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1220 Cards in this Set

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Best treatment for ventricular tachy in a pt with stable BP?
amidarone is drug of choice. lidocaine can also be used.
What type of arrhythmias can be treated by Digoxin?
atrial arrhythmias
Tx for sustained ventricular tachy with hemodynamic compromise?
Cardioversion
What role does carotid massage play in ventricular tachy?
None - useful for SUPRAventricular tachy (narrow complex)
What kind of pulse is found in aortic regurg?
bounding aka "water hammer"
What causes a bounding or water hammer pulse in aortic regurg?
AR is associated with an increased SV which produces an abrupt rise in the systolic BP and rapid distension of the peripheral arteries. Then during diastole, there is a regurg of blood back into the left ventricle, resulting in a low diastolic pressure and collapse of the peripheral arteries.
Fixed splitting of S2 plus a midsystolic pulmonary flow murmur?
ASD
Why is lidocaine not used prophylactically in patients with acute coronary sundromes to prevent ventricular fibrillation?
it increases the risk of asystole
3 most common causes of aortic stenosis?
senile calcific aortic stenosis, bicuspid aortic valve, and rheumatic heart disease.

S4 in aortic stenosis is common - atrial kick against a stiff left ventricle.
When is a pt at risk for ACUTE pericarditis after an MI?
first several days - diffuse ST elevations, esp with PR depressions are typical ECG findings.

Dressler syndrome is an immune-mediated pericarditis that can occur WEEKS to months after infarction.
Common complication 3-7 days after an MI?
ventricular free wall rupture - presents with rapid deterioration of the pt 2dry to pericardial tamponade -- pulseless electrical activity on ECG is common

OR

interventricular free wall rupture and papillary muscle rupture - presents with new onset systolic murmor
common LATE complication of anterior wall MI?
ventricular aneurysm - can occur days to months after the initial infarction.

will see persistent ST elevations on ECG. S/sx of CHF, ventricuar arrhythmias, mitral regur, and/or thrombus formation can be seen.
MILD hypovolemia can cause syncope in what population of pts?
elderly - they very poorly tolerate even what seems to be an insignificant loss of fluid - especially orthostatic syncope upon getting up in the morning.

BUN/Cr ratio is a useful indicator of dehydration.
Treatment of choice for DRessler's syndrome?
NSAIDS. Corticosteroids can be used in refractory cases or if NSAIDs are CI.

Anticoagulation should be avoided to prevent development of hemorrhagic pericardial effusion.
Most likely artery that is occluded in acute inferior wall MI?
Right coronary artery, especially if it is complicated by right ventricular infarction (hypotension) and bradycardia.
LAD occlusion causes?
anterior wall MI
What can confirm a diagnosis of malignant hypertension?
Presence of papilledema - always suspect malig HTN if very high BPs (>/= 200/140).

Pathologic change responsible for end-organ dmg is fibrinoid necrosis of small arterioles.
leading cause of mitral stenosis worldwide?
Rheumatic heart disease

The mitral stenosis classically presents later during pregnancy bc of the physiologically increased total blood volume. Pulmonary edema and atrial fib may also occur due to left atrial overload/enlargement.
Pharmacologic management of variant (or Prinzmetal's angina)?
calcium ch blockers and/or nitrates to prevent coronary vasoconstriction.

Non-selective beta blockers and aspirin should be avoided bc they can promote vasoconstriction. Aspirin may cause vasospasm via prostacyclin inhibition.
Greatest risk factor for variant angina?
smoking
When does variant angina classically occur?
at night and can be associated with transient ST elevation on ECG.
PITTING edema vs. non-pitting edema?
PITTING - due to increased movement of fluid from vascular space into interstitial space. Can be due to increased intravascular hydrostatic pressure (CHF, portal HTN), decreased plasma oncotic pressure (low albumin 2ndry to malnutrition, nephrotic sydnrome, cirrhosis), or increased capillary leak (burns, trauma, or infection).

non-pitting - due to lymphatic obstruction (lymphedema) or decreased lymphatic flow(myxedema from hypothyroidism)
First step in treating pt with a WITNESSED cardiac arrest?
defibrillation

if arrest is unwitnessed or greater than 4-5 minute lapse btn arrest and arrival of defibrillator, a 2-min trial of CPR should precede defibrillaiton.
tx for first degree heart block?
nothing - completely benign condition
A stenotic mitral valve causes increased left atrial pressure which in turn gets transmitted to the pulmonary vasculature. What symptoms can this increase in pulm vascular pressure cause?
exertional dyspnea, nocturnal cough, and hemoptysis (hemoptysis in particular should raise suspicion for mitral stenosis)
how do nitrates reduce chest pain in angina pectoris?
venodilation --> blood pools in systemic venous circulation --> decreases preload --> reduces ventricular volume and wall stress (stretch) --> decreased myocardial oxygen demand.

They also cause some ARTERIAL vasodilation with modest decrease in afterload and myocardial oxygen consumption but this is not main mechanism.
thiazide diuretic may cause electrolyte disturbances causing sudden syncope without warning signs. this is caused by?
ventricular arrhythmia - drug predisposis to this
s/sx of coarctation of the aorta?
majority of pts are asymptomatic - but common s/sx (when present) include headache, epistaxis, cold extremities, delayed femoral pulse, or HTN in the upper extremity. In adults, enlarged pulsatile collateral vessels may be palpated in the intercostal spaces anteriorly, in the axilla or in the interscapular area. Also, upper extremity may be preferentially well developed.
Almost pathognomonic for coarctation of aorta?
"3" sign -indentations of the aorta at the site of the coarctation and pre and post stenotic dilation along the left paramedian border.
Patent ductus arteriosus is associated with?
birth at high altitudes and maternal rubella infection.
aortic aneurysms present with what s/sx?
hoarseness, chest pain, dysphagia or a dry cough.
When is surgery indicated for an aortic aneurysm?
aneurysm > 6 cm in diameter, persistent pain, continued elevated BP or wide expansion of the aneurysm.
Why do pts with severe aortic stenosis have anginal chest pain?
due to increased myocardial oxygen demand 2dry to large left ventricular mass.
When is clopidogrel (plus aspirin) indicated for 2ndry prevention in a cardiac patient?
1) All patients with a UA/NSTEMI for at least 12 months (aspirin indefinitely)
2) post- PCI pts x 30 days for bare metal stents and 1 year for drug eluting stents. Drug eluting stents need a longer duration bc epithelialization occurs slowly.
How long is LMWH usually given post-MI?
first 48 hours typically
Classic physical exam findings for cardiac tamponade?
pulsus paradoxus and Beck's triad (hypotension, jugular venous distention, and muffled heart sounds)

pathophys: fluid fills in pericardial sac --> pressure riss above diastolic pressure of the ventricles --> ventricles less able to expand and accept venous return to the heart --> decreased preload, SV, and CO --> decrease in CO made worse by inspiration due to lower intrathoracic pressure --> more systemic venous blood return to right ventriclue --> intraventricular septum bows into the left vetricle causing further reduction of left ventricular filling
Why can a dual upstroke be present in HOCM?
occurs from midsystolic obstruction that develops as the heart contracts
What maneuver worsens the murmur of HOCM?
anything that decreases preload - valsava, standin g
Elevated BNP levels and an audible S3 are both signs of _____?
increased cardiac filling pressures due to volume overload.
Most useful test to assess coronary RE-occlusion after an MI?
CK-MB bc it returns to normal levesl within 1-2 days, while troponin T (genrally a more sensitive marker of cardiac injury) takes up to 10 days to return to normal after an MI.
Tx for hemodynamically stable SUPRAventricular tachy?
vagal maneuvers followed by adenosine and AV nodal blockers. adenosine decreases conduction through the AV node.

SVT should be suspected on ECG with a regular, narrow QRS complex tachy withOUT definite P waves.
What should be suspected in otherwise young healthy pts who develp s/sx of CHF including paroxysmal nocturnal dyspnea, dyspnea on exertion, peripheral edema, hepatomegaly, cardiomegaly, bilateral pleural effusions,a nd a third heart sound?
Dilated cardiomyopathy 2ndry to myocarditis should be high on the DDx. Coxsackie B virus is the most common cause.

Diagnosis is via echocardiogram which typically shows dilated ventricles and diffuse hypokinesia resulting in systolic dsyfunction (low EF).
Most effective lifestyle intervention for reducing blood pressure?
decreased consumption of alcohol. smoking cessation decreases a pt's risk of cardiovascular dz but does NOT improve blood pressure itself.
First line drugs for tx of cocaine-related cardiac ischemia?
benzodiazepines, nitrates, and aspirin - allays the anxiety and reduces the HTN and tachycardia

beta-blockers (Metoprolol) would be CI bc they aggravate cocaine-medited vasoCONStriction.
How long should a pt with an episode of rheumatic fever receive antibiotic prophylaxis with penicllin to prevent further attacks?
Treat until pt reaches age 18 to prevent repeat episodes which can worsen valvular function.
Most common cause of secondary HTN?
chronic oral contraceptive use - simply discontinuing its use can correct the problem
Tx for third degree heartblock?
pacemaker insertion

3rd degree or complete heart block is marked by complete indepenence of the P waves and QRS complexes.
Tx for subacute bacterial endocarditis?
empiric ABX until causative bacterium is identivied. Native valve bacterial endocardities is most commonly due to Streptococcus viridans, which is highly susceptible to IV penicillin G or IV ceftriaxone.
Intensive retrosternal pain that radiates to the back of the chest along with normal ECG strongly suggests?
aortic dissection - check BP in both arms and auscultate for diasolic murmur of aortic regurg. TEE is the preferred diagnostic tool (bc MRI and CT are time consuming) but before performing procedure, HTN should be controlled.
How does adenosine have diagnostic value in a suspected supraventricular tachycardia?
an SVT is usually terminated by adenosine whereas other tachycardias are simply slowed.
Review of renin-angiotensin-aldosterone axis...
renin is produced by the juxtaglomerular cells of the kidney in response to hypOperfusion. Renin cleaves angiotensinogen to agiotensin I. In turn, angiotensin I is converted into angiotensin II by ACE in the lungs. Angiotensin II is a potent vasoconstrictor. It also promotes vasopressin (ADH) release from the pituitary and aldosterone prodxn from the adrenal cortex. Aldosterone acts on the distal convoluted tubules and collecting ducts to promote sodium and water resorption (at the expense of potassium).
In a patient with an MI who develops a cold leg, one should get an ECHO to rule out?
thrombus in the left ventricle that may have embolized to the leg. An MI results in blood stasis in the akinetic part of the heart with resultant thrombus formation.
typical presentation for bacillary angiomatosis?
immunocompromised indvidual (e.g. AIDS, malignancy, undergoing chemo, organ transplant recipients) with non specific constitutional symptoms PLUS characteristic lesions of the skin and viscera (angioma-like blood vessel growths). This condition is caused by Bartonella henselae and Bartonella quintana. Antibiotic treatment causes lesion regression.
What should be suspected in a pt that has areflexic weakness in the upper extremities and dissociated anesthesia (loss of pain and temp with preserved position and vibration) in a "cape" distribution?
Syringomyelia - presence of a cavitary expansion of the spinal cord (known as a syringe) with destruction of the gray and white matter adjacent to and often communicating with the central canal. Most frequent site of involvement is the lower cervical or upper thoracic region. When syringes occur in the upper cervical cord and extend proximally to involve the medulla oblongata, the condition is called syringobulbia. Causes include congenital, trauma, inflammatory conditions,tumors, and idiopathic.
Strongest influence on long-term prognosis following an ST-elevation MI?
duration of time that passes before coronary blood flow is restored (via PTCA or fingrinolysis). Reperfusion injury can occur but benefits of reperfusion far outweigh the consequences of reperfusion injury.
Pt that presents with painLESS sub acute monocular vision loss?
DDx includes central retinal vein occlusion (CRVO) or central retinal artery occlusion (CRAO).

CRVO will show optic disk swelling, retinal hemorrhage, dilated veins, and cotton wool spots. CRAO shows pallor of the optic disk, a cherry red fovea, and boxcar segmentation of blood in the retinal VEINS.
Most common histologic lesion of diabetic nephropathy?
diffuse glomerulosclerosis but NODULAR glomerulosclerosis (with Kimmelstiel-Wilson nodules) is pathognomonic.

Dz progression can be slowed with strict glycemic control, treatment of HTN, and angiotensin axis blockade.
What can cause insoluble crystal precipitation in the tubular lumen leading to acute renal failure 2dry to renal tubular obstruction?
hyperuricemia from tumor lysis syndrome, indinavir, acyclovir, and sulfonamide therapy.

Inadequate hydration is a predisposing factor. Look for oliguria with elevated creatinine and BUN.
Best initial test in a patient with suspected hepatocellular carcinoma (typically caused by chronic viral hepatitis or cirrhosis)?
AFP which is frequently elevated in hepatocellular carcinoma but is NOT EXCLUDED by a normal AFP level. If AFP is elevated, imaging (CT or MRI) will be needed to detect the lesion. Biopsy may ultimately be necessary in many patients if a concerning lesion is found on imaging.

Note that ascites fluid cytology has a low yield for confirming diagnosis of hepatocellular carcinoma and generally not recommended.
Leukocytosis, anemia, and increased number of mature granulocytic forms (eg. segmented neutrophils and band forms on peripheral blood) with low leukocyte alkaline phosphatase score should raise suspicion for?
CML - typically seen after age 50. Presence of Philadelphia chromosome confirms dx.

The only other dzs that may cause a low leukocyte alkaline phosphatase are hypophosphatemia and paroxysmal nocturnal hemoglobinuria (PNH).
Elevated leukocyte alkaline phosphatase is characteristic of?
Leukemoid reaction
tartrate resistant acid phosphatase is present in ?
hairy cell eukemia
Adult treatment panel 3 recommendation for CHD or CHD risk equivalent (such as DM or PAD)?
Goal LDL < 100
Lifestyle modification @ >/= 100
Drug therapy @ >/= 130
Adult treatment panel 3 recommendation for 2+ risk factors for coronary heart disease?
Goal LDL < 130
Lifestyle modification @ >/= 130
Drug therapy @ >/= 160
Adult treatment panel 3 recommendation for 0-1 risk factors for coronary heart disease?
Goal LDL < 160
Lifestyle modification @ >/= 160
Drug therapy @ >/= 190
Risk factors for coronary heart disease?
men >/= 45
women >/= 55
HTN
cigarette smoking
HDL < 40
fam hx of premature CHD (male < 55, female <65)
CHD risk equivalents?
DM
symptomatic carotid artery dz
abdominal aortic aneurysm
peripheral artery dz
10-yr risk of CHD of 20% or higher
Decreases triglyceride levels and increases HDL concentrations?
Niacin - NOT considered first line for reducing LDL levels
Most common cause of fatal sporadic encephalitis in the U.S.?
Herpes encephalitis 2dry to HSV-1. Affects the temporal lobe of the brain and presents acutely (< 1 week) with focal neuro findings such as AMA, cranial nerve deficits, hemiparesis, dysphasia, aphasia, ataxia, or focal seizures. Fever is present in approx 90% of pts.

