition to end–organ damage– immediate treatment is indicated
2. urgency – inc BP alone without end–organ damage = hypertensive urgency rarely requires emergency treatment and can be managed with attempts to lower the BP over a 24 hour period

Front 96

When patients present with markedly inc blood pressure what is it critical to access for?

Back 96

Signs of end–organ damage
1. Eyes– papilledema (swelling of the optic disc)
2. CNS – AMS or ICH –– hypertensive encephalopathy may develop (confusion etc)
3. Kidneys– renal failure or hematuria
4. Heart – unstable angina, MI, CHF with pulmonary edema, aortic dissection
5. Lungs– pulmonary edema

Front 97

Treatment of hypertensive URGENCY

Back 97

Lower blood pressure gradually with ORAL agents over the course of 24 hours

Front 98

Diagnosis of aortic coarctation
1. ECG findings
2. CXR findings

Back 98

1. ECG– LVH
2. CXR– notching of the ribs due to inc flow through the collaterals. Figure 3 appearance due to indentation of the aorta at the site of coarctation with dilation before and after the stenosis

Front 99

Diagnosis of PDA
1. CXR findings
2. Echo findings

Back 99

1. CXR– inc pulm vasc markings, dilated pulm arteries, enlarged cardiac silhouette, sometimes calcifications of the ductus arteriosus
2. Echo– PDA +/– turbulent blood flow`

Front 100

Pathophysiology of PDAs

Back 100

– large L––> R shunt results in Right Hear volume overload, PHTN, and RHF (ascites, HSM, JVD etc)
– cyanosis is a late finding
– may eventually see reversal of blood flow (R––>L)

Front 101

Treatment of Aortic Coarctation

Back 101

– Standard treatment is surgical decompression
– percutaneous balloon aortoplasty is also an option in selected cases

Front 102

Coarcation of the Aorta
1. definition
2. associations

Back 102

1. narrowing/occlusion of aorta usually at origin of Left subclavian near the ligamentum arteriosum ––> leads to obstruction between the proximal and distal aorta thus leading to inc afterload
2. associated with Turner syndrome

Front 103

Diagnosis of VSD
1. ECG findings
2. CXR
3. Echo findings

Back 103

1. biventricular hypertrophy predominates when the PVR is high
2. CXR– enlargement of the pulm artery, enlargement of the cardiac silhouette. As the PVR increases the L––> R shunt decreases and heart size decreases but PA size increases
3. VSD

Front 104

Pathophysiology of VSD

Back 104

1.Blood flows from LV (high pressure) into the RV (low pressure) through the VSD. this leads to inc pulm blood flow. As long as pulmonary vascular resistance (PVR) is lower the systemic vascular resistance (SVR) then flow is L ––> R. If PVR > SVR then shunt becomes R ––> L
2. Large defects leads to PHTN

Front 105

Clinical features of aortic coarctation

Back 105

– HTN in upper extremities and hypotension in the lower extremities
– well–developed upper body with under–developed lower hald
– mid–systolic murmur heard best over the back
– sx– HA, cold extremities, claudication with exercise and fatigue

Front 106

treatment of shock (general)

Back 106

1. ABCs – airway, breathing and circulation
2. Except for cardiogenic and sometimes neurogenic shock–– give large boluses of IV Fluids

Front 107

What signs/symptoms are common to all forms of shock?

Back 107

– decreased BP
– oliguria
– tachycardia – compensatory due to low BP
– AMS

Front 108

Initial approach to the patient in shock
1. findings supportive of different types of shock
2. initial steps to treatment

Back 108

1. Focused H & P – fever and infection site––> septic shock
– trauma, GI bleeding, vomiting––> hypovolemic shock
– h/o MI, angina or heart disease ––> cardiogenic shock
– JVD ––> cardiogenic shock
– spinal injury or neuro deficits ––> neurogenic shock
2. Stabilize and determine the cause– 2 large bore IVs, central line and art line, b. fluid bolus 500–1000cc, c. blood draw – CBC, elec, CR, BUN, PT/PTT, type and cross, d. ECG, CXR, e. pulse ox, f. vasopressors (dopamine or epi if unstable DESPITE fluids), g, if NOT sure what the cause is then do pulmonary catheter or echo

Front 109

Shock – general characteristics
1. definition
2. presentation
3. changes seen to what?

Back 109

1. underperfusion of tissues–– medical emergency. Supply does not meet demand
2. decreased BP plus malfunction of underperfused organ systems (lactic acidosis, renal –anuria/oliguria, CNS dysfunction (AMS)
3. C.O., SVR and volume status (assessed by JVP and PCWP) –– these vary depending on the type of shock

Front 110

treatment of superficial thrombophlebitis
1. need anticoag?
2. localized thrombophlebitis?
3. severe thrombophlebitis?
4. need for abx? if septic thrombophlebitis?

Back 110

1. No anticoagulation needed–– rarely causes PE
2. localized thrombophlebitis ––< mild analgesic (aspirin) is all that is required–– continue activity
3. severe thrombophlebitis (with pain and cellulitis) – a. bed rest, elevation, hot compresses, b. onse symptoms resolve –– ambulation and elastic stockings, c. no abx unless suppurative–– need adequate drainage, d. septic thrombophlebitis–– usually due to infection of IV cannula –– remove and start IV abx

Front 111

Superficial thrombophlebitis
1. general characteristics
2. clinical features

Back 111

1. Vichow's triad is implicated (stasis, endothelial injury and hypercoaguable state). UE – at IV sites, LE – assoc with varicose veins (in greater saphenous system) – secondary to stasis of blood flow
2. pain and tenderness, induration, plus erythema long the course of vein. Tender cord may be palpated

Front 112

Perforating veins

Back 112

– connect superficial and deep venous systems
– valves allow flow from superficial to deep systems but not vice versa

Front 113

Prognosis of VTach

Back 113

– prognosis depends on presence of heart disease and whether VTach is sustained or non–sustained
– VTach after a MI leads to a poor prognosis especially if sustained
– If there is no underlying heart condition, then there is a good prognosis.

Front 114

Non–Sustained VTach

Back 114

–Brief self–limited runs of VTach
– usually asymptomatic
– when CAD and LV dysfunction are present, it is an independent risk factor for sudden cardiac death so do a thorough cardiac work–up in patients with non–sustained VT

Front 115

Torsades de pointes (TdP)

Back 115

– rapid polymorphic VT
– dangerous arrhythmia that often can lead to VFib
– associated wtih many factors that prolong QT interval (e.g. congenital, TCAs, anticholinergics, electrolyte abnormalities, ischemia)
– IV Magnesium stabilizes heart while you treat the underlying cause

Front 116

Sustained VTach definition

Back 116

– persists in absence of intervention
– lasts longer than 30 seconds and is almost always symptomatic
– often associated with marked hemodynamic compromise (dec BP or ischemia)
– LIFE THREATENING
– can progress to VFib

Front 117

Causes of VTach (6)– which is most common

Back 117

1. CAD with prior MI = most common cause
2. Active ischemia, hypotension
3. cardiomyopathies
4. congenital defects
5. prolonged QT syndrome
6. Drug toxicity

Front 118

Ventricular Tachycardia definition

Back 118

– rapid and repetitive firing of 3 or more PVCs in a row at a rate between 100–250 bpm
– AV dissocation present (i.e. sinus P waves continue with their cycle unaffected by Vtach)
– originates below the bundle of His

Front 119

Treatment of Wolff–Parkinson–White Syndrome

Back 119

1. Radio–frequency catheter ablation of one arm of the re–entrant loop
2. Avoid drugs active on the AV node (e.g. digoxin) because they may accelerate conduction through the accessory pathway (type IA + IC antiarrhytmics are better choices)

Front 120

ECG diagnosis of WPW syndrome

Back 120

– narrow complex tachycardia, short PR interval + DELTA WAVE (upward deflection seen before the QRS complex)

Front 121

Wolff–Parkinson–White (WPW) syndrome– definition

Back 121

– accessory conduction pathway from atria to ventricles causes premature ventricular excitation because it lacks the delay seen in the AV node.
– May lead to paroxysmal tachycardia by 2 mechanisms
a. orthodromic reciprocating tachy – impulse through AV node (anterograde) –– depolarizes ventricles –– retrograde impulse through accessory pathway redepolarizes the atrai –– re–entry loop (no delta waves)
b. supraventricular tachy (afib or aflutter)–– usually AV node only allows certain impulses through accessory pathway but everything gets through allowing for inc HR and hemodynamic instability

Front 122

Treatment for paroxsymal SVT

Back 122

1. Vagal maneuvers ––> block re–entry mechanism by delaying AV conduction
2. Pharmacologic Treatment– IV adenosine – agent of choice. Short duration, that decreases sinoatrial activity and AV nodal activity. IV verapamil and IV esmolol or digoxin.
3. Direct Current Cardioversion if drugs are not effective or patient is unstable
4. Prevention– digoxin usually is the drug of choice. Verapamil or beta–blockers are alternatives. Radiofrequency catheter ablation of either the AV node or the accessory tract

Front 123

Side effects of adenosine

Back 123

– Headache
– flushing
– shortness of breath
– chest pain
– n/v

Front 124

Causes of paroxsymal Vtach (PVST)

Back 124

1. ischemic heart disease
2. digoxin toxicity= PVST with 2:1 ratio is most common
3. AV node re–entry
4. atrial flutter with RVR
5. AV reciprocating tachy (accessory pathway)
6. excessive caffeine intake or EtOH

Front 125

Most common cause of Supraventricular Tachycardia (SVT)

Back 125

AV nodal re–entrant tachycardia

Front 126

Paroxsymal supraventricular tachycardia (PVST) pathophysiology (2 types)

Back 126

1. most commonly due to re–entrant tachycardia. 2 pathways (one fast and one slow), within the AV node– re–entrant circuit is in AV node. It is initiated or terminated by PACs. ECG shows narrow QRS complexes with no discernable p–waves. The p–waves are buried in the QRS complex
2. orthodromic AV re–entrant tachycardia– an accessory pathway between atria and ventricles that conducts retrograde. Initiated or terminated by PACs and PVCs. ECG shows narrow QRS complexes with p–waves that may or may not be seen. Re–entrant circuit is longer

Front 127

Colorectal cancer
1. how common?
2. most common type?

Back 127

1. 3rd most common cancer in the United States (in men and women)
2. Virtually all colorectal tumors arise from adenomas and the majority are endoluminal adenocarcinomas arising from the mucosa––>adenocarcinoma. Rarely there are carcinoid tumors, lymphomas, and Kaposi's sarcoma (HHV 8 in AIDS pts)

Front 128

Colorectal cancer (CRC) screening

Back 128

1. fecal occult blood test– poor sensitivity and specificity. PPV is only 20%, but all patients with a positive FOBT need a colonoscopy anyway
2. Digital rectal exam (DRE)– only about 10% of tumors are palpable by rectal examination
3. Colonscopy– the most sensitive and specific test–– the diagnostic study of choice for patients with a positive FOBT. Diagnostic and therapeutic–– biopsy or polypectomy.
4. Flexible sigmoidoscopy– can be used to reach teh area where approximately 50% to 70% of polyps and cancers occur (with a 60cm scope). Can be diagnostic in about 2/3 of all CRCs
5. Barium enema– evaluates entire colon– complementary to flex sig. Disadvantage is the any abnormal findings need to be evaluated by colonscopy
6. Carcinoembryonic antigen (CEA)– not useful for screening––useful for baseline and recurrence surveillance. Has some prognostic significance–– patients with a preoperative CEA >5 ng/mL have a worse prognosis.

Hint 128

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Front 129

Clinical staging of CRC

Back 129

CT scan of chest, abd, pelvis and by physical exam (ascites, hepatomegaly, lymphadenopathy etc)

Front 130

CRC patterns of spread (4)

Back 130

1. Direct extension– circumferentially and then through the bowel wall to later invade other abdominoperitoneal organs
2. Hematogenous– portal circulation to liver – liver is the most common site of distant spread. Or lumbar/vertebral veins to lungs
3. lymphatic– regionally
4. transperitoneal and intraluminal

Front 131

Risk factors for Colorectal Cancer (CRC)

Back 131

1. Age– everyone over the age of 50 years is at increased risk
2. adenomatous polyps– these are pre–malignant lesions, but most do not develop into cancer. villous adenomas have higher malignant potential than tubular adenomas. The larger the size and the greater the number of polyps the higher the risk of cancer
3. personal history of prior CRC of adenomatous polyps
4. Inflammatory bowel disease (IBD)
– both Ulcerative Colitis (UC) and Crohn's disease pose an increased risk for CRC, but UC poses a greater risk. Incidence of CRC is 5–10% at 20 years and 12–20% at 30 years with UC
5. Family history– multiple first degree relatives with CRC or any first–degree relative diagnosed with CRC or ademona under age 60
6. dietary factors– high fat, low–fiber diets
7. major polyposis syndromes (FAP, Gardner's syndrome, Turcot's syndrome, Peutz Jeghers, Familiar juvenile polyposis coli, hereditary non polyposis CRC (HNPCC)

Front 132

Familial adenomatous polyposis (FAP)
1. what is it?
2. what is the risk of CRC?
3. tx

Back 132

1. autosomal dominant disease characterized by hundreds of adenomatous polyps in the colon. the colon is always involved and the duodenum is involved in 90% of cases. Polyps may also form in the stomach, jejunum, and ileum.
2. The risk of CRc is 100% by the 3rd to 4th decade of life
3. prophylactic colectomy is usually recommended

Hint 132

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Front 133

Gardner's Syndrome
1. what is it?
2. what is the risk of CRC?

Back 133

– polyps plus osteoma, dental abnormalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts
– risk of CRC is 100% by age 40

Hint 133

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Front 134

Turcot's syndrome
1. inheritance pattern?
2. what does it affect?

Back 134

1. autosomal recessive
2. FAP tumors plus cerebellar medulloblastoma or gliobastoma multiforme
(think Turcots– turban–– affects your brain)

Hint 134

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Front 135

Peutz–Jeghers syndrome
1. what is it?
2. what are some clinical features?
3. malignant potential compared to ademonas?
4. which cancers are pts at increased risk for?
5. other potential complications?

Back 135

1. Single or multiple hamartomas that may be scattered through the entire GI tract: small bowel (78%), colon (60%), stomach (30%)
2. pigments spots around lips, oral mucosa, face, genitalia, and palmar surfaces
3. unlike adenoma, hamartomas have a very low malignant potential
4. slightly increased incidence in various carcinomas (e.g. stomach, ovary, breast, cervix, testicle, lung).
5. intussception or GI bleeding may occur

Hint 135

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Front 136

Familial juvenile polyposis coli

Back 136

1. rare, presents in childhood, only small risk of CRC
2. more than 10 and up to 100s of juvenile colon polyps

Front 137

Hereditary Nonpolyposis CRC (HNPCC– Lynch syndrome)

Back 137

1. lynch syndrome I– site specific CRC– early onset CRC, absence of antecedent multiple polyposis
2. lynch syndrome II– (cancer family syndrome)– all features of Lynch I plus increased number and early occurrence of other cancers (e.g. female genital tract, skin, stomach, pancreas, brain, breast, biliary tract)

Hint 137

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Front 138

Clinical features of CRC
1. most common symptom?
2. other symptoms

Back 138

1. the presence of symptoms is typically a manifestation of relatively advanced disease. Most symptoms include melena, hematochezia, abdominal pain, change in bowel habits, or unexplained iron deficiency anemia
2. Signs and symptoms are potentially common to all locations
a. abdominal pain is the most common presenting symptom. Can be caused by partial obstruction or peritoneal dissemination. Remember that CRC is the most common cause of large bowel obstruction in adults. Colonic perforation can lead to peritonitis and is the most life–threatening complication.
b. weight loss
c. blood in stool
d. may be asx

Front 139

Right–sided CRC tumors

Back 139

– obstruction is unusual because of the large luminal diameter (the cecum has the largest diameter of any part of the colon) allowing the tumor growth to go undetected
– common findings – occult blood in stool, iron deficiency anemia, and melena (because blood is partially digested by the time it comes out giving it a darker hue)
– triad of anemia, weakness and RLQ mass (occasionally)
– change in bowel uncommon

Hint 139

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Front 140

A patient presents with anemia, weakness and a RLQ mass on exam– what is a likely diagnosis?

Back 140

Right sided colon cancer

Front 141

Left–sided CRC tumors

Back 141

– the descending colon has a smaller diameter than the right so signs of obstruction are more common
– change in bowel are more common– alternating diarrhea and constipation–– narrowing of the stools – "pencil stools"
– hematochezia is more common (red blood–– since it doesn't have as far to go as in the case of a right sided tumor– the blood is less digested/dark)

Hint 141

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Front 142

Rectal cancer
1. how common
2. symptoms and signs

Back 142

– 20–30% of all CRCs
– hematochezia– most common symptom
– tenesmus– feeling the need to pass stool constantly even though the colon is empty– can be very painful
– rectal mass– feeling of incomplete evacuation of stool (due to mass)

Hint 142

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Front 143

Treatment of CRC
1. only cure
2. role of CEA levels
3. role of adjuvant therapy (chemo and radiation)
4. F/U
5. when do recurrences usually happen?

Back 143

1. Surgery is the only curative treatment of CRC– surgical resection of tumor containing bowel as well as resection of regional lymphatics
2. CEA level should be obtained before surgery– can given an indication of prognosis (> 5ng/mL = worse px), also used for F/U
3. chemo and radiation use depends on the stage of the cancer
4. F/U is important and varies
a. Stool guaiac test
b. annual CT of abd/pelvis and CXR for up to 5 yrs
c. colonoscopy at 1 yr and then every 3 years
d. CEA levels are check periodically (ever 3–6 months). – a subsequent increase in CEA is sensitive marker of recurrence. Often, 2nd look operations are based on elevated CEA levels post–op. Very high levels suggest liver involvement
5. about 90% of recurrences occur within 3 years after surgery

Front 144

Nonneoplastic colon polyps (types, which is most common?)

Back 144

1. benign lesions with no malignant potential
a. hyperplastic (metaplastic) polyps are the most common (90%) nonneoplastic polyps–– generally remain small and asx
b. no specific therapy required, but they can be difficult to distinguish from neoplastic polyps and so are commonly removed
c. juvenile polyps–– typically in children younger than 10 years are high vascular and common so they should be removed
d. inflammatory polyps– pseudopolyps–– associated with UC

Front 145

Adenomatous polyps
1. three types – and corresponding malignancy potential
2. what features help determine malignant potential?
3. treatment

Back 145

benign lesions, but have significant malignant potential, precursors of adenocarcinoma
1. can be one of three types–– villous, tubulovillous, and tubular. tubular is the most common– up to 60–80%–– smallest of malignancy. villous has greatest risk of malignancy
2. can determine malignant potential by following:
a. size– the larger the polyp the greater the malignant potential
b. histologic type– see above
c. atypia of cells (increased nuclear to cytoplasmic ratio etc)
d. Sessile (flat– more likely to be malignant) vs pedunculated (on a stalk)
3. tx– complete removal of the polyp

Front 146

Diverticulosis
1. cause
2. risk factors
3. prevalence with age
4. most common site affected

Back 146

1. Caused by increased intraluminal pressure– inner layer of colon bulges through focal area of weakness in colon wall (usually an area of blood vessel penetration)
2. Risk factors– low fiber diets– constipation causes intraluminal pressures to increase. Positive family history
3. prevalence increases with age
4. The most common location is the sigmoid colon–– however diverticular may occur anywhere in the colon

Hint 146

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Front 147

Clinical features of diverticulosis
1. sx

Back 147

– usually asymptomatic and discovered incidentally on barium edema or colonscopy done for another reason
– may have vague LLQ discomfort, bloating, constipation/diarrhea etc
– only 10–20% become symptomatic–– develop complications such as diverticular bleeding or diverticulitis

Front 148

Diagnosis (test of choice, etc)

Back 148

1. Test of choice– barium enema
2. abdominal Xrays are usually normal and are not diagnostic

Front 149

Treatment of diverticulosis

Back 149

1. High fiber foods (such as bran) to increase stool bulk
2. psyllium (if patient cannot tolerate bran)– dietary fiber not absorbed by the small intestine

Front 150

Complications of diverticulosis

Back 150

1. Painless rectal bleeding (up to 40% of patients) – bleeding is usually clinically insignificant and stops spontaneously. No further treatment is necessary in these patients. Bleeding can be severe in about 5% of patients. In many cases the bleeding stops spontaneously. Colonoscopy may be performed to locate the site of bleeding (or mesenteric angiography in certain cases). If bleeding is persistent and/or recurrent, surgery may be needed (segmental colectomy)
2. Diverticulitis– Occurs when feces become impacted in the diverticulum, leading to erosion and microperforation. Can be complicated or uncomplicated. Uncomplicated diverticulitis account for most cases and refers to diverticulitis without abscess formation, colovesical fistula (into bladder) , obstruction, and free colonic perforation

Front 151

Diverticulitis
1. cause
2. complicated vs uncomplicated
3. clinical features

Back 151

1. occurs in 15–25% of patients with diverticulosis when feces become impacted in the diverticulum, leading to erosion and microperforation
2. complications include– free colonic perforation, colovesical fistula (fistula between bowel and bladder– 50% of fistulas arising from diverticulitis), abscess formation, obstruction
3. clinical features– fever, LLQ pain, leukocytosis. May also see alteration in bowel habits (constipation or diarrhea), vomiting and sometimes a painful mass on rectal exam if inflammation is near the rectum
– lower GI bleeding is rare in diverticulitis but common in diverticulosis

Front 152

Diagnosis of Diverticulitis

Back 152

1. CT Scan of abdomen and pelvis with oral and IV contrast is the test of choice–– may reveal a swollen, edematous bowel wall or an abscess
2. Abdominal xrays are helpful in ruling out potential causes of LLQ pain, ileus, obstruction (indicated by air–fluid levels), distention and perforation

Front 153

Treatment of diverticulitis
1. mainstays of treatment
2. when is surgery indicated?

Back 153

1. uncomplicated diverticulitis is managed by IV antibiotics, bowel rest (NPO), IV Fluids. Mild episodes can be treated on an outpatient basis if patient is reliable and has few or no comorbid conditions. If symptoms persist after 3–4 days, surgery may be necessary. Antbiotics should be continued for 7–10 days. After successful treatment, about 1/3 have recurrence.
– Surgery is recommended for recurrent episodes (resection of the involved segment)
– Complicated diverticulitis–– surgery is indicated

Front 154

Angiodysplasia–

Back 154

Tortuous, dilated veins in the submucosa of the colon (usually proximal) wall
– a common cause of lower GI bleeding in patients over the age of 60
– bleeding is usually low grade, but 15% of patients may have massive hemorrhage if veins rupture
– diagnosed by colonoscopy (preferred over angiography)
– in about 90% of patients, bleeding stops spontaneously
– It can frequently be treated by colonoscopic coagulation of the lesion. If bleeding persists, a right hemicolectomy should be considered

Hint 154

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Front 155

Acute Mesenteric Ischemia
1. cause
2. 4 causes
3. mortality

Back 155

1. Results from a compromised blood supply, usually due to superior mesenteric vessels
2. 4 causes–
a. Arterial embolism (50% of cases), almost all emboli are of cardiac origin (atrial fibrillation, MI, valvular disease),
b. Arterial thrombosis (25% of cases)– most of these patients have atherosclerotic disease (coronary artery disease (CAD, PVD, stroke) at other site, Acute occlusions occurs over pre–existing atherosclerotic disease. The acute event may be due to decrease in cardiac output (e.g. resulting from MI, CHF, or plaque rupture), Collateral circulation has usually developed.
c. Non–occlusive mesenteric ischemia (20% of cases) – due to splanchnic vasoconstriction secondary to low cardiac output, typically seen in critically ill elderly patients.
d. Venous thrombosis (<10% of cases)– many predisposing factors –– e.g infection, hypercoaguable states, oral contraceptives, portal HTN, malignancy, pancreatitis
3. mortality– the overall mortality rate for all types is about 60–70%. If bowel infarction has occurred, the mortality rate can exceed 90%

Front 156

Clinical features of acute mesenteric ischemia

Back 156

1. classic presentation is acute onset of severe abdominal pain disproportionate to physical findings–– pain is due to ischemia and possibly infarction of intestines, analogous to MI in CAD
– the abdominal examination may appear benign even when there is severe ischemia which can lead to a delay in diagnosis
– the acuteness and severity of the pain vary depending on the type of acute mesenteric ischemia
– anorexia, vomiting
– GI bleeding (mild)
– peritonitis, sepsis, and shock may be present in advanced disease

Front 157

Diagnosis of acute mesenteric ischemia

Back 157

1. mesenteric angiography– definitive diagnostic test
2. obtain a plain film of the abdomen to exclude other causes of abdominal pain
3. "Thumbprinting" on barium enema is due to thickened edematous mucosal folds

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Front 158

Treatment of acute mesenteric ischemia

Back 158

1. supportive measures– IV Fluids and broad spectrum antibiotics
2. direct intra–arterial infusion of papervine– vasodilator into the the superior mesenteric system during arteriography is the therapy of choice for all arterial causes of acute mesenteric ischemia. This relieves the occlusion and vasospasm
3. Direct intra–arterial infusion of thrombolytics or embolectomy may be indicated in some patients with embolic acute mesenteric ischemia
4. heparin anticoagulation is the treatment of choice for venous thrombosis
5. surgery (resection of non–viable bowel) may be needed in all types of acute mesenteric ischemia if signs of peritonitis develop

Front 159

Chronic Mesenteric Ischemia
1. Cause
2. Symptoms
3. Diagnosis
4. Treatment

Back 159

1. Caused by atherosclerotic occlusive disease of the main mesenteric vessels (celiac artery, superior and inferior mesenteric arteries)
2. Abdominal angina– dull pain, typically postprandial (when there is increased demand for splanchnic blood flow)–– analogous to anginal pain in CAD, significant weight loss may occur secondary to this
3. Mesenteric ateriography to confirm
4. Surgical revascularization – leads to pain relief in 90% of cases

Front 160

Ogilvie's Syndrome
1. what is it?
2. What are the common causes?
3. How diagnosed?
4. treatment

Back 160

1. An unusual problem in which signs, symptoms, and radiographic evidence of large bowel obstruction are present, but there is no mechanical obstruction
2. Common causes– recent surgery or trauma, serious medical illness (e.g. sepsis, malignancy) and medications (narcotics, psychotropic drugs, anticholinergics)
3. The diagnosis cannot be confirmed until mechanical obstruction of the colon is excluded
4. Treatment– stopping any offending agent (e.g. narcotics) and supportive measures (IV Fluids, electrolyte repletion), decompression with gentle enemas or NG suction may be helpful, however if this fails then colonoscopic decompression is usually successful, with surgical decompression and cecostomy/colostomy as a last resort

Front 161

Pseudomembranous Colitis
1. aka
2. cause–– and when does it happen in relation to this?

Back 161

1. antibiotic associated colitis– many patients do not have grossly visible pseudomembranes
2. Antibiotic treatment kills organisms that normally inhibit the growth of Clostridium difficile, leading to its overgrowth and toxin production.
– almost all antibiotics have been associated with it, but the most frequently implicated are Clindamycin, Ampicillin and cephalosporins
– symptoms usually begin within the first week of antibiotic therapy– however, it can start up to 6 weeks after cessation of antibiotic treatment
– disease severity varies widely

Front 162

Clinical features of pseudomembranous colitis/ c. diff

Back 162

1. profuse watery diarrhea (usually NO blood or mucus)
2. crampy abdominal pain
3. Toxic megacolon (in severe cases) with risk of perforation

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Front 163

Diagnosis of pseudomembranous colitis/c. difficile

Back 163

1. Demonstration of C. difficile toxins in the stool is diagnostic, but results take about 24 hours (95% sensitivity)
2. Flexible sigmoidoscopy is the most rapid test and is diagnostic, but because of comfort/expense it is infrequently used
3. Abd Xray to r/o toxic megacolon and perforation
4. leukocytosis is very common

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Front 164

Treatment of pseudomembranous colitis/c. difficile
(including recurrence risk and adjuvant therapy)

Back 164

1. Discontinue the offending agent/antibiotic if possible
2. Metronidazole (flagyl) is the drug of choice but cannot be used in infants or pregnant patients
3. Oral vancomycin can be used if the patient is resistant to metronidazole or cannot tolerate it
– regardless of the choice of antibiotic, recurrence may occur within 2–8 weeks after stopping the antibiotic. This occurs in 15–35% of successfully treated patients
– Cholestyramine may be used as an adjuvant treatment to improve diarrhea

Front 165

Colonic Volvulus
1. definition
2. potential complications
3. most common sites affected

Back 165

1. Twisting of the a loop of intestine about its mesenteric attachment site
2. may result in obstruction or vascular compromise with the potential for necrosis and/or perforation if untreated
3. most common site is the sigmoid colon (75% of all cases), and the cecum (25% of all cases)

Front 166

Risk factors for volvulus (sigmoid vs cecal volvulus)

Back 166

1. chronic illness, age, institionalization, and CNS disease increase the risk of sigmoid volvulus
2. cecal volvulus– due to congenital lack of fixation of the right/descending colon and tends to occur in younger patients
3. chronic constipation, laxative abuse, and antimotility drugs
4. prior abdominal surgery

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Front 167

Clinical features of volvulus

Back 167

1. Acute onset of colicky abdominal pain
2. obstipation (no passing gas or stool) and abdominal distention
3. anorexia, nausea and vomiting

Front 168

Diagnosis of volvulus

Back 168

1. Plain films of the abdomen– a. sigmoid volvulus– omega loop sign (or bent inner–tube shape)– indicates a dilated sigmoid colon. b. cecal volvulus– distention of the cecum and small bowel– coffee bean sign indicates a large air–fluid level in the RLQ
2. Sigmoidoscopy– preferred diagnostic and therapeutic test for sigmoid volvulus–– can treat during this procedure by untwisting and decompressing the bowel in many cases
3. barium enema– reveals the narrowing of the colon at the point where it is twisted "bird's beak"

DO NOT perform barium enema if strangulation is suspected.

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Front 169

Treatment of volvulus
1. sigmoid
2. cecal

Back 169

1. sigmoid volvulus– nonoperative reduction– decompression via sigmoidoscopy is successful in 70% of cases. The recurrent rate is high so elective sigmoid colon resection is recommended
2. cecal volvulus– emergent surgery is indicated

DO NOT perform barium enema if strangulation is suspected

Front 170

Cirrhosis
1. definition
2. reversible vs irreversible

Back 170

1. chronic liver disease characterized by fibrosis, disruption of the liver architecture, and widespread nodules in the liver. The fibrous tissue replaces damaged or dead hepatocytes
2. cirrhosis is generally irreversible when advanced. In early stages, specific treatment of the cause of cirrhosis may improve or reverse the condition. The point at which the disease becomes irreversible is unclear.

Front 171

What does the distortion of liver anatomy cause in cirrhosis (2 major events)?