CSF analysis shows lymphocytic pleocytosis, increased number of erythrocytes (due to hemorrhagic destruction of the temporal lobe), and elevated protein levels. MRI is the preferred method of imaging as CT may be normal in up to 50% of pts. Focal EEG findings (prominent intermittent high amplitude slow waves) occur in > 70-80%.

PCR analysis of HSV DNA in the spinal fluid is the gold std of diagnosis.
India ink preparation is used to detect?
cryptococcal meningitis in immunocompromised patients.
What may simulate an iron deficiency anemia (microcytic/hypochromic) but with iron studies that reveal ELEVATED serum iron levels and decreased TIBC?
Sideroblastic anemia resulting from defective heme synthesis, most commonly due to pyridoxine-dependent impairment in early steps of protoporphyrin synthesis. Often caused by alcoholism or drugs such as isoniazid.

Microscopy reveals two gropus of RBCs ("dimorphic" RBC population) - microcytic and hypochromic.
Pt with signs of ischemia (parasthesia, change in temperature, and non-detectable radial arterial pulsations) BUT NORMAL neuro exam is suspicious for?
embolus of the upper extremity arterial bed, specifically the radial artery. Immediate anticoagulation with heparin and surgical intervention (i.e. embolectomy) are crucial bc can lead to tissue death and amputation if not effectively treated in hours.
Diagnostic study of choice in multiple sclerosis?
MRI which shows white matter dz
Reliable screening test for hemochromatosis?
Percent transferrin saturation (greater than 45%) and serum ferritin level (greater than 1000 microg/L).
Complications of hemachromatosis?
chronic liver disease or cirrhosis, hepatocellular carcinoma, diabetes, pancreatic insufficiency, skin pigmentation
First step in management of acute pyelonephritis?
Blood and urine cultures FIRST, followed by IV antibiotics.

Acute pyelonephritis can lead to gram-negative sepsis so it is important to determine the causative agent, evaluate for bacteremia, and check for drug resistant organisms.

Fluoroquinolones or ceftriaxones can be used for treatment.
When does acute pyelonephritis become complicated?
progression to renal corticomedullary abscess, perinephric abscess, emphysematous pyelonephritis, or papillary necrosis. Typically occurs in pts with DM, kidney stones, or other urologic abnormalities.
When is CT or ultrasound indicated in the mgmt of acute pyelo?
if fever or clinical symptoms persist after 48-72 hours of appropriate antimicrobial therapy to r/o obstruction, abscess, or other complications.
what is allergic conjunctivitis?
an acute hypersensitivity reaction caused by environmental exposure to allergens. Characterized by intense itching, hyperemia, tearing, conjunctival edema, and eyelid edema but NO vision disturbances. Usually a positive family or personal history of asthma, seasonal rhinitis, atopic dermatitis, food allergies, or urticaria. Condition usually subsides wi 24 hours even wo treatment. Topical antihistamines, artificial tears, and cool compresses can help.
What is atopic keratoconjunctivitis?
SEVERE form of ocular allergy with itching, tearing, THICK mucus d/c, photophobia, and blurred vision.
What is blepharitis?
chronic inflammatory condition involving lid margins bilaterally. Crusty d/c is seen clinging to lashes in ANTERIOR blepharitis whereas hyperemic lid margins with telangiectasias are seen in POSTERIOR blepharitis.
What is dacrocystitis?
infection of the lacrimal sac due to obstruction of the nasolacrimal duct. It is characterized by pain, swelling, tenderness, and redness in the tear sac area. Mucous or pus can be expressed.
Classic presentation of Guillain-Barre syndrome?
ascending paralysis, areflexia and sensory changes 3-4 wks after a URI or gastroenteritis, PLUS albumino-cytologic dissociation (elevated protein despite normal cell count). Also can have cranial nerve paralysis and autonomic dysfunction.
Tx for Guillan-Barre syndrome?
IV immunoglobulin and plasmapheresis.
Major signs/sx for Waldenstrom's macroglobulinemia:
1) increased size of the spleen, liver, and some lymph nodes
2) Tiredness, usually due to anemia
3) Tendency to bleed/bruise easily
4) night sweats
5) headache and dizziness
6) various visual problems (opthalmoscopy may show dilated, segmented, and tortuous retinal veins)
7) pain and numbness in the extremities due to a predominantly demyelinating sensorimotor neuropathy.
Diagnostic clues for Waldenstrom's macroglobulinemia?
an IgM spike on electrophoresis which causes hyperviscosity of the blood (seen for example by retinal vein engorgement).
Pts with multiple myeloma may present with similar symptoms but the involved immunoglobulins are usually IgG or IgA. Further, they rarely have hyperviscosity sindromes such as retinal vein engorgement.
Management of newly diagnosed iron deficiency anemia in an elderly pt?
Secondary to chronic GI blood loss until proven otherwise. Colonoscopy should be next step in mgmt. A single negative occult blood test does not exclude the possiblity of GI bleeding.
Clinical features of interstitial nephritis?
fever, rash, and arthralgias. May be accompanied by peripheral eosinophilia, hematuria, sterile pyuria, eosinophiluria, and urine WBC casts.

70% of cases are caused by drugs such as cephalosporins, penicillins, sulfonamides, sulfonamide containing diuretics, NSAIDs, rifampin, phenytoin, and allopurinol. Discontinuing drug is the treatment.
What drugs provide a survival benefit in CHF pts?
ACE-I, ARBs, beta-blockers, and spironolactones.

Digoxin and loop diuretics (furosemide) provide symptomatic relief but no survival benefit.
Warfarin inhibits?
synthesis of Vit K dependent factors II, VII, IX, X, protein C and protein S.
Antibiotic choice for prophylaxis/treatment of infections caused by human or dog bites?
Amoxicillin-clavulanate (covers polymicrobial infections)
Main mechanism of kidney damage in SLE?
immune-complex mediated which activates complement leading to low serum C3.
Mechanism of kidney damage in post-strep glomerulonephritis?
immune-complex mediated which activates complement leading to low serum C3.
Management of spontaneous subconjunctival hemorrhage?
A benign finding that requires no treatment. Minor bruising that may be due to simple trauma from rubbing eyes, violent coughing spells, or hypertensive episodes. Usually disppears in 24-28 hours.
Role of dihydropyridine calcium channel blockers (such as nifedipine) in ACS pts?
contraindicated bc can worsen cardiac ischemia via peripheral vasodilation and reflex tachy.

NON-dihydropyridines (diltiazem and verapamil) can be used in STEMI pts with ongoing ischemia after beta-blockers have been administered but even then, they do not improve mortality.
Classic findings of erysipelas?
sharply demarcated, erythematous, edematous, tender skin lesion with raised borders. Legs are most frequently-involved site.

Most frequently implicated organism is group A beta-hemolytic streptococcus (S. pyogenes).
Population most at risk of developing SLE?
young, african-american women aged 20-40 years.
common SLE s/sx?
fatigue, painLESS oral ulcers, non-deforming arthritis (commonly affecting MCP/PIP hand joints) in 90%, low grade fever, weight loss, malar or discoid rash, hematologic abnormalities (thrombocytopenia and leukopenia), serositis, and proteinuria.
What pathological mechanism underlies exophthalmos of Graves disease?
1) sympathetic nervous system mediated lid retraction.
2) autoimmune attack on extraocular muscles wherein lymphocytes infiltrate the EOMs and orbital fat causing edema, proliferation of local interstitial fibroblasts, and deposition of glycosaminoglycans. End result is fibrosis and edema with EOM enlargement that pushes the lobe outward.

May be bilateral or unilateral!

Eye "grittiness" or "sandiness" and excessive tearing may occur due to corneal exposure and keratitis resulting from inability to completely close eyelids over protruding eyeball.
First step in management of a diabetic ulcer?
Proper wound care and debridement followed by antibiotics.
Most common nephropathy associated with carcinoma?
Membranous nephropathy; however, minimal change disease is a well-known complication of Hodgkin's lymphoma.
Acanthosis nigricans is associated with?
1) insulin resistant states such as DM, acromegaly, obesity, and others
2) GI (or GU) malignancies
Reversible risk factors for premature atrial contractions?
tobacco and alcohol. beta-blockers are often helpful in pts who are symptomatic
Suspect what if there are signs of hypopituitarism plus headaches and bitemporal blindness?
craniopharyngiomas (benign suprasellar tumors).

In chidlren, retarded growth is the most prominent feature 2dry to low growth hormone and thyroid hormone. Sexual dysfunction is more prominent in adults. Women can present with amenorrhea. Tumor compresses optic chiasm causing bitemporal blindess. Headaches are due to an increased intracranial pressure.

TX is surgery and/or radiotherapy.
Tremor that is somewhat suppressed at rest and exacerbated toward the end of a goal-directed movement?
essential tremor-first line tx is propranalol especially if the pt is hypertensive. Other possibilities include anticonvulsants such as primidone and topiramate.
Tremor that is worst at rest and improves with intentional movement?
Resting tremor associated with Parkinson's.
Most common malignancy of the liver?
Metastasis from another primary source
Most common cause of hydatid cysts of the liver?
Cystic echinococcosis is cuased by the tapeworm Echinococcus granulosus mostly in immigrants or pts that live in the SW region of the country and are exposed to SHEEP and DOGS. Microscopic exam reveals encapsulated and calcified cyst that contains fluid and budding cells.
alpha feto protein is commonly elevated in which liver dz?
hepatocellular carcinoma
Suspect what if there is a solitary epithelial tumor of the liver (usually in the right hepatic lobe) in a middle-aged woman with a lengthy hx of oral contraceptive usage?
hepatic adenoma (benign condition)
Neoplasm of the liver characterized by vascular spaces that are lined with malignant cells?
hepatic angiosarcoma - rare neoplasm more common in older men exposed to toxins such as vinal chloride gas, arsenic compounds, and thorium oxide.
vomitus gastric contents are rich in?
hydrogen, chloride, and potassium
Remember what about heterophile antibodies used to dx infectious mono?
very sensitive and specific but may be negative early in illness.
Mechanism of hypercalcemia in pts with tumors that are metastatic to bone?
local osteolysis by production of CYTOKINES such as IL-1 and tumor necrosis factor (TNF).
Pathogenesis of chronic cough 2ndry to ACE-I?
Related to an accumulation of the inflammatory or proinflammatory mediators bradykinin, substance P, thromboxanes, and prostaglandins.
In mechanical ventilation, pO2 provides a measure of oxygenation and is influenced by _______ and ________ while pCO2 provides a measure of ventilation and is affected mainly by ________ and ________.
pO2: FiO2 and PEEP levels

pCO2: Respiratory rate and tidal volume.
Mechanical ventilation improves oxygenation by providing an increased fraction of inspired oxygen (FiO2) and by providing PEEP to prevent alveolar collapse.
Typical goal FiO2?
Initially, pts are usually given high FiO2 (~ 80% or 0.8), pending the results of the first blood gas analysis. Based on results, FiO2 should be decreased to prevent oxygen toxicity; typically below 50-60% is desirable. Goal is to maintain paO2 >/= 60!! PEEP can also be adjusted to increase/decrease the number of alveoli available for gas exchange and maintain adequate oxygenation.
Criterion for initiating home oxygen in COPD patients?
PaO2 < 55 mmHg or SaO2 < 88%.

Pts with signs of pulmonary htn or hematocrit > 55% should be started on home oxygen when the PaO2 < 60 mmHg.

The dose of oxygen should be titrated such that SaO2 is maintained at >90% during sleep, normal waking hours, and at rest. Survival benefits are significant when used for a minimum of 15 hours per day.
Acidosis accompanied by hypercarbia (elevated pCO2) and a normal/elevated serum bicarb is diagnostic of a?
respiratory acidosis (often caused by hypOventilation)

Note: post-ictal state can cause apnea/hypoapnea during prologned seizures or an aspiration event.
Pathogenesis of aspirin sensitivity syndrome?
a 'psuedo-allergic' reaction due to prostaglandin/leukotriene misbalance. Aspirin is a cyclooxygenase inhibitor --> arachidonate diverges from blocked COXs to a 5-lipoxygenase pathway --> accumulation of leukotrienes and changed prostaglandin/leukotriene balance triggers characteristic reactions (bronchoconstriction, polyp formation).

Tx includes avoidance of NSAIDs and the use of leukotriene receptor ANTagonists (drug of choice).
Very high yield!
Common cause of upper lobe cavitary lung lesions in immigrant patients?
TB
Recommended therapy for an acute bacterial exacerbation of COPD?
supplemental oxygen, inhaled bronchodilators (beta-2 agonests or anticholinergics such as ipratropium), broad-spectrum ABX, a 2-week corticosteroid taper, and smoking cessation.

Care must be taken with supplemental oxygen bc it can suprress the hypoxia-fueled respiratory drive in COPD pts.
An important cause of pneumonia in HIV/AIDS patients?
Pneumocystis jiroveci (carinii) pneumonia - hypoxia occurs 2ndry to alveolar and interstitial inflammation causing areas of V/Q mismatch. This manifests as an increase in the alveolar-arterial oxygen gradient.
Symptoms that help distinguish Legionella from other causes of community acquired pneumonia?
1) high-grade vever
2) GI symptoms
3) confusion
What will be a common finding on sputum gram stain for Legionella pneumophila?
Many neutrophils but no organisms bc it is a Gram-negative rod that stains poorly and is primarily intracellular.
Commonly spread by cooling towers and water supplies. Travel-associated infection is well-documented.
Diagnosis and treatment of Legionella pneumophila CAP?
Dx is confirmed by urine antigen testing or culture on charcoal agar. Tx with azithromycin or levofloxacin.
NEW clubbin in a pt with COPD often indicates?
lung cancer - interestingly finger clubbing is RARELY a feature of COPD.
Alveolar hypoventilation (as in COPD exacerbation) can cause?
confusion, somnolence, coma, and tonic-clonic seizures. Sedatives should be avoided in these pts as they can exacerbate alveolar hypoventilation.
Only two modalities shown to decrease mortality in COPD?
home oxygen therapy and smoking cessation
Non-cardiogenic pulmonary edema aka ARDS can develop in what settings?
sepsis, severe bleeding, pneumonia, toxic ingestion, or burns when release of inflammatory mediators cause increased alveolar capillary permeability and resultant pulmonary edema.
How can cardiogenic pulmonary edema be distinguished from non-cardiogenic?
Measurement of pulmonary capillary wedge pressure (PCWP).