Back 171

1. Decreased blood flow through the liver with subsequent hypertension in the portal circulation (portal hypertension)–– this has widespread manifestations, including ascites, peripheral edema, splenomegaly, and varicosity of veins "back stream" in the circulation (gut, butt, caput–– gastric/esophageal varices, internal hemorrhoids, and caput medusa–dilated abdominal veins)
2. hepatocellular failure–– leads to impairment of biochemical functions, such as decreased albumin synthesis and decreased clotting factor synthesis

Front 172

Assessment of hepatic functional reserve in cirrhosis

Back 172

1. Child's classification– estimates hepatic reserve in liver failure–– used to measure disease severity and is a predictor of morbidity and mortality (based on ascites, bilirubin, encephalopathy, nutritional status, and albumin)
2. Child's class C indicates the most severe disease, while class A is milder

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Front 173

Causes of cirrhosis (10)

Back 173

1. Alcoholic liver disease – most common cause. Refers to a range of conditions from fatty liver (reversible, due to acute ingestion) to cirrhosis (irreversible). 15–20% of heavy drinkers develop alcoholic cirrhosis
2. Chronic hepatitis B or C infections– next most common causes
3. Drugs (acetaminophen toxicity, methotrexate)
4. Autoimmune hepatitis
5. Primary Biliary Cirrhosis (PBC), Secondary biliary cirrhosis
6. Inherited metabolic diseases (hemachromatosis, Wilson's disease)
7. Hepatic congestion secondary to right–sided heart failure, constrictive pericarditis
8. Alpha–1 antitrypsin deficiency (also causes emphysema)
9. hepatic veno–occlusive disease– can occur after a bone marrow transplantation
10. Non–alcoholic steatohepatitis (NASH)

Front 174

Clinical features of cirrhosis

Back 174

1. some patients have no overt clinical findings, especially early in the disease
2. patients may have signs or symptoms suggestive of one or more of the complications of cirrhosis (portal hypertension, varices, ascites, hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis (SBP), hyperestrinism, Coagulopathy, Hepatocellular carcinoma (HCC)

Front 175

Treatment of portal hypertension

Back 175

TIPS – transjugular intrahepatic porto–systemic shunt

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Front 176

Esophageal varices
1. evaluation
2. clinical features
3. treatment

Back 176

1. variceal hemorrhage has a high mortality rate. patients with cirrhosis should be evaluated to document the presence of varices and risk of hemorrhage–– if present prophylactic measures should be taken such as non–selective beta blocker
2. massive hematemesis, melena, and exacerbation hepatic encephalopathy.
3. Fluids to maintain BP. IV abx prophylactically. IV octreotide is initiated and and continued for 3–5 days. Perform emergent upper GI endoscopy once the patient is stabilized for diagnosis and treatment of hemorrhage either with variceal band ligation or sclerotherapy. Give beta blockers in the long term to prevent re–bleeding
– rectal hemorrhoids and caput medusae (distension of abdominal wall vessels are also possible)

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Front 177

Ascites
1. definition
2. clinical features
3. diagnosis
4. treatment

Back 177

1. accumulation of fluid in the peritoneal cavity due to portal HTN – increased hydrostatic pressure and hypoalbuminemia – decreased oncotic pressure
2. abdominal distention, shifting dullness, and fluid wave
3. abd ultrasound can detect as little as 30 mL of fluid. Diagnostic paracentesis determines whether ascites is due to portal HTN or another process–– indications include new onset ascites, worsening ascites or suspected spontaneous bacterial peritonitis
4. treatment– bed rest, low sodium diet, and diuretics (furosemide and spironolactone), perform therapeutic paracentesis if tense ascites, shortness of breath or early satiety present. Peritoneovenous shunt or TIPS to reduce portal HTN

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Front 178

Hepatic encephalopathy
1. cause (build up of?)
2. how prevalent in cirrhosis?
3. precipitants?

Back 178

1. toxic metabolites (there are many but ammonia is believed to be the most important)–– normally detoxified by the liver– accumulates and reaches the brain
2. occurs in 50% of cirrhosis to varying extent
3. alkalosis, hypokalemia (due to diuretics), sedating drugs (narcotics, sleep meds), systemic infection and hypovolemia

Front 179

Hepatic encephalopathy
1. clinical features
2. treatment

Back 179

1. decreased mental function, confusion, poor concentration, even stupor or coma.
– asterexis – "flapping tremor"– have the patient extend arms and dorsiflex the hands – not specific
– rigidity, hyperreflexia
– fetor hepaticus–– musty odor of breath
2. lactulose – prevents absorption of ammonia– metabolism of lactulose by bacteria in the colon favors formation of NH4+, which poorly absorbed from the GI tract–– thereby promoting excretion of ammonia
– neomycin – antibiotic– neomycin – kills bowel flora, so decreases ammonia production by intestinal bacteria
– diet: limit protein to 30–40 g/day

Front 180

Hepatorenal syndrome
1. what is it indicative of?
2. definition
3. precipitants
4. clinical features
5. treatment

Back 180

1. indicates end–stage liver disease
2. progressive renal failure in advanced liver disease, secondary to renal hypoperfusion resulting from vasoconstriction of renal vessels
– this is a functional renal failure– kidneys are normal in terms of morphology, and no specific causes of renal dysfunction are evident. Does not respond to volume expansion
3. precipitated by infection or diuretics
4. clinical features– azotemia (inc BUN), oliguria, hyponatremia, hypotension, low urine output (<10 mEq/L)
5. Liver transplantation is the only cure–– in general the prognosis is very poor, and the condition is usually fatal without liver transplant

Front 181

Spontaneous Bacterial Peritonitis (SBP)
1. definition
2. etiologic agents
3. clinical features
4. diagnosis
5. treatment

Back 181

1. infected ascitic fluid, occurs in up to 20% of patients hospitalized for ascites
– usually occurs in patients with ascites caused by end–stage liver disease–– associated with a high mortality – 20–30%
– high recurrence rate – up to 70% in the first year
2. e. coli (most common), klebsiella, strep pneumo
3. clinical features– abd pain, fever, vomiting, rebound tenderness, may lead to sepsis
4. diagnosis established by paracentesis and examination of ascitic fluid for WBCs (esp PMNs), gram stain with culture and sensitivities (WBC > 500, PMN >250)
– positive ascites culture – culture negative SBP is common as well
5. treatment0 broad spectrum antbiotics– give specific antibiotic therapy once the organism is identified. clinical improvement should be seen in 24–48 hours.
– repeat paracentesis in 2–3 days to document decrease is ascitic fluid PMN (<250)

Front 182

Hyperestrinism is liver failure/cirrhosis

Back 182

1. spider angiomas– dilated cutaneous arterioles with central red spot and reddish extensions that radiate outward like a spider's web
2. palmar erythema
3. gynecomastia
4. testicular atrophy

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Front 183

Coagulopathy secondary to liver failure
1. cause – what is elevated in terms of clotting tests?
2. treatment

Back 183

decreased clotting factors– prolonged PT (prothrombin time)––liver uses vitamin K to synthesize clotting factors in this pathway (II, VII, IX, X). PTT may be prolonged in severe disease
– vitamin K is ineffective in treatment because it cannot be used by a diseased liver
2. treatment – fresh frozen plasma (FFP)

Front 184

signs of acute liver failure

Back 184

– coagulopathy
– jaundice
– hypoglycemia (liver stores glycogen)
– hepatic encephalopathy
– infection
– elevated LFTs
– any complication associated with cirrhosis

Front 185

What should you look for in diagnosing SBP?

Back 185

– fever and change in mental status in a patient with ascites
– if not treated early the mortality is high– so always be suspicious in a patient with ascites and do the diagnostic paracentesis early

Front 186

Wilson's disease
– deficiency of what?
– inheritance pattern?
– build up of?
– when diagnosed typically?

Back 186

1. autosomal recessive disease of copper metabolism
– normally excess copper is excreted by the liver, but the liver of patients with wilson's disease cannot do so because there is usually a deficiency in ceruloplasmin– a copper biding protein necessary for copper excretion
– copper accumulates in hepatocytes causing them to die
– copper leaks into plasma and accumulates in other organ including kidney, cornea and brain
– most often apparent during childhood/adolescence (after age 5) and the majority of cases is present between 5 to 35
–– picture is of a Kayser–Fleischer ring–– build up of copper in the cornea– –does not interfere with vision

– also known as hepatolenticular disease as it effects the liver and brain

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Front 187

Clinical features of Wilson's disease

Back 187

1. liver disease (most common initial manifestation)– varies but may include acute hepatitis, cirrhosis, and/or fulminant liver failure
2. Kayser–Fleisher rings– yellowish rings in the cornea caused by copper deposition–– does not interfere with vision
3. CNS findings–– extrapyramidal signs (EPS)– parkinsonian symptoms (resting tremor, rigidity, bradykinesia), chorea, drooling, incoordination due to copper deposition in the basal ganglia
– psychiatric disturbances–– depression, neuroses, personality changes, psychosis
4. Renal involvement– aminoaciduria, nephrocalcinosis

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Front 188

Diagnosis of Wilson's disease

Back 188

1. hepatic disease– elevated LFTs, impaired synthesis of clotting factors and albumin
2. decreased ceruloplasmin levels–– although levels within the normal range do not exclude the diagnosis
3. liver biopsy– inc copper conc
4. if diagnosed first degree relatives must be screened

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Front 189

Treatment of Wilson's disease

Back 189

1. Chelating agents – D–penicillamine– removes and detoxifies the excess copper deposits
2. Zinc – prevents uptake of dietary copper. Given alone to presymptomatic or pregnant patients or in conjuction with chelating agents in symptomatic patients
3. Liver transplantation – if unresponsive to therapy or fulminant liver failure
4. monitor patient's copper levels, urinary copper excretion, ceruloplasmin, and liver function– physical examination for signs of liver or neurologic disease, psych health

Front 190

Hemochromatosis
1. cause
2. involved organs
3. secondary hemochromatosis

Back 190

1. autosomal recessive disease of iron absorption
– excessive iron absorption in the intestine leads to accumulation of iron (as ferritin and hemosiderin) in various organs. Over many years, fibrosis in the involved organs occurs secondary to hydoxyl free radicals that are generated by excess iron
2. affected organs –– liver (primary organ) , pancreas, heart, skin, joints, thyroid, gonads, hypothalamus

– secondary hemochromatosis can also occur with multiple transfusions or in chronic hemolytic anemias

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Front 191

Hepatocellular Adenoma
1. definition
2. risk factors
3. symptoms
4. malignant potential
5. Diagnosis
6. Treatment

Back 191

Benign liver tumor– most often seen in young women (15–40 years of age)
2. Risk factors include OCP use, female sex, and anabolic steroid use
3. May be asymptomatic or can have RUQ pain and fullness
4. Malignant potential is low (<1%), however the adenoma may rupture– leading to hemoperitoneum and hemorrhage
5. Dx by CT scan, US, hepatic arteriography (most accurate but invasive)
6. Treatment– discontinue OCPs. surgically resect tumors >5cm that do not regress after stopping OCPs due to risk of rupture

Front 192

Cavernous Hemangiomas
1. definition
2. symptoms
3. complications
4. diagnosis
5. treatment

Back 192

1. vascular tumors that are usually small and asymptomatic. Most common type of benign liver tumor.
2. As the size of the tumor increases (e.g. due to pregnancy or OCP use) the sx increase and may include RUQ pain and mass
3. Complications are uncommon unless the tumor is very large and may include rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF secondary to large AV shunt and gastric outlet obstruction
4. Diagnose with US or CT with contrast. Biopsy is C/I due to risk of rupture
5. Most cases do not require treatment

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Front 193

Focal Nodular Hyperplasia
1. definition
2. symptoms
3. Treatment

Back 193

1. benign liver tumor without malignant potential that occurs in women of reproductive age. No association with OCPs!!
2. Usually asymptomatic although hepatomegaly may be present.
3. Treatment not necessary in most cases

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Front 194

3 types of benign liver tumors

Back 194

1. Hepatocellular Adenoma
2. Cavernous Hemangioma
3. Focal Nodular Hyperplasia

Front 195

Hepatocellular Carcinoma
1. prevalence& where is it common
2. 2 pathologic types

Back 195

1. HCC – 80% of primary liver cancers–– common in Africa and Asia although rare in U.S.
2. Nonfibrolamellar (most common) – assoc with Hep B, C amd cirrhosis– usually unresectable and with a very short survival time (months)
– fibrolamellar– usually not assoc with hep b,c or cirrhosis– usually resectable with a longer survival time– most common in adolescents and you adults

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Front 196

Risk factors for hepatocellular carcinoma

Back 196

1. Cirrhosis– especially in association with alcohol or hepatitis B or C– HCC develops in 10% of cirrhotic patient
2. chemical carcinogens– aflatoxin, vinyl chloride, thorotrast
3. Alpha–1–antitrypsin (AAT) deficiency
4. Hemachromatosis, Wilson's disease
5. Schitosomiasis
6. Hepatic ademona (10% risk of malignant transformation)
7. cigarette smoking
8. glycogen storage disease (type 1)

Front 197

Clinical features of hepatocellular carcinoma

Back 197

1. abdominal pain (painful hepatomegaly)
2. weight loss, anorexia, fatigue
3. signs and symptoms of chronic liver disease– portal HTN, ascites, jaundice
4. paraneoplastic syndromes– erythrocytosis, thrombocytosis, hypercalcemia, carcinoid syndrome, hypertrophic pulmonary osteodystrophy, hypoglycemia, high cholesterol

Front 198

Diagnosis of Hepatocellular Carcinoma

Back 198

1. Liver biopsy– required for definitive diagnosis
2. lab tests– hep B and C serology, LFTs, coags
3. Imaging studies– US, CT chest, abd, pelvis, MRI or MRI if surgery is an option
4. tumor marker elevation– AFP (alpha fetaprotein) is a useful screen tool as AFP may be elevated in 40–70% of patients with HCC– also helps monitor response to therapy

Front 199

Treatment and prognosis of Hepatocellular Carcinoma (HCC)

Back 199

1. Liver resection (in 10% of patients who have resectable tumors)– liver regenerates
2. Liver transplant if diagnosis is made early

Prognosis– If unresectable– less than 1 year, if resectable then 25% of patients are alive at 5 years

Front 200

What should you suspect in patients with cirrhosis and a palpable liver mass + inc AFP?

Back 200

hepatocellular carcinoma

Front 201

Nonalcoholic Steatohepatitis (NASH)
1. definition
2. associations
3. symptoms
4. how discovered?
5. treatment

Back 201

1. histology of the liver is identical to that in patients with alcoholic liver disease but these patients do not have a history of alcohol disease
2. associated with obesity, hyperlipidemia, diabetes mellitus
3. usually asymptomatic with a benign course (but cirrhosis develops in 10–15%)
4. Typically discovered on routine laboratory tests (mild elevation in ALT and AST)
5. No clearly established treatment

Front 202

Gilbert's syndrome
1. what is it?
2. what lab test is abn?
3. what are exacerbating factors?
4. how usually discovered/symptoms
5. treatment

Back 202

1. occurs in up to 7% of the population – autosomal dominant condition in which there is decreased activity of hepatic UGT)
2. common cause of isolated elevation of unconjugated bilirubin
3. exacerbated by fasting (crash diets), fever, alcohol, and infection
4. asymptomatic in most cases but occasionally mild jaundice maybe present
5. liver biopsy results are normal and usually no treatment is necessary

Front 203

Hemobilia
1. definition
2. causes
3. clinical features
4. diagnosis
5. treatment

Back 203

1. blood draining into the duodenum via the common bile duct– source of bleeding can be anywhere along the biliary tract, the liver or the ampullary region
2. causes– trauma (most common), papillary thyroid carcinoma, surgery (cholecystectomy), CBD exploration, tumors, infection
3. GI bleeding (melena, hematemesis), jaundice, and RUQ pain
4. Arteriogram is diagnostic– Upper GI endoscopy shows blood coming out of the ampulla of vater
5. treatment– resuscitation (may require transfusion)– if bleeding is severe, surgery is necessary (options include ligation of hepatic arteries, or arteriogram with embolization of vessels)

Front 204

Polycystic Liver Cysts
1. cause/inheritance
2. symptoms
3. treatment

Back 204

1. autosomal dominant– usually associated with polycystic kidney disease. PCKD often results in renal failure and is the main determinant of prognosis whereas liver cysts rarely lead to hepatic fibrosis and liver failure
2. usually asymptomatic, although some patients have abd pain and upper abd mass
3. treatment is usually not needed

Front 205

Hydatid Liver Cysts
1. cause
2. symptoms
3. treatment

Back 205

1. caused by infection from the tapeworm, Echinococcus granulosus. Cysts most commonly occur in the right lobe of the liver
2. small cysts are asymptomatic, larger cysts may cause RUQ pain and rupture into the peritoneal cavity causing fatal anaphylactic shock
3. Treatment– surgical resection (caution to avoid spilling cyst contents into peritoneal cavity). Give mebendazole after surgery

Front 206

Pyogenic Liver Abscess
1. most common cause
2. causative organisms
3. clinical features
4. diagnosis
5. treatment

Back 206

1. most common cause is biliary tract obstruction– obstruction of bile flow allows bacterial proliferation. Other causes include GI infection (diverticulitis, appendicitis) with spread via portal venous system and penetrating liver trauma (GSW, surgery)
2. Causative organisms include E. coli, Klebsiella, enteroccus, and anaerobes
3. fever, malaise, anorexia, weight loss, nausea, vomiting, RUQ pain, and jaundice– patients appear quite ill
4. Diagnosed by ultrasound or CT scan, elevated LFTs
5. fatal if untreated. Treatment (IV antibiotics and percutaneous drainage of abscess) reduces mortality to about 5–20%. Surgical drainage is sometimes necessary

Front 207

Amebic liver abscess
1. who is it most common in? transmission?
2. cause?
3. symptoms
4. diagnosis
5. treatment

Back 207

1. Most common in men (9:1), particularly in homosexual men, transmitted through fecal–oral contact
2. caused by intestinal amebiasis (entamoeba histolytica)– the amoebea reach the liver via the hepatic portal vein
3. fever, RUQ pain, nausea/vomting, HSM, diarrhea
4. serological testing (IgG enzyme immunoassay) establishes diagnosis, LFTs are often elevated. The E. histolytica antigen test (detects protozoa in stool) – not sensitive. Imaging studies (US, CT) identify abscess, but it is difficult to distinguish from pyogenic abscess
4. IV metronidazole is effective treatment in most cases. Therapeutic aspiration of abscess may be necessary if the abscess is large (high risk of rupture) or there is no response to medical therapy

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Budd–Chiari Syndrome
1. definition
2. course
3. causes
4. clinical features
5. dx
6. tx

Back 208

1. Liver disease caused by occlusion of the hepatic venous outflow, which leads to hepatic congestion and subsequent microvascular trauma
2. course is variable, but most cases are indolent, with gradual development of portal HTN and progressive deterioration of liver function. Rarely disease is severe and leads to acute liver failure
3. causes– hypercoaguable states, myeloproliferative disorders (polycythemia vera), pregnancy, chronic inflammatory diseases, infection, various cancers, trauma. Idiopathic 40%
4. resemble those of cirrhosis– hepatomegaly, jaundice, ascites, abd pain, variceal bleeding
5. dx– hepatic venography, serum ascites albumin gradient > 1.1 g/dL
6. tx– medical tx is usually unsatisfactory (anticoagulation, thrombolytics, diuretics). Surgery is eventually needed in most cases (balloon angioplasty with stent placement in inferior vena cava, portocaval shunts). liver transplant if cirrhosis is present

Front 209

Jaundice
1. definition
2. when evident? at what level?
3. conjugated vs unconjugated bilirubin

Back 209

1. yellow coloration of skin, mucous membranes, and sclerae due to overproduction or underclearance of bilirubin
2. clinical jaundice usually becomes evident when total bilirubin is > 2 mg/dL
3. conjugated (direct) bilirubin– loosely bound to albumin and therefore water soluble– gets excreted in the urine causing it to look dark. Nontoxic.
– unconjugated (indirect) bilirubin– tightly bound to albumin and therefore not water soluble and cannot be excreted in the urine even when blood levels are high. Toxic unbound form can cross the blood–brain barrier and cause neuro deficits

Front 210

Causes of conjugated hyperbilirubinemia

Back 210

1. decreased intrahepatic excretion of bilirubin
– hepatocellular disease (viral or alcoholic hepatitis, cirrhosis)
– inherited disorders (Dubin–Johnson syndrome, Rotor's syndrome)
– drug induced (OCPs)
– Primary biliary cirrhosis (PBC)
– primary sclerosis cholangitis (PSC)

2. extrahepatic biliary obstruction
– gallstones
– carcinoma in the head of the pancreas
– cholangiocarcinoma
– periampullary tumors
– extrahepatic biliary atresia
–

Front 211

Causes of unconjugated hyperbilirubinemia

Back 211

1. Excess production of bilirubin– hemolytic anemias
2. Reduced hepatic uptake of bilirubin or impaired conjugation
– Gilbert's syndrome
– drugs – (sulfonamides, penicillin, rifampin, radiocontrast agents)
– Crigler Najjar syndrome type I and type II
– physiologic jaundice of the newborn– immaturity of conjugating system
– diffuse liver disease (hepatitis, cirrhosis)

Front 212

Diagnosis and treatment of hyperbilirubinemia

Back 212

1. serum levels of conjugated and unconjugated bilirubin
2. if unconjugated hyperbilirubinemia – check a CBC, reticulocyte count, hemoglobin, LDH, and peripheral smear (may aid in the diagnosis of hemolysis as the cause of jaundice)
3. if conjugated hyperbilirubinemia–– LFTs may point to the cause
4. US or CT to assess biliary tract for obstruction or anatomic changes
5. additional tests (Endoscopic Retrograde Cholangiopancreatography – ERCP) or percutaneous transhepatic cholangiography– depending on findings of above
6. liver biopsy may be indicated in some cases to determine cause of injury

–treatment– treat the underlying cause. May want to give cholestyramine– bile acid sequestrant

Front 213

Liver Function Tests
1. what are they? What is most sensitive and specific for liver disease?
2. what indicates alcohol as a cause?
3. mild elevation indicates?
4. moderate elevation indicates?
5. severe elevation indicates?
6. what if patient has cirrhosis?

Back 213

1. Aminotransferases – ALT and AST
– ALT is more sensitive and specific than AST for liver damage
2. ALT and AST usually have a similar increase with the exception being alcoholic hepatitis – in which the AST–ALT ratio may be > 2:1
3. if ALT and AST levels are mildly elevated (low hundred) think of chronic viral hepatitis or acute alcoholic hepatitis
4. If ALT and AST are moderately elevated (high hundreds to 1000s) – think of acute viral hepatitis
5. if ALT and AST are severely elevated (>10,000) – extensive hepatic necrosis has occurred. Typical causes include– ischemia, shock liver (prolonged hypotension or circulatory collapse), acetaminophen toxicity, severe viral hepatitis
6. NOTE: liver transaminases are often normal or even low in patients with cirrhosis (without any active cell necrosis) or metastatic liver disease because the number of functioning hepatocytes is markedly reduced

Front 214

What are potential causes of elevated ALT and AST?

Back 214

A– Autoimmune hepatitis
B– hepatitis B
C– hepatitis C
D– drugs or toxins
E– Ethanol
F– fatty liver (hypertriglyceridemia)
G– growths (tumors)
H– hemodynamic disorders (e.g. CHF)
I– Iron– hemochromatosis, Copper (wilson's disease) or AAT deficiency

Front 215

Alkaline Phosphatase (ALK–P)
1. what does it measure?
2. what if levels are very high (10 fold increase)?
3. What should you also measure with this?

Back 215

– Not specific to liver– also found in bone, gut, and placenta
1. ALK–Phos is elevated when there is an obstruction of bile flow (e.g. cholestasis) in any part of the biliary tree. Normal levels make cholestasis unlikely
2. If levels are very high (10–fold increase), think of extrahepatic biliary tract obstruction or intrahepatic cholestasis (e.g. PBC or drug induced cirrhosis)
3. If levels are elevated, measure GGT (gamma–glutamyl–transferase) level to make sure the elevation is hepatic in origin (rather than bone or intestinal). If the GGT is also elevated, this strongly suggests a hepatic origin. If the GGT level is normal, but ALK–P is elevated, consider pregnancy or bone disease

Front 216

What can cause a decreased albumin level?

Back 216

– chronic liver disease
– nephrotic syndrome
– malnutrition
– inflammatory states (burns, sepsis, trauma)

Front 217

Prothrombin time (PT)

Back 217

The liver synthesizes clotting factors I, II, V, VII, IX, X, XII and XIII–– the function of which is reflected by PT
– PT is not prolonged until most of the liver's synthetic capacity is lost– which corresponds to advanced liver disease

Front 218

Cholelithiasis
1. definition
2. 3 types

Back 218

1. refers to stones in the gallbladder (gallstones)
2. There are 3 types of stones – a. cholesterol stones (yellow to green)– associated with: obesity, diabetes, and hyperlipidemia, multiple pregnancies, OCPs, Crohn's disease, ileal resection, advanced age, Native American ancestry, cirrhosis, cystic fibrosis
b. Pigment stones– black stones are usually found in the gallbladder and are associated with either hemolysis (e.g. sickle cell disease, thalassemia, hereditary spherocytosis, artificial cardiac valves) or alcoholic cirrhosis.
– brown stones are usually found in the bile ducts and are associated with biliary tract infections
c. Mixed stones have components of both cholesterol and pigment stones and account for the majority of stones

Front 219

Clinical features of cholelithiasis

Back 219

– most cases are asymptomatic. Majority of patients found to have incidental gallstones will remain asymptomatic.
– biliary colic is the cardinal symptom of gallstones and is due to temporary obstruction of the cystic duct by a gallstone. Pain occurs as the gallbladder contracts against this obstruction.
– pain is typically located in the RUQ or epigastrium and may be mild, moderate, or severe
– patients classically report pain after eating and at night
– Boas' sign – referred right scapular pain of biliary colic

Front 220

Diagnosis of cholelithiasis

Back 220

1. RUQ ultrasound has high sensitivity and specificity (>95%) for stones > 2 mm.
2. CT and MRI are alternatives

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Front 221

Treatment of cholelithiasis

Back 221

1. No treatment if the patient is asymptomatic
2. Elective cholecystectomy for patients with recurrent bouts of biliary colic

Front 222

Complications of cholelithiasis

Back 222

1. cholecystitis (chronic or acute) with prolonged obstruction of cystic duct
2. choledocholithiasis with its associated complications
3. gallstone ileus– lack of peristalsis
4. malignancy

Front 223

What fraction of patients with biliary colic will develop acute cholecystitis within 2 years?

Back 223

1/3

Front 224

What causes the pain in acute cholecystitis? biliary colic?

Back 224

Pain in acute cholecystitis is secondary to gallbladder wall inflammation, whereas the pain of biliary colic is secondary to contraction of the gallbladder against an obstructed cystic duct. The pain of acute cholecystitis persists for several days, whereas the pain of biliary colic lasts only a few hours.

Front 225

Acute cholecystitis
1. definition/cause
2. chronic cholecystitis?
3. what percent of patients with gallstones will develop this?

Back 225

1. obstruction of the cystic duct (not infection) induces acute inflammaion of the gallbladder wall
2. chronic cholecystitis may develop with recurrent bouts of acute cholecystitis
3. 10% of patients with gallstones will develop acute cholecystitis

Front 226

Symptoms of acute cholecystitis?

Back 226

– pain is always present and is located in RUQ or epigastrium. It may radiate to the right shoulder or scapula
– nausea and vomiting, anorexia

Front 227

Signs of acute cholecystitis on exam?

Back 227

– RUQ tenderness, rebound tenderness in RUQ
– Murphy's sign is pathognomonic– inspiratory arrest during deep palpation of the RUQ, not present in many cases (if this happens with US–– it is called a sonographic Murphy's)
– Hypoactive bowel sounds
– low–grade fever, leukocytosis

Front 228

Diagnosis of acute cholecystitis?

Back 228

1. RUQ ultrasound is the test of choice– high sensitivity and specificity. Findings include thickened gallbladder wall and pericholecystic fluid, distended gallbladder, and presence of stone(s)
2. CT scan is as accurate as ultrasound but is more sensitive in identifying complications of acute cholecystitis such as perforation, abscess and pancreatitis
3. Radionucleotide scan (hepatoiminodiacetic acid– HIDA)
– used when US is inconclusive. Its sensitivity and specificity parallel that of US. If HIDA is normal, acute cholecystitis can be ruled out.
– A positive HIDA scan means the gallbladder is not visualized
– If gallbladder is not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed

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Front 229

Treatment of acute cholecystitis

Back 229

1. patient should be admitted. Conservative measures include hydration with IV fluids, bowel rest (NPO), IV antibiotics, analgesics and correction of any electrolyte abnormalities
2. surgery– cholecystectomy is indicated in most patients with symptomatic gallstones. Early cholecystectomy is preferred (first 24 to 48 hours). Recurrence rate with nonsurgical treatment is as high as 70%. Timing of surgery depends on the severity of the symptoms and patients risk assessment for surgery, but in most patients, early cholecystectomy is preferred.

Front 230

Acalculous Cholecystitis
1. what is it?
2. cause/associations?
3. signs and symptoms?
4. diagnosis
5. treatment

Back 230

1. Acute cholecystitis without stones obstructing the cystic duct (up to 10% of the patients with acute cholecystitis)
2. usually idiopathic and seen in patients with severe underlying illness; possible association with dehydration, ischemia, burns, severe trauma, and post–operative state
3. signs and symptoms are the same as acute cholecystitis
4. diagnosis may be difficult because patients with this condition are often severely ill and have other medical problems, so clinical features are less apparent
5. emergent cholecystectomy is the treatment of choice. For patients who are too ill for surgery, perform percutaneous drainage of the gallbladder with cholecystostomy

Front 231

Choledocholithiasis
1. definition
2. primary vs secondary stones?

Back 231

1. gallstones in the common bile duct (CBD)
2. primary versus secondary stones. Primary stones originate in the CBD (usually pigmented stones), Secondary stones originate in the gallbladder and then pass into the CBD (usually cholesterol or mixed stones).
– 95% of CBD stones are secondary

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Front 232

Clinical features of choledocholithiasis

Back 232

1. patients may be asymptomatic for years
2. symptoms when present include RUQ pain or epigastric pain and jaundice

Front 233

Diagnosis of choledocholithiasis

Back 233

1. laboratory tests– total and direct bilirubin levels are elevated as well as alk–phos
2. RUQ US is usually the initial study, but is not a sensitive study for choledocholithiasis. It detects CBD stones in only 50% of the cases, so it cannot be used to rule out the diagnosis.
3. ERCP (endoscopic retrograde cholangiopancreatography) is the gold standard (sensitivity and specificity is 95%) and should follow US. ERCP is diagnostic and therapeutic.
4. PTC (percutaneous transhepatic cholangiography) is an alternative to ERCP

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Front 234

Treatment of choledocholithiasis

Back 234

1. ERCP with sphincterotomy and stone extraction with stent placement (successful in 90% of patients)
2. laparoscopic choledocholithotomy (in select cases)

Front 235

Cholangitis
1. definition and causes
2. treatment

Back 235

1. infection of the biliary tract secondary to obstruction, which leads to biliary stasis and bacterial overgrowth
– choledocholithiasis accounts for 60% of cases
– other causes include pancreatic and biliary neoplasm, postoperative strictures, invasive procedures such as ERCP or PTC and choledochal cysts
2. cholangitis is a potentially life–threatening illness and requires emergency treatment

Front 236

Clinical features of cholangitis

Back 236

1. Charcot's triad– RUQ pain, jaundice and fever–– this classic triad is present in only 50–70% of cases
2. Reynold's pentad– charcot's triad plus septic shock and altered mental status (CNS depression–– e.g. coma, disorientation)
3. patient is acutely ill, and abdominal symptoms may be lacking or may go unrecognized

Front 237

Diagnosis of cholangitis
1. initial study
2. lab findings
3. cholangiography options (2)– when would you choose each?