PCWP > 18 mmHg -- pulmonary edema 2dry to impaired left ventricular fxn.

PCWP < 18 mmHg -- NON-cardiogenic etiology
Non-invasive positive pressure ventilation (NIPPV) should be tried before intubation and mechanical ventilation in a pt with respiratory distress because?
Better alveolar ventilation and less fiatigue of respiratory muscles.

Recommended in pts with a pH < 7.35 or PaCO2 > 45 mmHg or respiratory rate > 25/min.
When is non-invasive positive pressure ventilation contraindicated?
pts who are septic, hypotensive, or dysrhythmic.
Characteristic change in FEV1/FVC in COPD patients versus restrictive lung dz?
decreased in COPD due to reduction of mainly FEV1.

normal ratio in restrictive lung dz.
DLCO (diffusion capacity) may help distinguish between what two COPD entities?
it is decreased in emphysema and normal in chronic bronchitis
Suspect what with presence of a mobile cavitary mass (crescent radiolucency next to a rounded mass) in the lung which presents with intermittent hemoptysis?
Aspergilloma - cavitations are due to destruction of underlying pulmonary parenchyma. Mobile mass is due to debris and hyphae coalescing to form a fungus ball.
Number one cause of chronic cough in nonsmokers?
postnasal drip
Most specific test available for GERD?
24-hour pH recording - usually used in pts with chest pain or chronic cough when esophagoscopy is negative.
Suspect what in COPD pts with catastrophic worsening of their respiratory symptoms?
spontaneous secondary pneumothorax - destruction of alveolar sacs and formation of large airspaces (generally in the UPPER lobes) are predisposing factors.
In addition to panlobular emphysema, pts with alpha-1 antitrypsin deficiency are also at risk for _________?
liver disease

note: AAT is an enzyme that counteracts NEUTROPHIL ELASTASE. Uninhibited elastase causes bullous changes of the lungs.
Goal INR in pts with prosthetic heart valves?
2.5-3.5
how long should a pt with a VTE be treated with oral anticoagulation?
At least 3 months if there is a reversible risk factor and for 6-12 months in pts with idiopathic DVT.
The proximal deep veins include?
iliac, femoral and popliteal
Potential therapies for patients with obesity hypoventilation syndrome?
weight loss, ventilator support, oxygen therapy and progestins (a respiratory stimulant).
cause of obesity hypoventilation sydrome aka Pickwickian sydrome?
decreased lung compliance
Suspect what if a loculated, abnormally contured effusion with adjacent pulmonary consolidation is seen on CXR?
empyema, an intrapleural collection of pus - most commonly due to bacterial seeding from an untreated pneumonia.

Often unrepsonsive to antibiotics bc infection progresses to a mixed aerobic and anaerobic bacterial population.
How can bronchiectasis be identified on CT?
presence of dilated bronchi with thickened walls. Hemoptysis, sometimes massive to the point of requiring bronchial artery emoblization is a potential complication.
Treat an ANaerobic lung infection (suspected due to foul-smelling sputum) with what ABX?
Clindamycin
Common responsible antigens in hypersensitivity pneumonitis?
aerosolized bird droppings ("bird facier's lung") and molds associated with farming ("farmer's lung")
Typical presentation of hypersensitivity pneumonitis?
acute episodes of cough, breathlessness, fever, and malaise that occur within 4-6 hours of antigenic exposure. Chronic exposure may cause weight loss, clubbing, and "honeycombing" of the lung. Management is avoidance of the responsible antigen.
In pneumonia pts, placing the consolidated lung segment in a dependent position can increase right-to-left shunt. Why?
Alveoli of consolidated lung segments are filled with exudate and do not participate in pulmonary gas exchange, so their ventilation is essentially zero, i.e. blood perfusing consolidated areas is not oxygenated. These positions decrease the patient's oxygen saturation levels which is the same theory as an increased R-to-L shunt.
Mainstay therapy for ARDS?
Mechanical ventilation with LOW tidal volumes and PEEP. Levels up to 15 of PEEP may be necessary in ARDS pts.

Note: potential complications of PEEP include barotrauma and tension pneumothorax.
What may help distinguish asthma from COPD?
FEV1 measurement before and after bronchodilator treatment - demonstrates reversibility if greater than 15% improvement of FEV1 is seen. Reversibility is more consistent with asthma; however a certain subset of pts with COPD also show positive bronchodilator response indicating an overlap of pathophysiology may exist.
Presentation of blastomycosis?
pulmonary and CXR findings similar to TB and histoplasmosis however systemic blastomycosis may cause skin ulcerations and lytic bone lesions.

Note: found endemically in the Great Lakes, Mississippi and Ohio River basins. Wisconsin has the HIGHEST rate of infection.
Coccidiodomycosis is endemic to what part of the US?
Southwestern

Causes fungal infection of the lungs that can lead to fever, cough, and night sweats. X-pulmonary manifestations include skin, skeleton, and MENINGES.
Definitive diagnostic test for bronchiectasis?
high-resolution CT scan
Suspect what in a pt with an asymptomatic pulmonary nodule that resides in Mississippi?
Histoplasma capsulatum - endemic to Mississippi and Ohio River valleys and Central America. Found in soil with a high concentration of bird or bat guano droppings.

Note: chronic cavitary pulmonary histoplasmosis (which is a fatal form) usually develps in older COPD pts. Disseminated histoplasmosis is seen in immunocompromised pts.
Bacteria commonly responsible for acute exacerbation of COPD?
S. pneumoniae, H. influenza, and M. catarrhalis. All pts suspected with a bacterial pneumonia should have a CXR as the first step and then ABX wo waiting for sputum gram stain or cultures.
How long before Warfarin becomes therapeutic in treatment of a VTE?
4-5 days which is why concurrent heparin for 5 days should be used.
Drugs of choice for in-patient treatment of community acquired pneumonia?
newer antipneumoccocal quinolones like levofloxacin or moxifloxacin.

For outpatient therapy, either azithromycin or doxycyline can be used.
What is an important interaction of ciprofloxacin and erythromycin with theophylline?
decreases theophylline clearance and raises plasma concentration with possibility of theophylline toxicity. Toxicity manifests as CNS timulation (headache, insomnia), GI disturbance (N/V), and cardiac toxicity (arrhythmia). Mechanisms responsible for toxicity may include phosphodiesterase inhibition, adenosine antagonism, and stimulation of epinephrine.
Typical FEV1/FVC ratio in COPD?
less than 0.7
Suspect what with asymmetric breath sounds immediately after intubation?
Right mainstem bronchus intubation - a relatively common complication of endotracheal intubation. Ideally the tip of the endotracheal tube should be between the vocal cords and the carina. CXR confirms diagnosis and slight withdrawal of the tube resolves the complication.
Left-sided endocarditis commonly sends septic emoli to where?
regions rich in blood supply such as the brain, kidneys, liver, and spleen.
Drug of choice in a pt who presents with stable angina AND hypertension?
beta-blocker - increases the threshold for the development of an anginal episode and controls the hypertension. They are also believed to be cardioprotective bc they decrease the sympathetic output to the heart.
What makes a test reliabile?
similar results on repeat measurements. reliability is maximal when random error is minimal.
What makes a test valid or accurate?
The test's ability to measure what it is supposed to measure. To determine validity, results must be compared to those obtained from the gold standard test.
When should a patient be screened for bladder cancer?
never due to its relatively low incidence and poor positive predictive value.
The two phases involved in the pathogenesis of metabolic alkalosis?
generation phase - vomiting results in the loss of gastric fluids high in HCl, NaCl, and water. The loss of hydrogen ions as HCl results in unbalanced retention of HCO3- leading to a metabolic alkalosis.

maintenance phase - volume loss in the vomitus causes a decrease in the ECV volume leading to decreased renal perfusion pressure. The kidneys respond by increasing activation of the renin-angiotensin-aldosterone system. Aldosterone promotes retention of water at the expense of H+ and K+ loss in the urine. This action of aldosterone is what causes the hypokalemia and a contraction alkalosis.

First step in management - restoration of the ECF volume with IV normal saline and potassium.
Possible mechanism of adverse effects such as myopathy of statins?
decreased synthesis of products unrelated to cholesterol products such as reduced CoQ10 production.
Mechanism of action of statin?
inhibits HMG-CoA reductase which is the rate-limiting enzyme in the synthesis of cholesterol that converts HMG-CoA to mevalonate.
When is an AIDS pt at risk for CMV retinitis?
When CD4 count falls below 50. Pts may be asymptomatic with characteristic fundoscopic findings of yellow-white patches of retinal opacification and hemorrhages. Tx is ganciclovir or foscarnet.
Suspect what if there is necrosis involving the inner layers of the retina that appear as white, fluffy lesions surrounded by retinal edema and vitritis?
ocular toxoplasmosis in an immunocompromised host. More than 50% will also have encephalitis.
Suspect what in an older pt that presents with fever, malaise, and a burning/itching sensation of the periorbital region with examination revealing a vesicular rash in the distribution of the cutaneous branch of the first divison of the trigeminal nerve?
Herpes zoster opthalmicus caused by varicella-zoster. Usually in the elderly but may also be a presenting sign in HIV pts that predict increased risk of progression to AIDS.
A saw-tooth pattern of P waves that do not all conduct QRS complexes?
atrial flutter due to a re-entrant rhythm within the atria. A 2:1, 3:1, or 4:1 heart block is often seen.
A P-wave that is morphologically distinct from those originating in the sinus node; will also occur prematurely and may not conduct to the ventricles?
atrial ectopy
Suspect what in a pt with diffuse telangiectasias, recurrent severe epistaxis, and widespread AV malformations in the mucous membranes, skin, GI tract or even the liver, brain, and lung?
Osler-Weber-Rendu sydrome aka hereditary telangiectasia.

Note: AVMs in the lungs can shunt blood from the right to the left side of the heart causing chronic hypoxemia and a reactive polycythemia. They can also present as massive hemoptysis.
The use of anti-estrogen, tamoxifen, reduces the risk of recurrence of breast cancer from the original site or a new breast site, but increases the risk of ________, _______, and _______?
endometrial cancer, uterine sarcoma and venous thrombosis.

Tamoxifen has a mixed agonist and antagonist activity.
Diarrhea due to Vibrio parahaemolyticus is usually transmitted by the ingestion of ?
seafood including shrimp, crab, and raw oysters
Post-splenectomy pts are at increased risk for sepsis from encapsulated organisms due?
impaired antibody-mediated opsonization in phagocytosis - antibodies produced by germinal center plasma cells enter the systemic circulation to bind specific antigens and facilitate phagocytosis via opsonization which is not possible in asplenic pts.
Fever every 48 hours occurs with what type of malaria?
P. vivax and P. ovale
Fever every 72 hours occurs with what type of malaria?
P. malariae
Type of malaria with no periodicity?
P. faciparum - most malaria deaths are due to faciparam malaria
"Smudge cells" are characteristically seen in?
CLL - a disease of mostly older patients. Pts are often asymptomatic and diagnosed due to incidental finding of lymphocytosis with a peripheral blood fil showing small, mature-appearing lymphocytes. Symptomatic pateints usually c/o lymphadenopathy.
What indicates a poor prognosis in CLL?
thrombocytopenia
Chronology of disease progression in measles caused by Paramyxovirus?
1) exposure to the virus transmitted via respiratory droplets.
2) Prodrome of cough, coryza, and conjunctivitis after 10 days
3) Koplik's spots appear ~48 hours BEFORE skin rash and slowly fade once the rash appears.
4) Rash is initially over the face and then spreads to cover trunk and extremeties.

Koplik's spots are red spots with bluish specks over the buccal mucosa opposite the premolar tooth.
Complications are pneumonia, Vit A deficiency, and bronchiectasis. Late complications include immunosuppression and subacute sclerosing panencephalitis.
What type of thyroid cancer has the propensity for early hematogenous spread to the lung, brain, and bones?
Follicular thyroid cancers - they can be differentiated from follicular adenomas by histopathological demonstration of invasion of the capsule and blood vessels.
Most common thyroid malignancy?
Papillary throid cancer characterized by psammoma bodies. Fine needle aspiration biopsy reveals large cells with ground glass cytoplasm, and pale nuclei with inclusion bodies and central grooving.
Prognosis of papillary thyroid cancer?
excellent even in the presence of metastasis
sensory and reflex abnormalities on PE generally indicate?
neuropathies due to peripheral nerve problems
What should be suspected with absent/diminished reflexes at rest but improved muscular strength with repetitive tasks?
PREsynaptic membrane damage, i.e. Lambert-Eaton syndrome
paraplegia/quadriplegia with sensory abnormalities and urinary retention/incontinence on PE generally indicates?
some type of myelopathy originating from damage to the spinal cord
Even with therapeutic range INRs, there is significant risk of _______ with warfarin treatment?
Retroperitoneal hematoma - should be suspected with back pain and hemodynamic compromise. Dx with an abdominal CT.
DOC for trigeminal neuralgia?
carbamazepine - effective in approx 80% of cases.

Note: Risk of aplastic anemia; therefore routine CBC should be included in follow up management.
Tx for cluster headaches?
Sumatriptan and high-flow oxygen
Untreated hyperthyroid pts are at risk for?
Rapid bone loss resulting from increased osteoclastic activity (from direct effects of the thyroid hormones) AND cardiac tachyarrhythmias including A-fib.
Toxic adenomas causing hyperthyroidism do not cause proptosis as in Grave's disease bc?
there is no autoimmune process underlying the disease
Glucocorticoids cause what classic changes on blood cells?
1) Leukocytosis due to neutrophilia
2) Diminished eosinophils
3) Lymphopenia
DOC for treatment of myasthenia gravis?
oral anticholinesterase such as pyridostigmine or neostigmine. Atropine (anticholinergic agent) can be used to prevent muscarinic side effects of anti-ACh therapy.

Note: edrophonium can be used to diagnose MG but is no longer used
What is a complication that can arise in pts requiring multiple blood transusions or immediately after surgery that manifests as hyperactive deep tendon reflexes, muscle cramps, and sometimes convusions?
hypOcalcemia resulting from volume expansion and hypOaluminemia PLUS decreased IONIZED calcium due to citrate binding.