Back 237

1. RUQ ultrasound is the initial study
2. laboratory findings– hyperbilirubinemia, leukocytosis, mild elevation in serum transaminases
3. cholangiography (either PTC or ERCP)
– this is the definitive test, but it should not be performed during the acute phase of the illness.
– Once cholangitis resolves, proceed with PTC or ERCP to identify the underlying problem and plan treatment
– perform PTC when the duct system is dilated (per US) and ERCP when the duct system is normal

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Front 238

Treatment of cholangitis

Back 238

1. IV antibiotics and IV Fluids
– close monitoring of hemodynamics, BP, urine output (UOP),
2. Most patients respond rapidly. Once the patient has been afebrile for 48 hours then proceed with cholangiography (PTC or ERCO) for evaluation of the underlying condition
3. decompress the CBP via PTC (catheter drainage), ERCP (sphincterotomy) or laparotomy (T–tube insertion) once the patient is stabilized, or emergently if the condition does not respond to antibiotics

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Front 239

Carcinoma of the gallbladder
1. what type are they most often and who do they occur in?
2. associations/ risk factors
3. clinical features
4. treatment
5. prognosis

Back 239

1. most are adenocarcinomas. Typically occur in the elderly
2. associated with gallstones in most cases, other risk factors include cholecystoenteric fistula and porcelain gallbladder
3. Clinical features are non–specific and suggest extrahepatic bile duct obstruction: jaundice, biliary colic, weight loss, anorexia, and RUQ mass. Palpable gallbladder is a sign of advanced disease.
4. difficult to remove with surgery: cholecystectomy versus radical cholecystectomy (with wedge resection of liver and lymph node dissection) depending on the depth of invasion
5. prognosis is dismal – more than 90% of patients die of advanced disease within 1 year of diagnosis. Disease often goes undetected until it is advanced.

Front 240

Primary Sclerosing Cholangitis (PSC)
1. definition/general characteristics
2. associations

Back 240

1. a chronic idiopathic progressive disease of intrahepatic and/or extrahepatic bile ducts characterized by thickening of the bile duct walls and narrowing of their lumens, leading to cirrhosis, portal hypertension and liver failure
2. their is a strong association with ulcerative colitis (less so with Crohn's disease). UC is present in 50–70% with PSC, often the UC may dominate the clinical picture. (NOTE– the course of PSC is unaffected by colectomy done for UC)

Front 241

Clinical features of primary sclerosing cholangitis (PSC)

Back 241

– signs and symptoms begin insidiously
– chronic cholestasis findings, including jaundice and pruritis; all patients eventually present with chronic obstructive jaundice
– other symptoms: fatigue, malaise and weight loss

Front 242

Diagnosis of primary sclerosing cholangitis

Back 242

1. ERCP and PTC are diagnostic studies of choice– see multiple area of bead–like stricturing and dilations of the intrahepatic and extrahepatic ducts
2. laboratory tests show cholestatic LFTS– inc LFTs plus inc direct bili, plus inc alk–phos

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Front 243

treatment of primary sclerosing cholangitis

Back 243

1. there is no curative treatment other than liver transplantation
2. when a dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile duct dilitation may relieve symptoms
3. use cholestyramine for symptomatic relief (to decrease pruritis) – bile acid sequestant that binds to it and prevents it from being reabsorped. The insoluble compound is then excreted in the feces

Front 244

Primary Biliary Cirrhosis (PBC)
1. definition – what is affected?
2. course?
3. cause?
4. who is most often affected?

Back 244

1. chronic and progressive cholestatic liver disease characterized by destruction of the intrahepatic bile ducts with portal inflammation and scarring
2. it is a slowly progressive disease with a variable course. It may progress to cirrhosis and end–stage liver failure
3. It is an autoimmune disease that is often associated with other autoimmune disorders
4. most common in middle–aged women

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Front 245

Clinical features of primary biliary cirrhosis (PBC)

Back 245

1. fatigue
2. pruritus (early in the course of the disease)
3. jaundice (late in the course)
4. RUQ discomfort
5. xanthoma and xanthalesmata (cholesterol deposits)
6. osteoporosis
7. portal HTN (with resultant sequelae)

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Front 246

Diagnosis of Primary Biliary Cirrhosis (PBC)
1. labs
2. biopsy findings
3. Imaging

Back 246

1. labs– cholestatic LFTs (inc alk phos)
2. positive anti–mitochondrial antibodies (AMAs) found in 90% to 95% of patients. This is the hallmark of the disease (specificity of 98%). If serum is positive for AMAs, perform a liver biopsy to confirm diagnosis
3. abd US or CT scan to rule out biliary obstruction

Front 247

Cholangiocarcinoma
1. definition
2. mean age of diagnosis?
3. 3 regions affected– what is most common?
4. prognosis
5. risk factors

Back 247

1. tumor of the intrahepatic and extrahepatic bile ducts: most are adenocarcinomas
2. mean age of diagnosis is in the 7th decade
3. Located in three regions: proximal third of the CBD (most common, also called Klatskin's tumor), distal extrahepatic (best change of resectability), intrahepatic (least common)
4. prognosis is dismal– survival is less than 1 year after diagnosis
5. risk factors – ulcerative colitis, choledochal cysts, clonorchis sinesis (Chinese liver fluke) – hong kong

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Front 248

Clinical features of cholangiocarcinoma

Back 248

1. obstructive jaundice and associated symptoms (dark urine, clay–colored/acholic stools) and pruritis
2. weight loss

Front 249

Diagnosis of cholangiocarcinoma

Back 249

1. cholangiography (PTC or ERCP)– for diagnosis and assessment of resectability
2. If the patient has an unresectable tumor (more likely the case with proximal than distal bile duct tumors), stent placement is an option during either PTC or ERCP and may relieve biliary obstruction

Front 250

Treatment of cholangiocarcinoma

Back 250

1. most patients do have resectable tumors at the time of diagnosis
2. the survival rate is low despite aggressive chemotherapy, stenting or biliary drainage

Front 251

Choledochal cysts
1. definition and who is most likely to be affected?
2. clinical features?
3. complications
4. diagnosis
5. treatment

Back 251

1. cystic dilations of biliary tree involving either the extrahepatic or intrahepatic ducts or both–– more common in women (4:1)
2. clinical features: epigastric pain, jaundice, fever, and RUQ mass
3. Complications – cholangiocarcinoma (most feared complication– risk is about 20% over 20 years), hepatic abscess, recurrent cholangitis/pancreatitis, rupture, biliary obstruction, cirrhosis, and portal HTN
4. US is the best non–invasive test and ERCP is definitive for diagnosis
5. Treatment is surgery: complete resection of the cyst with biliary–enteric anastomosis to restore continuity of biliary system with the bowels

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Front 252

Bile Duct Stricture
1. causes–– what is most common?
2. clinical features?
3. complications?
4. treatment

Back 252

1. most common cause is iatrogenic injury (prior biliary surgery such as cholecystectomy, liver transplantation), other causes include recurring choledocholithiasis, chronic pancreatitis, and primary sclerosing cholangitis (PSC)
2. clinical features are those of obstructive jaundice
3. complications can be life–threatening and include– secondary biliary cirrhosis, liver abscess, and ascending cholangitis
4. treatment involves endoscopic stenting (preferred) or surgical bypass if obstruction is complete or if endoscopic therapy fails

Front 253

Biliary dyskinesia

Back 253

1. motor dysfunction of the spincter of Oddi, which leads to recurrent episodes of biliary colic without any evidence of gallstones on diagnostic studies such as US, CT, and ERCP
2. Diagnosis is made by HIDA scan (once the gallbladder is filled with labeled radionucleotide, give cholecystokinin (CCK) intravenously, then determine the EF of the gallbladder. If the EF is low, dyskinesia is likely.
3. Treatment options – laparoscopic cholecystectomy, endoscopic sphincterotomy

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Front 254

1. Pathogenesis of appendicitis
2. peak age of incidence

Back 254

a. The lumen of the appendix is obstructed by hyperplasia of lymphoid tissue (60% of cases), a fecalith (35% of cases), a foreign body, or other rare causes (parasite or carcinoid tumor)– 5% of cases
b. obstruction leads to stasis (of fluid and mucus), which promotes bacterial overgrowth leading to inflammation
c. distention of the appendix can compromise blood supply. The resulting ischemia can lead to infarction or necrosis if untreated. Necrosis can result in appendiceal perforation and ultimately peritonitis
2. peak incidence is in the teens to mid–20s. Prognosis is far worse in infants and elderly patients (high rate of perforation)

Front 255

Symptoms of acute appendicitis

Back 255

1. Abdominal pain– classically starts in the epigastrium as ill–defined pain, moves toward umbilicus, and then to RLQ. with distention of the appendix, the parietal peritoneum may become irritate, leading to sharp pain
2. anorexia always present. Appendicitis is unlikely if the patient is hungry
3. nausea and vomiting (typically follow pain)

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Front 256

Signs of acute appendicitis

Back 256

1. tenderness in RLQ (maximal tenderness at McBurney's point– 2/3 of the distance from the umbilicus to the right anterior superior iliac spine)
2. rebound tenderness, guarding, diminished bowel sounds
3. low grade fever (may spike if perforation is present)
4. Rovsing's sign– deep palpation in the LLQ causes referred pain in the RLQ
5. Psoas sign– RLQ pain when right thigh is extended as patient lies on left side
6. Obturator sign– pain in the RLQ when flexed right thigh is internally rotated when patient is supine

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Front 257

Diagnosis of acute appendicitis

Back 257

** Acute appendicitis is a clinical diagnosis. Laboratory findings (mild leukocytosis) are only supportive. Radiographs or other imaging studies re unnecessary unless the diagnosis is uncertain or the presentation is atypical
– CT scan (sensitivity of 98% to 100%)–– lowers the false positive rate significantly
– ultrasound (sensitivity of 90%)

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Front 258

Treatment of acute appendicitis
– risk of false positive?

Back 258

–appendectomy (usually laparoscopic)
– up to 20% of patients who are diagnosed with acute appendicitis are found to have a normal appendix during surgery. Because the illness is potentially life–threatening, this is an acceptable risk EVEN DURING PREGNANCY

Front 259

Carcinoid tumors and carcinoid syndrome
– origination and secretion?
– most common site?

Back 259

1. carcinoid tumors originate from neuroendocrine cells and secrete serotonin
2. the most common site for these tumors is in the appendix, but they can be found in a variety of locations (small bowel, rectum, bronchus, kidney and pancreas)

Front 260

Pathogenesis of acute pancreatitis

Back 260

1. Inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion

Front 261

2 forms of acute pancreatitis

Back 261

1. Mild – (75% have mild to moderate) – responds well to supportive treatment
2. severe (up to 25%)– necrotizing pancreatitis– significant morbidity and mortality

Front 262

Causes of acute pancreatitis

Back 262

1. alcohol abuse (40%)
2. Gallstones (40%) – the gallstone passes into the bile duct and blocks the ampulla of vater (where bile enters the duodenum)
3. post ERCP– pancreatitis occurs in up to 10% of patients undergoing ERCP
4. viral infections– mumps, Coxackie virus B
5. drugs – sulfonamides, thiazide diuretics, furosemide, estrogens, HIV meds etc
6. post–operative complication (high mortality rate)
7. scorpion bites
8. pancreas divisum (controversial)– congenital problem
9. pancreatic cancer
10. hypertriglyceridemia, hypercalcemia
11. uremia
12. blunt abdominal trauma – most common cause of pancreatitis in young children

(IGETSMASHED pneumonic)

Front 263

Symptoms of acute pancreatitis

Back 263

1. abdominal pain, usually in the epigastric region–– may radiate to the back (50% of patients)
– often steady, dull, and severe, worse when supine and after meals
2. nausea and vomiting, anorexia

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Front 264

Signs of acute pancreatitis

Back 264

1. low grade fever, tachycardia, hypotension, leukocytosis
2. epigastric tenderness, abdominal distention
3. decreased or absent bowel sounds indicate partial ileus
4. the following signs are seen with hemorrhagic pancreatitis as blood tracks along fascial planes
– grey turner's sign– flank ecchymoses
– cullen's sign– periumbilical ecchymoses (pictured)
– fox's sign– ecchymosis of the umbilical ligament

Hint 264

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Front 265

Diagnosis of pancreatitis – Labs
1. What labs should you order? What is most specific for acute pancreatitis?
2. prognostic predictors

Back 265

1. Lab tests
– serum amylase is the most common test– but many conditions cause hyperamalasemia (non–specific) and its absence does not rule out acute pancreatitis (non–sensitive) However, if levels are more than 5 times the upper limit of normal, there is a high specificity for acute pancreatitis
–– serum lipase – more specific for pancreatitis than amylase
2. LFTs – to identify cause (gallstone pancreatitis) – inc Alk phos
3. hyperglycemia, hypoxemia, and leukocytosis may also be present
4. Order the following to assess for prognosis (ranson's criteria) –– glucose, calcium, hematocrit, BUN, arterial blood gas (PaO2, base deficit), LDH, AST, WBC count

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Front 266

Why does hypocalcemia occur in acute pancreatitis?

Back 266

Due to fat saponification – fat necrosis binds calcium

Front 267

Diagnosis of acute pancreatitis – Imaging

Back 267

1. Abdominal xray– limited role in the diagnosis of acute pancreatitis
– more helpful in ruling out other diagnosis– such as intestinal perforation (free air). The presence of calcifications can suggest chronic pancreatitis.
– In some cases, one may see a sentinel loop (area of air–filled bowel usually in the LUQ, which is a sign of localized ileus) or colon cutoff sign (air–filled segment of the transverse colon abruptly ending or "cutting off" at the region of pancreatic inflammation
2. abdominal ultrasound– can help in identifying cause of pancreatitis – gallstone. Useful for following up pseudocysts or abscesses
3. CT scan of the abdomen– most accurate test for the diagnosis of acute pancreatitis and for identifying complications of the disease
– indicated in patients with severe acute pancreatitis
4. ERCP indications – severe gallstone pancreatitis with biliary obstruction, to identify uncommon causes of acute pancreatitis if disease is recurrent

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Front 268

Complications of acute pancreatitis

Back 268

1. Pancreatic necrosis (may be sterile or infected)
– sterile pancreatic necrosis – infection may develop, but half of all cases resolve spontaneously. These patients should be monitored closely in an ICU. Prophylactic antibiotics is controversial but if necrosis involves more than 30% of pancreas, antibiotics should be strongly considered
– infected pancreatic necrosis – high mortality rate (results in multiple organ failure in 50% of cases), surgical debridement and antibiotics indicated
– the only way to distinguish sterile from infected necrosis is via CT–guided percutaneous aspiration with gram stain/culture of the aspirate
2. pancreatic pseudocyst– encapsulated fluid collection that appears 2 to 3 weeks after an acute attack–– unlike a true cyst, it lacks an epithelial lining
– complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough or if located in the head of the pancreas– it may cause compression of the CBD
– diagnosis by CT scan = study of choice
– treatment – cysts > 5cm– drain either percutaneously or surgically, <5 cm – observation
3. hemorrhagic pancreatitis – characterized by cullen's sign, grey turner's sign, and fox's sign, CT Scan with IV contrast is the study of choice
4. Adult respiratory distress syndrome – a life–threatening complication with high mortality rate
5. pancreatic ascites/pleural effusion– the most common cause is inflammation of peritoneal surfaces
6. ascending cholangitis – due to gallstone in ampulla of vater, leading to infection of biliary tract
7. pancreatic abscess (rare) – develops over to 4–6 weeks and is less life–threatening than infected pancreatic necrosis

Front 269

pancreatic pseudocyst
1. what is it?
2. complications
3. diagnosis
4. treatment

Back 269

1. pancreatic pseudocyst– encapsulated fluid collection that appears 2 to 3 weeks after an acute attack–– unlike a true cyst, it lacks an epithelial lining
2. complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough or if located in the head of the pancreas– it may cause compression of the CBD
3. diagnosis by CT scan = study of choice
4. treatment – cysts > 5cm– drain either percutaneously or surgically, <5 cm – observation

Hint 269

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Front 270

Treatment of mild acute pancreatitis

Back 270

mild pancreatitis treatment
– Bowel rest (NPO),
– IV fluids – patients may have severe intravascular volume depletion. Correct electrolyte abnormalities
– pain control – but be cautious in giving narcotics. Fentanyl and meperidine are preferred over morphine which causes an increase in sphincter of oddi pressure
– NG tube if severe nausea/vomiting or ileus present, routine use is controversial

Front 271

Treatment of severe acute pancreatitis

Back 271

If severe– patient should be admitted to the ICU. Early enteral nutrition in the first 72 hours is recommended through a nasojejunal tube.
– if the severe acute pancreatitis has not resolved in a few days, supplement parenteral nutrition should be started.
– if more than 30% of the pancreas is necrosed, prophylactic antibiotics (imipenem) should be considered to prevent infection (which has high morbidity and mortality)

Front 272

Prognosis of acute pancreatitis

Back 272

Ranson's criteria is used to determine prognosis and mortality rates
– patients with more than 3 or 4 of Ranson's criteria should be monitored in the ICU setting

Hint 272

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Front 273

Chronic pancreatitis
1. definition
2. what is impaired?
3. causes?

Back 273

1. persistent or continuing inflammation of the pancreas, with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts (areas of stricture/dilation– "chain of lakes" appearance on ERCP)– eventually results in irreversible destruction of the pancreas
2. The endocrine and exocrine functions of the pancreas are impaired
3. Chronic alcoholism is the most common cause (>80% of cases).
– other causes include hereditary pancreatitis, tropical pancreatitis, and idiopathic chronic pancreatitis

Hint 273

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Front 274

Clinical features of chronic pancreatitis

Back 274

1. severe pain in the epigastrium– recurrent or persistent abdominal pain
– often accompanied by nausea and vomiting
– may be aggravated by a drinking episode or by eating
– radiates to the back (in 50% of cases)
2. weight loss due to malabsorption, alcohol abuse and diabetes. Steatorrhea secondary to malabsorption

Front 275

Diagnosis of chronic pancreatitis

Back 275

1. CT scan– the initial study of choice. It may show calcifications not seen on plain films. Mild to moderate cases may not be detectable, so a normal CT does not necessarily rule out chronic pancreatitis
2. abdominal radiograph– the presence of pancreatic calcifications is 95% specific, but is found in only 30% of cases
3. ERCP is the gold standard– but is not done routinely because it is invasive
4. laboratory studies are not helpful in the diagnosis. Serum amylase and lipase levels are not elevated in chronic pancreatitis

Front 276

Complications of chronic pancreatitis

Back 276

1. narcotic addiction – probably the most common complication
2. diabetes mellitus/impaired glucose tolerance
– caused by progressive loss of islets of langerhans
– eventually appears in up to 70% of patients
3. Malabsorption/steatorrhea
– caused by pancreatic exocrine insufficiency– occurs when pancreatic enzyme secretion decreases significantly
– late manifestation of chronic pancreatitis
4. pseudocyst formation
5. pancreatic ductal dilation
6. CBD obstruction – may occur secondary to fibrosis in head of the gland
7. vitamin B12 malabsorption
8. effusions (e.g. pleural, pericardial, peritoneal)
9. pancreatic carcinoma – patients with chronic pancreatitis have an increased risk

Front 277

Treatment of chronic pancreatitis

Back 277

1. Non–operative management
– narcotic analgesics for pain
– bowel rest (NPO)
– pancreatic enzymes and H2 blockers (give simultaneously)

Hint 277

– pancreatic enzymes inhibit CCK release and thus decrease pancreatic secretions after meals. H2 blockers inhibit gastric acid secretion, preventing degradation of the pancreatic enzyme supplements by gastric acid
– insulin – may be necessary due to severe pancreatic endocrine insufficiency
– alcohol abstinence
– frequent, small volume, low–fat meals– may improve abdominal pain
2. Surgery– main goal is relief of incapacitating abdominal pain
– pancreaticojejunostomy– pancreatic duct drainage procedure to decompress dilated pancreatic duct– most common procedure
– pancreatic resection – distal pancreatectomy, whipple's procedure

Front 278

Characteristics of pancreatic cancer
1. most common demographic affected
2. anatomic location
3. risk factors
4. prognosis

Back 278

1. most common in elderly patients (75% of patients are > 60 years old), rare before age 40– more common in African Americans
2. Anatomic location – a. pancreatic head (75% of cases), b. pancreatic body – 20% of cases, c. pancreatic tail – 5–10% of cases
3. Risk factors– cigarette smoking (most clearly establish risk), chronic pancreatitis, diabetes, heavy alcohol use, exposure to chemicals– benzidene and b–naphthylamine
4. the prognosis is dismal– most patients die within months of diagnosis

Hint 278

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Front 279

Clinical features of pancreatic cancer

Back 279

1. abdominal pain (90% of patients) – may be vague and dull ache
2. jaundice – most common with carcinoma of head of pancreas– less than 10% of patients with cancer involving body and tail of pancreas have jaundice. Indicated obstruction of intrapancreatic CBD and is a sign of advanced disease
3. weight loss (common due to decreased food intake and malabsorption), anorexia
4. recent onset of glucose intolerance, but the diabetes is mild
5. depression, weakness and fatigue
6. migratory thrombophlebitis– develops in 10% of patients
7. courvoisier's sign– palpable gallbladder = present in 30% of patients with cancer in the head of the pancreas, presents without pain

** The early clinical findings of pancreatic cancer are very vague and nonspecific. By the time a diagnosis is made, most patients have an incurable level of advanced disease

Hint 279

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Front 280

painless jaundice and palpable gall bladder

Back 280

Courvoisier's sign – pancreatic carcinoma in the head of the pancreas (30%)
– however painless jaundice is not common in pancreatic cancer

Hint 280

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Front 281

Diagnosis of pancreatic cancer

Back 281

1. ERCP is the most sensitive test for diagnosing pancreatic cancer. It can also distinguish cancer of the head of the pancreas from tumors of the CBD, duodenum, ampulla, and lymphomas which have a more favorable prognosis
2. CT scan is the preferred test for diagnosis and assessment of disease spread
3. tumor markers – CA19–9 (sensitivity of 83% and specificity of 82%), CEA (sensitivity of 56% and specificity of 75%)

Front 282

Treatment of pancreatic cancer

Back 282

1. Surgical resection (whipple's procedure – pancreaticoduodectomy) is the only hope of cure–– however, only a minority of tumors are resectable (roughly 10%). The prognosis is grim even after resection, with a 5–year survival of 10%
2. If the tumor is unresectable and biliary obstruction is present, perform PTC (percutaneous cholangiopancreatography) or ERCP with stent placement across the obstruction for palliation

Hint 282

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Front 283

Anatomic difference between upper and lower GI bleed –– where do you draw the line?

Back 283

Upper GI bleeds occur above the ligament of Treitz in the duodenum, whereas lower GI bleeds occur below this point

Hint 283

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Front 284

Causes of upper GI bleeds

Back 284

1. peptic ulcer disease (PUD)– duodenal ulcer (25% of cases), gastric ulcer (20% of cases), gastritis (25% of cases)
2. reflux esophagitis
3. esophageal varices (10% of cases) – venous bleeding
4. gastric varices
5. gastric erosions, duodenitis
6. Mallory–Weiss tear
7. hemobilia
8. dieulafoy's vascular malformation– submucosal dilated arterial lesions that can cause massive GI bleeding
9. aortoenteric fistula– after aortic surgery (ask about prior aortic aneurysm/graft)–– rare but lethal cause of GI bleeding
10. Neoplasm– bleeding is not rapid– usually not an emergency

Front 285

Causes of lower GI bleeds

Back 285

1. diverticulosis (40% of cases)– most common source of GI bleeding in patients over age 60, usually painless
2. angiodysplasia– (40% of cases)– second most common source of GI bleeding in patients over age 60
3. IBD– (UC, Crohn's disease)
4. colorectal carcinoma
5. colorectal adenomatous polyps
6. ischemic colitis
7. hemorrhoids, anal fissures
8. small intestinal bleeding – diagnosed by excluding upper GI and colonic bleeding

Front 286

What is hematemesis and what does it suggest?

Back 286

vomiting blood–– suggests an upper GI bleed (bleeding proximal to the ligament of Treitz). Indicates moderate to severe bleeding that may be ongoing
– if massive bleed may see signs of volume depletion and signs and symptoms of anemia–– fatigue, pallor, dyspnea

Front 287

What is "coffee ground emesis" and what does it suggest?

Back 287

darker, "coffee ground" appearing emesis which suggests an upper GI bleeding at a lower rate–– enough time for the blood to be partly digested and take on the appearance of coffee grounds

Front 288

What is "melena" and what does it suggest?

Back 288

Black, tarry, liquid, foul–smelling stool
–– caused by degradation of hemoglobin by bacteria in the colon–– presence of melena indicates that blood has remained in the GI tract for several hours
– the further the bleeding site is from the rectum, the more likely it is for melena to occur
– note that dark stools can also result from bismuth, iron, spinach, charcoal and licorice
– melena suggests upper GI bleeding 90% of the time. Occasionally, the jejunum or ileum is the source. It is unusual for melena to be caused by a colonic lesion, but if it is, the ascending colon is the most likely site

Hint 288

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Front 289

What is "Hematochezia" and what does it suggest?

Back 289

– Bright red blood per rectum
– this usually represents a lower GI source (typically left colon or rectum)–– consider diverticulosis, AVM, hemorrhoids or colon cancers
– it may result from massive upper GI bleeding that is very brisk (5–10% of time)

Front 290

What is "occult" blood in the stool?

Back 290

– blood that is discovered on fecal occult blood test–– cannot be seen grossly.
– source of bleeding may be anywhere along the GI tract

Front 291

what should you always ask patients with GI bleeding?

Back 291

If they are on NSAIDs/aspirin, clopidogrel (plavix) or other anticoagulants

Front 292

what should you always think of when you see a lower GI bleed or positive fecal occult blood test in someone over 40?

Back 292

Colon cancer until proven otherwise

Front 293

Aortoenteric fistula

Back 293

– a rare but potential lethal cause of GI bleed
– classic presentation is a patient with a history (sometimes remote) of aortic graft surgery that develops a small amount of GI bleeding involving the duodenum before having a fatal, massive hemorrhage hours to weeks later
– perform endoscopy or surgery during this small window of opportunity to prevent death

Front 294

What tests should you order in a patient with GI bleeding?
a. hematochezia
b. hematemesis
c. melena
d. occult blood

Back 294

a. hematochezia– first rule out anorectal cause (hemorrhoids). Colonoscopy should be the initial test because colon cancer is the main concern in all patients over 50
b. hematemesis– upper GI endoscopy is the initial test
c. Melena– upper endoscopy is usually the initial test because the most likely bleeding site is the upper GI tract. Order a colonoscopy if no bleeding site is identified from the endoscopy
d. occult blood– colonoscopy is the initial test is more cases as colon cancer is the main concern. Order an upper endoscopy if no bleeding site is identified from the colonscopy

Front 295

Laboratory tests for diagnosis GI bleeds

Back 295

1. stool guaiac for occult blood
2. hemoglobin/hematocrit–– may not be decreased in acute bleeds. A hemoglobin level > 7 to 8 g/dL is generally acceptable in young, healthy patients without active bleeding, however most elderly patients (especially those with cardiac disease) should have a hgb > g/dL
3. A low MCV is suggestive of iron deficiency anemia (chronic blood loss). Patients with acute bleeding have normocytic RBCs
4. Coagulation profile (platelets, PT, PTT and INR)
5. LFTs, renal function (BUN, Cr)
6. The BUN–Creatinine ratio is elevated with upper GI bleeding. This is suggestive of upper GI bleeding if patient has no renal insufficiency. The higher the ratio, the more likely the bleeding is from an upper GI source

Front 296

Role of upper endoscopy in evaluating a GI bleed
– when should it be performed?

Back 296

– most accurate diagnostic test in evaluation of upper GI bleeding
– both diagnostic and potentially therapeutic (coagulate bleeding vessel)
– most patients with upper GI bleeding should have upper endoscopy within the first 24 hours

Front 297

Role of nasogastric tube (NG tube) in evaluation of upper GI bleeding?

Back 297

– often the initial procedure for determining whether GI bleeding is from an upper or lower GI source
– use the NG tube to empty the stomach to prevent aspiration
– false–negative findings are possible if upper GI bleeding is intermittent or from a lesion in the duodenum
– Evaluation of aspirate– bile present, but no blood (upper GI bleed unlikely––probably from site distal to liagment of Treitz), bright red blood or "coffee ground emesis" (upper GI bleed), non–bloody aspirate––clear gastric fluid (upper GI bleed unlikely, but cannot be ruled out definitively (source may possibly be in the duodenum)

Front 298

Role of anoscopy or proctosigmoidoscopy in evaluation of GI bleed

Back 298

can exclude an anal/rectal source. Perform this if there is no obvious bleeding from hemorrhoids

Front 299

role of colonoscopy in the evaluation of GI bleeding

Back 299

– identifies the site of lower GI bleeding in >70% of cases and can also be therapeutic

Front 300

Role a of a bleeding/radionucleotide scan in evaluating GI bleeding

Back 300

– reveals bleeding even with a low rate of blood loss
– it does NOT localize the lesion, it only identifies continued bleeding
– its role is controversial, but it may help determine whether angiography is needed

Front 301

Role of arteriography in evaluation of GI bleeding

Back 301

– definitively locates the point of bleeding
– mostly used in patients with lower GI bleeding
– should be performed during active bleeding
– potentially therapeutic (embolization or intra–arterial vasopressin infusion)

Front 302

role of exploratory laparotomy in evaluation of GI bleed

Back 302

LAST RESORT

Front 303

Treatment of GI bleed– all patients

Back 303

If patient is hemodynamically unstable, resuscitation is always a top priority
– Remember the ABCs. Once the patient is stabilized, obtain a diagnosis
– supplemental O2
– place 2 large bore IV lines. Give fluids or blood if patient is volume depleted.
– draw blood for hgb, hct, platelets, PT and PTT. Monitor hgb q 4–8 hours until the patient's hemoglobin has been stable for at least 24 hours
– type and crossmatch adequate blood (PRBCs). Transfuse as clinical condition demands (e.g. shock, patients with cardiopulmonary disease etc)

Front 304

Treatment of upper GI bleed

Back 304

esophagogastroduodenoscopy (EGD/upper endoscopy) with coagulation of the bleeding vessel. If the bleeding continues, repeat endoscopic therapy or proceed with surgical intervention (ligation of the bleeding vessel)

Hint 304

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Front 305

Treatment of lower GI bleeding

Back 305

– colonscopy– polyp excision, injection, laser, cautery
– arteriographic vasoconstrictor infusion
– surgical resection of involved area– last resort

Front 306

Indications for surgery in GI bleed

Back 306

1. hemodynamically unstable patient who has not responded to IV fluid, transfusion, endoscopic intervention or correction of coagulopathies
2. severe initial bleed or recurrence of bleed after endoscopic treatment
3. continued bleeding for more than 24 hours
4. visible vessel at base of ulcer (30% to 50% chance of rebleed)
5. ongoing transfusion requirement (5 unites within the first 4–6 hours)

Front 307

Two types of esophageal carcinoma

Back 307

1. squamous cell carcinoma (used to be 90% of cases)
2. Adenocarcinoma – on the rise, risk factors include GERD–– now accounts for 50% of new cases in the US

Front 308

Squamous cell carcinoma of the esophagus
1. what population is the most affected?
2. where is it most common within the esophagus?
3. what are the risk factors?