Note: severe hypOmagnesemia may mimic hypocalcemia bc it causes decreased PTH secretion and decreased peripheral responsiveness to PTH.
When is aspirin indicated as the ONLY antithrombotic therap in a pt with atrial fibrillation?
IN an otherwishe healthy pt with "lone" atrial fibrillation in the absence of other risk factors for stroke (CHADS2).
Indications for thyroid function tests?
1) hyperlipidemia, esp high LDL
2) unexplained hypOnatremia
3) elevated serum muscle enzymes
Drugs of choice for treating/preventing chemo-induced N/V?
serotonin ANTagonists that block 5HT3 receptors such as ondansetron. Corticosteroids are sometimes added to the regimen for better prophylaxis.
A rare malignancy that often arises in Hispanic and Southwestern Native American females with a hx of gallstones?
Gallbladder carcinoma - typically diagnosed after cholecystectomy. If discovered while still confined to the lamina propria of the gallbladder, a simple cholecystectomy results in a cure rate of 73-100% and is considered sufficient treatment.
Negative predictive value varies with?
pretest probability of a dz - a pt with high probability of having a dz will have a low NPV whereas a pt with low probability of having a dz will have a high NPV.
Known side effects of anti-tubercular therapy?
peripheral neuropathy due to pyridoxine deficiency (Vit B6) and hepatitis
Light's criteria to distinguish an exudative pleural effusion from one that is transudative:
1) pleural fluid protein/serum protein ration > 0.5
2) pleural fluid LDH/serum LDH ratio > 0.6
3) pleural fluid LDH greater than 2/3 of the upper limit of normal for serum LDH
How to determine if a pleural effusion is complicated?
Complicated fluids have:
1) a positive gram stain or cultures
2) pH < 7.2
3) glucose level < 60 mg/dL

Complicated effusions require a chest tube drainage.
Prophylaxis for a cluster headache?
prophylaxis is key to mgmt and includes verapamil, lithium, and ergotamine. Tx of acute attacks is inhalation of 100% oxygen and subcutaneous sumatriptan.
Tx for acute exacerbations of MS?
corticosteroids; beta-interferon or glatiramer acetate is used to decrease the frequency of exacerbations.
Evaluation for diarrhea in HIV-infected pts should include?
stool culture, examination for ova and parasites, and test for C. difficile toxin.
Suspect what in a pt over 50 years old with pain and stiffness in the neck, shoulders, and pelvic girdle with an elevated ESR and morning stiffness lasting OVER 1 hour?
polymyalgia rheumatica - treatment when NOT associated with giant cell arteritis is low-dose prednisone.

Note: pts indicate that pain is in the soft tissues and not the joints.
Characteristic findings in brain death?
ABSENT cortical and brain stem functions such as pupillary light rxn, heart acceleration after atropine injection, or spontaneous respiration.

The spinal cord may still be functioning; terhefore, deep tendon reflexes may be present.
Management of pts with probable benign prostatic hyperplasia based on hx and rectal exam?
urinalysis and serum creatinine to assess for infection, obstruction, or hematuria. Abnormalities warrant furter investigation.
Life threatening complication of succinylcholine used during rapid-sequence intubation?
Hyperkalemia leading to life-threatening arrhythmias - should not be used in pts at high risk for hyperkalemia such as those with crush/burn injuries more than 8 hours old (due to high risk of rhabdomyolysis), demyelinating syndromes like Guillain-Barre, and tumor lysis syndrome.

Vecuronium or rocuronium are better choice in these pts.
Most common cause of death in acromegaly?
cardiovascular accounting for ~ 38-62%.

acromegaly results from: high GH-->excess prodxn of IGF-1 --> excessive/abnormal bone and soft tissue growth including the heart leading to cardiomyopathy
What can help prevent contrast-induced nephropathy in pts with a hx of DM or chronic renal insufficiency (elevated baseline creatinine)?
Adequate IV hydration with isotonic bicarbonate or normal saline AND administration of acetylcysteine.

Contast-induced nephropathy presents as a transient spike in creatinine within 24 hours of contrast administration with a return to normal renal function within 5-7 days.
Suspect what in a pt older than 60 years with back pain that radiates to the buttocks/thighs and numbness/parasthesias that are worse during walking and lumbar extension and better with lumbar flexion?
Lumbar spinal stenosis due to two factors:
1) enlarging osteophytes at facet joints
2) hypertrophy of the ligamentum flavum

Dx via MRI.
Common extracolonic manifestations of inflammatory bowel dz?
1) skin findings such as erythema nodosum and pyoderma gangrenosum.
2) episcleritis
3) arthritis
4) cholangitis

p-ANCA is positive in ulcerative colitis.
What do inflammatory bowel dz and ankylosing spondylitis have in common?
HLA-B27 and presentation of arthritis is similar (low back pain/stiffness worse in the morning and improved with activity; plain radiographs show sacroiliac joint inflammation).
Suspect what with sharply localized pain over the anteromedial part of the tibial plateau just below the joint line of the knee (with possible complaints of exacerbation of pain while sleeping on one's side)?
Anserine bursitis - the result of abnormal gait, overuse, or trauma. A valgus stress test does NOT reproduce pain, thereby ruling out damage to the medial collateral ligament and XR will be normal. Treatment is rest, ice, and maneuvers that reduce pressure on the bursa. Corticosteroid injections into the bursa are helpful.
Most appropriate step in management of a pt with suspected recurrence of gouty arthritis?
synovial fluid analysis bc gouty arthritis cannot be reliably distinguished from septic arthritis (which can rapidly dstro the involved joint) or pseudogout based upon history and exam alone.

Synovial fluid analysis will reveal a WBC count of 2,000-50,000/ml and needle-shaped, NEGatively birefringent crystals under polarized light. Gram stain and culture will be negative.
Most appropriate step in managment of a young patient presenting with progressive low back pain and spinal stiffness of >3 month duration that typically improves with exercise?
XR demonstrating fused sacroiliac joints and/or bamboo spine caused by ankylosing spondylitis. It is a seronegative (negative for rheumatoid factor and ANA)spondyloarthropathy with a strong association with HLA-B27 (>90%).
Most likely diagnosis in a pt that is awakened by severe, acute pain in the great toe and describes occasional pruritus that can be "unbearable" after a hot bath?
Polycythemia vera-related gout. Myeloproliferative disorders are common causes of uric acid overproduction that can precipitate attacks of gouty arthritis.

Note: Polycythemia vera commonly causes splenomegaly and characteristic pruritis (due to histamine release from an increased number of circulating basophils).
Treatment of fibromyalgia?
Improves with TCAs and exercise.

Seen in women 20-50 years and is associated with fatigue, poor sleep, and depression.
A common complication of advanced osteoporosis?
compression fracture of the vertebrae - usually manifests as acute back pain withOUT any obvious preceding trauma. PE will show local tenderness and a normal neuro and musculoskeletal exam.

Note: Glucocorticoids predispose a pt to osteoporosis.

Note: Absent ankle reflex can be seen in elderly pts as part of the normal aging process.
Common complication of giant cell or temporal arteritis?
aortic aneurysms due to the involvement of the branches of the aorta. Pts should be followed with serial chest X-rays.
signs and symptoms of temporal arteritis?
symptoms such as headache, jaw claudication, muscle fatigue, and visual disturbance. PE may show scalp tenderness and a decreased temporal artery pulse. ESR is greater than 50 typically.
Prophylaxis for gout?
Allopurinol and probenecid - there is some risk of inducing uric acid RENAL stones with probenicid, so allopurinol is the first line agent.
Presentation of drug-induced serum sickness?
Symptoms of fever, urticaria, and arthralgias begin 1-2 weeks after administration of a drug such as penicillin, amoxicillin, TMP-SMX or cefaclor. Most commonly occurs in young children when a VIRAL infection is treated with an antibiotic agent.
How does degenerative joint disease (osteoartritis aka "wear and tear" arthritis) present?
Adults over 40 with indolent but progressive pain of the hands and weight bearing joints that is exacerbated by exercise and relieved by rest BUT sometimes with MILD morning stiffness (LESS than 30-60 minutes unlike rheumatoid arthritis). Unlike autoimmune processes, systemic symptoms are absent. Effusions may occur but joint will remain cool to touch. Bony crepitus, bony enlargement, and painful or decreased range of motion are common on exam. Synovial fluid analysis will reveal fewer than 2,000 WBC, no organisms, and no crystals.
What will a plain film of an osteoarthritic joint show?
narrowed joint space with osteophyte formation and subchondral sclerosis/cysts.
How many WBCs can be seen on synovial fluid analysis with septic arthritis?
> 50,000
What should be suspected with proximal muscle weakness PLUS an elevated ESR AND CK?
an inflammatory myopathy such as polymyositis or dermatomyositis - confirmed by muscle biopsy. Classic cutaneous findings include a rash over the face (with periorbital edema known as heliotrope sign), chst and lateran neck (called shawl sign), and on the knucles, elbows, and knees (Gottron's sign). Lichenoid papules overlying joints are known as Gottron's papules. Treated with high-dose corticosteroids.
Auto-antibody associated with dermatomyositis?
anti-Mi-2 (against helicase).
What type of regular screening should a pt with dermatomyositis undergo?
Cancer screening - over 10% will develop an internal malignancy, most commonly an ovarian cancer.
Suspect what if a woman in the fifth or sixth decade complanes of keratoconjunctivitis sicca (xerophthalmia, dry eyes), xerostomia (dry mouth), and other associated problems such as dental caries and difficulty swallowing?
Sjogren syndrome - diagnosed by the either the presence of lymphocytic infiltration of the salivary glands or serum autoantibodies against SSA (Ro) and/or SSB (La).

PE may reveal enlargement and firmness to palpation of the salivary glands. Due to the antimicrobial and lubricating properties of normal amounts of saliva, there is an increased incidence of dental caries and difficulty swallowing with Sjogren's syndrome.
Next step in management in a pt with rheumatoid arthritis?
disease modifying anti--rheumatic drugs (DMARDs): methotrexate is the initial drug of choice.
What is diagnostic of rheumatoid arthritis?
Lab testing shows rheumatoid factor and anti-cyclic citrullinated peptide, while XR shows joint erosions, uxt-articular osteoporosis and narrowing of joint spaces (most commonly affecting the proximal interphalangeal and metacarpophalangeal joints).
initial drug of choice for osteoarthritis?
acetaminophen
Most frequent cause of prosthetic joint septic arthritis?
Staphylococcus aureus via hematogenous spread.
Important adverse effect with use of methotrexate?
Macrocytic anemia, sometimes even pancytopenia. Routine peripheral blood counts should be taken every 3 months.

Methotrexate works by inhibiting dihydrofolate reductase which can lead to folate depletion. The addition of folic acid supplements can alleviate or prevent this side effect.

Other side effects include, nausea, stomatitis, rash, hepatotoxicity, interstitial lung dz, alopecia, and fever.
Who is at highest risk for osteomyelitis?
injection drug uses, patients with sickle cell anemia, and immunosuppressed pts. The vertebrae is frequently involved site in IV drug abusers.

Platelet count is often high as a marker of inflammation/stress and the ESR is significantly elevated (>100) as well. MRI is the most sensitive diagnostic study. Treatment is long term IV ABX with or without surgery.
Most common septic arthritis in young, sexually active pts?
Neisseria gonorrhea which may present in one of two ways:
1) an asymetric polyarthrits (often with tenosynovitis and skin rash) OR
2) isolated purulent arthritis affecting one or a few joints.
**In some, an asymmetric polyarthritis will precede purulent monoarthritis.

Dx may be confirmed by gram stain of synovial fluid, blood cultures, urethral cultures or skin cultures.
What is tennis elbow?
Lateral epicondylitis that manifests as pain with supination or extension of the wrist and point tenderness just distal to the lateral epicondyle. Can be caused by a variety of activities that involve repeated forceful wrist extension and supination such as backhand in tennis or use of a screwdriver.

Underlying pathophysiology: degeneration of the extensor carpi radialis brevis tendon near the lateral epicondyle.
What does "neuropathic claudication" in lumbar spinal stenosis mean?
Exacerbation of leg symptoms with walking (similar to PVD). However, unlike PVD, the symptoms are positional. Extension (e.g. standing and DOWNhill walking) exacerbate symptos bc this narrows the spinal canal, whereas fexion (e.g. sitting and UPhill walking) improves symptoms bc it widens the spinal canal.
Manifestations of sarcoidosis?
cough, dyspnea, erythema nodosum, antrior uveitis, and acute polyarthrits.

CXR shows hilar adenopathy with or without reticulonodular infiltrates. Bioposy will reveal NONcaseating granulomas. Elevated serum ACE may be elevated.
Treatment for symptomatic sarcoidosis?
Systemic glucocorticoids. Asymptomatic sarcoidosis is often followed without treatment due to the high rate of spontaneous remission.
Lab and radiographic evidence that supports the diagnosis of psuedogout?
fever, leukocytosis with a left shift, and chondrocalcinosis (calcified articular cartilage). Synovial fluid analysis (needed for diagnosis) IDs rhomboid, positively birefringent crystals.
Settings that may precipitate pseudogout?
trauma, surgery, or medical illness.
Characteristics of SLE induced arthralgia/arthritis?
Affects greater than 90% of pts but is considered NON-deforming. Most commonly involves hands or knees. It is a migratory arthritis with pain that is often disproportionate to objective physical findings.
First line therapy for reactive arthritis?
NSAIDs
Triad for reactive arthritis (Reiter syndrome)?
conjunctivitis, Asymmetric oligoarthritis, and nongonococcal urethritis. Arthritis often involves knee and sacroiliac spine.

Note: mucocutaneous lesions (ulcers) and enthesitis (Achilles tendon pain) are common too!
Red flags that warrant investigation rather than conservative treatment of back pain?
1) Age over 50
2) Hx of previous cancer
3) Unexplained weight loss
4) Pain greater than 1 month duration
5) Nighttime pain causing difficulty with sleep
6) No response to previous therapy
7) Neurologic syndrome

**Initial test of choice is plain films to look for lytic lesions and compression fractures.
Pain aggravated by pushing, pulling, lifting the arm above the head, and lying on the affected shoulder is most likely due to?
Rotator cuff tear vs. rotator cuff tendonitis. Lidocaine injection can help distinguish btn the two - amelioration of pain with injection indicates tendonitis whereas no improvement indicates a tear. MRI is the study of choice for confirmation of diagnosis.
Most likely cause of proximal muscle weakness with associated fatiguability, tremor, anxiety, and weight loss?
Thyroid myopathy (in this case hypErthyroidism but can also be caused by hypothyroidism). Causes predominantly proximal muscle weakness. Search for additional symptoms of thyroid dysfunction to confirm diagnosis.
How to distinguish btn thyroid myopathy and myasthenia gravis causing proximal muscle weakness?
MG will more than likely involve eye and bulbar musculature whereas thyroid myopathy will not.
How can a viral arthritis be distinguished from other symmetric inflammatory arthritides (namely RA and SLE)
It tends to resolve within 2 months.

Positive rheumatoid factor may occur in RA, viral or bacterial infection, malignancy, and in normal individuals.

ANA is sensitive for SLE but can also be present in RA, hepatitis, and HIV. Weakly positive ANA can be found in approx 5% of normal individuals!

Treatment for viral arthritis is NSAIDs. Antiviral therapy is unnecessary as symptoms are self-limited.
What should be suspected if a pt complains of pain with active range of motion of the shoulder, passive internal rottion, and forward flexion but with no signs of deltoid atrophy?
Subacromial bursitis - typically occurs in the setting of chronic microtrauma to the supraspinatus tendon caused by overhead work and repeated overhead movements of the arm during work or sporting events. The tendon is traumatized by compression btn the acromian and the humeral head, and its vascular supply may be temporarily compromised during such episodes of compression. The subacromial bursa lies btn the acromian and the tendon of the supraspinatus muscle.
A tear of the proximal end of the long head of the bicep tendon is associated with?
rotator cuff injury and typically occurs during forceful flexion of the arm. Patients present with a prominent bulge in the midportion of the upper arm. Axillary nerve injury may occur as a result of anterior dislocation of the humerus out of the glenoid fossa.
The axillary nerve supplies?
the deltoid and the teres minor with motor innervation - palsy of this nerve would result in paralysis and ultimately denervation atrophy of these muscles.
Precipitating factors for osteonecrosis? (aka aseptic necrosis, avascular necrosis, ischemic necrosis, and osteochondritis dessicans)
Chronic corticosteroid use and chronic excessive ingestion of alcohol account for over 90% of cases. Other factors include trauma and antiphospholipid syndrome.

Pathogenesis: bone vasculature is disrupted --> bone and bone marrow infarction --> trabecular thinning --> ultimately causing collapse of the affected bone.

**process may take months to years and presents with ANTERIOR hip pain worsened by activity and relieved rest with progressive limitation of range of motion. Will ultimately cause joint instability and pain at rest.

MRI is the most sensitive test for this condition.
Suspect what if a pt complains of painful joints with the formation of tumor-like protrusions with lesions draining chalky white material?
Chronic tophaceous gout - begins with asymptomatic hyperuricemia and progresses to gouty arthritis, typically affecting the great toe first (called podagra). Uric acid crystals form in the renal tubules and collecting system resulting in nephrolithiasis. Urate crystals may deposit in the soft tissues forming tumors known as tophi which can ulcerate to drain chalky material.

Note: diuretics (especially HCT) have a hyperuricemic effect from hypovolemia-associated enhancement of uric acid reabsorption in the proximal tubule.
Suspect what with normal serum calcium and phophate levels BUT INCR alk phos and urinary hydroxyproline levels?
Paget disease of bone (osteitis deformans) - disorder of accelerated and disordered osteoclastic bone resorption of uncertain etiology. Incr bone resorption --> disorganized formation of lamellar or woven bone (inherently weaker than normally formed bone) --> pain and bowing of lower extremity weight bearing bones --> hypertrophy of skull compresses the vestibulocochlear nerve causing deafness.

Lab abnormalities include elevated alk phos plus urinary markers of bone degradation such as hydroxyproline, deoxypyridinoline, N-telopeptide and C-telopeptide.
CREST syndrome refers to what constellation of findings?
1) Calcinosis cutis - localized dystrophic deposition of calcium in the skin that appear as nodules typically on the upper extremities. May ulcerate and drain a chalky material like chronic tophaceous gout.
2) Raynaud phenomenon - acute bouts of digital ischemia in response to cold and may lead to digital necrosis.
3) Esophageal dysmotility - dysphagia and GERD
4) Sclerodactyly - fibrosis of skin on fingers distal to MCP joints resulting in "shiny appearance," flexion contractures, and joint pain.
5) Telangiectasias - "mat-like" patches most common on the face and palms.
What are firm, flesh-colored, NON-tender nodules found over pressure points such as the elbow and extensor surface of the proximal ulna?
rheumatoid nodules - almost all will have positive rheumatoid factor.
What are Heberden and Bouchard nodes?
hard, bony nodules over the DIP and PIP joints, respectively.
Mechanism involved that leads to joint trauma in neurogenic arthropathy aka Charcot's joint?
nerve damage - process starts with decreased pain, proprioception, and temperature perception. As normal neurologic input is lost, pts unknowingly traumatize their weight bearing joints. XR's will show loss of cartilage, osteophyte development, and loose bodies. Associated pain is typically mild. Management includes treating the underlying disease and providing mechanical devices (special shoes) to assist in weight bearing and decrease further trauma.
Diseases that can lead to neurogenic arthropathy aka Charcot's joint?
DM, peripheral nerve damage, syringomyelia, spinal cord injury, B12 deficiency, or tabes dorsalis.
In chronic gout, what may an XR of the joints show?
punched-out erosions with overhanging rim of cortical bone known as "rat bite" lesion.
Typical population that is affected by ankylosing spondylitis?
Young men (2-3:1 ratio compared to women) under 40 years of age (most frequently btn 20-30 years). Symptoms are typically worst in the morning and improve as the day progresses. Associated findings iclude arthritis of the peripheral joints and anterior uveitis.
Side effects of methotrexate treatment (first line drug for RA)?
stomatitis (ulcers), nausea, abdominal pain, fever, LFT elevation 2dry to hepatotoxicity and anemia 2dry to myelosuppression.
triad of Felty syndrome?
Rheumatoid arthritis, splenomegaly, and granulocytopenia with neutrophil < 2,000/mm3). Granulocytopenia generally does not occur until symptoms of arthrits have been present for over 10 years.
Suspect what in a patient over 50 years with NEW-onset temporal headache, jaw claudication, vision loss, or symptoms of polymyalgia rheumatica?
temporal arteritis - immediate empiric treatment with high dose steroids is necessary, especially to prevent visual loss.

Note: ESR will be elevated and temporal artery biopsy will provide definitive diagnosis.
Important preventative measures to prevent gouty attacks?
1) alcohol cessation: ethanol is metabolized to lactate, which competes with urate for renal excretion, leading to accumulation of urate in the body.
2) eating a low purine diet
3) avoiding drugs such as diuretics and pyrazinamide.

Tx of ACUTE attack: NSAIDs, colchicine, or steroids.
What are Baker cysts?
A result of excessive fluid production by an inflamed synovium that occurs in cases of RA, osteoarthritis, and cartilage tears. Excess fluid accumulation expands in the poplitieal bursa, creating a tender mass in the popliteal fossa. They can occasionally burst to release their contents into the calf, resulting in an appearance similar to a DVT.
Most prominent extraarticular manifestation of ankylosing spondylitis?
anterior uveitis
Bone demineralization is present in _________ and _________.
osteomalacia and osteoperosis.

osteomalacia is due to inadequate serum vitamin D, calcium or phosphorus resulting in demineralized osteoid. Osteoperosis is due to a decrease in bone mineral density.
Suspect what in a pt that has traveled to or is from an endemic area and presents with RUQ pain, diarrhea, leukocytosis, elevated alk phos, and tender liver mass on abdominal CT?
Amebiasis - most pts are asymptomatic but can develop liver abscess, dysentery, and other organ develpment. Those with liver abscess typically present with 1-2 weeks of fever, RUQ pain that starts wi 5 months of returning from an endemic aria, dysentery (1/3 of pts), and occasionally jaundice (<10% of pts).

Diagnosis is confirmed with ultrasound, CT, or MRI of SOLITARY liver lesion. Leukocytosis (>10,000) or an elevated alk phosphatase is also supportive. Serologic testing for antibodies should be performed to definitively r/o a pyogenic abscess. While awaiting serology results, treatment with oral metronidazole should be started which results in a cure for >90% within 7-10 days. If tests are negative or pt does not improve, alternative testing such as percutaneous drainage to rule out pyogenic abscess can be done.
Treatment for pyogenic abscess of liver?
Drainage and tx with oral metronidazole PLUS IV ceftriaxone.
POST cholecystectomy pain is due to one of three reasons:
1) common bile duct stone
2) sphincter of Oddi dysfunction
3) functional causes

Abnormal alkaline phosphatase or dilatation of biliary tree observed on ultrasound are indicators of either CBD stone or sphincter dysfunction. ERCP would be indicated to confirm and treat the condition, either through stone removal or sphincterotomy. No evidence of LFT abnormalities or dilation of biliary tree indicates functional pain with no obvious organic basis. Tx symptomatically with analgesics and reassurance.
Three major types of gallstones?
1) cholesterol
2) pigment
3) mixed

**cholesterol and mixed stones together comprise 80% of all gallstones in the Western population.
Pathogenesis of gallstones?
Water-INsoluble cholesterol is secreted in bile and converted into soluble micelles by bile acids and lecithin. Gallbladder hypomotility or excess cholesterol:bile salt ratio can cause cholesterol to precipitate into insoluble crystals which form gallstones.
Risk factors for formation of pigment gallstones?
chronic hemolysis (like in sickle cell anemia), chronic biliary tract infection or parasite infection; and advanced age.
Protective factors against development of gallstones?
low-carb diet, physical activity, consumption of caffeinated coffee, and aspirin or other NSAID usage.
Dx of cholelithiasis?
best confirmed with ultrasound. Tx for symptomatic cholelithiasis is laparoscopic cholecystectomy.
Treatment options for pregnant pts who experience repeated attacks of biliary colic?
cholecystectomy, preferably during the second trimester OR bile salt such as ursodeoxycholic acid to dissolve cholesterol stones. Gallstones frequently recur once treatment with bile salt is stopped, however.
Gallstones are common in what population?
fat, female, fertile woman of forty years.
Consider what diagnosis if a pregnant woman c/o intense pruritus, especially significant on the palms and soles and worse at night?
intrahepatic cholestasis - a fxnl disorder of bile formation that develops in the second and third trimesters of pregnancy and is characterized by intense, often intolerable generalized pruritus, especially significant on the palms and soles and worse at night.

Total bile acids are typically elevated and may be the only finding. If other liver studies indicating stasis are abnormal, it may include elevated alkaline phosphatase and total/direct bilirubin. Serum aminotransferases may be quite high, which requires ruling out viral hepatitis.
Treatment for intrahepatic cholestasis of pregnancy?
Relief and preventing complications! Relief is provided using ursodeoxycholic acid as it increases bile flow and can relieve pruritus. Maternal prognosis is good as condition resolves shortly after delivery with no hepatic sequelae. Condition may recur in subsequent pregnancy and affected women are at increased risk for developing gallstones.

Reducing complications is centered around the fetus bc known complications include fetal prematurity, meconium-stained amniotic fluid, and intrauterine demise. Preferred approach is early delivery once fetal lung maturity is established.
What is Reye syndrome?
fatty liver with encephalopathy seen exclusively in children younger than 15 years, and is preceded by a URI with influenza or varicella. Tx with aspirin (salicylates) significantly increases likelihood of developing Reye syndrome.

Characterized by headache, nausea/vomiting, excitability, delirium, combativeness, hypOglycemia, liver failure, and progressive CNS damage.
Morphological changes seen in liver showing Reye syndrome?
extensive fatty vacuolization of the liver withOUT inflammation due to diffuse mitochondrial injury.
Lab abnormalities found in Reye syndrome?
Elevated aminotransferases, ammonia levels, PT prolongation, hypOglycemia, and metabolic acidosis.
Treatment of Reye syndrome?
glucose with FFP and mannitol to cerebral edema.
Balloon degeneration with polymorphic cellular infiltrates seen in the liver indicates?
ACUTE alcoholic hepatitis
Panlobular mononuclear infiltration with hepatic cell necrosis with confluent hepatic cell necrosis connecting adjacent lobules (described as "bridging necrosis") in the liver indicates?
ACUTE viral hepatitis
CHRONIC active hepatitis has what morphological appearance?
mononuclear inflammatory cells that extend from portal areas to disrupt the limiting periportal plate of hepatocytes undergoing necrosis -- called "piecemeal" necrosis.
First diagnostic step in a pt suspected to have pancreatic cancer?
Abdominal ultrasound followed by abdominal CT if sono is nondiagnostic.
Prognosis of pancreatic cancer?
typically presents late and has a poor prognosis, even in those with potentially resectable mass. Five-year survival rate ranges from 10-30%, depending on nodal status.
Major risk factors for pancreatic carcinoma?
chronic pancreatitis, smoking, DM, and hereditary predisposition.
Typical presentation of pancreatic carcinoma?
Tumors of the pancreatic body or tail = pain and weight loss

Tumors of the pancreatic head = steatorrhea, weight loss, and jaundice.

**Pain is usually a dull upper abdominal (epigastric) pain that radiates to the back
Classic PE signs of pancreatic carcinoma?
Often PE is unremarkable aside from jaundice with an abdominal mass or ascites (present in only 20%). Metastatic disease may be indicated by a nontender but palpable gallbladder (Courvoisier's sign) OR left supraclavicular adenopathy (Virchow's node).
Tumor markers which may be elevated in pancreatic carcinoma?
CA 19-9 - but this can also be elevated in pts with jaundice and NO pancreatic cancer which reduces its utility as a screening tool. Postoperative monitoring of pancreatic cancer with CA 19-9 may be helpful in evaluating response to chemotherapy.
Most common underlying causes of cirrhosis?
chronic alcohol abuse and chronic viral hepatitis (mostly hep C but can also be caused by hep B).
How is infection with Echinococcus granulosus diagnosed?
Serology and CT showing "eggshell" calcification of a hepatic cyst.
Treatment of hydatid cysts from Echinococcus granulosus?
Aspiration is NOT indicated due to risk of anaphylactic shock secondary to spilling of cyst contents. Treatment is surgical resection under the cover of albendazole.
Classic criteria for acute cholecystitis?
1) usually develops after a large or fatty meal
2) sudden appearance of steady pain in the epigastrium or RUQ
3) Pain may radiate to right scapula
4) positive Murphy's sign - sharp arrest of inspiration with gallbladder palpation.
5) fever, vomiting, and leukocytosis.
6) Total bili may range from 1-4 mg/dL, and serum aminotransferases and alk phos are often mildly elevated.
Most likely cause of acute cholecystitis?
2ndry to gallstone formation in over 90% of cases, most commonly arising when a gallstone impacts in the cystic duct.

gallstone impacts cystic duct --> ingestion of fatty foods --> contraction of gallbladder against obstructed cystic duct causing severe colicky pain --> tissue behind duct obstruction becomes inflamed 2dry to bacterial overgrowth 2dry stasis --> subsequent ischemia can lead to gangree or perforation or abscess formation.
What should all patients with cirrhosis be screened for?
Esophageal varices by endoscopy. Primary prophylaxis to reduce the risk of bleeding is via beta blockers.
Two most common causes of acute pancreatitis?
alcohol and gallstones.

other major causes include medications and hypertriglyceridemia.
Why is ultrasound more sensitive than CT for detecting gallstones?
Many stones have bile and are isodense, therefore would not be seen on CT scan.
Initial diagnostic test in all pts suspected of experiencing a first attack of acute pancreatitis?
Ultrasound of the RUQ to search for the presence of gallstones. Abdominal CT scan is used to confirm the diagnosis of acute pancreatitis and identify complications.
What is a HIDA scan and what is it used for?
it helps track production and flow of bile from the liver to the intestine - an excellent tool to diagnose cystic duct OBSTRUCTION (cholecystitis). Not as useful in detecting nonobstructive gallstones (cholelithiasis).