Back 308

1. african american men
2. upper thoracic and mid thoracic esophagus. 1/3 may be in the distal 10 cm of the esophagus
3. alcohol and tobacco use, diet (nitrosamines, betel buts, chronic ingestion of hot foods and beverages such as tea), HPV, achalasia, Plummer–Vinson syndrome, caustic ingestion and nasopharyngeal carcinoma

Front 309

Adenocarcinoma of the esophagus
1. what population is the most affected?
2. where is it most common within the esophagus?
3. what are the risk factors?

Back 309

1. more common in caucasians and men (5:1 over women)
2. most common in distal third of esophagus/GE junction (in 80% of cases)
3. GERD and Barrett's esophagus are the main risk factors. Alcohol and tobacco are not as important as in SCC

Front 310

Prognosis for esophageal cancer of both types

Back 310

Very poor– 5 year survival rate is about 5% to 15% for both types

Front 311

Staging of esophageal cancer
I
IIa
IIb
III
IV

Back 311

I– tumor invades lamina propria or submucosa, nodes are negative
IIa. tumor invades the muscularis propria or adventitia, nodes negative
IIb. tumor invades up to the muscularis propria, positive regional nodes
III. tumor invades adventitia (positive regional nodes) or tumor invades adjacent structures (positive or negative nodes)
IV. distant mets

Front 312

Clinical features of esophageal carcinoma

Back 312

1. dysphagia– most common symptom (initially for solids only, then progression to liquids)
2. weight loss – second most common symptom
3. anorexia
4. odynophagia (pain with swallowing) – a late finding that suggests extraesophageal involvement (mediastinal invasion)
5. hematemesis– hoarseness of voice (recurrent laryngeal nerve involvement)
6. aspiration pneumonia– respiratory symptoms due to involvement of tracheobronchial tree
7. tracheoesophageal or bronchoesophageal fistula
8. chest pain

Front 313

Diagnosis of esophageal carcinoma

Back 313

1. barium swallow useful in the evaluation of dysphagia–– a presumptive diagnosis can be made
2. upper endoscopy with biopsy and brush cytology is required for definitive diagnosis in 95% of cases
3. transesophageal ultrasound helps determine the depth of penetration of the tumor and is the most reliable test for staging local cancer
4. full metastatic workup (e.g. CT chest/abdomen, CXR and bone scan)

Front 314

Treatment of esophageal cancer

Back 314

1. Palliation is the goal in most patients because the disease is usually advanced at presentation
2. surgery (esophagectomy) may be curative for patients with disease in stage 0, 1, or 2 a
3. chemotherapy plus radiation before surgery has been shown to prolong survival more than surgery alone

Front 315

Achalasia
1. definition
2. criteria for diagnosis

Back 315

1. acquired motor disorder of esophageal smooth muscle in which the lower esophageal sphincter (LES) fails to completely relax with swallowing and abnormal peristalsis of esophageal body replaces normal peristalsis of the esophageal body
2. Absolute criteria for diagnosis– incomplete relaxation of the LES, and aperistalsis of the esophagus

Front 316

Causes of achalasia

Back 316

1. the majority of cases in the US are idiopathic
2. in the US, adenocarcinoma of the proximal stomach is the second most common cause
3. Worldwide, Chagas' disease is an important cause

Front 317

Clinical features of achalasia

Back 317

1. dysphagia (odynophagia is less common)
– equal difficulty swallowing solids and liquids (in contrast to esophageal cancer, in which dysphagia for solids is greater than for liquids).
– patients tend to eat slowly and drink lots of water to wash down food. Also, they may twist their body, extend their neck, or walk about the room in effort to force food into their stomach
2. regurgitation–– food gets "stuck" in the esophagus and then comes back up. This may lead to regurgitation
3. chest pain
4. weight loss
5. recurrent pulmonary complications secondary to aspiration, which may cause lung abscesses, bronchiectasis or hemoptysis

Picture is of heller myotomy– one of the treatments for achalasia

Hint 317

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Front 318

Diagnosis of achalasia

Back 318

1. Barium swallow – "bird's beak"– beak–like narrowing of distal esophagus and a large, dilated esophagus proximal to the narrowing
2. Upper GI endoscopy– to rule out secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal cancer
3. manometry – to confirm the diagnosis– reveals failure of LES relaxation and aperistalsis of the esophageal body

Hint 318

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Front 319

Risk of esophageal carcinoma in patients with achalasia

Back 319

Sevenfold increase in the risk of esophageal cancer (usually SCC)
– it occurs in 10% of patients 15–25 years after the initial achalasia diagnosis.
– Often tumors go unnoticed (even when large) due to a dilated esophagus and chronic dysphagia. Therefore, perform a surveillance scope to detect the tumor at an early stage

Front 320

Treatment of achalasia

Back 320

1. Instruct the patient on adaptive measures– chew food to consistency of pea soup before swallowing. Sleep with trunk elevated, avoid eating before sleep.
2. Medical therapy
a. antimuscarinic agents (dicyclomine)– usually unsatisfactory
b. sublingual nitroglycerin, long–acting nitrates, and calcium channel blockers. May improve swallowing in early stages of achalasia (before esophageal dilatation occurs). Most useful in the short–term treatment of achalasia (before more definitive therapy)
3. Injecting of botulinum toxin into the LES during endoscopy. Blocks cholinergic activity in the LES. Can be effective in up to 65% of cases. however repeat procedure needs to be performed every 2 years.
4. forceful dilatation– can be mechanical, pneumatic, or hydrostatic. Pneumatic balloon dilatation is most effective. Lowers basal LES tone by disrupting the muscular ring. can be effective, there is a 5% risk of perforation
5. surgical
a. Heller myotomy– circular muscle layer of LEW is incised
b. usually reserved for patients who do not respond to dilation therapy
6. Early results a promising (80–90% of patients experience good to excellent palliation of dysphagia at 1 year)
7. Long term data is still needed

Hint 320

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Front 321

Diffuse esophageal spasm
1. definition/ general characteristics
2. clinical features
3. diagnosis

Back 321

1. Nonperistaltic spontaneous contraction of the esophageal body–– several segments of the esophagus contract simultaneously and prevent appropriate advancement of the food bolus. In contrast to achalasia, sphincter function is normal (normal LES pressure)
2. There is noncardiac chest pain that mimics angina and may radiate to the jaw, arms and back. Dysphagia is common, however there is no regurgitation of food usually.
3. Diagnosed by esophageal manometry – simultaneous, multiphasic, repetitive constractions that occur after a swallow, sphincter response is normal. Upper GI barium swallow shows "corkscrew esophagus"– in 50% of cases which represents multiple spontaneous contractions

Hint 321

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Front 322

Treatment of diffuse esophageal spasm

Back 322

1. In general, there is no completely effective therapy–– treatment failure rates are high
2. medical treatment involves nitrates and calcium channel blockers (decreases amplitude of contractions). Tricyclic antidepressants may provide symptomatic relief
3. esophagomyotomy is usually not performed, and its efficacy is controversial. Some support its use, whereas others only recommend it when a patient is incapacitated my symptoms

Front 323

2 types of esophageal hernia and characteristics of each

Back 323

1. sliding hiatal hernia (type 1) – accounts for 905 of cases. Both the gastroesophageal (GE) junction and a portion of the stomach herniate into the thorax through the esophageal hiatus (so that the GE junction is above the diaphragm)– this a common and benign finding that is associated with GERD
2. paraesophageal hiatal hernia – accounts for <5% of cases. The stomach herniates into the thorax through the esophageal hiatus, but the GE junction does not. It remains below the diaphragm. This uncommon hernia can become strangulated and should be repaired surgically. These tend to enlarge with tim, and the entire stomach may ultimately move into the thorax
3. type 3 hernia are a combination of type 1 and 2 and are treated as type 2 hernias (surgically)

Hint 323

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Front 324

Clinical features of esophageal hernias

Back 324

1. The majority of cases are asymptomatic and are discovered incidentally
2. possible symptoms include heartburn, chest pain, and dysphagia
3. complications of sliding hiatal hernias include GERD (most common), reflux esophagitis (with risk of Barrett's esophagus/cancer), and aspiration
4. Complications of paraesophageal hernias are potentially life–threatening and include obstruction, hemorrhage, incarceration and strangulation

Front 325

Diagnosis of esophageal hernias

Back 325

Barium upper GI series and upper endoscopy

Front 326

Treatment of esophageal hernias by type

Back 326

1. Type 1 hernias are treated medically (with antacids, small meals and elevation of the head after meals); 15% of cases may require surgery (Nissen's fundoplication) if there is no response to medical therapy or if there is evidence of esophagitis
2. Type 2 hernias treated with elective surgery due to risk of strangulation

Hint 326

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Front 327

Mallory–Weiss Syndrome

Back 327

1. mucosal tear at (or just below) the GE junction as a result of forceful vomiting or retching. It usually occurs after repeated episodes of vomiting, but it may occur after one episode
2. it is most commonly associated with binge drinking in alcoholics, but any disorder that causes vomiting can induce the mucosal tear
3. hematemesis is always present– it varies from streaks of blood in vomitus to massive bright red blood
4. upper endoscopy is diagnostic
5. most cases (90%) stop bleeding without any treatment
6. Treatment is surgery (oversewing the tear) or angiographic embolization if bleeding continues, but this is rarely necessary. Acid suppression is used to promote healing

Hint 327

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Front 328

Plummer–Vinson Syndrome

Back 328

1. key features: upper esophageal web (causes dysphagia), iron deficiency anemia, koilonychia (spoon–shaped fingernails), and atrophic oral mucosa
2. 10% of patients develop SCC of the oral cavity, hypopharynx or esophagus, therefore, this is considered a premalignant lesion
3. treatment: esophageal dilatation, correct nutritional deficiency

Hint 328

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Front 329

Schatzki's Ring
1. what is it?
2. symptoms
3. treatment
4. causes?
5. acid vs base ingestion
6. complications
7. treatment

Back 329

1. distal esophageal webs– a circumferential ring in the lower esophagus that is always accompanied by a sliding hiatal hernia
2. It is usually asymptomatic, but mild to moderate dysphagia may be present
3. If the patient is symptomatic (but has no reflux), consider esophageal dilatation. If the patient has reflux, consider antireflux surgery (e.g. nissen)
4. usually due to ingestion of alkali, bleach, or detergent
5. ingesting alkali is more dangerous than infesting acid because it may lead to liquefactive necrosis of the esophagus with full–thickness perforation. Acid ingestion does not cause full–thickness damage (only causes necrosis of esophageal mucosa). 6. Complications : stricture formation and risk of esophageal cancer
7. Treatment is esophagectomy if full thickness necrosis has occurred. Patient should avoid vomiting, gastric lavage, and all oral intake (can compound the original injury). Give the patient steroids and antibiotics. Perform bougienage for esophageal stricture

Hint 329

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Front 330

Mallory Weiss syndrome vs Boerhaave's syndrome

Back 330

During forceful vomiting, the marked increase in intra–abdominal pressure is transmitted to the esophagus. This can lead to two conditions, depending on the severity and location of the tear.
1. If the tear is mucosal at the GE junction, it is referred to as a mallory weiss tear
2. If the tear is transmural (causing esophageal perforation) it is referred to as Boerhaave's syndrome

picture– boerhaave's syndrome

Front 331

Esophageal diverticula
1. most common cause
2. most common type
3. mechanism of most common type
4 and 5. clinical features of most common type, age affected
6. traction diverticula
7.epiphrenic diverticula
8. diagnosis
9. treatment

Back 331

1. most esophageal diverticula are caused by an underlying motility disorder of the esophagus
2. Zenker's diverticulum is the most common type–– found in the upper 1/3 of the esophagus
3. Failure of the cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure. This causes outpouching of mucosa through an area of weakness in the pharyngeal constrictors
4. clinical features include dysphagia, regurgitation, halitosis, weight loss and chronic cough
5. It is typically seen in patients > 50 years old
6. traction diverticula– located in the midpoint of the esophagus near the tracheal bifurcation. It is due to traction from contiguous mediastinal inflammation and adenopathy (pulmonary tuberculosis). Tuberculosis causes hilar node scarring, which causes retraction of the esophagus. It is usually asymptomatic and does not require treatment
7. epiphrenic diverticuli– found in the lower 1/3 of the esophagus. It is usually associated with spastic esophageal dysmotility or achalasia. Symptoms of dysphagia are more often related to the underlying motility disorder, unless the diverticulum is very large
8. Barium swallow is the best diagnostic test for divertula.
9. Treatment of Zenker's diverticula is surgery. Cricopharyngeal myotomy has excellent results. Treatment of epiphrenic diverticula is esophagomytomy. Diverticulectomy is of secondary importance in both cases

Picture– Zenker's Diverticulum

Hint 331

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Front 332

Esophageal perforation
1. etiology
2. clinical features
3. diagnosis
4. treatment– stable vs unstable pt

Back 332

1. blunt trauma, medical tubes and instruments, forceful vomiting (Boerhaave's syndrome) that is associated with alcoholic binges and bulimia
2. pain (severe retrosternal/chest/shoulder pain), tachycardia, hypotension, tachypnea, fever, Hamman's sign (mediastinal crunch– produced by heart beating against air–filled tissues), pneumothorax, pleural effusion
3. contrast esophagram is the definitive diagnostic study (soluble gastrogafin swallow preferred), CXR0 usually shows air in the mediastinum
4. if the patient is stable and the perforation is small (draining into lumen)– medical management is appropriate – IV fluids, NPO, antibiotics, and H2 blockers
– if patient is ill and perforation is large– or there is communication into the pleural cavity, surgery should be performed within 24 hours of presentation (success rate is higher)

– if gastric/esophageal contents leak into the mediastinum or pleura, infection and septic sequela may result
– The time interval between esophageal perforation and surgery is the most important factor in determining survival. If surgery is delayed beyond 24 hours, the mortality rate and the likelihood of fistulization increase

Front 333

Peptic ulcer disease
1. most common causes
2. other causes

Back 333

1. most common causes– H. pylori infection, NSAIDs– inhibit prostoglandin production, which leads to impaired mucosal defenses. Zollinger–Ellison syndrome– acid hypersecretory states
2. Other causes– smoking– ulcers are twice as likely in smokers, alcohol and coffee– may exacerbate symptoms, but causal relationship is as yet unproven
3. other potential unproven causes– emotional stress, personality type A, and dietary factors

Front 334

Clinical features of peptic ulcer disease

Back 334

1. epigastric pain– aching or gnawing in nature
– nocturnal symptoms and effect of food on symptoms are variable
2. may be complicated by upper GI bleeding
3. other symptoms– n/v, early satiety, and weight loss

Front 335

Diagnosis
1. most accurate method?
2. most convenient test?
3. lab tests
4. if considering a dx of Zollinger Ellison syndrome?

Back 335

1. Endoscopy– most accurate test in diagnosing ulcers, essential in diagnosis of gastric ulcers because biopsy is necessary to r/o malignancy– duodenal ulcers not require biopsy. Preferred when severe or acute bleeding is present (can perform electrocautery of bleeding ulcers)
2. Barium swallow– sometimes used initially but is less reliable than endoscopy. Double contrast techniques preferred due to improved accuracy
3. lab tests– for diagnostic evaluation of h. pylori infection– a. biopsy: histologic evaluation of endoscopic biopsy is the gold standard
– urease detection via urea breath test – most convenient test (sensitivity and specificity > 95%). It documents active infection and helps to assess the results of antibiotic therapy
– serology – lower specificity – the presence of h. pylori does not necessarily indicate current infection–– antibodies to h. pylori can remain elevated for months or even years after eradication of infection. There may also be false positives because of PPIs, bismuth, many abx and GI bleeding
4. serum gastrin measurement– if considering Zollinger–Ellison syndrome as diagnosis

–– if a peptic ulcer is uncomplicated, a barium study or endoscopy is not needed initially. Initiate empiric therapy. However, if complications are suspected, order confirmatory tests

Hint 335

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Front 336

Medical Treatment of peptic ulcer disease

Back 336

1. Medical– the majority of patients with PUD can be successfully treated by curing H. pylori infection, avoidance of NSAIDs, and appropriate use of antisecretory drugs
a. supportive– discontinue aspirin, restrict alcohol use, but do not restrict any foods, stop smoking, decrease stress, avoid eating before bedtime (eating stimulates nocturnal gastric acid levels)
b. acid suppression – H2 blockers– accelerate healing of ulcers, PPIs– most effective antisecretory agents (although expensive), antacids – somewhat outdates for primary therapy and most appropriate for adjunctive therapy/symptom relief
c. Eradicate h. pylori with triple or quadruple therapy – once infection is cleared the recurrence rate is low. For initial therapy, triple therapy (PPI, amoxicillin, and clarithromycin), for 10 days to 2 weeks, For retreatment quadruple therapy – PPI, bismuth, and 2 antibiotics
d. cytoprotection – sulcralfate– faciliates ulcer healing, must be taken frequently, is costly and can cause GI upset. misoprostol– reduces risk of ulcer formation associated with NSAID use, is costly, and cause GI upset (commonly)
e. Treatment regimens
– if h. pylori test is positive, begin eradication therapy with either triple or quadruple therapy. Also begin acid–suppression with antacids, an H2 blocker or a PPI
– if the patient has an active NSAId induced ulcer, stop NSAID use (switch to acetaminophen), Also begin with either PPI or misoprostol. Continue for 4–8 weeks, depending on severity. Treat the h. pylori infection if present
– antisecretory drugs can be discontinued after 4–6 weeks in patients with uncomplicated ulcers who are asymptomatic. Patients at increased risk of recurrence (especially if underlying cause of ulcer is not reversed) may benefit from maintenance therapy
– h. pylori negative ulcers that NOT caused by NSAIDs can be treated with antisecretory drugs (H2 blockers or PPIs)

Front 337

Surgical treatment of peptic ulcer disease

Back 337

– rarely needed electively
– required for complications of PUD – bleeding perforation, gastric outlet obstruction

Front 338

Complications of Peptic ulcer disease

Back 338

1. perforation– acute severe abdominal pain, signs of peritonitis and hemodynamic instability– upright CXR or CT to detect free air under diaphragm. Tx– emergency surg to close perf and definitive ulcer operation– selective vagotomy or truncal vagotomy/pyloroplasty–– can progress to sepsis and death if untreated
2. gastric outlet obstruction– n/v of poorly digested food, epigastric fullness/early satiety and weight loss. Barium swallow and upper endoscopy, saline load test (empty stomach with NG tube, add 750 mL saline, aspirate after 30 min, test is positive if aspirate > 400mL. Tx– initially NG suction, replaced electrolyte/volume deficits. Supplemental nutrition if obstruction is longstanding. Surgery is eventually necessary in 75% of patients. Most common with duodenal ulcers and type III gastric ulcers
3. GI bleeding – bleeding may be slow (leading to anemic symptoms) or can be rapid and severe (leading to shock. Stool guaiac, upper GI. Tx– resuscitation, diagnose site of bleed via endoscopy and treat– perform surgery for acute bleeds that require transfusion of > 6 units. PUD is the most common cause of upper GI bleeding

Front 339

duodenal vs gastric ulcers

Back 339

1. duodenal ulcers– caused by increase in offensive factors (higher rates of basal and stimulated gastric acid secretion), 70–90% of patients have h. pylori, Low (malignancy is very rare) should undergo biopsy to r/o. The majority are located 1–2 cm distal to pylorus (usually on posterior wall). Usually occurs in younger patients (<40), assoc with blood type O, NSAIDs– RF, eating usually relieves pain (food in duodenum stimulates bicarb secretion). Nocturnal pain is more common than in gastric ulcers

2. gastric ulcer– caused by a decrease in defensive factors (gastric acid level is normal/low unless ulcer is pyloric or pre–pyloric). 60–70% of patients have h. pylori, high malignant potential (5–10% are malignant), 4 types depending on location – type I is most common– on lesser curvature of stomach – 70%, occurs in older patients > 40, assoc with blood type A, smoking – RF, eating makes it worse– stimulates acid secretion, complication rates are higher than with duodenal ulcers. Higher risk of recurrence with medical therapy alone

Front 340

Acute gastritis
1. definition
2. causes
3. symptoms
4. treatment
5. if no response to tx after 4–8 weeks?

Back 340

1. inflammation of the gastric mucosa
2. there are multiple causes– NSAIDs/aspirin, h. pylori infection, alcohol, heave cigarette smoking, or caffeine, extreme physiologic stress– e.g. shock, sepsis, burns
3. it can be either asymptomatic or cause epigastric pain. The relationship between eating and pain is not consistent
4. if epigastric pain is low/mod and is not associated with worrisome sx/findings, empiric therapy with acid suppression is appropriate. stop NSAIDs
5. If there is no positive response after 4–8 weeks of treatment, consider a diagnostic w/u (include upper GI endoscopy and US to r/o gallstones) and test for h. pylori

Front 341

Chronic gastritis
1. most common cause
2. progression
3. symptoms
4. complications

Back 341

1. the most common cause is h. pylori (over 80% of cases)
2. autoimmune gastritis leads to chronic atrophic gastritis with serum antiparietal and anti–intrinsic factor antibodies (possible development of pernicious anemia)
3. most patients with chronic gastritis due to h. pylri are asymptomatic and never develop complications. The condition may manifest as epigastric pain similar to PUD. Other associated symptoms are n/v and anorexia.
4. complications include PUD, gastric carcinoma, and mucosa–associated lymphoid tissue (MALT) lymphoma
5. upper endoscopy with biopsy is the test of choice for diagnosis of chronic gastritis. Other tests should be used to find the cause (usually h. pylori)

Front 342

Gastric cancer
1. most common type
2. where is it common geographically?
3. morphology

Back 342

1. majority are adenocarcinomas
2. gastric cancer is rare in the US but more common in Japan (relation to smoked foods?)
3. a. ulcerative carcinoma– ulcer through all layers
b. polypoid carcinoma– solid mass projects into stomach lumen
c. superficial spreading– most favorable prognosis
d. linitis plastic – "leather water bottle" – infiltrates early through all layers, stomach wall is thick and rigid, poor prognosis

Hint 342

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Front 343

Risk factors for gastric carcinoma

Back 343

1. severe atrophic gastritis, intestinal metaplasia, gastric dysplasia
2. adenomatous gastric polyps, chronic atrophic gastritis
3. h. pylori infection – 3–6–fold increase in risk
4. postantrectomy– many cases reported after Billroth II anastamosis – 15–20 yrs later
5. pernicious anemia – 3–fold increased risk
6. menetrier's disease – 10% develop cancer
7. high intake of preserved foods – high salt, nitrates, nitrites– smoked fish
8. blood type A

Front 344

Clinical features of gastric cancer

Back 344

1. abdominal pain and unexplained weight loss are the most common symptoms
2. reduced appetite, anorexia, dyspepsia, early satiety
3. n/v, anemia, melena, guaiac–positive stool

Front 345

Diagnosis of gastric carcinoma

Back 345

1. endoscopy with multiple biopsies– most accurate test
2. barium upper GI series– less accurate, but can complement upper endoscopy findings
3. abdominal CT scan– for staging and to detect presence of mets
4. FOBT

Front 346

Treatment of gastric carcinoma

Back 346

1. surgical resection with wide > 5 cm margins – total and subtotal gastrectomy with extended lymph node dissection
2. chemotherapy may be appropriate in some cases

Front 347

Gastric lymphoma

Back 347

1. a type of non–hodgkins lymphoma that arises in the stomach
2. clinical features are similar to those of adenocarcinomas of the stomach (e.g. abdomina pain, weight loss, anorexia)
3. complications include bleeding, obstruction, and perforation
4. diagnosis– EGD with biopsy is standard of diagnosi
5. tx– depends on stage of the disease and the presence of complications. options include surgical resection, radiation, and chemotherapy

Hint 347

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Front 348

What is the best test for evaluating a patient with epigastric pain?

Back 348

Upper GI endoscopy as it can diagnose PUD, gastritis and esophagitis. It can also rule out cancers of the esophagus and stomach, and h. pylori infection with biopsy

Front 349

What are the 3 main points to consider in small bowel obstruction?

Back 349

1. partial vs complete obstruction– with a partial obstruction, patients are able to pass gas or have bowel movements as opposed to a complete obstruction. However, patients with a complete obstruction may occasionally be able to pass gas or stool because they have residual stool or gas in the colon
2. Closed loop vs open loop obstruction
– with closed loop obstruction, the lumen is occluded at 2 points by an adhesive band or hernia ring. This can compromise the blood supply and require emergent surgery.
3. Proximal versus distal small bowel obstruction (SBO)– distal obstruction causes distention of the proximal bowel segments, making a diagnosis easier on plain film

Front 350

Pathophysiology of small bowel obstruction

Back 350

1. dehydration is the key event in SBO.
– Intestinal distention causes reflex vomiting, increased intestinal secretion proximal to the point of obstruction, and decreased absorption. This leads to hypochloremia, hypokalemia and metabolic alkalosis
2. The resulting hypovolemia leads to systemic findings such as tachycardia, hypotension, tachypnea, AMS, oliguria

Front 351

Causes of Small Bowel Obstruction

Back 351

1. Adhesions from previous abdominal surgery– most common cause in adults
2. Incarcerated hernias– second most common cause
3. Malignancy, intussusception, Crohn's disease, carcinomatosis, and superior mesenteric artery syndrome (compression of the third portion of the duodenum)

Front 352

Clinical features of small bowel obstruction

Back 352

1. crampy abdominal pain– if the pain is continuous and severe, strangulation may be present
2. N/v– may be feculent
3. obstipation – absence of stool and flatus
4. abdominal distention

Front 353

Diagnosis of small bowel obstruction

Back 353

1. Abdominal plain films– dilated loops of small bowel, air0fluid levels proximal to the point of obstruction (on upright film), and minimal gas in colon (if complete SBO)
2. Barium enema– to rue out colonic obstruction if plain films do not distinguish small from large bowel obstruction. This identifies the site of obstruction
3. Upper GI series– with small bowel follow through if above are not diagnostic

Front 354

Treatment of small bowel obstruction

Back 354

1. Nonoperative management– appropriate if bowel obstruction is incomplete and there is no fever, tachycardia, peritoneal signs, or leukocytosis
2. IV Fluids to establish adequate urine output, add potassium to fluids to correct hypokalemia (which is typically present)
3. NG tube to empty the stomach (gastric decompression)
4. Antibiotics
5. Surgery is indicated for complete obstruction, for partial obstruction that is persistent and/or associated with constant pain, or if strangulation is suspected. Perform an exploratory laparotomy with lysis of adhesions and resection of any necrotic bowel

Front 355

Paralytic Ileus
1. definition
2. causes
3. abd plain film appearance
4. diagnosis
5. treatment

Back 355

1. peristalsis is decreased or absent (no mechanical obstruction is present)
2. causes include medications (narcotics, drugs with anticholinergic effects), postoperative state (after abd surgery), spinal cord injury, shock, metabolic disorders (especially hypokalemia) and peritonitis
3. Abdominal plain films show a uniform distribution of gas in the small bowel, colon, and rectum (in contract to small bowel or colonic obstruction)
4. Failure to pass contrast medium beyond a fixed point is diagnostic
5. treatment– IV Fluids, NPO, correction of electrolyte imbalances (especially hypokalemia), NG suction if needed, and placement of a long tube if ileus persists postoperatively

Front 356

Celiac Sprue
1. what is it?
2. symptoms
3. diagnosis
4. treatment

Back 356

– characterized by hypersensitivity to gluten (in wheat products)
– results in weight loss, abdominal distention, bloating and diarrhea
– biopsy in proximal small bowel reveals flattening of villi, which causes malabsorption
– strict adherence to a gluten–free diet is essential

Front 357

Crohn's disease
1. definition
2. Distribution

Back 357

1. chronic transmural inflammatory disease that can affect any part of the GI tract (mouth to anus) but most commonly involves the small bowel (terminal ileum)
2. Distribution: There are three major patterns of disease.
– 40% of patients have disease in the terminal ileum and cecum
– 30% of patients have disease confined to the small intestine
– 25% of patients have disease confined to the colon
– Rarely, other parts of the GI tract may be involved (stomach, mouth, esophagus)

Front 358

Pathology of Crohn's disease

Back 358

1. Terminal ileum is the hallmark location, but other sites of GI tract may also be involved
2. Skip lesions– discontinuous involvement
3. Fistulae
4. luminal strictures
5. non–caseating granulomas
6. Transmural thickening and inflammation (full–thickness wall involvement) – results in narrowing of the lumen
7. Mesenteric "fat creeping" onto the antimesenteric border of the small bowel

Front 359

Clinical features of crohn's disease

Back 359

1. diarrhea (usually without blood)
2. malabsorption and weight loss (common)
3. abdominal pain (usually RLQ), n/v
4. fever, malaise
5. extraintestinal manifestations in 15–20% of cases (uveitis, arthritis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, apthous oral ulcers (cold sores), and nephrolithiasis

Hint 359

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Front 360

Epidemiology of inflammatory bowel disease–– who is it most common in?