Also known as cholescintigraphy, hepatobiliary scintigraphy, and hepatobiliary scan.
What is charcot's triad and what does it indicate?
Triad of fever, severe jaundice, and RUQ abdominal pain.

Indicates acute ascending cholangitis - an infection of the common bile duct.
What is Reynold's pentad and what does it indicate?
Charcot's triad of fever, severe jaundice, RUQ pain PLUS confusion and hypOtension.

Indicates suppurative cholangitis with need for urgent biliary decompression/drainage preferably by ERCP. Therapy typically includes sphincterotomy with stone removal and/or stent insertion.
Initial diagnostic test employed in suspected acute ascending cholangitis?
Ultrasound.
Treatment of acute ascending cholangitis?
after diagnosis with ultrasound, immediate supportive care and broad spectrum ABX. Sufficient in 80% of patients. Pts who do not respond to this treatment should undergo ERCP for biliary drainage. Early drainage can significantly decrease morbidity and mortality.
Most likely cause of acute pancreatitis in a patient with NO hx of alcohol use or gallstones but with the presence of eruptive xanthomas?
hypertriglyceridemia (over 1,000 mg/dL) - confirm with FASTING serum lipid profile
Downsides to using ursodeoxycholic acid for treating symptomatic cholelithiasis over surgical correction?
expensive, therapy is needed for several months before gallstones dissolve, 50% recurrence rate once the treatment is stopped.
What type of hyperbilirubinemia is found in Dubin-Johnson syndrome?
Conjugated!
How may a patient with Dubin-Johnson syndrome clinically present?
Icterus is evident but is typically otherwise normal. Icterus may be so mild that it only becomes evident in the context of a trigger such as illness, pregnancy, or oral contraceptive usage. ROUTINE labs are usually unremarkable including LFTs. Interestingly serum bilirubin can range from 2-5 mg/dL, but can ALSO be normal or extremely elevated! Diagnosis requires a direct bilirubin fraction of at least 50% and confirmation of high levels of urine coproporphyrin I (as opposed to coproporphyrin III in normal individuals). Total urine copropophyrin is in normal amounts.
Gross and histological appearance of liver in Dubin Johnson syndrome?
Grossly the liver is strikingly black. Histology shows dense pigment composed of epinephrine metabolites within the lysosomes.
What does hyperestrogenism in cirrhosis lead to?
gynecomastia, testicular atrophy, decreased body hair, spider angiomas, and palmar erythema
What stages of liver disease from alcoholism can be reversed by cessation?
fatty liver (steatosis), alcoholic hepatitis, and early fibrosis.

True cirrhosis with regenerative nodules is irreversible.
Two main causes of CONjugated hyperbilirubinemia?
1) intrahepatic causes from either intrahepatic obstruction (e.g. viral or autoimmune hepatitis, alcoholic hepatitis, drug reactions, 3rd trimester of pregnancy or postop states).

OR congenital defects in hepatic excretion (e.g. Dubin-Johnson, Rotor)

2) extrahepatic causes
What helps distinguish between the different causes for conjugated hyperbilirubinemia?
dominant aminotransferase elevation = hepatocellular disease

vs.
dominant alk phos elevation = intra- or extrahepatic biliary obstruction.

Those with predominant alk phos elevations should have an ultrasound or CT scan to rule out extrahepatic obstrcution. If nondiagnostic, next step is ERCP or PTC (percutaneous transhepatic cholangiogram).
Blood transfusions before what year are at risk for hep C or hep B?
screen for hep C if before 1992.

screen for hep B if before 1986.
What should be suspected in a patient with a palpable mass in the epigastrium 4 weeks after the onset of acute pancreatitis?
pseudocyst - not a true cyst as they lack an epithelial lining. Inflammatory fluid comprised of enzymes (amylase, lipase, enterokinase), tissue, and debris enclosed by a thick fibrous capsule. If amylase leaks out, serum amylase becomes markedly elevated.

Often resolves spontaneously so drain only if it persists for > 6 weeks, is greater than 5 cm in diameter, or becomes secondarily infected.

Note: ultrasound is the preferred means of imaging.
Treatment for hepatic encephalopathy?
1) correct precipitating factors such as hypOvolemia, GI bleeding, hypokalemia, metabolic alkolosis, hypoxia, sedative usage, hypoglycemia, and infection.

2) Lower blood ammonia level - typically with lactulose (a disachharide) that acidifies colonic contents thereby converting absorbable ammonia into nonabsorbable ammonium ION (an ammonia trap). Non-responders can be placed on ornithine-aspartate infusion or oral sodium benzoate.
3) Reduced-protein diet is recommended but not drastic limitation bc can lead to negative nitrogen balance.
Single most important test to assess the FUNCTION of the liver?
PT bc all clotting factors (except VIII) are made in the liver.
What would a progressive decrease in liver transaminase levels indicate?
either recovery from liver injury or that few hepatocytes are functional.
Marked increase in transaminases is indicative of?
ongoing tissue destruction in the liver.
Two drugs approved for treatment of CHRONIC hepatits B and what is an important predictor of response to these drugs?
interferon and lamivudine in patients with persistently elevated ALT levels, detectable serum HBsAg, HBeAg, and HBV DNA.

Degree of elevation of serum ALT is most important predictor of response to interferon and lamivudine - serum ALT should be more than 2 times the upper limit for a favorable response.

Note: in general, lamuvidine is more convenient (oral) with fewer side effects than interferon.
Vanishing bile duct syndrome (aka ductopenia) indicates?
primary biliary cirrhosis usually - rare!
Why does cirrhosis sometimes lead to decreased TSH, T4, and T3?
Primary pituitary failure -- hypothalamic-pituatary dysfunction can occur in pts with cirrhosis!
What is hepatic hydrothorax?
Transudative pleural effusions in patients with cirrhosis which are NOT 2dry to any underlying cardiac or pulmonary disease. Generally much more common on the right side and is thought to occur 2dry to small defects in the diaphragm which permit abdominal ascites fluid to pass into the pleural space.

Primary treatment is therapeutic thoracentesis followed by a salt restricted diet and diuretics. If that fails, the next best treatment is a transjugular intrahepatic portosystemic shunt (TIPS).
ALL chronic hepatitis C with elevated ALT, detectable HCV RNA, and histological evidence of chronic hepatitis of at least moderate grade are candidates for antiviral therapy with?
interferon and ribavirin - combination therapy has shown to be more beneficial than monotherapy.
Most common diseases causing liver metastasis?
primary tumors of the GI, lung and breast
Most important reversible risk factor for pancreatic cancer?
smoking

Note: alcohol consumption, gallstones, and coffee intake are not risk factors for pancreatic cancer.
What confirms diagnosis of Wilson's disease?
Gold standard for diagnosis is liver biopsy that demonstrates quantitative hepatic copper levels. More commonly, diagonsis is confirmed by the presence of low serum ceruloplasmin (particularly < 20 mg/dL) PLUS increased urinary copper excretion or Kayser-Fleischer rings.
Treatment for Wilson's dz?
First line meds include copper chelators like d-penicillamine or trientine. Oral zinc also helps as it prevents copper absorption. Liver transplantation may be the only option if there is fulminant hepatic failure or dz that does not respond to pharmacotherapy.
Pathogenesis of Wilson's dz?
genetic mutations causing poor copper metabolism by reducing the formation and secretion of ceruloplasmin and by decreasing the secretion of copper into the biliary system. Copper accumulates within the liver causing free radical damage and eventually leaks out and deposits in other tissues including the basal ganglia (hepatolenticular degeneration) and cornea.
The most serious form of acute pancreatitis that can lead to systemic hypotension and eventual shock?
Pancreatic necrosis - locally released and activated pancreatic enzymes can increase vascular permeability within and around the pancreas, leading to the loss of a large volume of plasma into the retroperitoneum. Release of pancreatic enzymes and other inflammatory mediators into the circulation can also cause SYSTEMIC inflammation, widespread vasodilation, capillary leak, and resultant hypotension.

Requires aggressive fluid resuscitation and ABX.
What serological marker helps diagnose acute hepatitis B during the "window" period when HBsAg has disappeared but anti-HBs has not appeared?
IgM anti-HBc. The IgG fraction of anti-HBc signals recovery from disease.
What signals active viral replication and infectivity of hepatitis B?
HBeAg - detectable shortly after appearance of HBsAg. Tends to disappear shortly after aminotransferase levels peak and before HBsAg is eliminated, and is followed by the appearance of anti-HBe. Should it persist for more than 3 months, there is increased likelihood of chronic hepatitis B.
What marker suggests the cessation of active viral replication and low infectivity in hepatitis B virus?
Anti-HBe
Risk factors for the development of pancreatic cancer?
family hx, chronic pancreatitis, smoking, DM, obesity, and a diet high in fat.

Alcoholism and gallstones are NOT risk factors.
What are choledochal cysts?
congenital abnormalities of the biliary tree characterized by dilation of the intra and/or extra hepatic biliary ducts or both. Most cases are related to an anomalous pancreaticobiliary junction, which leads to weakness and dilatation of the biliary wall due to the reflux of alkaline pancreatic secretions into the biliary tree.

Initial investigation of choice is an ultrasonogram followed by CT or MRI as needed.
Treatment for benign hepatic adenomas?
General consensus for all symptomatic hepatic adenomas is surgical resection. Complete regression of the tumor can happen with discontinuation of oral contraceptives but growth, rupture (risk approaches 40%), and malignant transformation (risk approaches 8-13%) can also take place.

Note: biopsy is contraindicated bc of risk of hemorrhage.
Where is the primary infection in a pt who has an amebic liver abscess?
in the colon leading to bloody diarrhea; the ameba is transported to the liver by portal circulation leading to liver abscesses.
First step in management of acute variceal bleeding?
Establish vascular access with two large bore IV needles or a central line. Fluid resuscitation should begin until necessary blood products can be transfused.

Next minimize risk of aspiration by securing airway and initiating gastric decompression with nasogastric aspiration.

Finally, control bleeding. Medical control of bleeding can start with vasoconstrictors like terlipressing (synthetic analogue of vasopressin), ocreotide, or somatostatin. Control of bleeding is established in 80% though rebleeding is very common especially during the 6 weeks following the initial hemorrhage.
What does fresh frozen plasma contain?
All clotting factors and plasma proteins and provides volume in hypotensive states.
What does cryoprecipitate contain?
factor VIII, Factor XIII, fibrinogen, and von Willebrand factor.
Suspect what in a pt with evidence of atherosclerotic vascular dz that presents with abdominap pain followed by bloody diarrhea but have MINimal abdominal exam findings?
ischemic colitis - most commonly in the splenic flexure bc it is supplied by end arteries.
Patients with ulcerative colitis should undergo routine surveillance for what?
colon cancer with yearly colonoscopies beginning 8-10 years after diagnosis.
An elevated _______ in a pt with ulcerative colitis should raise suspicion for?
an elevated alkaline phosphatase level raises suspicion for primary sclerosing cholangitis.
Suspect what in a pt with a 5-month hx of episodic retrosternal pain lasting about 15 minutes and precipitated by emotional stress and hot or cold food?
Diffuse esophageal spasm - diagnosed via manometry (motility study) that should repetitive, non-peristaltic, high amplitude contractions that are either spontaneous or after ergonovine stimulation.
Suspect what in a pt with cirrhosis and ascites that presents with fever and lethargy?
spontaneous bacterial peritonitis (SBP) - can be a subtle presentation. Fever and subtle changes in mental status are the most common signs with abdominal pain often LESS prominent than in peritonitis of other etiologies.

Diagnose with paracentesis - requires positive ascites fluid culture and PMN level greater than 250/mm3. Paracentesis should be done before ABX therapy. E. coli and Klebiella are the most common organisms - treat with third generation cephalosporin.
Suspect what in a pt with multiple episodes of thrombosis withOUT a clear precipitating factor?
hypercoagulability (clue can be elevated PT/PTT and fibrin split products).

In a younger patient the cause may be genetic whereas in an older patient the cause may be a primary malignancy.
triad of carcinoid syndrome:
flushing, valvular heart disease, and diarrhea

Note: elevated serotonin and its metabolites 5-hyroxyindole acetic acid (5-HIAA) are present in the blood and urine.
Pts with carcinoid syndrome are at risk of developing what vitamin deficiency?
niacin - due to the increased formation of serotonin from tryptophan. Tryptophan is needed to make niacin.

3 D's of niacin deficiency: diarrhea, dermatitis, and dementia
Suspect what in a pt with an enlarged NON-tender gallbladder and evidency of biliary obstruction?
carcinoma of the head of the pancreas - CT scan is the best initial test.
first step in management of uncomplicated diverticulosis?
high fiber intake
Suspect what in a pt with a hx of GERD that hs difficulty swallowing solids by not liquids withOUT anorexia or weight loss?
peptic esophageal stricture - caused by body's reparative response to chronic exposure to gastric acid. Strictures tend to appear as symmetric and circumferential narrowings on endoscopy.

Note: Adenocarcinoma generally occurs in pts who have had GERD for >20 years and presents with weight loss and Asymmetric narrowing of the esophageal lumen.
What type of peptic ulcer gets better after meals and what type gets worse after meals?
dudoenal ulcers = better after meals

gastric ulcer = worse after meals.
Treatment for duodenal ulcer disease?
90% are infected with H. pylori so ABX (amoxicillin plus clarithromycin) for eradicate causal organism and a proton-pump inhibitor for acid suppression.
Why does total parenteral nutrition increase the risk of gallstones?
TPN bypasses the gut therefore normal stimuli (fatty acids and protein in the duodenum) for the release of cholecystokinin (CCK) is impaired. CCK typically stimulates contraction of the gall bladder and bile release into the gut lumen. Without CCK, gall bladder stasis results in bile sludge which can lead to gall stone formation.
Suspect what in the absence of perstaltic waves in the lower 2/3 of the esophagus and significant decrease in lower esophageal sphincter tone?
esophageal dysmotility associated with scleroderma.

characteristic clues: "sticking sensation" in the throat or dysphagia accompanied by heartburn.
How to diagnose lactose intolerance?
Many ways:
1) Positive hydrogen breath test (after ingestion of lactose)
2) positive stool test for reducing substances
3) low stool pH and increased stool osmotic gap.

Note: there is NO steatorrhea
Most common cause of intermittent and occult lower GI bleeding in pts over the age of 65?
Angiodysplasia - a controversial clue may be a systolic ejection murmur at the right second intercostal space, most likely representing aortic stenosis. Can be seen on colonoscopy but often missed. Angiography is the gold standard test but rarely performed.
How can C. difficile-induced colitis be diagnosed?
cytotoxin assay in stool. Treat with oral/IV metronidazole. Oral (but NOT IV) vancomycin can also be used.
Lab tests that can help confirm hepatorenal syndrome?
Elevated creatinine and VERY low URINE sodium (< 10 mEq/L). Also, the absence of protein and blood in the urine is helpful bc it makes intrinsic renal disease less likely.
Pathogenesis of hepatorenal syndrome?
Pts with severe liver dz can develop generalized systemic vsodilation thought to be 2dry to generation of nitric oxide in the splanchnic circulation due to portal hypertension. This reduced peripheral vascular resistance causing renal hypoperfusion and pre-renal renal failure.
Anti-endomysial or anti-gliadin antibodies indicate?
celiac dz
anti-scl-70 antibodies indicate?
scleroderma
anti-centromeric antibodies indicate?
CREST syndrome
anti-mitochondrial antibodies indicate?
primary biliary cirrhosis
signs and symptoms of malabsorpton due to celiac dz?
1) bulky, foul-smelling floating stool
2) loss of muscle mass or subQ fat
3) pallor 2dry to iron deficiency anemia
4) bone pain due to osteomalacia
5) easy brusing due to vit K deficiency
6) hyperkeratosis due to Vit A deficiency.

Fatigue and weight loss are also common complaints.
Suspect what with steatorrhea and with a hx of severe intermittent epigastric pain?
chronic pancreatitis - look for alcohol consumption.
Differential for a pt with dysphagia for BOTH solids and liquids, as well as regurgitation?
Achalasia and pseudoachalasia (2dry to a neoplasm at the gastroesophageal junction).

Achalasia can be diagnosed with imaging studies showing a markedly dilated esophagus with decreased peristaltic contractions and smooth, "bird beak" tapering of the DISTAL esophagus. Achalasia results from degeneration of the neurons within the esophageal wall that control peristalsis. It is usualy idiopathic but can be 2dry to systemic disease (e.g. Chagas' disease, amyloidosis, and sarcoidosis).

An older pt (over 60) that also has weight loss should be evaluated for an underlying neoplasm via endoscopy.
What is toxic megacolon?
Symptoms of acute colitis with radiologic evidence of colonic dilation. Can rapidly progress to colonic perforation; therefore it is a medical emergency.
MCC of toxic megacolon?
ulcerative colitis.
Treatment for toxic megacolon?
it is a medical emergency - IV steroids are the drug of choice. Also, nasogastric decompression, IV fluids, antibiotics and bowel rest is needed.
Indication for esophagoscopy in management of GERD?
1) Empiric therapy with acid-suppressing drugs fails
2) pt has features of "complicated" disease (e.g. dysphagia, odynophagia, weight loss, overt or occult bleeding, and iron deficiency anemia) in addition to the typical symptoms of GERD (e.g. heartburn, regurgitation, or sour/bitter taste).
When is esophageal pH monitoring used for the management of GERD?
when empiric therapy fails AND endoscopy (aka esophagoscopy) is negative.
Diagnostic clues to chronic inflammatory diarrhea (such as IBD)?
weight loss and inflammatory changes in the blood such as anemia, elevated ESR, acute phase reactants, and reactive thrombocytosis. Positive occult blood or positive stool leukocytes are also important clues bc they are usually absent in other types of diarrhea (such as secretory and osmotic).
Suspect what in a pt with back pain, anemia, renal dysfunction, and elevated ESR?
multiple myeloma. another characterisitc finding in MM is hypErcalcemia from bone lysis caused by plasmocyte-released humoral factors.
Manifestations of hypERcalcemia?
severe constipation, anorexia, weakness, increased urination, or neurologic abnormalities (e.g. confusion or lethargy).
Always consider ________ as a cause of constipation.
hypERcalcemia
What explains the "shifting" phenomenon of abdominal pain from the peri-umbilical to the right lower quadrant that is classic for acute appendicitis?
In the initial stages, only the viscera are inflamed. Afferent visceral pain fibers from the appendix accompany sympathetic nerves and enter the spinal cord at the T10 segment which explains the peri-umbilical pain. Subsequent inflammation of the parietal peritoneum and skeletal muscles cause somatic pain which is well localized (RLQ) and more severe in intensity.
Stepwise approach to treatment for ascites:
1) sodium and water restriction
2) spironolactone
3) loop diuretic (not more than 1 L/day of diuresis bc can cause hepato-renal syndrome)
4) frequent abdominal paracentesis with/without albumin infusion (2-4 L/day, less aggressive if renal function is borderline).
Important risk factors for adenocarcinoma of the esophagus versus squamous cell carcinoma of the esophagus?
adenocarcinoma - Barrett's esophagus and GERD

squamous cell CA - smoking and alcohol are important ones among many others
What should be suspected in an adult immigrant patient who presents with high-grade fever, a severe sore throat with odynophagia and drooling, stridor upon respiration and tenderness to palpation over the larynx?
Epiglottitis - can still occur by Hib (especially in those from other countries) or Streptococcus pyogenes.
What part of the GI does Crohn's disease involve?
any component from the mouth to the anus, characteristically with skip areas of involvement. Even apthous mouth ulcers can be a component of the disease.

Note: Granulomas are identified pathologically in up to 30% of patients with Crohn's disease.
Suspect what in an elderly patient with poorly controlled diabetes that presents with ear pain and drainage?
Malignant otitis externa - most commonly caused by Pseudomonas aeruginosa. Ear pain and drainage is not responsive to topical medications. Granulation tissue may be seen within the ear canal. Progression of infection can lead to osteomyelitis of the skull base and destruction of the facial nerve. CT or MRI can be used to confirm the diagnosis.
Treat malignant otitis externa with what type of antibiotics?
SYSTEMIC abx that cover for Pseudomonas. TOPICAL abx are ineffective!
It is important to distinguish between what two differentials when a patient presents with a swollen and painful eye accompanied by fever but has a normal fundoscopy?
Orbital cellulitis (infection of the fat and muscles within the orbit) VS. preseptal cellulitis (infection that involves only the superficial tissues).

Protrusion of the eyeball (proptosis) and decreased visual acuity are usually only seen with orbital cellulitis. CT can be helpful if the clinical presentation is indeterminate or if there is concern for abscess. Treat requires IV broad spectrum ABX.

Note: Cavernous sinus thrombosis sometimes presents similarly to orbital cellulitis but is more often BIlateral with inolvement of cranial nerve III (resulting in ptosis) and V as well as early visual loss. Fudoscopy is usually NOT normal and reveals papilledema and dilated tortuous retinal veins.
Suspect what in a patient with hard to remove white patches in the oral mucosa?
leukoplakia that may lead to squamous cell carcinoma - caused by chronic irritation to the oral mucosa due to smoking, alcohol, or ill-fitting dentures.
Suspect what in a child patient who presents with continued ear drainage for several weeks despite appropriate abx therapy?
cholesteatomas - can be congenital or acquired. Congenital lesions are in pts around the age of 5 or younger. Acquired lesions are due to chronic middle ear disease that leads to formation of a retraction pocket in the tympanic membrane, which can fill with granulation tissue and skin debris. Complications of cholesteatomas include hearing loss, cranial nerve palsies, vertigo, brain abscesses or even meningits. Refer to an otolaryngologist!!
What disease consists of the following features: asthma, chronic rhinosinusitis, nasal polyposis, and bronchospasm or nasal congestion following the ingestion of aspirin or NSAIDs?
Aspirin exacerbated respiratory disease (AERD) - examination will reveal bilat, grey, glistening mucoid masses in the nasal cavities.

Note: food tastes bland secondary to anosmia from nasal congestion.
Suspect what in a patient who presents with severe, sharp headaches, low-grade fever, periorbital edema, and cranial nerve palsies?
cavernous sinus thrombosis (CST) - most are 2dry to a skin infection located in the medial aspect of the face (around eyes and nose) but ethmoid or sphenoid sinusitis can also cause this condition. Headache is usually the most common EARLY symptom, partly due to neuropathic pain from the irritation of V1 and V2 branches of the trigeminal nerve (which explains sharpness and location in the upper face). Cranial nerves III, IV, V1, V2 and VI all pass through the cavernous sinus and can be affected by CST. Low-grade fever and periorbital edema occur several days later due to impaired venous flow in the orbital veins.

Dx with MRI or CT with contrast of the orbits. Tx with IV broad spectrum abx. Sometimes anticoagulation, glucocorticoid therapy or surgery may be needed as well.
Suspect what in a patient who presents with a combination of vertigo, ear fullness, tinnitus, and hearing loss?
Meniere's disease - resulting from distention of the endolymphatic compartment of the inner ear. Episodes of vertigo last 20 min to 24 hours in addition to low frequency, sensorineural hearing loss and tinnitus. Acute symptoms may include vomiting, postural instability, and nystagmus. Triggers that increase endolymphatic retention should be avoided including alcohol, caffeine, nicotine, and high salt foods. A strict, salt restricted diet of 2-3 grams/day is recommended as initial therapy.
What s/sx should lead to suspicion for a diagnosis OTHER than UNcomplicated pharyngitis or tonsillitis?
1) a muffled voice or "hot potato voice"
2) deviation of the uvula
3) prominent UNIlateral lymphadenopathy

This condition is likely peritonsillar abscess and can be fatal! Treatment includes needle aspiration of the peritonsillar abscess and initiation of IV abx.
Dense intramembranous deposits that stain for C3 from a renal biopsy is a characteristic microscopic finding for?
membranoproliferative glomerulonephritis, type 2 - pts present with nephrotic range proteinuria and hematuria. It is caused by IgG antibodies (termed C3 nephritic factor) directed against C3 convertase of the alternative complement pathway.
What are most kidney stones composed of?
75-90% are composed of calcium oxalate (envelope-shaped on microscopy). Small bowel disease, surgical resection or chronic diarrhea can lead to malabsorption of fatty acids. unabsorbed fatty acids chelate calcium --> more oxalic acid free for absorption --> more likely calcium oxalate stones!
Calcium phosphate stones are common in?
primary hyperparathyroidism and renal tubular acidosis.
Uric acid stones (10-15% of renal stones) are common when?
urine is acidic or there is increased cell turnover (hyperuricemia). Dehydration is an important risk factor. Persistent stones due to hyperuricosuria can be treated with purine-restricted diet and allopurinol.
Cysteine stones (< 1% of renal stones) are seen in?
inborn error of metabolism leading to increased excretion of cysteine.
Struvite stones (10-15% of renal stones) are common when?
urine is alkaline bc of infection with urease producing bacteria (e.g. Proteus).
Most common causes of calcium stones?
1) idiopathic hypercalciuria: hypercalciuria, normal SERUM calcium, and absent metabolic dz. *most common form of hypercalciuria.
2) hypercalciuria due to systemic disorders (primary hyperparathyroidism, sarcoidosis)
3) hyperuricosuria
4) hyperoxaluria (due to large amounts of Vit C or green leafy vegetables or 2dry to IBD/short bowel syndrome).
5) Decreased urinary citrate
6) Renal tubular acidosis
7) chronic dz in urine output -- leads to precipitation of calcium salts.
Treatment for calcium oxalate urolithiasis (in order of importance)?
1) increased fluid intake (> 3L per day)
2)normal or increased calcium diet (1000 mg/dL is RDA)
3) dietary sodium restriction (<100 mEq/dL)
4) oxalate restriction (i.e. dark roughage, chocolate, and vitamin C)
5) decreased dietary proteins (i.e. beef, fish, eggs, and poultry.)
Medical treatment for urolithiasis?
Thiazides/amiloride diuretics - decreases urinary calcium excretion (primarily by inducing mild volume depletion which leads to a compensatory rise in proximal reabsorption of sodium and calcium) and prevents the precipitation of calcium in the urine.
What DM drug should be discontinued in patients with acute renal failure, hepatic failure, or sepsis?
Metformin - all increase the chance of developing lactic acidosis

Note: Pioglitazone is contraindicated in liver failure.
Hyperkalemia with significant changes should be rapdily treated with?
calcium gluconate to stabilize the heart cell membranes but effects are short-lived; therefore, agents to reduce the serum concentration of potassium such as insulin and/or sodium polystyrene sulfonate will also be necessary too!
Suspect what in a pt that presents with recurrent episodes of hematuria beginning several days after an upper respiratory infection (serum complement levels are normal)?
IgA nephropathy and post-streptococcal glomerulonephritis are major causes of hematuria after an URI. IgA nephropathy is the MOST common cause in adults and usually occurs less than 5 days after the URI. Post-strep glomerulonephritis averages 10 days after pharyngitis and 21 days for impetigo.
Treatment for overflow incontinence due to diabetic autonomic neuropathy?
Aside from strict glycemic control, intermittent catheterization and cholinergic medications such as bethanechol are options. Heavy alcohol intake may contribute so cessation is important.