Back 360

– more common in caucasians than other racial groups
– particularly common in Jewish populations
– mean age of onset is 15–35 years of age

Front 361

Course of crohn's disease

Back 361

– chronic indolent course characterized by unpredictable flares and remissions
– the effectiveness of medical treatment decreases with advancing disease and complications eventually develop, requiring surgery
– There is no cure, and recurrence is common even after surgery

Front 362

Treatment of paralytic ileus

Back 362

– usually resolves with time or when the cause is addressed medically
– surgery is usually not needed

Front 363

Diagnosis of crohn's disease

Back 363

1. endoscopy (sigmoidoscopy or colonoscopy) with biopsy– typical findings are apthous ulcers, cobblestone appearance, pseudopolyps, patchy (skip) lesions
2. barium enema
3. upper GI with small bowel follow–through

Hint 363

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Front 364

Complications of crohn's disease

Back 364

1. fistulae– between colon and other segments of the intestine (enteroenteral), bladder (enterovescial), vagina (enterovaginal), and skin (enterocutaneous)
2. anorectal disease (in 30% of patients)– fissures, abscesses and perianal fistulas
3. SBO (in 20–30% of patients) is the most common indication for surgery. Initially it is due to edema and spasm of bowel with intermittent signs of obstruction, later, scarring and thickening of bowel cause chronic narrowing of the lumen
4. malignancy– increased risk of colonic and small bowel tumors (but less than with UC)
5. Malabsorption of B12 and bile acids (both occur in the terminal ileum)
6. Cholelithiasis may occur secondary to decreased bile acid absorption
7. Nephrolithiasis– increased colonic absorption of dietary oxalate can lead to calcium oxalate kidney stones
8. Aphthous ulcers of lips, gingiva, and buccal mucosa (common)
9. toxic megacolon– less common in crohn's than in UC
10. growth retardation
11. narcotic abuse, psychosocial issues due to chronicity and often disabling nature of the disease

Hint 364

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Front 365

Medical Treatment of crohn's disease

Back 365

1. Sulfazalazine – this is useful if the colon is involved– 5–ASA (mesalamine) is the active compound and is released in the colon– it more useful in UC. 5–ASA compounds block prostoglandin release and serve to reduce inflammation. There are preparations of 5–ASA that are more useful in distal small bowel disease
2. Metronidazole (flagyl)– if no response to 5–ASA
3. systemic corticosteroids (prednisone) for acute exacerbations and if no response to metronidazole
4. Immunosuppressants (azathioprine, 6–mercaptopurine) – in conjunction with steroids if the patient does not respond to the above agents
5. bile acid sequestrants –cholestyramine or colestipol– for patients with ileal disease who cannot absorb bile acids
6. anti–diarrheal agents are generally NOT a good choice–– may cause ileus

Front 366

Surgical treatment of crohn's disease

Back 366

– eventually required in most patients
– reserve for complications of crohn's disease
– involves segmental resection of involved bowel
– disease recurrence after surgery is high– up to 50% of patients experience disease recurrence at 10 years post–op
– indications for surgery include SBO, fistulae (especially between bowel and bladder, vagina), disabling disease, and perforation or abscess
– nutritional supplementation and support– parenteral nutrition is sometimes necessary

Front 367

Ulcerative colitis (UC)
1. definition and age at presentation
2. distribution

Back 367

1. chronic inflammatory disease of the colon or rectal mucosa that may occur at any age, but usually begins in adolescence of young adulthood
2. UC involves the rectum in ALL cases and can involve the colon either partially or entirely.
– Rectum alone (in 10% of cases)
– rectum and left colon (in 40% of cases)
– rectum, left colon and right colon (in 30% of cases),
– pancolitis (in 30% of cases)
– the small bowel is not usually involved in UC, but it may reach the distal ileum in a small percentage of patients ("backwash ileitis" in 10% of cases)

Front 368

Clinical course of ulcerative colitis

Back 368

The course is unpredictable and variable and is characterized by periodic exacerbations and periods of complete remission.
– less than 5% of patients have an initial attack without any recurrence

Front 369

Pathology of ulcerative colitis

Back 369

1. uninterrupted involvement of the rectum and/or colon – NO skip lesions
2. inflammation is no transmural as in crohn's–– it is limited to the mucosa, and submucosa
3. PMNs accumulate in the crypts of the colon (crypt abscesses)

Hint 369

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Front 370

Clinical features (wide range of presentation)

Back 370

1. hematochezia – may start as non bloody diarrhea and then progress to bloody as disease progresses
2. abdominal pain
3. bowel movements are frequent but small
4. fever, anorexia, and weight loss (severe cases)
5. tenesmus (rectal dry heaves)
6. Extraintestinal symptoms (jaundice, uveitis, arthritis, skin lesions)

Front 371

Diagnosis of ulcerative colitis

Back 371

1. stool cultures for c. diff, ova, and parasites– to rulre out infectious causes of diarrhea
2. fecal leukocytes
3. WBCs can appear in UC, ischemic colitis and or infectious diarrhea
4. colonoscopy– to assess the extent of disease and the presence of any complications

Front 372

Complications of ulcerative colitis

Back 372

1. iron deficiency anemia
2. hemorrhage
3. electrolyte disturbances and dehydration secondary to diarrhea
4. strictures, benign and malignant (usually malignant)
5. colon cancer– the risk correlates with extent and duration of colitis. In distal proctitis there is no increased risk of CRC
6. sclerosing cholangitis – the course is not parallel with bowel disease and is not prevented by colectomy
7. cholangiocarcinoma– half of all bile duct cancers are associated with UC
8. Toxic megacolon– leading cause of death in UC and affects <5% of patients. It is associated with risk of colonic perforation
9. growth retardation
10. narcotic abuse
11. psychosocial issues (e.g. depression) due to chronicity and often disabling nature of the disease

Front 373

Medical Treatment of ulcerative colitis

Back 373

1. Medical
a. systemic corticosteroids are used for acute exacerbations
b. sulfasalazine (topical application as a suppository) is the mainstay of treatment. Preferred over topical steroids because they are effective as maintenance therapy. Remission rates are as high as 93%. 5–ASA (mesalazine) is the active component. 5–ASA enemas can be used for proctitis and distal colitis
c. immunosuppressive agents in patients with refractory disease may prevent relapses but are not effective for acute attacks

Front 374

Surgical Treatment of ulcerative colitis

Back 374

– often curative (unlike Crohn's disease) and involves total colectomy
– indications for surgery include:
– severe disease that is debilitating, refractory, and unresponsive to medical therapy
– toxic megacolon (risk of perforation), obstruction (due to stricture), severe hemorrhage, and perforation
– fulminant exacerbation that does not respond to steroids
– evidence of colon cancer of increased risk of colon cancer
– growth failure or failure to thrive in children
– systemic complications

Front 375

Colorectal cancer
1. how common?
2. most common type?

Back 375

1. 3rd most common cancer in the United States (in men and women)
2. Virtually all colorectal tumors arise from adenomas and the majority are endoluminal adenocarcinomas arising from the mucosa––>adenocarcinoma. Rarely there are carcinoid tumors, lymphomas, and Kaposi's sarcoma (HHV 8 in AIDS pts)

Front 376

Colorectal cancer (CRC) screening

Back 376

1. fecal occult blood test– poor sensitivity and specificity. PPV is only 20%, but all patients with a positive FOBT need a colonoscopy anyway
2. Digital rectal exam (DRE)– only about 10% of tumors are palpable by rectal examination
3. Colonscopy– the most sensitive and specific test–– the diagnostic study of choice for patients with a positive FOBT. Diagnostic and therapeutic–– biopsy or polypectomy.
4. Flexible sigmoidoscopy– can be used to reach teh area where approximately 50% to 70% of polyps and cancers occur (with a 60cm scope). Can be diagnostic in about 2/3 of all CRCs
5. Barium enema– evaluates entire colon– complementary to flex sig. Disadvantage is the any abnormal findings need to be evaluated by colonscopy
6. Carcinoembryonic antigen (CEA)– not useful for screening––useful for baseline and recurrence surveillance. Has some prognostic significance–– patients with a preoperative CEA >5 ng/mL have a worse prognosis.

Hint 376

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Front 377

Clinical staging of CRC

Back 377

CT scan of chest, abd, pelvis and by physical exam (ascites, hepatomegaly, lymphadenopathy etc)

Front 378

CRC patterns of spread (4)

Back 378

1. Direct extension– circumferentially and then through the bowel wall to later invade other abdominoperitoneal organs
2. Hematogenous– portal circulation to liver – liver is the most common site of distant spread. Or lumbar/vertebral veins to lungs
3. lymphatic– regionally
4. transperitoneal and intraluminal

Front 379

Risk factors for Colorectal Cancer (CRC)

Back 379

1. Age– everyone over the age of 50 years is at increased risk
2. adenomatous polyps– these are pre–malignant lesions, but most do not develop into cancer. villous adenomas have higher malignant potential than tubular adenomas. The larger the size and the greater the number of polyps the higher the risk of cancer
3. personal history of prior CRC of adenomatous polyps
4. Inflammatory bowel disease (IBD)
– both Ulcerative Colitis (UC) and Crohn's disease pose an increased risk for CRC, but UC poses a greater risk. Incidence of CRC is 5–10% at 20 years and 12–20% at 30 years with UC
5. Family history– multiple first degree relatives with CRC or any first–degree relative diagnosed with CRC or ademona under age 60
6. dietary factors– high fat, low–fiber diets
7. major polyposis syndromes (FAP, Gardner's syndrome, Turcot's syndrome, Peutz Jeghers, Familiar juvenile polyposis coli, hereditary non polyposis CRC (HNPCC)

Front 380

Familial adenomatous polyposis (FAP)
1. what is it?
2. what is the risk of CRC?
3. tx

Back 380

1. autosomal dominant disease characterized by hundreds of adenomatous polyps in the colon. the colon is always involved and the duodenum is involved in 90% of cases. Polyps may also form in the stomach, jejunum, and ileum.
2. The risk of CRc is 100% by the 3rd to 4th decade of life
3. prophylactic colectomy is usually recommended

Hint 380

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Front 381

Gardner's Syndrome
1. what is it?
2. what is the risk of CRC?

Back 381

– polyps plus osteoma, dental abnormalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts
– risk of CRC is 100% by age 40

Hint 381

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Front 382

Turcot's syndrome
1. inheritance pattern?
2. what does it affect?

Back 382

1. autosomal recessive
2. FAP tumors plus cerebellar medulloblastoma or gliobastoma multiforme
(think Turcots– turban–– affects your brain)

Hint 382

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Front 383

Peutz–Jeghers syndrome
1. what is it?
2. what are some clinical features?
3. malignant potential compared to ademonas?
4. which cancers are pts at increased risk for?
5. other potential complications?

Back 383

1. Single or multiple hamartomas that may be scattered through the entire GI tract: small bowel (78%), colon (60%), stomach (30%)
2. pigments spots around lips, oral mucosa, face, genitalia, and palmar surfaces
3. unlike adenoma, hamartomas have a very low malignant potential
4. slightly increased incidence in various carcinomas (e.g. stomach, ovary, breast, cervix, testicle, lung).
5. intussception or GI bleeding may occur

Hint 383

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Front 384

Familial juvenile polyposis coli

Back 384

1. rare, presents in childhood, only small risk of CRC
2. more than 10 and up to 100s of juvenile colon polyps

Front 385

Hereditary Nonpolyposis CRC (HNPCC– Lynch syndrome)

Back 385

1. lynch syndrome I– site specific CRC– early onset CRC, absence of antecedent multiple polyposis
2. lynch syndrome II– (cancer family syndrome)– all features of Lynch I plus increased number and early occurrence of other cancers (e.g. female genital tract, skin, stomach, pancreas, brain, breast, biliary tract)

Hint 385

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Front 386

Clinical features of CRC
1. most common symptom?
2. other symptoms

Back 386

1. the presence of symptoms is typically a manifestation of relatively advanced disease. Most symptoms include melena, hematochezia, abdominal pain, change in bowel habits, or unexplained iron deficiency anemia
2. Signs and symptoms are potentially common to all locations
a. abdominal pain is the most common presenting symptom. Can be caused by partial obstruction or peritoneal dissemination. Remember that CRC is the most common cause of large bowel obstruction in adults. Colonic perforation can lead to peritonitis and is the most life–threatening complication.
b. weight loss
c. blood in stool
d. may be asx

Front 387

Right–sided CRC tumors

Back 387

– obstruction is unusual because of the large luminal diameter (the cecum has the largest diameter of any part of the colon) allowing the tumor growth to go undetected
– common findings – occult blood in stool, iron deficiency anemia, and melena (because blood is partially digested by the time it comes out giving it a darker hue)
– triad of anemia, weakness and RLQ mass (occasionally)
– change in bowel uncommon

Hint 387

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Front 388

A patient presents with anemia, weakness and a RLQ mass on exam– what is a likely diagnosis?

Back 388

Right sided colon cancer

Front 389

Left–sided CRC tumors

Back 389

– the descending colon has a smaller diameter than the right so signs of obstruction are more common
– change in bowel are more common– alternating diarrhea and constipation–– narrowing of the stools – "pencil stools"
– hematochezia is more common (red blood–– since it doesn't have as far to go as in the case of a right sided tumor– the blood is less digested/dark)

Hint 389

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Front 390

Rectal cancer
1. how common
2. symptoms and signs

Back 390

– 20–30% of all CRCs
– hematochezia– most common symptom
– tenesmus– feeling the need to pass stool constantly even though the colon is empty– can be very painful
– rectal mass– feeling of incomplete evacuation of stool (due to mass)

Hint 390

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Front 391

Treatment of CRC
1. only cure
2. role of CEA levels
3. role of adjuvant therapy (chemo and radiation)
4. F/U
5. when do recurrences usually happen?

Back 391

1. Surgery is the only curative treatment of CRC– surgical resection of tumor containing bowel as well as resection of regional lymphatics
2. CEA level should be obtained before surgery– can given an indication of prognosis (> 5ng/mL = worse px), also used for F/U
3. chemo and radiation use depends on the stage of the cancer
4. F/U is important and varies
a. Stool guaiac test
b. annual CT of abd/pelvis and CXR for up to 5 yrs
c. colonoscopy at 1 yr and then every 3 years
d. CEA levels are check periodically (ever 3–6 months). – a subsequent increase in CEA is sensitive marker of recurrence. Often, 2nd look operations are based on elevated CEA levels post–op. Very high levels suggest liver involvement
5. about 90% of recurrences occur within 3 years after surgery

Front 392

Nonneoplastic colon polyps (types, which is most common?)

Back 392

1. benign lesions with no malignant potential
a. hyperplastic (metaplastic) polyps are the most common (90%) nonneoplastic polyps–– generally remain small and asx
b. no specific therapy required, but they can be difficult to distinguish from neoplastic polyps and so are commonly removed
c. juvenile polyps–– typically in children younger than 10 years are high vascular and common so they should be removed
d. inflammatory polyps– pseudopolyps–– associated with UC

Front 393

Adenomatous polyps
1. three types – and corresponding malignancy potential
2. what features help determine malignant potential?
3. treatment

Back 393

benign lesions, but have significant malignant potential, precursors of adenocarcinoma
1. can be one of three types–– villous, tubulovillous, and tubular. tubular is the most common– up to 60–80%–– smallest of malignancy. villous has greatest risk of malignancy
2. can determine malignant potential by following:
a. size– the larger the polyp the greater the malignant potential
b. histologic type– see above
c. atypia of cells (increased nuclear to cytoplasmic ratio etc)
d. Sessile (flat– more likely to be malignant) vs pedunculated (on a stalk)
3. tx– complete removal of the polyp

Front 394

Diverticulosis
1. cause
2. risk factors
3. prevalence with age
4. most common site affected

Back 394

1. Caused by increased intraluminal pressure– inner layer of colon bulges through focal area of weakness in colon wall (usually an area of blood vessel penetration)
2. Risk factors– low fiber diets– constipation causes intraluminal pressures to increase. Positive family history
3. prevalence increases with age
4. The most common location is the sigmoid colon–– however diverticular may occur anywhere in the colon

Hint 394

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Front 395

Clinical features of diverticulosis
1. sx

Back 395

– usually asymptomatic and discovered incidentally on barium edema or colonscopy done for another reason
– may have vague LLQ discomfort, bloating, constipation/diarrhea etc
– only 10–20% become symptomatic–– develop complications such as diverticular bleeding or diverticulitis

Front 396

Diagnosis (test of choice, etc)

Back 396

1. Test of choice– barium enema
2. abdominal Xrays are usually normal and are not diagnostic

Front 397

Treatment of diverticulosis

Back 397

1. High fiber foods (such as bran) to increase stool bulk
2. psyllium (if patient cannot tolerate bran)– dietary fiber not absorbed by the small intestine

Front 398

Complications of diverticulosis

Back 398

1. Painless rectal bleeding (up to 40% of patients) – bleeding is usually clinically insignificant and stops spontaneously. No further treatment is necessary in these patients. Bleeding can be severe in about 5% of patients. In many cases the bleeding stops spontaneously. Colonoscopy may be performed to locate the site of bleeding (or mesenteric angiography in certain cases). If bleeding is persistent and/or recurrent, surgery may be needed (segmental colectomy)
2. Diverticulitis– Occurs when feces become impacted in the diverticulum, leading to erosion and microperforation. Can be complicated or uncomplicated. Uncomplicated diverticulitis account for most cases and refers to diverticulitis without abscess formation, colovesical fistula (into bladder) , obstruction, and free colonic perforation

Front 399

Diverticulitis
1. cause
2. complicated vs uncomplicated
3. clinical features

Back 399

1. occurs in 15–25% of patients with diverticulosis when feces become impacted in the diverticulum, leading to erosion and microperforation
2. complications include– free colonic perforation, colovesical fistula (fistula between bowel and bladder– 50% of fistulas arising from diverticulitis), abscess formation, obstruction
3. clinical features– fever, LLQ pain, leukocytosis. May also see alteration in bowel habits (constipation or diarrhea), vomiting and sometimes a painful mass on rectal exam if inflammation is near the rectum
– lower GI bleeding is rare in diverticulitis but common in diverticulosis

Front 400

Diagnosis of Diverticulitis

Back 400

1. CT Scan of abdomen and pelvis with oral and IV contrast is the test of choice–– may reveal a swollen, edematous bowel wall or an abscess
2. Abdominal xrays are helpful in ruling out potential causes of LLQ pain, ileus, obstruction (indicated by air–fluid levels), distention and perforation

Front 401

Treatment of diverticulitis
1. mainstays of treatment
2. when is surgery indicated?

Back 401

1. uncomplicated diverticulitis is managed by IV antibiotics, bowel rest (NPO), IV Fluids. Mild episodes can be treated on an outpatient basis if patient is reliable and has few or no comorbid conditions. If symptoms persist after 3–4 days, surgery may be necessary. Antbiotics should be continued for 7–10 days. After successful treatment, about 1/3 have recurrence.
– Surgery is recommended for recurrent episodes (resection of the involved segment)
– Complicated diverticulitis–– surgery is indicated

Front 402

Angiodysplasia–

Back 402

Tortuous, dilated veins in the submucosa of the colon (usually proximal) wall
– a common cause of lower GI bleeding in patients over the age of 60
– bleeding is usually low grade, but 15% of patients may have massive hemorrhage if veins rupture
– diagnosed by colonoscopy (preferred over angiography)
– in about 90% of patients, bleeding stops spontaneously
– It can frequently be treated by colonoscopic coagulation of the lesion. If bleeding persists, a right hemicolectomy should be considered

Hint 402

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Front 403

Acute Mesenteric Ischemia
1. cause
2. 4 causes
3. mortality

Back 403

1. Results from a compromised blood supply, usually due to superior mesenteric vessels
2. 4 causes–
a. Arterial embolism (50% of cases), almost all emboli are of cardiac origin (atrial fibrillation, MI, valvular disease),
b. Arterial thrombosis (25% of cases)– most of these patients have atherosclerotic disease (coronary artery disease (CAD, PVD, stroke) at other site, Acute occlusions occurs over pre–existing atherosclerotic disease. The acute event may be due to decrease in cardiac output (e.g. resulting from MI, CHF, or plaque rupture), Collateral circulation has usually developed.
c. Non–occlusive mesenteric ischemia (20% of cases) – due to splanchnic vasoconstriction secondary to low cardiac output, typically seen in critically ill elderly patients.
d. Venous thrombosis (<10% of cases)– many predisposing factors –– e.g infection, hypercoaguable states, oral contraceptives, portal HTN, malignancy, pancreatitis
3. mortality– the overall mortality rate for all types is about 60–70%. If bowel infarction has occurred, the mortality rate can exceed 90%

Front 404

Clinical features of acute mesenteric ischemia

Back 404

1. classic presentation is acute onset of severe abdominal pain disproportionate to physical findings–– pain is due to ischemia and possibly infarction of intestines, analogous to MI in CAD
– the abdominal examination may appear benign even when there is severe ischemia which can lead to a delay in diagnosis
– the acuteness and severity of the pain vary depending on the type of acute mesenteric ischemia
– anorexia, vomiting
– GI bleeding (mild)
– peritonitis, sepsis, and shock may be present in advanced disease

Front 405

Diagnosis of acute mesenteric ischemia

Back 405

1. mesenteric angiography– definitive diagnostic test
2. obtain a plain film of the abdomen to exclude other causes of abdominal pain
3. "Thumbprinting" on barium enema is due to thickened edematous mucosal folds

Hint 405

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Front 406

Treatment of acute mesenteric ischemia

Back 406

1. supportive measures– IV Fluids and broad spectrum antibiotics
2. direct intra–arterial infusion of papervine– vasodilator into the the superior mesenteric system during arteriography is the therapy of choice for all arterial causes of acute mesenteric ischemia. This relieves the occlusion and vasospasm
3. Direct intra–arterial infusion of thrombolytics or embolectomy may be indicated in some patients with embolic acute mesenteric ischemia
4. heparin anticoagulation is the treatment of choice for venous thrombosis
5. surgery (resection of non–viable bowel) may be needed in all types of acute mesenteric ischemia if signs of peritonitis develop

Front 407

Chronic Mesenteric Ischemia
1. Cause
2. Symptoms
3. Diagnosis
4. Treatment

Back 407

1. Caused by atherosclerotic occlusive disease of the main mesenteric vessels (celiac artery, superior and inferior mesenteric arteries)
2. Abdominal angina– dull pain, typically postprandial (when there is increased demand for splanchnic blood flow)–– analogous to anginal pain in CAD, significant weight loss may occur secondary to this
3. Mesenteric ateriography to confirm
4. Surgical revascularization – leads to pain relief in 90% of cases

Front 408

Ogilvie's Syndrome
1. what is it?
2. What are the common causes?
3. How diagnosed?
4. treatment

Back 408

1. An unusual problem in which signs, symptoms, and radiographic evidence of large bowel obstruction are present, but there is no mechanical obstruction
2. Common causes– recent surgery or trauma, serious medical illness (e.g. sepsis, malignancy) and medications (narcotics, psychotropic drugs, anticholinergics)
3. The diagnosis cannot be confirmed until mechanical obstruction of the colon is excluded
4. Treatment– stopping any offending agent (e.g. narcotics) and supportive measures (IV Fluids, electrolyte repletion), decompression with gentle enemas or NG suction may be helpful, however if this fails then colonoscopic decompression is usually successful, with surgical decompression and cecostomy/colostomy as a last resort

Front 409

Pseudomembranous Colitis
1. aka
2. cause–– and when does it happen in relation to this?

Back 409

1. antibiotic associated colitis– many patients do not have grossly visible pseudomembranes
2. Antibiotic treatment kills organisms that normally inhibit the growth of Clostridium difficile, leading to its overgrowth and toxin production.
– almost all antibiotics have been associated with it, but the most frequently implicated are Clindamycin, Ampicillin and cephalosporins
– symptoms usually begin within the first week of antibiotic therapy– however, it can start up to 6 weeks after cessation of antibiotic treatment
– disease severity varies widely

Front 410

Clinical features of pseudomembranous colitis/ c. diff

Back 410

1. profuse watery diarrhea (usually NO blood or mucus)
2. crampy abdominal pain
3. Toxic megacolon (in severe cases) with risk of perforation

Hint 410

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Front 411

Diagnosis of pseudomembranous colitis/c. difficile

Back 411

1. Demonstration of C. difficile toxins in the stool is diagnostic, but results take about 24 hours (95% sensitivity)
2. Flexible sigmoidoscopy is the most rapid test and is diagnostic, but because of comfort/expense it is infrequently used
3. Abd Xray to r/o toxic megacolon and perforation
4. leukocytosis is very common

Hint 411

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Front 412

Treatment of pseudomembranous colitis/c. difficile
(including recurrence risk and adjuvant therapy)

Back 412

1. Discontinue the offending agent/antibiotic if possible
2. Metronidazole (flagyl) is the drug of choice but cannot be used in infants or pregnant patients
3. Oral vancomycin can be used if the patient is resistant to metronidazole or cannot tolerate it
– regardless of the choice of antibiotic, recurrence may occur within 2–8 weeks after stopping the antibiotic. This occurs in 15–35% of successfully treated patients
– Cholestyramine may be used as an adjuvant treatment to improve diarrhea

Front 413

Colonic Volvulus
1. definition
2. potential complications
3. most common sites affected

Back 413

1. Twisting of the a loop of intestine about its mesenteric attachment site
2. may result in obstruction or vascular compromise with the potential for necrosis and/or perforation if untreated
3. most common site is the sigmoid colon (75% of all cases), and the cecum (25% of all cases)

Front 414

Risk factors for volvulus (sigmoid vs cecal volvulus)

Back 414

1. chronic illness, age, institionalization, and CNS disease increase the risk of sigmoid volvulus
2. cecal volvulus– due to congenital lack of fixation of the right/descending colon and tends to occur in younger patients
3. chronic constipation, laxative abuse, and antimotility drugs
4. prior abdominal surgery

Hint 414

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Front 415

Clinical features of volvulus

Back 415

1. Acute onset of colicky abdominal pain
2. obstipation (no passing gas or stool) and abdominal distention
3. anorexia, nausea and vomiting

Front 416

Diagnosis of volvulus

Back 416

1. Plain films of the abdomen– a. sigmoid volvulus– omega loop sign (or bent inner–tube shape)– indicates a dilated sigmoid colon. b. cecal volvulus– distention of the cecum and small bowel– coffee bean sign indicates a large air–fluid level in the RLQ
2. Sigmoidoscopy– preferred diagnostic and therapeutic test for sigmoid volvulus–– can treat during this procedure by untwisting and decompressing the bowel in many cases
3. barium enema– reveals the narrowing of the colon at the point where it is twisted "bird's beak"

DO NOT perform barium enema if strangulation is suspected.

Hint 416

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Front 417

Treatment of volvulus
1. sigmoid
2. cecal

Back 417

1. sigmoid volvulus– nonoperative reduction– decompression via sigmoidoscopy is successful in 70% of cases. The recurrent rate is high so elective sigmoid colon resection is recommended
2. cecal volvulus– emergent surgery is indicated

DO NOT perform barium enema if strangulation is suspected

Front 418

Cirrhosis
1. definition
2. reversible vs irreversible

Back 418

1. chronic liver disease characterized by fibrosis, disruption of the liver architecture, and widespread nodules in the liver. The fibrous tissue replaces damaged or dead hepatocytes
2. cirrhosis is generally irreversible when advanced. In early stages, specific treatment of the cause of cirrhosis may improve or reverse the condition. The point at which the disease becomes irreversible is unclear.

Front 419

What does the distortion of liver anatomy cause in cirrhosis (2 major events)?

Back 419

1. Decreased blood flow through the liver with subsequent hypertension in the portal circulation (portal hypertension)–– this has widespread manifestations, including ascites, peripheral edema, splenomegaly, and varicosity of veins "back stream" in the circulation (gut, butt, caput–– gastric/esophageal varices, internal hemorrhoids, and caput medusa–dilated abdominal veins)
2. hepatocellular failure–– leads to impairment of biochemical functions, such as decreased albumin synthesis and decreased clotting factor synthesis

Front 420

Assessment of hepatic functional reserve in cirrhosis

Back 420

1. Child's classification– estimates hepatic reserve in liver failure–– used to measure disease severity and is a predictor of morbidity and mortality (based on ascites, bilirubin, encephalopathy, nutritional status, and albumin)
2. Child's class C indicates the most severe disease, while class A is milder

Hint 420

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Front 421

Causes of cirrhosis (10)

Back 421

1. Alcoholic liver disease – most common cause. Refers to a range of conditions from fatty liver (reversible, due to acute ingestion) to cirrhosis (irreversible). 15–20% of heavy drinkers develop alcoholic cirrhosis
2. Chronic hepatitis B or C infections– next most common causes
3. Drugs (acetaminophen toxicity, methotrexate)
4. Autoimmune hepatitis
5. Primary Biliary Cirrhosis (PBC), Secondary biliary cirrhosis
6. Inherited metabolic diseases (hemachromatosis, Wilson's disease)
7. Hepatic congestion secondary to right–sided heart failure, constrictive pericarditis
8. Alpha–1 antitrypsin deficiency (also causes emphysema)
9. hepatic veno–occlusive disease– can occur after a bone marrow transplantation
10. Non–alcoholic steatohepatitis (NASH)

Front 422

Clinical features of cirrhosis

Back 422

1. some patients have no overt clinical findings, especially early in the disease
2. patients may have signs or symptoms suggestive of one or more of the complications of cirrhosis (portal hypertension, varices, ascites, hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis (SBP), hyperestrinism, Coagulopathy, Hepatocellular carcinoma (HCC)

Front 423

Treatment of portal hypertension

Back 423

TIPS – transjugular intrahepatic porto–systemic shunt

Hint 423

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Front 424

Esophageal varices
1. evaluation
2. clinical features
3. treatment

Back 424

1. variceal hemorrhage has a high mortality rate. patients with cirrhosis should be evaluated to document the presence of varices and risk of hemorrhage–– if present prophylactic measures should be taken such as non–selective beta blocker
2. massive hematemesis, melena, and exacerbation hepatic encephalopathy.
3. Fluids to maintain BP. IV abx prophylactically. IV octreotide is initiated and and continued for 3–5 days. Perform emergent upper GI endoscopy once the patient is stabilized for diagnosis and treatment of hemorrhage either with variceal band ligation or sclerotherapy. Give beta blockers in the long term to prevent re–bleeding
– rectal hemorrhoids and caput medusae (distension of abdominal wall vessels are also possible)

Hint 424

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Front 425

Ascites
1. definition
2. clinical features
3. diagnosis
4. treatment

Back 425

1. accumulation of fluid in the peritoneal cavity due to portal HTN – increased hydrostatic pressure and hypoalbuminemia – decreased oncotic pressure
2. abdominal distention, shifting dullness, and fluid wave
3. abd ultrasound can detect as little as 30 mL of fluid. Diagnostic paracentesis determines whether ascites is due to portal HTN or another process–– indications include new onset ascites, worsening ascites or suspected spontaneous bacterial peritonitis
4. treatment– bed rest, low sodium diet, and diuretics (furosemide and spironolactone), perform therapeutic paracentesis if tense ascites, shortness of breath or early satiety present. Peritoneovenous shunt or TIPS to reduce portal HTN

Hint 425

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Front 426

Hepatic encephalopathy
1. cause (build up of?)
2. how prevalent in cirrhosis?
3. precipitants?

Back 426

1. toxic metabolites (there are many but ammonia is believed to be the most important)–– normally detoxified by the liver– accumulates and reaches the brain
2. occurs in 50% of cirrhosis to varying extent
3. alkalosis, hypokalemia (due to diuretics), sedating drugs (narcotics, sleep meds), systemic infection and hypovolemia

Front 427

Hepatic encephalopathy
1. clinical features
2. treatment

Back 427

1. decreased mental function, confusion, poor concentration, even stupor or coma.
– asterexis – "flapping tremor"– have the patient extend arms and dorsiflex the hands – not specific
– rigidity, hyperreflexia
– fetor hepaticus–– musty odor of breath
2. lactulose – prevents absorption of ammonia– metabolism of lactulose by bacteria in the colon favors formation of NH4+, which poorly absorbed from the GI tract–– thereby promoting excretion of ammonia
– neomycin – antibiotic– neomycin – kills bowel flora, so decreases ammonia production by intestinal bacteria
– diet: limit protein to 30–40 g/day

Front 428

Hepatorenal syndrome
1. what is it indicative of?
2. definition
3. precipitants
4. clinical features
5. treatment

Back 428

1. indicates end–stage liver disease
2. progressive renal failure in advanced liver disease, secondary to renal hypoperfusion resulting from vasoconstriction of renal vessels
– this is a functional renal failure– kidneys are normal in terms of morphology, and no specific causes of renal dysfunction are evident. Does not respond to volume expansion
3. precipitated by infection or diuretics
4. clinical features– azotemia (inc BUN), oliguria, hyponatremia, hypotension, low urine output (<10 mEq/L)
5. Liver transplantation is the only cure–– in general the prognosis is very poor, and the condition is usually fatal without liver transplant

Front 429

Spontaneous Bacterial Peritonitis (SBP)
1. definition
2. etiologic agents
3. clinical features
4. diagnosis
5. treatment

Back 429

1. infected ascitic fluid, occurs in up to 20% of patients hospitalized for ascites
– usually occurs in patients with ascites caused by end–stage liver disease–– associated with a high mortality – 20–30%
– high recurrence rate – up to 70% in the first year
2. e. coli (most common), klebsiella, strep pneumo
3. clinical features– abd pain, fever, vomiting, rebound tenderness, may lead to sepsis
4. diagnosis established by paracentesis and examination of ascitic fluid for WBCs (esp PMNs), gram stain with culture and sensitivities (WBC > 500, PMN >250)
– positive ascites culture – culture negative SBP is common as well
5. treatment0 broad spectrum antbiotics– give specific antibiotic therapy once the organism is identified. clinical improvement should be seen in 24–48 hours.
– repeat paracentesis in 2–3 days to document decrease is ascitic fluid PMN (<250)

Front 430

Hyperestrinism is liver failure/cirrhosis

Back 430

1. spider angiomas– dilated cutaneous arterioles with central red spot and reddish extensions that radiate outward like a spider's web
2. palmar erythema
3. gynecomastia
4. testicular atrophy

Hint 430

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Front 431

Coagulopathy secondary to liver failure
1. cause – what is elevated in terms of clotting tests?
2. treatment

Back 431

decreased clotting factors– prolonged PT (prothrombin time)––liver uses vitamin K to synthesize clotting factors in this pathway (II, VII, IX, X). PTT may be prolonged in severe disease
– vitamin K is ineffective in treatment because it cannot be used by a diseased liver
2. treatment – fresh frozen plasma (FFP)

Front 432

signs of acute liver failure

Back 432

– coagulopathy
– jaundice
– hypoglycemia (liver stores glycogen)
– hepatic encephalopathy
– infection
– elevated LFTs
– any complication associated with cirrhosis

Front 433

What should you look for in diagnosing SBP?

Back 433

– fever and change in mental status in a patient with ascites
– if not treated early the mortality is high– so always be suspicious in a patient with ascites and do the diagnostic paracentesis early

Front 434

Wilson's disease
– deficiency of what?
– inheritance pattern?
– build up of?
– when diagnosed typically?

Back 434

1. autosomal recessive disease of copper metabolism
– normally excess copper is excreted by the liver, but the liver of patients with wilson's disease cannot do so because there is usually a deficiency in ceruloplasmin– a copper biding protein necessary for copper excretion
– copper accumulates in hepatocytes causing them to die
– copper leaks into plasma and accumulates in other organ including kidney, cornea and brain
– most often apparent during childhood/adolescence (after age 5) and the majority of cases is present between 5 to 35
–– picture is of a Kayser–Fleischer ring–– build up of copper in the cornea– –does not interfere with vision

– also known as hepatolenticular disease as it effects the liver and brain

Hint 434

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Front 435

Clinical features of Wilson's disease

Back 435

1. liver disease (most common initial manifestation)– varies but may include acute hepatitis, cirrhosis, and/or fulminant liver failure
2. Kayser–Fleisher rings– yellowish rings in the cornea caused by copper deposition–– does not interfere with vision
3. CNS findings–– extrapyramidal signs (EPS)– parkinsonian symptoms (resting tremor, rigidity, bradykinesia), chorea, drooling, incoordination due to copper deposition in the basal ganglia
– psychiatric disturbances–– depression, neuroses, personality changes, psychosis
4. Renal involvement– aminoaciduria, nephrocalcinosis

Hint 435

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Front 436

Diagnosis of Wilson's disease

Back 436

1. hepatic disease– elevated LFTs, impaired synthesis of clotting factors and albumin
2. decreased ceruloplasmin levels–– although levels within the normal range do not exclude the diagnosis
3. liver biopsy– inc copper conc
4. if diagnosed first degree relatives must be screened

Hint 436

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Front 437

Treatment of Wilson's disease

Back 437

1. Chelating agents – D–penicillamine– removes and detoxifies the excess copper deposits
2. Zinc – prevents uptake of dietary copper. Given alone to presymptomatic or pregnant patients or in conjuction with chelating agents in symptomatic patients
3. Liver transplantation – if unresponsive to therapy or fulminant liver failure
4. monitor patient's copper levels, urinary copper excretion, ceruloplasmin, and liver function– physical examination for signs of liver or neurologic disease, psych health

Front 438

Hemochromatosis
1. cause
2. involved organs
3. secondary hemochromatosis

Back 438

1. autosomal recessive disease of iron absorption
– excessive iron absorption in the intestine leads to accumulation of iron (as ferritin and hemosiderin) in various organs. Over many years, fibrosis in the involved organs occurs secondary to hydoxyl free radicals that are generated by excess iron
2. affected organs –– liver (primary organ) , pancreas, heart, skin, joints, thyroid, gonads, hypothalamus

– secondary hemochromatosis can also occur with multiple transfusions or in chronic hemolytic anemias

Hint 438

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Front 439

Hepatocellular Adenoma
1. definition
2. risk factors
3. symptoms
4. malignant potential
5. Diagnosis
6. Treatment

Back 439

Benign liver tumor– most often seen in young women (15–40 years of age)
2. Risk factors include OCP use, female sex, and anabolic steroid use
3. May be asymptomatic or can have RUQ pain and fullness
4. Malignant potential is low (<1%), however the adenoma may rupture– leading to hemoperitoneum and hemorrhage
5. Dx by CT scan, US, hepatic arteriography (most accurate but invasive)
6. Treatment– discontinue OCPs. surgically resect tumors >5cm that do not regress after stopping OCPs due to risk of rupture

Front 440

Cavernous Hemangiomas
1. definition
2. symptoms
3. complications
4. diagnosis
5. treatment

Back 440

1. vascular tumors that are usually small and asymptomatic. Most common type of benign liver tumor.
2. As the size of the tumor increases (e.g. due to pregnancy or OCP use) the sx increase and may include RUQ pain and mass
3. Complications are uncommon unless the tumor is very large and may include rupture with hemorrhage, obstructive jaundice, coagulopathy, CHF secondary to large AV shunt and gastric outlet obstruction
4. Diagnose with US or CT with contrast. Biopsy is C/I due to risk of rupture
5. Most cases do not require treatment

Hint 440

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Front 441

Focal Nodular Hyperplasia
1. definition
2. symptoms
3. Treatment

Back 441

1. benign liver tumor without malignant potential that occurs in women of reproductive age. No association with OCPs!!
2. Usually asymptomatic although hepatomegaly may be present.
3. Treatment not necessary in most cases

Hint 441

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Front 442

3 types of benign liver tumors

Back 442

1. Hepatocellular Adenoma
2. Cavernous Hemangioma
3. Focal Nodular Hyperplasia

Front 443

Hepatocellular Carcinoma
1. prevalence& where is it common
2. 2 pathologic types

Back 443

1. HCC – 80% of primary liver cancers–– common in Africa and Asia although rare in U.S.
2. Nonfibrolamellar (most common) – assoc with Hep B, C amd cirrhosis– usually unresectable and with a very short survival time (months)
– fibrolamellar– usually not assoc with hep b,c or cirrhosis– usually resectable with a longer survival time– most common in adolescents and you adults

Hint 443

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Front 444

Risk factors for hepatocellular carcinoma

Back 444

1. Cirrhosis– especially in association with alcohol or hepatitis B or C– HCC develops in 10% of cirrhotic patient
2. chemical carcinogens– aflatoxin, vinyl chloride, thorotrast
3. Alpha–1–antitrypsin (AAT) deficiency
4. Hemachromatosis, Wilson's disease
5. Schitosomiasis
6. Hepatic ademona (10% risk of malignant transformation)
7. cigarette smoking
8. glycogen storage disease (type 1)

Front 445

Clinical features of hepatocellular carcinoma

Back 445

1. abdominal pain (painful hepatomegaly)
2. weight loss, anorexia, fatigue
3. signs and symptoms of chronic liver disease– portal HTN, ascites, jaundice
4. paraneoplastic syndromes– erythrocytosis, thrombocytosis, hypercalcemia, carcinoid syndrome, hypertrophic pulmonary osteodystrophy, hypoglycemia, high cholesterol

Front 446

Diagnosis of Hepatocellular Carcinoma

Back 446

1. Liver biopsy– required for definitive diagnosis
2. lab tests– hep B and C serology, LFTs, coags
3. Imaging studies– US, CT chest, abd, pelvis, MRI or MRI if surgery is an option
4. tumor marker elevation– AFP (alpha fetaprotein) is a useful screen tool as AFP may be elevated in 40–70% of patients with HCC– also helps monitor response to therapy

Front 447

Treatment and prognosis of Hepatocellular Carcinoma (HCC)

Back 447

1. Liver resection (in 10% of patients who have resectable tumors)– liver regenerates
2. Liver transplant if diagnosis is made early

Prognosis– If unresectable– less than 1 year, if resectable then 25% of patients are alive at 5 years

Front 448

What should you suspect in patients with cirrhosis and a palpable liver mass + inc AFP?

Back 448

hepatocellular carcinoma

Front 449

Nonalcoholic Steatohepatitis (NASH)
1. definition
2. associations
3. symptoms
4. how discovered?
5. treatment

Back 449

1. histology of the liver is identical to that in patients with alcoholic liver disease but these patients do not have a history of alcohol disease
2. associated with obesity, hyperlipidemia, diabetes mellitus
3. usually asymptomatic with a benign course (but cirrhosis develops in 10–15%)
4. Typically discovered on routine laboratory tests (mild elevation in ALT and AST)
5. No clearly established treatment

Front 450

Gilbert's syndrome
1. what is it?
2. what lab test is abn?
3. what are exacerbating factors?
4. how usually discovered/symptoms
5. treatment

Back 450

1. occurs in up to 7% of the population – autosomal dominant condition in which there is decreased activity of hepatic UGT)
2. common cause of isolated elevation of unconjugated bilirubin
3. exacerbated by fasting (crash diets), fever, alcohol, and infection
4. asymptomatic in most cases but occasionally mild jaundice maybe present
5. liver biopsy results are normal and usually no treatment is necessary

Front 451

Hemobilia
1. definition
2. causes
3. clinical features
4. diagnosis
5. treatment

Back 451

1. blood draining into the duodenum via the common bile duct– source of bleeding can be anywhere along the biliary tract, the liver or the ampullary region
2. causes– trauma (most common), papillary thyroid carcinoma, surgery (cholecystectomy), CBD exploration, tumors, infection
3. GI bleeding (melena, hematemesis), jaundice, and RUQ pain
4. Arteriogram is diagnostic– Upper GI endoscopy shows blood coming out of the ampulla of vater
5. treatment– resuscitation (may require transfusion)– if bleeding is severe, surgery is necessary (options include ligation of hepatic arteries, or arteriogram with embolization of vessels)

Front 452

Polycystic Liver Cysts
1. cause/inheritance
2. symptoms
3. treatment

Back 452

1. autosomal dominant– usually associated with polycystic kidney disease. PCKD often results in renal failure and is the main determinant of prognosis whereas liver cysts rarely lead to hepatic fibrosis and liver failure
2. usually asymptomatic, although some patients have abd pain and upper abd mass
3. treatment is usually not needed

Front 453

Hydatid Liver Cysts
1. cause
2. symptoms
3. treatment

Back 453

1. caused by infection from the tapeworm, Echinococcus granulosus. Cysts most commonly occur in the right lobe of the liver
2. small cysts are asymptomatic, larger cysts may cause RUQ pain and rupture into the peritoneal cavity causing fatal anaphylactic shock
3. Treatment– surgical resection (caution to avoid spilling cyst contents into peritoneal cavity). Give mebendazole after surgery

Front 454

Pyogenic Liver Abscess
1. most common cause
2. causative organisms
3. clinical features
4. diagnosis
5. treatment

Back 454

1. most common cause is biliary tract obstruction– obstruction of bile flow allows bacterial proliferation. Other causes include GI infection (diverticulitis, appendicitis) with spread via portal venous system and penetrating liver trauma (GSW, surgery)
2. Causative organisms include E. coli, Klebsiella, enteroccus, and anaerobes
3. fever, malaise, anorexia, weight loss, nausea, vomiting, RUQ pain, and jaundice– patients appear quite ill
4. Diagnosed by ultrasound or CT scan, elevated LFTs
5. fatal if untreated. Treatment (IV antibiotics and percutaneous drainage of abscess) reduces mortality to about 5–20%. Surgical drainage is sometimes necessary

Front 455

Amebic liver abscess
1. who is it most common in? transmission?
2. cause?
3. symptoms
4. diagnosis
5. treatment

Back 455

1. Most common in men (9:1), particularly in homosexual men, transmitted through fecal–oral contact
2. caused by intestinal amebiasis (entamoeba histolytica)– the amoebea reach the liver via the hepatic portal vein
3. fever, RUQ pain, nausea/vomting, HSM, diarrhea
4. serological testing (IgG enzyme immunoassay) establishes diagnosis, LFTs are often elevated. The E. histolytica antigen test (detects protozoa in stool) – not sensitive. Imaging studies (US, CT) identify abscess, but it is difficult to distinguish from pyogenic abscess
4. IV metronidazole is effective treatment in most cases. Therapeutic aspiration of abscess may be necessary if the abscess is large (high risk of rupture) or there is no response to medical therapy

Hint 455

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Front 456

Budd–Chiari Syndrome
1. definition
2. course
3. causes
4. clinical features
5. dx
6. tx

Back 456

1. Liver disease caused by occlusion of the hepatic venous outflow, which leads to hepatic congestion and subsequent microvascular trauma
2. course is variable, but most cases are indolent, with gradual development of portal HTN and progressive deterioration of liver function. Rarely disease is severe and leads to acute liver failure
3. causes– hypercoaguable states, myeloproliferative disorders (polycythemia vera), pregnancy, chronic inflammatory diseases, infection, various cancers, trauma. Idiopathic 40%
4. resemble those of cirrhosis– hepatomegaly, jaundice, ascites, abd pain, variceal bleeding
5. dx– hepatic venography, serum ascites albumin gradient > 1.1 g/dL
6. tx– medical tx is usually unsatisfactory (anticoagulation, thrombolytics, diuretics). Surgery is eventually needed in most cases (balloon angioplasty with stent placement in inferior vena cava, portocaval shunts). liver transplant if cirrhosis is present

Front 457

Jaundice
1. definition
2. when evident? at what level?
3. conjugated vs unconjugated bilirubin

Back 457

1. yellow coloration of skin, mucous membranes, and sclerae due to overproduction or underclearance of bilirubin
2. clinical jaundice usually becomes evident when total bilirubin is > 2 mg/dL
3. conjugated (direct) bilirubin– loosely bound to albumin and therefore water soluble– gets excreted in the urine causing it to look dark. Nontoxic.
– unconjugated (indirect) bilirubin– tightly bound to albumin and therefore not water soluble and cannot be excreted in the urine even when blood levels are high. Toxic unbound form can cross the blood–brain barrier and cause neuro deficits

Front 458

Causes of conjugated hyperbilirubinemia

Back 458

1. decreased intrahepatic excretion of bilirubin
– hepatocellular disease (viral or alcoholic hepatitis, cirrhosis)
– inherited disorders (Dubin–Johnson syndrome, Rotor's syndrome)
– drug induced (OCPs)
– Primary biliary cirrhosis (PBC)
– primary sclerosis cholangitis (PSC)

2. extrahepatic biliary obstruction
– gallstones
– carcinoma in the head of the pancreas
– cholangiocarcinoma
– periampullary tumors
– extrahepatic biliary atresia
–

Front 459

Causes of unconjugated hyperbilirubinemia

Back 459

1. Excess production of bilirubin– hemolytic anemias
2. Reduced hepatic uptake of bilirubin or impaired conjugation
– Gilbert's syndrome
– drugs – (sulfonamides, penicillin, rifampin, radiocontrast agents)
– Crigler Najjar syndrome type I and type II
– physiologic jaundice of the newborn– immaturity of conjugating system
– diffuse liver disease (hepatitis, cirrhosis)

Front 460

Diagnosis and treatment of hyperbilirubinemia

Back 460

1. serum levels of conjugated and unconjugated bilirubin
2. if unconjugated hyperbilirubinemia – check a CBC, reticulocyte count, hemoglobin, LDH, and peripheral smear (may aid in the diagnosis of hemolysis as the cause of jaundice)
3. if conjugated hyperbilirubinemia–– LFTs may point to the cause
4. US or CT to assess biliary tract for obstruction or anatomic changes
5. additional tests (Endoscopic Retrograde Cholangiopancreatography – ERCP) or percutaneous transhepatic cholangiography– depending on findings of above
6. liver biopsy may be indicated in some cases to determine cause of injury

–treatment– treat the underlying cause. May want to give cholestyramine– bile acid sequestrant

Front 461

Liver Function Tests
1. what are they? What is most sensitive and specific for liver disease?
2. what indicates alcohol as a cause?
3. mild elevation indicates?
4. moderate elevation indicates?
5. severe elevation indicates?
6. what if patient has cirrhosis?

Back 461

1. Aminotransferases – ALT and AST
– ALT is more sensitive and specific than AST for liver damage
2. ALT and AST usually have a similar increase with the exception being alcoholic hepatitis – in which the AST–ALT ratio may be > 2:1
3. if ALT and AST levels are mildly elevated (low hundred) think of chronic viral hepatitis or acute alcoholic hepatitis
4. If ALT and AST are moderately elevated (high hundreds to 1000s) – think of acute viral hepatitis
5. if ALT and AST are severely elevated (>10,000) – extensive hepatic necrosis has occurred. Typical causes include– ischemia, shock liver (prolonged hypotension or circulatory collapse), acetaminophen toxicity, severe viral hepatitis
6. NOTE: liver transaminases are often normal or even low in patients with cirrhosis (without any active cell necrosis) or metastatic liver disease because the number of functioning hepatocytes is markedly reduced

Front 462

What are potential causes of elevated ALT and AST?

Back 462

A– Autoimmune hepatitis
B– hepatitis B
C– hepatitis C
D– drugs or toxins
E– Ethanol
F– fatty liver (hypertriglyceridemia)
G– growths (tumors)
H– hemodynamic disorders (e.g. CHF)
I– Iron– hemochromatosis, Copper (wilson's disease) or AAT deficiency

Front 463

Alkaline Phosphatase (ALK–P)
1. what does it measure?
2. what if levels are very high (10 fold increase)?
3. What should you also measure with this?

Back 463

– Not specific to liver– also found in bone, gut, and placenta
1. ALK–Phos is elevated when there is an obstruction of bile flow (e.g. cholestasis) in any part of the biliary tree. Normal levels make cholestasis unlikely
2. If levels are very high (10–fold increase), think of extrahepatic biliary tract obstruction or intrahepatic cholestasis (e.g. PBC or drug induced cirrhosis)
3. If levels are elevated, measure GGT (gamma–glutamyl–transferase) level to make sure the elevation is hepatic in origin (rather than bone or intestinal). If the GGT is also elevated, this strongly suggests a hepatic origin. If the GGT level is normal, but ALK–P is elevated, consider pregnancy or bone disease

Front 464

What can cause a decreased albumin level?

Back 464

– chronic liver disease
– nephrotic syndrome
– malnutrition
– inflammatory states (burns, sepsis, trauma)

Front 465

Prothrombin time (PT)

Back 465

The liver synthesizes clotting factors I, II, V, VII, IX, X, XII and XIII–– the function of which is reflected by PT
– PT is not prolonged until most of the liver's synthetic capacity is lost– which corresponds to advanced liver disease

Front 466

Cholelithiasis
1. definition
2. 3 types

Back 466

1. refers to stones in the gallbladder (gallstones)
2. There are 3 types of stones – a. cholesterol stones (yellow to green)– associated with: obesity, diabetes, and hyperlipidemia, multiple pregnancies, OCPs, Crohn's disease, ileal resection, advanced age, Native American ancestry, cirrhosis, cystic fibrosis
b. Pigment stones– black stones are usually found in the gallbladder and are associated with either hemolysis (e.g. sickle cell disease, thalassemia, hereditary spherocytosis, artificial cardiac valves) or alcoholic cirrhosis.
– brown stones are usually found in the bile ducts and are associated with biliary tract infections
c. Mixed stones have components of both cholesterol and pigment stones and account for the majority of stones

Front 467

Clinical features of cholelithiasis

Back 467

– most cases are asymptomatic. Majority of patients found to have incidental gallstones will remain asymptomatic.
– biliary colic is the cardinal symptom of gallstones and is due to temporary obstruction of the cystic duct by a gallstone. Pain occurs as the gallbladder contracts against this obstruction.
– pain is typically located in the RUQ or epigastrium and may be mild, moderate, or severe
– patients classically report pain after eating and at night
– Boas' sign – referred right scapular pain of biliary colic

Front 468

Diagnosis of cholelithiasis

Back 468

1. RUQ ultrasound has high sensitivity and specificity (>95%) for stones > 2 mm.
2. CT and MRI are alternatives

Hint 468

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Front 469

Treatment of cholelithiasis

Back 469

1. No treatment if the patient is asymptomatic
2. Elective cholecystectomy for patients with recurrent bouts of biliary colic

Front 470

Complications of cholelithiasis

Back 470

1. cholecystitis (chronic or acute) with prolonged obstruction of cystic duct
2. choledocholithiasis with its associated complications
3. gallstone ileus– lack of peristalsis
4. malignancy

Front 471

What fraction of patients with biliary colic will develop acute cholecystitis within 2 years?

Back 471

1/3

Front 472

What causes the pain in acute cholecystitis? biliary colic?

Back 472

Pain in acute cholecystitis is secondary to gallbladder wall inflammation, whereas the pain of biliary colic is secondary to contraction of the gallbladder against an obstructed cystic duct. The pain of acute cholecystitis persists for several days, whereas the pain of biliary colic lasts only a few hours.

Front 473

Acute cholecystitis
1. definition/cause
2. chronic cholecystitis?
3. what percent of patients with gallstones will develop this?

Back 473

1. obstruction of the cystic duct (not infection) induces acute inflammaion of the gallbladder wall
2. chronic cholecystitis may develop with recurrent bouts of acute cholecystitis
3. 10% of patients with gallstones will develop acute cholecystitis

Front 474

Symptoms of acute cholecystitis?

Back 474

– pain is always present and is located in RUQ or epigastrium. It may radiate to the right shoulder or scapula
– nausea and vomiting, anorexia

Front 475

Signs of acute cholecystitis on exam?

Back 475

– RUQ tenderness, rebound tenderness in RUQ
– Murphy's sign is pathognomonic– inspiratory arrest during deep palpation of the RUQ, not present in many cases (if this happens with US–– it is called a sonographic Murphy's)
– Hypoactive bowel sounds
– low–grade fever, leukocytosis

Front 476

Diagnosis of acute cholecystitis?

Back 476

1. RUQ ultrasound is the test of choice– high sensitivity and specificity. Findings include thickened gallbladder wall and pericholecystic fluid, distended gallbladder, and presence of stone(s)
2. CT scan is as accurate as ultrasound but is more sensitive in identifying complications of acute cholecystitis such as perforation, abscess and pancreatitis
3. Radionucleotide scan (hepatoiminodiacetic acid– HIDA)
– used when US is inconclusive. Its sensitivity and specificity parallel that of US. If HIDA is normal, acute cholecystitis can be ruled out.
– A positive HIDA scan means the gallbladder is not visualized
– If gallbladder is not visualized 4 hours after injection, diagnosis of acute cholecystitis is confirmed

Hint 476

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Front 477

Treatment of acute cholecystitis

Back 477

1. patient should be admitted. Conservative measures include hydration with IV fluids, bowel rest (NPO), IV antibiotics, analgesics and correction of any electrolyte abnormalities
2. surgery– cholecystectomy is indicated in most patients with symptomatic gallstones. Early cholecystectomy is preferred (first 24 to 48 hours). Recurrence rate with nonsurgical treatment is as high as 70%. Timing of surgery depends on the severity of the symptoms and patients risk assessment for surgery, but in most patients, early cholecystectomy is preferred.

Front 478

Acalculous Cholecystitis
1. what is it?
2. cause/associations?
3. signs and symptoms?
4. diagnosis
5. treatment

Back 478

1. Acute cholecystitis without stones obstructing the cystic duct (up to 10% of the patients with acute cholecystitis)
2. usually idiopathic and seen in patients with severe underlying illness; possible association with dehydration, ischemia, burns, severe trauma, and post–operative state
3. signs and symptoms are the same as acute cholecystitis
4. diagnosis may be difficult because patients with this condition are often severely ill and have other medical problems, so clinical features are less apparent
5. emergent cholecystectomy is the treatment of choice. For patients who are too ill for surgery, perform percutaneous drainage of the gallbladder with cholecystostomy

Front 479

Choledocholithiasis
1. definition
2. primary vs secondary stones?

Back 479

1. gallstones in the common bile duct (CBD)
2. primary versus secondary stones. Primary stones originate in the CBD (usually pigmented stones), Secondary stones originate in the gallbladder and then pass into the CBD (usually cholesterol or mixed stones).
– 95% of CBD stones are secondary

Hint 479

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Front 480

Clinical features of choledocholithiasis

Back 480

1. patients may be asymptomatic for years
2. symptoms when present include RUQ pain or epigastric pain and jaundice

Front 481

Diagnosis of choledocholithiasis

Back 481

1. laboratory tests– total and direct bilirubin levels are elevated as well as alk–phos
2. RUQ US is usually the initial study, but is not a sensitive study for choledocholithiasis. It detects CBD stones in only 50% of the cases, so it cannot be used to rule out the diagnosis.
3. ERCP (endoscopic retrograde cholangiopancreatography) is the gold standard (sensitivity and specificity is 95%) and should follow US. ERCP is diagnostic and therapeutic.
4. PTC (percutaneous transhepatic cholangiography) is an alternative to ERCP

Hint 481

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Front 482

Treatment of choledocholithiasis

Back 482

1. ERCP with sphincterotomy and stone extraction with stent placement (successful in 90% of patients)
2. laparoscopic choledocholithotomy (in select cases)

Front 483

Cholangitis
1. definition and causes
2. treatment

Back 483

1. infection of the biliary tract secondary to obstruction, which leads to biliary stasis and bacterial overgrowth
– choledocholithiasis accounts for 60% of cases
– other causes include pancreatic and biliary neoplasm, postoperative strictures, invasive procedures such as ERCP or PTC and choledochal cysts
2. cholangitis is a potentially life–threatening illness and requires emergency treatment

Front 484

Clinical features of cholangitis

Back 484

1. Charcot's triad– RUQ pain, jaundice and fever–– this classic triad is present in only 50–70% of cases
2. Reynold's pentad– charcot's triad plus septic shock and altered mental status (CNS depression–– e.g. coma, disorientation)
3. patient is acutely ill, and abdominal symptoms may be lacking or may go unrecognized

Front 485

Diagnosis of cholangitis
1. initial study
2. lab findings
3. cholangiography options (2)– when would you choose each?

Back 485

1. RUQ ultrasound is the initial study
2. laboratory findings– hyperbilirubinemia, leukocytosis, mild elevation in serum transaminases
3. cholangiography (either PTC or ERCP)
– this is the definitive test, but it should not be performed during the acute phase of the illness.
– Once cholangitis resolves, proceed with PTC or ERCP to identify the underlying problem and plan treatment
– perform PTC when the duct system is dilated (per US) and ERCP when the duct system is normal

Hint 485

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Front 486

Treatment of cholangitis

Back 486

1. IV antibiotics and IV Fluids
– close monitoring of hemodynamics, BP, urine output (UOP),
2. Most patients respond rapidly. Once the patient has been afebrile for 48 hours then proceed with cholangiography (PTC or ERCO) for evaluation of the underlying condition
3. decompress the CBP via PTC (catheter drainage), ERCP (sphincterotomy) or laparotomy (T–tube insertion) once the patient is stabilized, or emergently if the condition does not respond to antibiotics

Hint 486

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Front 487

Carcinoma of the gallbladder
1. what type are they most often and who do they occur in?
2. associations/ risk factors
3. clinical features
4. treatment
5. prognosis

Back 487

1. most are adenocarcinomas. Typically occur in the elderly
2. associated with gallstones in most cases, other risk factors include cholecystoenteric fistula and porcelain gallbladder
3. Clinical features are non–specific and suggest extrahepatic bile duct obstruction: jaundice, biliary colic, weight loss, anorexia, and RUQ mass. Palpable gallbladder is a sign of advanced disease.
4. difficult to remove with surgery: cholecystectomy versus radical cholecystectomy (with wedge resection of liver and lymph node dissection) depending on the depth of invasion
5. prognosis is dismal – more than 90% of patients die of advanced disease within 1 year of diagnosis. Disease often goes undetected until it is advanced.

Front 488

Primary Sclerosing Cholangitis (PSC)
1. definition/general characteristics
2. associations

Back 488

1. a chronic idiopathic progressive disease of intrahepatic and/or extrahepatic bile ducts characterized by thickening of the bile duct walls and narrowing of their lumens, leading to cirrhosis, portal hypertension and liver failure
2. their is a strong association with ulcerative colitis (less so with Crohn's disease). UC is present in 50–70% with PSC, often the UC may dominate the clinical picture. (NOTE– the course of PSC is unaffected by colectomy done for UC)

Front 489

Clinical features of primary sclerosing cholangitis (PSC)

Back 489

– signs and symptoms begin insidiously
– chronic cholestasis findings, including jaundice and pruritis; all patients eventually present with chronic obstructive jaundice
– other symptoms: fatigue, malaise and weight loss

Front 490

Diagnosis of primary sclerosing cholangitis

Back 490

1. ERCP and PTC are diagnostic studies of choice– see multiple area of bead–like stricturing and dilations of the intrahepatic and extrahepatic ducts
2. laboratory tests show cholestatic LFTS– inc LFTs plus inc direct bili, plus inc alk–phos

Hint 490

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Front 491

treatment of primary sclerosing cholangitis

Back 491

1. there is no curative treatment other than liver transplantation
2. when a dominant stricture causes cholestasis, ERCP with stent placement for biliary drainage and bile duct dilitation may relieve symptoms
3. use cholestyramine for symptomatic relief (to decrease pruritis) – bile acid sequestant that binds to it and prevents it from being reabsorped. The insoluble compound is then excreted in the feces

Front 492

Primary Biliary Cirrhosis (PBC)
1. definition – what is affected?
2. course?
3. cause?
4. who is most often affected?

Back 492

1. chronic and progressive cholestatic liver disease characterized by destruction of the intrahepatic bile ducts with portal inflammation and scarring
2. it is a slowly progressive disease with a variable course. It may progress to cirrhosis and end–stage liver failure
3. It is an autoimmune disease that is often associated with other autoimmune disorders
4. most common in middle–aged women

Hint 492

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Front 493

Clinical features of primary biliary cirrhosis (PBC)

Back 493

1. fatigue
2. pruritus (early in the course of the disease)
3. jaundice (late in the course)
4. RUQ discomfort
5. xanthoma and xanthalesmata (cholesterol deposits)
6. osteoporosis
7. portal HTN (with resultant sequelae)

Hint 493

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Front 494

Diagnosis of Primary Biliary Cirrhosis (PBC)
1. labs
2. biopsy findings
3. Imaging

Back 494

1. labs– cholestatic LFTs (inc alk phos)
2. positive anti–mitochondrial antibodies (AMAs) found in 90% to 95% of patients. This is the hallmark of the disease (specificity of 98%). If serum is positive for AMAs, perform a liver biopsy to confirm diagnosis
3. abd US or CT scan to rule out biliary obstruction

Front 495

Cholangiocarcinoma
1. definition
2. mean age of diagnosis?
3. 3 regions affected– what is most common?
4. prognosis
5. risk factors

Back 495

1. tumor of the intrahepatic and extrahepatic bile ducts: most are adenocarcinomas
2. mean age of diagnosis is in the 7th decade
3. Located in three regions: proximal third of the CBD (most common, also called Klatskin's tumor), distal extrahepatic (best change of resectability), intrahepatic (least common)
4. prognosis is dismal– survival is less than 1 year after diagnosis
5. risk factors – ulcerative colitis, choledochal cysts, clonorchis sinesis (Chinese liver fluke) – hong kong

Hint 495

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Front 496

Clinical features of cholangiocarcinoma

Back 496

1. obstructive jaundice and associated symptoms (dark urine, clay–colored/acholic stools) and pruritis
2. weight loss

Front 497

Diagnosis of cholangiocarcinoma

Back 497

1. cholangiography (PTC or ERCP)– for diagnosis and assessment of resectability
2. If the patient has an unresectable tumor (more likely the case with proximal than distal bile duct tumors), stent placement is an option during either PTC or ERCP and may relieve biliary obstruction

Front 498

Treatment of cholangiocarcinoma

Back 498

1. most patients do have resectable tumors at the time of diagnosis
2. the survival rate is low despite aggressive chemotherapy, stenting or biliary drainage

Front 499

Choledochal cysts
1. definition and who is most likely to be affected?
2. clinical features?
3. complications
4. diagnosis
5. treatment

Back 499

1. cystic dilations of biliary tree involving either the extrahepatic or intrahepatic ducts or both–– more common in women (4:1)
2. clinical features: epigastric pain, jaundice, fever, and RUQ mass
3. Complications – cholangiocarcinoma (most feared complication– risk is about 20% over 20 years), hepatic abscess, recurrent cholangitis/pancreatitis, rupture, biliary obstruction, cirrhosis, and portal HTN
4. US is the best non–invasive test and ERCP is definitive for diagnosis
5. Treatment is surgery: complete resection of the cyst with biliary–enteric anastomosis to restore continuity of biliary system with the bowels

Hint 499

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Front 500

Bile Duct Stricture
1. causes–– what is most common?
2. clinical features?
3. complications?
4. treatment

Back 500

1. most common cause is iatrogenic injury (prior biliary surgery such as cholecystectomy, liver transplantation), other causes include recurring choledocholithiasis, chronic pancreatitis, and primary sclerosing cholangitis (PSC)
2. clinical features are those of obstructive jaundice
3. complications can be life–threatening and include– secondary biliary cirrhosis, liver abscess, and ascending cholangitis
4. treatment involves endoscopic stenting (preferred) or surgical bypass if obstruction is complete or if endoscopic therapy fails

Front 501

Biliary dyskinesia

Back 501

1. motor dysfunction of the spincter of Oddi, which leads to recurrent episodes of biliary colic without any evidence of gallstones on diagnostic studies such as US, CT, and ERCP
2. Diagnosis is made by HIDA scan (once the gallbladder is filled with labeled radionucleotide, give cholecystokinin (CCK) intravenously, then determine the EF of the gallbladder. If the EF is low, dyskinesia is likely.
3. Treatment options – laparoscopic cholecystectomy, endoscopic sphincterotomy

Hint 501

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Front 502

1. Pathogenesis of appendicitis
2. peak age of incidence

Back 502

a. The lumen of the appendix is obstructed by hyperplasia of lymphoid tissue (60% of cases), a fecalith (35% of cases), a foreign body, or other rare causes (parasite or carcinoid tumor)– 5% of cases
b. obstruction leads to stasis (of fluid and mucus), which promotes bacterial overgrowth leading to inflammation
c. distention of the appendix can compromise blood supply. The resulting ischemia can lead to infarction or necrosis if untreated. Necrosis can result in appendiceal perforation and ultimately peritonitis
2. peak incidence is in the teens to mid–20s. Prognosis is far worse in infants and elderly patients (high rate of perforation)

Front 503

Symptoms of acute appendicitis

Back 503

1. Abdominal pain– classically starts in the epigastrium as ill–defined pain, moves toward umbilicus, and then to RLQ. with distention of the appendix, the parietal peritoneum may become irritate, leading to sharp pain
2. anorexia always present. Appendicitis is unlikely if the patient is hungry
3. nausea and vomiting (typically follow pain)

Hint 503

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Front 504

Signs of acute appendicitis

Back 504

1. tenderness in RLQ (maximal tenderness at McBurney's point– 2/3 of the distance from the umbilicus to the right anterior superior iliac spine)
2. rebound tenderness, guarding, diminished bowel sounds
3. low grade fever (may spike if perforation is present)
4. Rovsing's sign– deep palpation in the LLQ causes referred pain in the RLQ
5. Psoas sign– RLQ pain when right thigh is extended as patient lies on left side
6. Obturator sign– pain in the RLQ when flexed right thigh is internally rotated when patient is supine

Hint 504

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Front 505

Diagnosis of acute appendicitis

Back 505

** Acute appendicitis is a clinical diagnosis. Laboratory findings (mild leukocytosis) are only supportive. Radiographs or other imaging studies re unnecessary unless the diagnosis is uncertain or the presentation is atypical
– CT scan (sensitivity of 98% to 100%)–– lowers the false positive rate significantly
– ultrasound (sensitivity of 90%)

Hint 505

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Front 506

Treatment of acute appendicitis
– risk of false positive?

Back 506

–appendectomy (usually laparoscopic)
– up to 20% of patients who are diagnosed with acute appendicitis are found to have a normal appendix during surgery. Because the illness is potentially life–threatening, this is an acceptable risk EVEN DURING PREGNANCY

Front 507

Carcinoid tumors and carcinoid syndrome
– origination and secretion?
– most common site?

Back 507

1. carcinoid tumors originate from neuroendocrine cells and secrete serotonin
2. the most common site for these tumors is in the appendix, but they can be found in a variety of locations (small bowel, rectum, bronchus, kidney and pancreas)

Front 508

Pathogenesis of acute pancreatitis

Back 508

1. Inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion

Front 509

2 forms of acute pancreatitis

Back 509

1. Mild – (75% have mild to moderate) – responds well to supportive treatment
2. severe (up to 25%)– necrotizing pancreatitis– significant morbidity and mortality

Front 510

Causes of acute pancreatitis

Back 510

1. alcohol abuse (40%)
2. Gallstones (40%) – the gallstone passes into the bile duct and blocks the ampulla of vater (where bile enters the duodenum)
3. post ERCP– pancreatitis occurs in up to 10% of patients undergoing ERCP
4. viral infections– mumps, Coxackie virus B
5. drugs – sulfonamides, thiazide diuretics, furosemide, estrogens, HIV meds etc
6. post–operative complication (high mortality rate)
7. scorpion bites
8. pancreas divisum (controversial)– congenital problem
9. pancreatic cancer
10. hypertriglyceridemia, hypercalcemia
11. uremia
12. blunt abdominal trauma – most common cause of pancreatitis in young children

(IGETSMASHED pneumonic)

Front 511

Symptoms of acute pancreatitis

Back 511

1. abdominal pain, usually in the epigastric region–– may radiate to the back (50% of patients)
– often steady, dull, and severe, worse when supine and after meals
2. nausea and vomiting, anorexia

Hint 511

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Front 512

Signs of acute pancreatitis

Back 512

1. low grade fever, tachycardia, hypotension, leukocytosis
2. epigastric tenderness, abdominal distention
3. decreased or absent bowel sounds indicate partial ileus
4. the following signs are seen with hemorrhagic pancreatitis as blood tracks along fascial planes
– grey turner's sign– flank ecchymoses
– cullen's sign– periumbilical ecchymoses (pictured)
– fox's sign– ecchymosis of the umbilical ligament

Hint 512

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Front 513

Diagnosis of pancreatitis – Labs
1. What labs should you order? What is most specific for acute pancreatitis?
2. prognostic predictors

Back 513

1. Lab tests
– serum amylase is the most common test– but many conditions cause hyperamalasemia (non–specific) and its absence does not rule out acute pancreatitis (non–sensitive) However, if levels are more than 5 times the upper limit of normal, there is a high specificity for acute pancreatitis
–– serum lipase – more specific for pancreatitis than amylase
2. LFTs – to identify cause (gallstone pancreatitis) – inc Alk phos
3. hyperglycemia, hypoxemia, and leukocytosis may also be present
4. Order the following to assess for prognosis (ranson's criteria) –– glucose, calcium, hematocrit, BUN, arterial blood gas (PaO2, base deficit), LDH, AST, WBC count

Hint 513

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Front 514

Why does hypocalcemia occur in acute pancreatitis?

Back 514

Due to fat saponification – fat necrosis binds calcium

Front 515

Diagnosis of acute pancreatitis – Imaging

Back 515

1. Abdominal xray– limited role in the diagnosis of acute pancreatitis
– more helpful in ruling out other diagnosis– such as intestinal perforation (free air). The presence of calcifications can suggest chronic pancreatitis.
– In some cases, one may see a sentinel loop (area of air–filled bowel usually in the LUQ, which is a sign of localized ileus) or colon cutoff sign (air–filled segment of the transverse colon abruptly ending or "cutting off" at the region of pancreatic inflammation
2. abdominal ultrasound– can help in identifying cause of pancreatitis – gallstone. Useful for following up pseudocysts or abscesses
3. CT scan of the abdomen– most accurate test for the diagnosis of acute pancreatitis and for identifying complications of the disease
– indicated in patients with severe acute pancreatitis
4. ERCP indications – severe gallstone pancreatitis with biliary obstruction, to identify uncommon causes of acute pancreatitis if disease is recurrent

Hint 515

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Front 516

Complications of acute pancreatitis

Back 516

1. Pancreatic necrosis (may be sterile or infected)
– sterile pancreatic necrosis – infection may develop, but half of all cases resolve spontaneously. These patients should be monitored closely in an ICU. Prophylactic antibiotics is controversial but if necrosis involves more than 30% of pancreas, antibiotics should be strongly considered
– infected pancreatic necrosis – high mortality rate (results in multiple organ failure in 50% of cases), surgical debridement and antibiotics indicated
– the only way to distinguish sterile from infected necrosis is via CT–guided percutaneous aspiration with gram stain/culture of the aspirate
2. pancreatic pseudocyst– encapsulated fluid collection that appears 2 to 3 weeks after an acute attack–– unlike a true cyst, it lacks an epithelial lining
– complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough or if located in the head of the pancreas– it may cause compression of the CBD
– diagnosis by CT scan = study of choice
– treatment – cysts > 5cm– drain either percutaneously or surgically, <5 cm – observation
3. hemorrhagic pancreatitis – characterized by cullen's sign, grey turner's sign, and fox's sign, CT Scan with IV contrast is the study of choice
4. Adult respiratory distress syndrome – a life–threatening complication with high mortality rate
5. pancreatic ascites/pleural effusion– the most common cause is inflammation of peritoneal surfaces
6. ascending cholangitis – due to gallstone in ampulla of vater, leading to infection of biliary tract
7. pancreatic abscess (rare) – develops over to 4–6 weeks and is less life–threatening than infected pancreatic necrosis

Front 517

pancreatic pseudocyst
1. what is it?
2. complications
3. diagnosis
4. treatment

Back 517

1. pancreatic pseudocyst– encapsulated fluid collection that appears 2 to 3 weeks after an acute attack–– unlike a true cyst, it lacks an epithelial lining
2. complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (duodenum, stomach, transverse colon) if large enough or if located in the head of the pancreas– it may cause compression of the CBD
3. diagnosis by CT scan = study of choice
4. treatment – cysts > 5cm– drain either percutaneously or surgically, <5 cm – observation

Hint 517

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Front 518

Treatment of mild acute pancreatitis

Back 518

mild pancreatitis treatment
– Bowel rest (NPO),
– IV fluids – patients may have severe intravascular volume depletion. Correct electrolyte abnormalities
– pain control – but be cautious in giving narcotics. Fentanyl and meperidine are preferred over morphine which causes an increase in sphincter of oddi pressure
– NG tube if severe nausea/vomiting or ileus present, routine use is controversial

Front 519

Treatment of severe acute pancreatitis

Back 519

If severe– patient should be admitted to the ICU. Early enteral nutrition in the first 72 hours is recommended through a nasojejunal tube.
– if the severe acute pancreatitis has not resolved in a few days, supplement parenteral nutrition should be started.
– if more than 30% of the pancreas is necrosed, prophylactic antibiotics (imipenem) should be considered to prevent infection (which has high morbidity and mortality)

Front 520

Prognosis of acute pancreatitis

Back 520

Ranson's criteria is used to determine prognosis and mortality rates
– patients with more than 3 or 4 of Ranson's criteria should be monitored in the ICU setting

Hint 520

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Front 521

Chronic pancreatitis
1. definition
2. what is impaired?
3. causes?

Back 521

1. persistent or continuing inflammation of the pancreas, with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts (areas of stricture/dilation– "chain of lakes" appearance on ERCP)– eventually results in irreversible destruction of the pancreas
2. The endocrine and exocrine functions of the pancreas are impaired
3. Chronic alcoholism is the most common cause (>80% of cases).
– other causes include hereditary pancreatitis, tropical pancreatitis, and idiopathic chronic pancreatitis

Hint 521

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Front 522

Clinical features of chronic pancreatitis

Back 522

1. severe pain in the epigastrium– recurrent or persistent abdominal pain
– often accompanied by nausea and vomiting
– may be aggravated by a drinking episode or by eating
– radiates to the back (in 50% of cases)
2. weight loss due to malabsorption, alcohol abuse and diabetes. Steatorrhea secondary to malabsorption

Front 523

Diagnosis of chronic pancreatitis

Back 523

1. CT scan– the initial study of choice. It may show calcifications not seen on plain films. Mild to moderate cases may not be detectable, so a normal CT does not necessarily rule out chronic pancreatitis
2. abdominal radiograph– the presence of pancreatic calcifications is 95% specific, but is found in only 30% of cases
3. ERCP is the gold standard– but is not done routinely because it is invasive
4. laboratory studies are not helpful in the diagnosis. Serum amylase and lipase levels are not elevated in chronic pancreatitis

Front 524

Complications of chronic pancreatitis

Back 524

1. narcotic addiction – probably the most common complication
2. diabetes mellitus/impaired glucose tolerance
– caused by progressive loss of islets of langerhans
– eventually appears in up to 70% of patients
3. Malabsorption/steatorrhea
– caused by pancreatic exocrine insufficiency– occurs when pancreatic enzyme secretion decreases significantly
– late manifestation of chronic pancreatitis
4. pseudocyst formation
5. pancreatic ductal dilation
6. CBD obstruction – may occur secondary to fibrosis in head of the gland
7. vitamin B12 malabsorption
8. effusions (e.g. pleural, pericardial, peritoneal)
9. pancreatic carcinoma – patients with chronic pancreatitis have an increased risk

Front 525

Treatment of chronic pancreatitis

Back 525

1. Non–operative management
– narcotic analgesics for pain
– bowel rest (NPO)
– pancreatic enzymes and H2 blockers (give simultaneously)

Hint 525

– pancreatic enzymes inhibit CCK release and thus decrease pancreatic secretions after meals. H2 blockers inhibit gastric acid secretion, preventing degradation of the pancreatic enzyme supplements by gastric acid
– insulin – may be necessary due to severe pancreatic endocrine insufficiency
– alcohol abstinence
– frequent, small volume, low–fat meals– may improve abdominal pain
2. Surgery– main goal is relief of incapacitating abdominal pain
– pancreaticojejunostomy– pancreatic duct drainage procedure to decompress dilated pancreatic duct– most common procedure
– pancreatic resection – distal pancreatectomy, whipple's procedure

Front 526

Characteristics of pancreatic cancer
1. most common demographic affected
2. anatomic location
3. risk factors
4. prognosis

Back 526

1. most common in elderly patients (75% of patients are > 60 years old), rare before age 40– more common in African Americans
2. Anatomic location – a. pancreatic head (75% of cases), b. pancreatic body – 20% of cases, c. pancreatic tail – 5–10% of cases
3. Risk factors– cigarette smoking (most clearly establish risk), chronic pancreatitis, diabetes, heavy alcohol use, exposure to chemicals– benzidene and b–naphthylamine
4. the prognosis is dismal– most patients die within months of diagnosis

Hint 526

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Front 527

Clinical features of pancreatic cancer

Back 527

1. abdominal pain (90% of patients) – may be vague and dull ache
2. jaundice – most common with carcinoma of head of pancreas– less than 10% of patients with cancer involving body and tail of pancreas have jaundice. Indicated obstruction of intrapancreatic CBD and is a sign of advanced disease
3. weight loss (common due to decreased food intake and malabsorption), anorexia
4. recent onset of glucose intolerance, but the diabetes is mild
5. depression, weakness and fatigue
6. migratory thrombophlebitis– develops in 10% of patients
7. courvoisier's sign– palpable gallbladder = present in 30% of patients with cancer in the head of the pancreas, presents without pain

** The early clinical findings of pancreatic cancer are very vague and nonspecific. By the time a diagnosis is made, most patients have an incurable level of advanced disease

Hint 527

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Front 528

painless jaundice and palpable gall bladder

Back 528

Courvoisier's sign – pancreatic carcinoma in the head of the pancreas (30%)
– however painless jaundice is not common in pancreatic cancer

Hint 528

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Front 529

Diagnosis of pancreatic cancer

Back 529

1. ERCP is the most sensitive test for diagnosing pancreatic cancer. It can also distinguish cancer of the head of the pancreas from tumors of the CBD, duodenum, ampulla, and lymphomas which have a more favorable prognosis
2. CT scan is the preferred test for diagnosis and assessment of disease spread
3. tumor markers – CA19–9 (sensitivity of 83% and specificity of 82%), CEA (sensitivity of 56% and specificity of 75%)

Front 530

Treatment of pancreatic cancer

Back 530

1. Surgical resection (whipple's procedure – pancreaticoduodectomy) is the only hope of cure–– however, only a minority of tumors are resectable (roughly 10%). The prognosis is grim even after resection, with a 5–year survival of 10%
2. If the tumor is unresectable and biliary obstruction is present, perform PTC (percutaneous cholangiopancreatography) or ERCP with stent placement across the obstruction for palliation

Hint 530

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Front 531

Anatomic difference between upper and lower GI bleed –– where do you draw the line?

Back 531

Upper GI bleeds occur above the ligament of Treitz in the duodenum, whereas lower GI bleeds occur below this point

Hint 531

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Front 532

Causes of upper GI bleeds

Back 532

1. peptic ulcer disease (PUD)– duodenal ulcer (25% of cases), gastric ulcer (20% of cases), gastritis (25% of cases)
2. reflux esophagitis
3. esophageal varices (10% of cases) – venous bleeding
4. gastric varices
5. gastric erosions, duodenitis
6. Mallory–Weiss tear
7. hemobilia
8. dieulafoy's vascular malformation– submucosal dilated arterial lesions that can cause massive GI bleeding
9. aortoenteric fistula– after aortic surgery (ask about prior aortic aneurysm/graft)–– rare but lethal cause of GI bleeding
10. Neoplasm– bleeding is not rapid– usually not an emergency

Front 533

Causes of lower GI bleeds

Back 533

1. diverticulosis (40% of cases)– most common source of GI bleeding in patients over age 60, usually painless
2. angiodysplasia– (40% of cases)– second most common source of GI bleeding in patients over age 60
3. IBD– (UC, Crohn's disease)
4. colorectal carcinoma
5. colorectal adenomatous polyps
6. ischemic colitis
7. hemorrhoids, anal fissures
8. small intestinal bleeding – diagnosed by excluding upper GI and colonic bleeding

Front 534

What is hematemesis and what does it suggest?

Back 534

vomiting blood–– suggests an upper GI bleed (bleeding proximal to the ligament of Treitz). Indicates moderate to severe bleeding that may be ongoing
– if massive bleed may see signs of volume depletion and signs and symptoms of anemia–– fatigue, pallor, dyspnea

Front 535

What is "coffee ground emesis" and what does it suggest?

Back 535

darker, "coffee ground" appearing emesis which suggests an upper GI bleeding at a lower rate–– enough time for the blood to be partly digested and take on the appearance of coffee grounds

Front 536

What is "melena" and what does it suggest?

Back 536

Black, tarry, liquid, foul–smelling stool
–– caused by degradation of hemoglobin by bacteria in the colon–– presence of melena indicates that blood has remained in the GI tract for several hours
– the further the bleeding site is from the rectum, the more likely it is for melena to occur
– note that dark stools can also result from bismuth, iron, spinach, charcoal and licorice
– melena suggests upper GI bleeding 90% of the time. Occasionally, the jejunum or ileum is the source. It is unusual for melena to be caused by a colonic lesion, but if it is, the ascending colon is the most likely site

Hint 536

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Front 537

What is "Hematochezia" and what does it suggest?

Back 537

– Bright red blood per rectum
– this usually represents a lower GI source (typically left colon or rectum)–– consider diverticulosis, AVM, hemorrhoids or colon cancers
– it may result from massive upper GI bleeding that is very brisk (5–10% of time)

Front 538

What is "occult" blood in the stool?

Back 538

– blood that is discovered on fecal occult blood test–– cannot be seen grossly.
– source of bleeding may be anywhere along the GI tract

Front 539

what should you always ask patients with GI bleeding?

Back 539

If they are on NSAIDs/aspirin, clopidogrel (plavix) or other anticoagulants

Front 540

what should you always think of when you see a lower GI bleed or positive fecal occult blood test in someone over 40?

Back 540

Colon cancer until proven otherwise

Front 541

Aortoenteric fistula

Back 541

– a rare but potential lethal cause of GI bleed
– classic presentation is a patient with a history (sometimes remote) of aortic graft surgery that develops a small amount of GI bleeding involving the duodenum before having a fatal, massive hemorrhage hours to weeks later
– perform endoscopy or surgery during this small window of opportunity to prevent death

Front 542

What tests should you order in a patient with GI bleeding?
a. hematochezia
b. hematemesis
c. melena
d. occult blood

Back 542

a. hematochezia– first rule out anorectal cause (hemorrhoids). Colonoscopy should be the initial test because colon cancer is the main concern in all patients over 50
b. hematemesis– upper GI endoscopy is the initial test
c. Melena– upper endoscopy is usually the initial test because the most likely bleeding site is the upper GI tract. Order a colonoscopy if no bleeding site is identified from the endoscopy
d. occult blood– colonoscopy is the initial test is more cases as colon cancer is the main concern. Order an upper endoscopy if no bleeding site is identified from the colonscopy

Front 543

Laboratory tests for diagnosis GI bleeds

Back 543

1. stool guaiac for occult blood
2. hemoglobin/hematocrit–– may not be decreased in acute bleeds. A hemoglobin level > 7 to 8 g/dL is generally acceptable in young, healthy patients without active bleeding, however most elderly patients (especially those with cardiac disease) should have a hgb > g/dL
3. A low MCV is suggestive of iron deficiency anemia (chronic blood loss). Patients with acute bleeding have normocytic RBCs
4. Coagulation profile (platelets, PT, PTT and INR)
5. LFTs, renal function (BUN, Cr)
6. The BUN–Creatinine ratio is elevated with upper GI bleeding. This is suggestive of upper GI bleeding if patient has no renal insufficiency. The higher the ratio, the more likely the bleeding is from an upper GI source

Front 544

Role of upper endoscopy in evaluating a GI bleed
– when should it be performed?

Back 544

– most accurate diagnostic test in evaluation of upper GI bleeding
– both diagnostic and potentially therapeutic (coagulate bleeding vessel)
– most patients with upper GI bleeding should have upper endoscopy within the first 24 hours

Front 545

Role of nasogastric tube (NG tube) in evaluation of upper GI bleeding?

Back 545

– often the initial procedure for determining whether GI bleeding is from an upper or lower GI source
– use the NG tube to empty the stomach to prevent aspiration
– false–negative findings are possible if upper GI bleeding is intermittent or from a lesion in the duodenum
– Evaluation of aspirate– bile present, but no blood (upper GI bleed unlikely––probably from site distal to liagment of Treitz), bright red blood or "coffee ground emesis" (upper GI bleed), non–bloody aspirate––clear gastric fluid (upper GI bleed unlikely, but cannot be ruled out definitively (source may possibly be in the duodenum)

Front 546

Role of anoscopy or proctosigmoidoscopy in evaluation of GI bleed

Back 546

can exclude an anal/rectal source. Perform this if there is no obvious bleeding from hemorrhoids

Front 547

role of colonoscopy in the evaluation of GI bleeding

Back 547

– identifies the site of lower GI bleeding in >70% of cases and can also be therapeutic

Front 548

Role a of a bleeding/radionucleotide scan in evaluating GI bleeding

Back 548

– reveals bleeding even with a low rate of blood loss
– it does NOT localize the lesion, it only identifies continued bleeding
– its role is controversial, but it may help determine whether angiography is needed

Front 549

Role of arteriography in evaluation of GI bleeding

Back 549

– definitively locates the point of bleeding
– mostly used in patients with lower GI bleeding
– should be performed during active bleeding
– potentially therapeutic (embolization or intra–arterial vasopressin infusion)

Front 550

role of exploratory laparotomy in evaluation of GI bleed

Back 550

LAST RESORT

Front 551

Treatment of GI bleed– all patients

Back 551

If patient is hemodynamically unstable, resuscitation is always a top priority
– Remember the ABCs. Once the patient is stabilized, obtain a diagnosis
– supplemental O2
– place 2 large bore IV lines. Give fluids or blood if patient is volume depleted.
– draw blood for hgb, hct, platelets, PT and PTT. Monitor hgb q 4–8 hours until the patient's hemoglobin has been stable for at least 24 hours
– type and crossmatch adequate blood (PRBCs). Transfuse as clinical condition demands (e.g. shock, patients with cardiopulmonary disease etc)

Front 552

Treatment of upper GI bleed

Back 552

esophagogastroduodenoscopy (EGD/upper endoscopy) with coagulation of the bleeding vessel. If the bleeding continues, repeat endoscopic therapy or proceed with surgical intervention (ligation of the bleeding vessel)

Hint 552

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Front 553

Treatment of lower GI bleeding

Back 553

– colonscopy– polyp excision, injection, laser, cautery
– arteriographic vasoconstrictor infusion
– surgical resection of involved area– last resort

Front 554

Indications for surgery in GI bleed

Back 554

1. hemodynamically unstable patient who has not responded to IV fluid, transfusion, endoscopic intervention or correction of coagulopathies
2. severe initial bleed or recurrence of bleed after endoscopic treatment
3. continued bleeding for more than 24 hours
4. visible vessel at base of ulcer (30% to 50% chance of rebleed)
5. ongoing transfusion requirement (5 unites within the first 4–6 hours)

Front 555

Two types of esophageal carcinoma

Back 555

1. squamous cell carcinoma (used to be 90% of cases)
2. Adenocarcinoma – on the rise, risk factors include GERD–– now accounts for 50% of new cases in the US

Front 556

Squamous cell carcinoma of the esophagus
1. what population is the most affected?
2. where is it most common within the esophagus?
3. what are the risk factors?

Back 556

1. african american men
2. upper thoracic and mid thoracic esophagus. 1/3 may be in the distal 10 cm of the esophagus
3. alcohol and tobacco use, diet (nitrosamines, betel buts, chronic ingestion of hot foods and beverages such as tea), HPV, achalasia, Plummer–Vinson syndrome, caustic ingestion and nasopharyngeal carcinoma

Front 557

Adenocarcinoma of the esophagus
1. what population is the most affected?
2. where is it most common within the esophagus?
3. what are the risk factors?

Back 557

1. more common in caucasians and men (5:1 over women)
2. most common in distal third of esophagus/GE junction (in 80% of cases)
3. GERD and Barrett's esophagus are the main risk factors. Alcohol and tobacco are not as important as in SCC

Front 558

Prognosis for esophageal cancer of both types

Back 558

Very poor– 5 year survival rate is about 5% to 15% for both types

Front 559

Staging of esophageal cancer
I
IIa
IIb
III
IV

Back 559

I– tumor invades lamina propria or submucosa, nodes are negative
IIa. tumor invades the muscularis propria or adventitia, nodes negative
IIb. tumor invades up to the muscularis propria, positive regional nodes
III. tumor invades adventitia (positive regional nodes) or tumor invades adjacent structures (positive or negative nodes)
IV. distant mets

Front 560

Clinical features of esophageal carcinoma

Back 560

1. dysphagia– most common symptom (initially for solids only, then progression to liquids)
2. weight loss – second most common symptom
3. anorexia
4. odynophagia (pain with swallowing) – a late finding that suggests extraesophageal involvement (mediastinal invasion)
5. hematemesis– hoarseness of voice (recurrent laryngeal nerve involvement)
6. aspiration pneumonia– respiratory symptoms due to involvement of tracheobronchial tree
7. tracheoesophageal or bronchoesophageal fistula
8. chest pain

Front 561

Diagnosis of esophageal carcinoma

Back 561

1. barium swallow useful in the evaluation of dysphagia–– a presumptive diagnosis can be made
2. upper endoscopy with biopsy and brush cytology is required for definitive diagnosis in 95% of cases
3. transesophageal ultrasound helps determine the depth of penetration of the tumor and is the most reliable test for staging local cancer
4. full metastatic workup (e.g. CT chest/abdomen, CXR and bone scan)

Front 562

Treatment of esophageal cancer

Back 562

1. Palliation is the goal in most patients because the disease is usually advanced at presentation
2. surgery (esophagectomy) may be curative for patients with disease in stage 0, 1, or 2 a
3. chemotherapy plus radiation before surgery has been shown to prolong survival more than surgery alone

Front 563

Achalasia
1. definition
2. criteria for diagnosis

Back 563

1. acquired motor disorder of esophageal smooth muscle in which the lower esophageal sphincter (LES) fails to completely relax with swallowing and abnormal peristalsis of esophageal body replaces normal peristalsis of the esophageal body
2. Absolute criteria for diagnosis– incomplete relaxation of the LES, and aperistalsis of the esophagus

Front 564

Causes of achalasia

Back 564

1. the majority of cases in the US are idiopathic
2. in the US, adenocarcinoma of the proximal stomach is the second most common cause
3. Worldwide, Chagas' disease is an important cause

Front 565

Clinical features of achalasia

Back 565

1. dysphagia (odynophagia is less common)
– equal difficulty swallowing solids and liquids (in contrast to esophageal cancer, in which dysphagia for solids is greater than for liquids).
– patients tend to eat slowly and drink lots of water to wash down food. Also, they may twist their body, extend their neck, or walk about the room in effort to force food into their stomach
2. regurgitation–– food gets "stuck" in the esophagus and then comes back up. This may lead to regurgitation
3. chest pain
4. weight loss
5. recurrent pulmonary complications secondary to aspiration, which may cause lung abscesses, bronchiectasis or hemoptysis

Picture is of heller myotomy– one of the treatments for achalasia

Hint 565

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Front 566

Diagnosis of achalasia

Back 566

1. Barium swallow – "bird's beak"– beak–like narrowing of distal esophagus and a large, dilated esophagus proximal to the narrowing
2. Upper GI endoscopy– to rule out secondary causes of achalasia (gastric carcinoma) and retention esophagitis or esophageal cancer
3. manometry – to confirm the diagnosis– reveals failure of LES relaxation and aperistalsis of the esophageal body

Hint 566

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Front 567

Risk of esophageal carcinoma in patients with achalasia

Back 567

Sevenfold increase in the risk of esophageal cancer (usually SCC)
– it occurs in 10% of patients 15–25 years after the initial achalasia diagnosis.
– Often tumors go unnoticed (even when large) due to a dilated esophagus and chronic dysphagia. Therefore, perform a surveillance scope to detect the tumor at an early stage

Front 568

Treatment of achalasia

Back 568

1. Instruct the patient on adaptive measures– chew food to consistency of pea soup before swallowing. Sleep with trunk elevated, avoid eating before sleep.
2. Medical therapy
a. antimuscarinic agents (dicyclomine)– usually unsatisfactory
b. sublingual nitroglycerin, long–acting nitrates, and calcium channel blockers. May improve swallowing in early stages of achalasia (before esophageal dilatation occurs). Most useful in the short–term treatment of achalasia (before more definitive therapy)
3. Injecting of botulinum toxin into the LES during endoscopy. Blocks cholinergic activity in the LES. Can be effective in up to 65% of cases. however repeat procedure needs to be performed every 2 years.
4. forceful dilatation– can be mechanical, pneumatic, or hydrostatic. Pneumatic balloon dilatation is most effective. Lowers basal LES tone by disrupting the muscular ring. can be effective, there is a 5% risk of perforation
5. surgical
a. Heller myotomy– circular muscle layer of LEW is incised
b. usually reserved for patients who do not respond to dilation therapy
6. Early results a promising (80–90% of patients experience good to excellent palliation of dysphagia at 1 year)
7. Long term data is still needed

Hint 568

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Front 569

Diffuse esophageal spasm
1. definition/ general characteristics
2. clinical features
3. diagnosis

Back 569

1. Nonperistaltic spontaneous contraction of the esophageal body–– several segments of the esophagus contract simultaneously and prevent appropriate advancement of the food bolus. In contrast to achalasia, sphincter function is normal (normal LES pressure)
2. There is noncardiac chest pain that mimics angina and may radiate to the jaw, arms and back. Dysphagia is common, however there is no regurgitation of food usually.
3. Diagnosed by esophageal manometry – simultaneous, multiphasic, repetitive constractions that occur after a swallow, sphincter response is normal. Upper GI barium swallow shows "corkscrew esophagus"– in 50% of cases which represents multiple spontaneous contractions

Hint 569

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Front 570

Treatment of diffuse esophageal spasm

Back 570

1. In general, there is no completely effective therapy–– treatment failure rates are high
2. medical treatment involves nitrates and calcium channel blockers (decreases amplitude of contractions). Tricyclic antidepressants may provide symptomatic relief
3. esophagomyotomy is usually not performed, and its efficacy is controversial. Some support its use, whereas others only recommend it when a patient is incapacitated my symptoms

Front 571

2 types of esophageal hernia and characteristics of each

Back 571

1. sliding hiatal hernia (type 1) – accounts for 905 of cases. Both the gastroesophageal (GE) junction and a portion of the stomach herniate into the thorax through the esophageal hiatus (so that the GE junction is above the diaphragm)– this a common and benign finding that is associated with GERD
2. paraesophageal hiatal hernia – accounts for <5% of cases. The stomach herniates into the thorax through the esophageal hiatus, but the GE junction does not. It remains below the diaphragm. This uncommon hernia can become strangulated and should be repaired surgically. These tend to enlarge with tim, and the entire stomach may ultimately move into the thorax
3. type 3 hernia are a combination of type 1 and 2 and are treated as type 2 hernias (surgically)

Hint 571

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Front 572

Clinical features of esophageal hernias

Back 572

1. The majority of cases are asymptomatic and are discovered incidentally
2. possible symptoms include heartburn, chest pain, and dysphagia
3. complications of sliding hiatal hernias include GERD (most common), reflux esophagitis (with risk of Barrett's esophagus/cancer), and aspiration
4. Complications of paraesophageal hernias are potentially life–threatening and include obstruction, hemorrhage, incarceration and strangulation

Front 573

Diagnosis of esophageal hernias

Back 573

Barium upper GI series and upper endoscopy

Front 574

Treatment of esophageal hernias by type

Back 574

1. Type 1 hernias are treated medically (with antacids, small meals and elevation of the head after meals); 15% of cases may require surgery (Nissen's fundoplication) if there is no response to medical therapy or if there is evidence of esophagitis
2. Type 2 hernias treated with elective surgery due to risk of strangulation

Hint 574

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Front 575

Mallory–Weiss Syndrome

Back 575

1. mucosal tear at (or just below) the GE junction as a result of forceful vomiting or retching. It usually occurs after repeated episodes of vomiting, but it may occur after one episode
2. it is most commonly associated with binge drinking in alcoholics, but any disorder that causes vomiting can induce the mucosal tear
3. hematemesis is always present– it varies from streaks of blood in vomitus to massive bright red blood
4. upper endoscopy is diagnostic
5. most cases (90%) stop bleeding without any treatment
6. Treatment is surgery (oversewing the tear) or angiographic embolization if bleeding continues, but this is rarely necessary. Acid suppression is used to promote healing

Hint 575

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Front 576

Plummer–Vinson Syndrome

Back 576

1. key features: upper esophageal web (causes dysphagia), iron deficiency anemia, koilonychia (spoon–shaped fingernails), and atrophic oral mucosa
2. 10% of patients develop SCC of the oral cavity, hypopharynx or esophagus, therefore, this is considered a premalignant lesion
3. treatment: esophageal dilatation, correct nutritional deficiency

Hint 576

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Front 577

Schatzki's Ring
1. what is it?
2. symptoms
3. treatment
4. causes?
5. acid vs base ingestion
6. complications
7. treatment

Back 577

1. distal esophageal webs– a circumferential ring in the lower esophagus that is always accompanied by a sliding hiatal hernia
2. It is usually asymptomatic, but mild to moderate dysphagia may be present
3. If the patient is symptomatic (but has no reflux), consider esophageal dilatation. If the patient has reflux, consider antireflux surgery (e.g. nissen)
4. usually due to ingestion of alkali, bleach, or detergent
5. ingesting alkali is more dangerous than infesting acid because it may lead to liquefactive necrosis of the esophagus with full–thickness perforation. Acid ingestion does not cause full–thickness damage (only causes necrosis of esophageal mucosa). 6. Complications : stricture formation and risk of esophageal cancer
7. Treatment is esophagectomy if full thickness necrosis has occurred. Patient should avoid vomiting, gastric lavage, and all oral intake (can compound the original injury). Give the patient steroids and antibiotics. Perform bougienage for esophageal stricture

Hint 577

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Front 578

Mallory Weiss syndrome vs Boerhaave's syndrome

Back 578

During forceful vomiting, the marked increase in intra–abdominal pressure is transmitted to the esophagus. This can lead to two conditions, depending on the severity and location of the tear.
1. If the tear is mucosal at the GE junction, it is referred to as a mallory weiss tear
2. If the tear is transmural (causing esophageal perforation) it is referred to as Boerhaave's syndrome

picture– boerhaave's syndrome

Front 579

Esophageal diverticula
1. most common cause
2. most common type
3. mechanism of most common type
4 and 5. clinical features of most common type, age affected
6. traction diverticula
7.epiphrenic diverticula
8. diagnosis
9. treatment

Back 579

1. most esophageal diverticula are caused by an underlying motility disorder of the esophagus
2. Zenker's diverticulum is the most common type–– found in the upper 1/3 of the esophagus
3. Failure of the cricopharyngeal muscle to relax during swallowing leads to increased intraluminal pressure. This causes outpouching of mucosa through an area of weakness in the pharyngeal constrictors
4. clinical features include dysphagia, regurgitation, halitosis, weight loss and chronic cough
5. It is typically seen in patients > 50 years old
6. traction diverticula– located in the midpoint of the esophagus near the tracheal bifurcation. It is due to traction from contiguous mediastinal inflammation and adenopathy (pulmonary tuberculosis). Tuberculosis causes hilar node scarring, which causes retraction of the esophagus. It is usually asymptomatic and does not require treatment
7. epiphrenic diverticuli– found in the lower 1/3 of the esophagus. It is usually associated with spastic esophageal dysmotility or achalasia. Symptoms of dysphagia are more often related to the underlying motility disorder, unless the diverticulum is very large
8. Barium swallow is the best diagnostic test for divertula.
9. Treatment of Zenker's diverticula is surgery. Cricopharyngeal myotomy has excellent results. Treatment of epiphrenic diverticula is esophagomytomy. Diverticulectomy is of secondary importance in both cases

Picture– Zenker's Diverticulum

Hint 579

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Front 580

Esophageal perforation
1. etiology
2. clinical features
3. diagnosis
4. treatment– stable vs unstable pt

Back 580

1. blunt trauma, medical tubes and instruments, forceful vomiting (Boerhaave's syndrome) that is associated with alcoholic binges and bulimia
2. pain (severe retrosternal/chest/shoulder pain), tachycardia, hypotension, tachypnea, fever, Hamman's sign (mediastinal crunch– produced by heart beating against air–filled tissues), pneumothorax, pleural effusion
3. contrast esophagram is the definitive diagnostic study (soluble gastrogafin swallow preferred), CXR0 usually shows air in the mediastinum
4. if the patient is stable and the perforation is small (draining into lumen)– medical management is appropriate – IV fluids, NPO, antibiotics, and H2 blockers
– if patient is ill and perforation is large– or there is communication into the pleural cavity, surgery should be performed within 24 hours of presentation (success rate is higher)

– if gastric/esophageal contents leak into the mediastinum or pleura, infection and septic sequela may result
– The time interval between esophageal perforation and surgery is the most important factor in determining survival. If surgery is delayed beyond 24 hours, the mortality rate and the likelihood of fistulization increase

Front 581

Peptic ulcer disease
1. most common causes
2. other causes

Back 581

1. most common causes– H. pylori infection, NSAIDs– inhibit prostoglandin production, which leads to impaired mucosal defenses. Zollinger–Ellison syndrome– acid hypersecretory states
2. Other causes– smoking– ulcers are twice as likely in smokers, alcohol and coffee– may exacerbate symptoms, but causal relationship is as yet unproven
3. other potential unproven causes– emotional stress, personality type A, and dietary factors

Front 582

Clinical features of peptic ulcer disease

Back 582

1. epigastric pain– aching or gnawing in nature
– nocturnal symptoms and effect of food on symptoms are variable
2. may be complicated by upper GI bleeding
3. other symptoms– n/v, early satiety, and weight loss

Front 583

Diagnosis
1. most accurate method?
2. most convenient test?
3. lab tests
4. if considering a dx of Zollinger Ellison syndrome?

Back 583

1. Endoscopy– most accurate test in diagnosing ulcers, essential in diagnosis of gastric ulcers because biopsy is necessary to r/o malignancy– duodenal ulcers not require biopsy. Preferred when severe or acute bleeding is present (can perform electrocautery of bleeding ulcers)
2. Barium swallow– sometimes used initially but is less reliable than endoscopy. Double contrast techniques preferred due to improved accuracy
3. lab tests– for diagnostic evaluation of h. pylori infection– a. biopsy: histologic evaluation of endoscopic biopsy is the gold standard
– urease detection via urea breath test – most convenient test (sensitivity and specificity > 95%). It documents active infection and helps to assess the results of antibiotic therapy
– serology – lower specificity – the presence of h. pylori does not necessarily indicate current infection–– antibodies to h. pylori can remain elevated for months or even years after eradication of infection. There may also be false positives because of PPIs, bismuth, many abx and GI bleeding
4. serum gastrin measurement– if considering Zollinger–Ellison syndrome as diagnosis

–– if a peptic ulcer is uncomplicated, a barium study or endoscopy is not needed initially. Initiate empiric therapy. However, if complications are suspected, order confirmatory tests

Hint 583

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Front 584

Medical Treatment of peptic ulcer disease

Back 584

1. Medical– the majority of patients with PUD can be successfully treated by curing H. pylori infection, avoidance of NSAIDs, and appropriate use of antisecretory drugs
a. supportive– discontinue aspirin, restrict alcohol use, but do not restrict any foods, stop smoking, decrease stress, avoid eating before bedtime (eating stimulates nocturnal gastric acid levels)
b. acid suppression – H2 blockers– accelerate healing of ulcers, PPIs– most effective antisecretory agents (although expensive), antacids – somewhat outdates for primary therapy and most appropriate for adjunctive therapy/symptom relief
c. Eradicate h. pylori with triple or quadruple therapy – once infection is cleared the recurrence rate is low. For initial therapy, triple therapy (PPI, amoxicillin, and clarithromycin), for 10 days to 2 weeks, For retreatment quadruple therapy – PPI, bismuth, and 2 antibiotics
d. cytoprotection – sulcralfate– faciliates ulcer healing, must be taken frequently, is costly and can cause GI upset. misoprostol– reduces risk of ulcer formation associated with NSAID use, is costly, and cause GI upset (commonly)
e. Treatment regimens
– if h. pylori test is positive, begin eradication therapy with either triple or quadruple therapy. Also begin acid–suppression with antacids, an H2 blocker or a PPI
– if the patient has an active NSAId induced ulcer, stop NSAID use (switch to acetaminophen), Also begin with either PPI or misoprostol. Continue for 4–8 weeks, depending on severity. Treat the h. pylori infection if present
– antisecretory drugs can be discontinued after 4–6 weeks in patients with uncomplicated ulcers who are asymptomatic. Patients at increased risk of recurrence (especially if underlying cause of ulcer is not reversed) may benefit from maintenance therapy
– h. pylori negative ulcers that NOT caused by NSAIDs can be treated with antisecretory drugs (H2 blockers or PPIs)

Front 585

Surgical treatment of peptic ulcer disease

Back 585

– rarely needed electively
– required for complications of PUD – bleeding perforation, gastric outlet obstruction

Front 586

Complications of Peptic ulcer disease

Back 586

1. perforation– acute severe abdominal pain, signs of peritonitis and hemodynamic instability– upright CXR or CT to detect free air under diaphragm. Tx– emergency surg to close perf and definitive ulcer operation– selective vagotomy or truncal vagotomy/pyloroplasty–– can progress to sepsis and death if untreated
2. gastric outlet obstruction– n/v of poorly digested food, epigastric fullness/early satiety and weight loss. Barium swallow and upper endoscopy, saline load test (empty stomach with NG tube, add 750 mL saline, aspirate after 30 min, test is positive if aspirate > 400mL. Tx– initially NG suction, replaced electrolyte/volume deficits. Supplemental nutrition if obstruction is longstanding. Surgery is eventually necessary in 75% of patients. Most common with duodenal ulcers and type III gastric ulcers
3. GI bleeding – bleeding may be slow (leading to anemic symptoms) or can be rapid and severe (leading to shock. Stool guaiac, upper GI. Tx– resuscitation, diagnose site of bleed via endoscopy and treat– perform surgery for acute bleeds that require transfusion of > 6 units. PUD is the most common cause of upper GI bleeding

Front 587

duodenal vs gastric ulcers

Back 587

1. duodenal ulcers– caused by increase in offensive factors (higher rates of basal and stimulated gastric acid secretion), 70–90% of patients have h. pylori, Low (malignancy is very rare) should undergo biopsy to r/o. The majority are located 1–2 cm distal to pylorus (usually on posterior wall). Usually occurs in younger patients (<40), assoc with blood type O, NSAIDs– RF, eating usually relieves pain (food in duodenum stimulates bicarb secretion). Nocturnal pain is more common than in gastric ulcers

2. gastric ulcer– caused by a decrease in defensive factors (gastric acid level is normal/low unless ulcer is pyloric or pre–pyloric). 60–70% of patients have h. pylori, high malignant potential (5–10% are malignant), 4 types depending on location – type I is most common– on lesser curvature of stomach – 70%, occurs in older patients > 40, assoc with blood type A, smoking – RF, eating makes it worse– stimulates acid secretion, complication rates are higher than with duodenal ulcers. Higher risk of recurrence with medical therapy alone

Front 588

Acute gastritis
1. definition
2. causes
3. symptoms
4. treatment
5. if no response to tx after 4–8 weeks?

Back 588

1. inflammation of the gastric mucosa
2. there are multiple causes– NSAIDs/aspirin, h. pylori infection, alcohol, heave cigarette smoking, or caffeine, extreme physiologic stress– e.g. shock, sepsis, burns
3. it can be either asymptomatic or cause epigastric pain. The relationship between eating and pain is not consistent
4. if epigastric pain is low/mod and is not associated with worrisome sx/findings, empiric therapy with acid suppression is appropriate. stop NSAIDs
5. If there is no positive response after 4–8 weeks of treatment, consider a diagnostic w/u (include upper GI endoscopy and US to r/o gallstones) and test for h. pylori

Front 589

Chronic gastritis
1. most common cause
2. progression
3. symptoms
4. complications

Back 589

1. the most common cause is h. pylori (over 80% of cases)
2. autoimmune gastritis leads to chronic atrophic gastritis with serum antiparietal and anti–intrinsic factor antibodies (possible development of pernicious anemia)
3. most patients with chronic gastritis due to h. pylri are asymptomatic and never develop complications. The condition may manifest as epigastric pain similar to PUD. Other associated symptoms are n/v and anorexia.
4. complications include PUD, gastric carcinoma, and mucosa–associated lymphoid tissue (MALT) lymphoma
5. upper endoscopy with biopsy is the test of choice for diagnosis of chronic gastritis. Other tests should be used to find the cause (usually h. pylori)

Front 590

Gastric cancer
1. most common type
2. where is it common geographically?
3. morphology

Back 590

1. majority are adenocarcinomas
2. gastric cancer is rare in the US but more common in Japan (relation to smoked foods?)
3. a. ulcerative carcinoma– ulcer through all layers
b. polypoid carcinoma– solid mass projects into stomach lumen
c. superficial spreading– most favorable prognosis
d. linitis plastic – "leather water bottle" – infiltrates early through all layers, stomach wall is thick and rigid, poor prognosis

Hint 590

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Front 591

Risk factors for gastric carcinoma

Back 591

1. severe atrophic gastritis, intestinal metaplasia, gastric dysplasia
2. adenomatous gastric polyps, chronic atrophic gastritis
3. h. pylori infection – 3–6–fold increase in risk
4. postantrectomy– many cases reported after Billroth II anastamosis – 15–20 yrs later
5. pernicious anemia – 3–fold increased risk
6. menetrier's disease – 10% develop cancer
7. high intake of preserved foods – high salt, nitrates, nitrites– smoked fish
8. blood type A

Front 592

Clinical features of gastric cancer

Back 592

1. abdominal pain and unexplained weight loss are the most common symptoms
2. reduced appetite, anorexia, dyspepsia, early satiety
3. n/v, anemia, melena, guaiac–positive stool

Front 593

Diagnosis of gastric carcinoma

Back 593

1. endoscopy with multiple biopsies– most accurate test
2. barium upper GI series– less accurate, but can complement upper endoscopy findings
3. abdominal CT scan– for staging and to detect presence of mets
4. FOBT

Front 594

Treatment of gastric carcinoma

Back 594

1. surgical resection with wide > 5 cm margins – total and subtotal gastrectomy with extended lymph node dissection
2. chemotherapy may be appropriate in some cases

Front 595

Gastric lymphoma

Back 595

1. a type of non–hodgkins lymphoma that arises in the stomach
2. clinical features are similar to those of adenocarcinomas of the stomach (e.g. abdomina pain, weight loss, anorexia)
3. complications include bleeding, obstruction, and perforation
4. diagnosis– EGD with biopsy is standard of diagnosi
5. tx– depends on stage of the disease and the presence of complications. options include surgical resection, radiation, and chemotherapy

Hint 595

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Front 596

What is the best test for evaluating a patient with epigastric pain?

Back 596

Upper GI endoscopy as it can diagnose PUD, gastritis and esophagitis. It can also rule out cancers of the esophagus and stomach, and h. pylori infection with biopsy

Front 597

What are the 3 main points to consider in small bowel obstruction?

Back 597

1. partial vs complete obstruction– with a partial obstruction, patients are able to pass gas or have bowel movements as opposed to a complete obstruction. However, patients with a complete obstruction may occasionally be able to pass gas or stool because they have residual stool or gas in the colon
2. Closed loop vs open loop obstruction
– with closed loop obstruction, the lumen is occluded at 2 points by an adhesive band or hernia ring. This can compromise the blood supply and require emergent surgery.
3. Proximal versus distal small bowel obstruction (SBO)– distal obstruction causes distention of the proximal bowel segments, making a diagnosis easier on plain film

Front 598

Pathophysiology of small bowel obstruction

Back 598

1. dehydration is the key event in SBO.
– Intestinal distention causes reflex vomiting, increased intestinal secretion proximal to the point of obstruction, and decreased absorption. This leads to hypochloremia, hypokalemia and metabolic alkalosis
2. The resulting hypovolemia leads to systemic findings such as tachycardia, hypotension, tachypnea, AMS, oliguria

Front 599

Causes of Small Bowel Obstruction

Back 599

1. Adhesions from previous abdominal surgery– most common cause in adults
2. Incarcerated hernias– second most common cause
3. Malignancy, intussusception, Crohn's disease, carcinomatosis, and superior mesenteric artery syndrome (compression of the third portion of the duodenum)

Front 600

Clinical features of small bowel obstruction

Back 600

1. crampy abdominal pain– if the pain is continuous and severe, strangulation may be present
2. N/v– may be feculent
3. obstipation – absence of stool and flatus
4. abdominal distention

Front 601

Diagnosis of small bowel obstruction

Back 601

1. Abdominal plain films– dilated loops of small bowel, air0fluid levels proximal to the point of obstruction (on upright film), and minimal gas in colon (if complete SBO)
2. Barium enema– to rue out colonic obstruction if plain films do not distinguish small from large bowel obstruction. This identifies the site of obstruction
3. Upper GI series– with small bowel follow through if above are not diagnostic

Front 602

Treatment of small bowel obstruction

Back 602

1. Nonoperative management– appropriate if bowel obstruction is incomplete and there is no fever, tachycardia, peritoneal signs, or leukocytosis
2. IV Fluids to establish adequate urine output, add potassium to fluids to correct hypokalemia (which is typically present)
3. NG tube to empty the stomach (gastric decompression)
4. Antibiotics
5. Surgery is indicated for complete obstruction, for partial obstruction that is persistent and/or associated with constant pain, or if strangulation is suspected. Perform an exploratory laparotomy with lysis of adhesions and resection of any necrotic bowel

Front 603

Paralytic Ileus
1. definition
2. causes
3. abd plain film appearance
4. diagnosis
5. treatment

Back 603

1. peristalsis is decreased or absent (no mechanical obstruction is present)
2. causes include medications (narcotics, drugs with anticholinergic effects), postoperative state (after abd surgery), spinal cord injury, shock, metabolic disorders (especially hypokalemia) and peritonitis
3. Abdominal plain films show a uniform distribution of gas in the small bowel, colon, and rectum (in contract to small bowel or colonic obstruction)
4. Failure to pass contrast medium beyond a fixed point is diagnostic
5. treatment– IV Fluids, NPO, correction of electrolyte imbalances (especially hypokalemia), NG suction if needed, and placement of a long tube if ileus persists postoperatively

Front 604

Celiac Sprue
1. what is it?
2. symptoms
3. diagnosis
4. treatment

Back 604

– characterized by hypersensitivity to gluten (in wheat products)
– results in weight loss, abdominal distention, bloating and diarrhea
– biopsy in proximal small bowel reveals flattening of villi, which causes malabsorption
– strict adherence to a gluten–free diet is essential

Front 605

Crohn's disease
1. definition
2. Distribution

Back 605

1. chronic transmural inflammatory disease that can affect any part of the GI tract (mouth to anus) but most commonly involves the small bowel (terminal ileum)
2. Distribution: There are three major patterns of disease.
– 40% of patients have disease in the terminal ileum and cecum
– 30% of patients have disease confined to the small intestine
– 25% of patients have disease confined to the colon
– Rarely, other parts of the GI tract may be involved (stomach, mouth, esophagus)

Front 606

Pathology of Crohn's disease

Back 606

1. Terminal ileum is the hallmark location, but other sites of GI tract may also be involved
2. Skip lesions– discontinuous involvement
3. Fistulae
4. luminal strictures
5. non–caseating granulomas
6. Transmural thickening and inflammation (full–thickness wall involvement) – results in narrowing of the lumen
7. Mesenteric "fat creeping" onto the antimesenteric border of the small bowel

Front 607

Clinical features of crohn's disease

Back 607

1. diarrhea (usually without blood)
2. malabsorption and weight loss (common)
3. abdominal pain (usually RLQ), n/v
4. fever, malaise
5. extraintestinal manifestations in 15–20% of cases (uveitis, arthritis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, apthous oral ulcers (cold sores), and nephrolithiasis

Hint 607

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Front 608

Epidemiology of inflammatory bowel disease–– who is it most common in?

Back 608

– more common in caucasians than other racial groups
– particularly common in Jewish populations
– mean age of onset is 15–35 years of age

Front 609

Course of crohn's disease

Back 609

– chronic indolent course characterized by unpredictable flares and remissions
– the effectiveness of medical treatment decreases with advancing disease and complications eventually develop, requiring surgery
– There is no cure, and recurrence is common even after surgery

Front 610

Treatment of paralytic ileus

Back 610

– usually resolves with time or when the cause is addressed medically
– surgery is usually not needed

Front 611

Diagnosis of crohn's disease

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1. endoscopy (sigmoidoscopy or colonoscopy) with biopsy– typical findings are apthous ulcers, cobblestone appearance, pseudopolyps, patchy (skip) lesions
2. barium enema
3. upper GI with small bowel follow–through

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Complications of crohn's disease

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1. fistulae– between colon and other segments of the intestine (enteroenteral), bladder (enterovescial), vagina (enterovaginal), and skin (enterocutaneous)
2. anorectal disease (in 30% of patients)– fissures, abscesses and perianal fistulas
3. SBO (in 20–30% of patients) is the most common indication for surgery. Initially it is due to edema and spasm of bowel with intermittent signs of obstruction, later, scarring and thickening of bowel cause chronic narrowing of the lumen
4. malignancy– increased risk of colonic and small bowel tumors (but less than with UC)
5. Malabsorption of B12 and bile acids (both occur in the terminal ileum)
6. Cholelithiasis may occur secondary to decreased bile acid absorption
7. Nephrolithiasis– increased colonic absorption of dietary oxalate can lead to calcium oxalate kidney stones
8. Aphthous ulcers of lips, gingiva, and buccal mucosa (common)
9. toxic megacolon– less common in crohn's than in UC
10. growth retardation
11. narcotic abuse, psychosocial issues due to chronicity and often disabling nature of the disease

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Medical Treatment of crohn's disease

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1. Sulfazalazine – this is useful if the colon is involved– 5–ASA (mesalamine) is the active compound and is released in the colon– it more useful in UC. 5–ASA compounds block prostoglandin release and serve to reduce inflammation. There are preparations of 5–ASA that are more useful in distal small bowel disease
2. Metronidazole (flagyl)– if no response to 5–ASA
3. systemic corticosteroids (prednisone) for acute exacerbations and if no response to metronidazole
4. Immunosuppressants (azathioprine, 6–mercaptopurine) – in conjunction with steroids if the patient does not respond to the above agents
5. bile acid sequestrants –cholestyramine or colestipol– for patients with ileal disease who cannot absorb bile acids
6. anti–diarrheal agents are generally NOT a good choice–– may cause ileus

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Surgical treatment of crohn's disease

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– eventually required in most patients
– reserve for complications of crohn's disease
– involves segmental resection of involved bowel
– disease recurrence after surgery is high– up to 50% of patients experience disease recurrence at 10 years post–op
– indications for surgery include SBO, fistulae (especially between bowel and bladder, vagina), disabling disease, and perforation or abscess
– nutritional supplementation and support– parenteral nutrition is sometimes necessary

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Ulcerative colitis (UC)
1. definition and age at presentation
2. distribution

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1. chronic inflammatory disease of the colon or rectal mucosa that may occur at any age, but usually begins in adolescence of young adulthood
2. UC involves the rectum in ALL cases and can involve the colon either partially or entirely.
– Rectum alone (in 10% of cases)
– rectum and left colon (in 40% of cases)
– rectum, left colon and right colon (in 30% of cases),
– pancolitis (in 30% of cases)
– the small bowel is not usually involved in UC, but it may reach the distal ileum in a small percentage of patients ("backwash ileitis" in 10% of cases)

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Clinical course of ulcerative colitis

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The course is unpredictable and variable and is characterized by periodic exacerbations and periods of complete remission.
– less than 5% of patients have an initial attack without any recurrence

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Pathology of ulcerative colitis

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1. uninterrupted involvement of the rectum and/or colon – NO skip lesions
2. inflammation is no transmural as in crohn's–– it is limited to the mucosa, and submucosa
3. PMNs accumulate in the crypts of the colon (crypt abscesses)

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Clinical features (wide range of presentation)

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1. hematochezia – may start as non bloody diarrhea and then progress to bloody as disease progresses
2. abdominal pain
3. bowel movements are frequent but small
4. fever, anorexia, and weight loss (severe cases)
5. tenesmus (rectal dry heaves)
6. Extraintestinal symptoms (jaundice, uveitis, arthritis, skin lesions)

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Diagnosis of ulcerative colitis

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1. stool cultures for c. diff, ova, and parasites– to rulre out infectious causes of diarrhea
2. fecal leukocytes
3. WBCs can appear in UC, ischemic colitis and or infectious diarrhea
4. colonoscopy– to assess the extent of disease and the presence of any complications

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Complications of ulcerative colitis

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1. iron deficiency anemia
2. hemorrhage
3. electrolyte disturbances and dehydration secondary to diarrhea
4. strictures, benign and malignant (usually malignant)
5. colon cancer– the risk correlates with extent and duration of colitis. In distal proctitis there is no increased risk of CRC
6. sclerosing cholangitis – the course is not parallel with bowel disease and is not prevented by colectomy
7. cholangiocarcinoma– half of all bile duct cancers are associated with UC
8. Toxic megacolon– leading cause of death in UC and affects <5% of patients. It is associated with risk of colonic perforation
9. growth retardation
10. narcotic abuse
11. psychosocial issues (e.g. depression) due to chronicity and often disabling nature of the disease

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Medical Treatment of ulcerative colitis

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1. Medical
a. systemic corticosteroids are used for acute exacerbations
b. sulfasalazine (topical application as a suppository) is the mainstay of treatment. Preferred over topical steroids because they are effective as maintenance therapy. Remission rates are as high as 93%. 5–ASA (mesalazine) is the active component. 5–ASA enemas can be used for proctitis and distal colitis
c. immunosuppressive agents in patients with refractory disease may prevent relapses but are not effective for acute attacks

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Surgical Treatment of ulcerative colitis

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– often curative (unlike Crohn's disease) and involves total colectomy
– indications for surgery include:
– severe disease that is debilitating, refractory, and unresponsive to medical therapy
– toxic megacolon (risk of perforation), obstruction (due to stricture), severe hemorrhage, and perforation
– fulminant exacerbation that does not respond to steroids
– evidence of colon cancer of increased risk of colon cancer
– growth failure or failure to thrive in children
– systemic complications