Note: pts will have high post-void residual volumes in the bladder.
Suspect what in a patient who presents with palpable purpura, proteinuria, hematuria, and other nonspecific findings such as arthralgias, hepatosplenomegaly, peripheral neuropathy and hypocomplementemia?
Mixed essential cryogloulinemia. Most patients also have hepatitis C.
Two treatment options for end stage renal disease?
dialysis or renal transplantation. Renal transplant is always preferred due to better survival rates and quality of life. A living RELATED donor is best, followed by a living non-related donor and lastly a cadaveric donor.
What qualifies a cystitis infection as complicated?
infections in women who are pregnant, the very young or the very old, diabetics, immunocompromised, or those who have abnormal anatomy of the GU tract.
Management of uncomplicated cystitis?
Urine cultures are not indicated. Oral TMP/SMX and nitrafurantoin are the preferred empiric abx.
Drug that is used to treat serious gram-negative infections but are potentially nephrotoxic?
Aminoglycosides - drug levels and renal function must be monitored closely during therapy.
Suspect what in a young patient that presents with recurrent episodes of hematuria and proteinuria, sensorineural deafness, and a family hx of renal failure?
Alport's syndrome - microscopy shows alternating areas of thinned and thickened capillary loops with splitting of the glomerular basement membrane.
Most common causes of nephrotic syndrome not secondary to a systemic disease are?
minimal change disease, membranous nephropathy, and focal segmental glomerulosclerosis. Minimal change dz is most common in children. The other two are most common in adults, with more than 1/2 of cases in African American patients. FSGS also has an association with obesity, heroin use, and HIV.
Definition of nephrotic syndrome?
heavy proteinuris (> 3g/24 hours), hypoalbuminemia, and peripheral edema.
Pathogenesis of analgesic-induced papillary necrosis?
chronic tubulointerstitial damage - results from papillary ischemia induced by analgesic-mediated vasoconstriction of medullary blood vessels (vasa recta). Sometimes hematuria is prominent, and clots may form causing renal colic.
Peculiar side effect of rifampin?
red to orange discoloration of body fluids including urine, saliva, sweat, and tears.
How to distinguish between the following:
1) chronic bacterial prostatitis
2) inflammatory chronic prostatitis
3) non-inflammatory chronic prostatitis
4) acute bacterial prostatitis
All may present with irritative voiding symptoms.
1) Afebrile pts, normal urinalysis, prostatic secretions show leukocyte count > 10 WBCs/HPF and culture of secretions is POSITIVE.
2) Afebrile pts, normal urinalysis, prostatic secreatons show leukocyte count > 10 WBCs/HPF and culture of secretions is NEGATIVE.
3) Afebrile pts, normal urinalysis, prostatic secretions show a NML number of leukocytes and culture of secretions is NEGATIVE.
4) FEBRILE pt, suprapubic/perineal pain, exquisitely tender prostate is noted on rectal exam, urinalysis shows bacteruria and pyuria.
Tx for dehydration?
IV sodium-containing crystalloid solutions (usually 0.9% NaCl)

Classic signs of dehydration: dry mucosa, marginally high hematocrit and serum electrolytes, BUN/Cr ratio > 20.
Suspect what if a pt with typical renal colic does not show a stone on plain film?
1) radiolucent stone (uric acid stone)
2) calcium stones less than 1-3 mm in diameter
3) non-stone causes (obstruction by a blood clot or tumor)

All will likely show on an ultrasound or CT scan.
Cause and treatment of uric acid stones?
Commonly caused by unusually low urine pH levels (which may be due to a defect in renal ammonia secretion) and hyperuricosuria.

Hydration plus alkalinization of urine to pH > 6.5 with oral potassium bicarbonate or potassium citrate since uric acid stones are highly soluble in alkaline urine.

Also a low-purine diet with/wo allopurinol can be helpful depending on the presence of hyperuricosuria.
First step in management of acute renal failure/kidney injury due to possible urinary retention?
Foley catheterization - it can resolve various post renal obstructions and monitor urine output in prerenal and intrinsic renal failure.

Note: Urine sediment analysis is helpful in differentiating between prerenal and intrinsic renal failure. Muddy brown casts indicate acute tubular nephritis while eosinophilic casts indcate AIN.

IV fluids are critical in prerenal acute kidney injury caused by hypovolemia. In ADEquately hydrated patients with recent-onset oliguria due to prerenal or certain intrinsic renal causes, a loop diuretic to avoid volume overload can be helpful.
Meds commonly known to cause hyperkalemia?
ACE-I, NSAIDs, and potassium-sparing diuretics (such as amiloride and spironolactone).
EKG changes due to hyperkalemia?
early: peaked T waves

followed by prolonged PR interval and QRS duration, and eventual loss of P waves. Progressive widening of the QRS complex and merging with the T wave produces a sine-wave pattern. This can progress to V-fib or asystole.
Management of hyperkalemia?
10 mL of 10% calcium gluconate to stabilize the myocardial membrane WHEN signs of cardiac toxicity are present or potassium level > 6.5. Follow with insulin and/or beta-2 agonists to shift potassium into cells. Sodium bicarbonate can also be used for this purpose.

Slower acting treatments to increase potassium excretion include loop and thiazide diuretics IF renal function of pt is intact.

Dialysis is reserved for those with renal failure and severe life-threatening hyperkalemia unresponsive to conservative measures.
A simple renal cyst should NOT have the following findings:
1) multilocular mass
2) thickened, irregular walls
3) thickened septae within the mass
4) contrast enhancement

simple renal cysts are most common in patients over age 50. They do not require further evaluation.
Suspect what in a male patient with fever, painful enlargement of the testes, and irritative voiding?
acute epididymitis - In younger patients, it is usually caused by sexualy transmitted organisms such as C. trachomatis or N. gonorrhea and is assocated with urethritis (pain at the tip of the penis and urethral discharge). In older men, it is usually non-sexually transmitted and caused by gram negative rods such as E. coli and is associated with a UTI.
Varicoceles that FAIL to empty when a patient is recumbent should always raise suspicion for?
renal cell carcinoma - scrotal varicoceles are usually on the left side and due to obstruction of the gonadal vein where it enters the renal vein.

Most pts with RCC are Asymptomatic until the dz is advanced. Classic triad of flank pain,hematuria, and a palpable abdominal renal mass is uncommon (10% of patients). CT scan of the abdomen is the most sensitive and specific for diagnosing renal cell carcinoma.
Diagnostic procedure of choice for detecting renal stones?
CT withOUT contrast bc it can detect radioopaque (calcium) as well as radiolucent (uric acid) stones.
Dietary recommendations for patients with renal calculi are:
1) DECR dietary protein and oxalate
2) DECR sodium intake
3) INCR fluid intake
4) INCR dietary calcium
Why are patients with nephrotic syndrome at an increased risk for stroke or MI?
because of abnormal lipid metabolism (including elevated LDL and/or a low HDL) as well as intrinsic hypercoagulability (tends to affect the venous more than the arterial system, particularly the renal veins). Both factors lead to accelerated atherosclerosis! Aggressive management including statins or other meds to lower cholesterol is indicated.
It is important to consider what diagnosis in a male patient who presents with symptoms of a UTI?
acute prostatitis because acute CYSTitis is uncommon in men! Pts with prostatitis may also complain of pain in the perineal region and a tender, boggy prostate is often found on PE. Most appropriate next step in order to help direct antibiotic therapy is a mid-stream urine sample. Prostatic massage should be avoided as it can result in bacteremia. Urethral catheterization should be avoided due to inflammation involving the urethra. If urinary retention develops, suprapubic catheterization may be necessary.
When should a diagnosis for membranous glomerulonephritis in a CHILD with nephrotic syndrome be suspected considering minimal change disease is overall the most common cause?
In a pt with active Hepatitis B infection, particularly if the HBeAg is positive (possibly due to deposition of HBeAg itself in the glomeruli).
What should be suspected in a pt that presents with a hx of rheumatoid arthritis, enlarged kidneys, hepatomegaly, generalized edema, and 4+ proteinuria?
Amyloidosis causing nephrotic syndrome. Note that rheumatoid arthritis predisposis to amyloidosis. Renal biopsy will show amyloid deposits that exhibit apple-green birefringence under POLARIZED light after staining with Congo red.
What should be suspected in a patient with a hx of CRF that presents with abnormal hemostasis but normal PT, PTT, and platelet counts?
uremic coagulopathy - BT is reflective of platelet function and is usually prolonged. The platelet count is normal but there is platelet dysfunction that causes bleeding.
Treatment of choice for a uremic coagulopathy?
DDAVP - increases the release of factor VIII:von Willebrand factor multimers from endothelial storage sites. Platelet transfusion is not indicated bc the transfused platelets quickly become inactive.

Note: Major defect in uremic coagulopathies involves platelet-vessel wall and platelet-platelet interactions. Several uremic toxins have been implicated, the chief among which is guanidinosuccinic acid.
Which antidiabetic drug causes some weight loss?
Meformin - assess pt's renal status before starting on metformin
Algorithm for Cushing's disease:
1) 24-hr urinary free cortisol as a screening test - 90% of patients will have values greater than 90 microgram/24 hr.

2) Low dose dexamethasone test can also be used as a screening test - in patients wo any pathology, ACTH levels should decrease whereas in Cushing's, ACTH levels remain high.

3) Once a screening test is positive, plasma ACTH levels determine the etiology of the syndrome. Plasma ACTH levels > 20 pg/mL can occur in Cushing's and ectopic ACTH production.

4) High-dose dexamethasone suppression test can distinguish btn Cushing's and ectopic ACTH production. In Cushing's, the 24-hr urinary cortisol or serum cortisol levels will decrease by 50% of basal cortisol levels. NO suppression indicates ectopic ACTH prodxn.

This is explained by the fact that excess ACTH secretion from pituitary adenomas are only relatively resistant to negative feedback whereas most ectopic tumors are completely resistant to feedback inhibition.

Also, RAPD develoment of symptoms (hypokalemic alkalosis, pigmentation, and hypertension) is more indicative of ectopic secretion.
Management of diabetic gastroparesis includes:
1) improved glycemic control (delayed gastric emptying makes this difficult to achieve, often leading to post-meal hypOglycemia after insulin injection.
2) Small, frequent meals
3) Dopamine antagonists (e.g. metoclopramide, domperidone) before meals.
4) Bethanechol
5) Erythromycin - this drug interacts with motilin receptors and can promote gastric emptying
6) Cisapride - available only through manufacturer after documentation of need for drug and thorough assessment of the individual's risk factors for cardiac arrhythmia.
How does diabetic autonomic neuropathy of the GI tract manifest?
1) stomach involvment leads to gastroparesis with anorexia, n/v, abdominal bloating, and early satiety
2) small intestine involvement causes diarrhea due to bacterial overgrowth
3) large intestine involvement presents with constipation.
What is megestrol acetate used for?
anorexia associated with cancer
How to detect factitious thyrotoxicosis?
Signs/symptoms of hyperthyroidism but NO goiter or exophthalmos. Low TSH and elevated T3/T4. 24-hr radioiodine uptake test shows diffusely decreased iodine uptake by the thyroid. Biopsy shows follicular atrophy.
What causes hypertension in hyperthyroid states?
caused by hyperdynamic circulation - predominantly systolic hypertension and an increase in pulse pressure
What causes hypertension in hypOthyroid states?
increased systemic vascular resistance - predeominantly diastolic htn
Indications for parathyroidectomy?
Needed for all SYMPTOMATIC patients with primary hyperparathyroidism.

Criterion for ASYMPtomatic patients with primary hyperparathyroidism are:
1) serum calcium at least 1 mg/dL above the upper limit of normal
2) young age (< 50 years old)
3) bone mineral density less than T-2.5 at any site.
4) Reduced renal function.
What two differentials should be considered when lab results show hypercalcemia, hypophosphatemia, and inappropriately elevated PTH levels?
primary hyperparathyroidism and familial hypocalciuric hypercalcemia.

24-hr urinary calcium test helps distinguish the two. Levels > 200 mg indicate primary hyperparathyroidism while levels < 100 mg indicate the latter.
What is a sestambi scan?
Surgeons use it to assess and localize parathyroid adenomas for guidance to surgical approach.
Why is corrected calcium important?
It takes hypoalbuminemia into account. Albumin plays an important role in homeostasis of the 3 forms of calcium: ionized (active) form 45%, albumin-bound 40%, and bound to inorganic/organic anions 15%. Pts with low albumin may have low TOTAL plasma calcium but normal levels of ionized calcium therefore remain healthy.

For every 1 g/dL change in serum albumin from 4 g/dL, total calcium should be expected to decrease by 0.8 mg/dL.
Most prominent cause of primary adrenal insufficiency in developING countries?
adrenal tuberculosis - also, CT scan often shows calcification of both adrenal glands. tx is lifelong replacement with glucocorticoids and mineralocorticoids.
Most prominent cause of primary adrenal insufficiency in developED countries?
autoimmune adrenalitis (more than 80% of patients with primary adrenal insufficiency)
What is cosyntropin?
synthetic ACTH - should cause a rise in serum cortisol
Two etiologies of early morning hypERglycemia?
1) inadequate insulin dosage
2) Somogyi effect

Measurement of 3AM blood glucose is helpful in distinguishing the two. 3AM hypOglycemia will cause an incease in levels of counterregulatory hormones (i.e. epinephrine, norepinephrine, glucagon), which consequently increase the rate of glycogenolysis and gluconeogenesis. This eventually cuases elevation of the morning blood glucose level.
Lab values that confirm a diagnosis of SIADH?
low PLASMA osmolality (<280 mOsm/kg) with high URINE osmolality (>100-150 mOsm/Kg).

These patients are characterized by hypOtonic (i.e. low PLASMA osmolarity) hopOnatremia with euvolemia due to persistently elevated ADH levels in the absence of appropriate stimuli for vasopressin release.

Note: one cause for SIADH is NSAID therapy
First line treatment for micro- versus macroprolactinomas?
Medical treatment for both bc it not only results in normalization of prolactin levels but also significant reduction in tumor size! Use dopaminergic agents such as bromocriptine and cabergoline. Cabergoline is a new drug with fewer side effects.
Definition of a microprolactinoma?
less than 10 mm in diameter - manifests as amenorrhea and galactorrhea in women and hypogonadism in males. Usually does not cause problems with other pituitary hormones or a mass effect.
TSH-secreting pituitary adenomas lead to...
excess TSH levels which stimulate thyroid gland. Elevated circulating thyroid hormone levels with inappropriately normal/elevated TSH levls is characteristic.

Note: pathophysiology generally involves the overproduction of the ALPHA-subunit of TSH.
Most appropriate initial management of DKA?
rapid IV administration of normal saline and REGular insulin.

Note: bicarb administration is usually NOT indicated due to adverse effects.
Criteria to make diagnosis of DKA?
1) blood glucose > 250
2) pH < 7.3 or low serum bicarb < 15-20 mmol/L
3) detection of plasma ketones
Most common risk factor for foot ulcerations?
Diabetic neuropathy (seen in 80% of diabetics with foot ulcers) - even more than peripheral vascular disease and smoking.
Suspect what in a patient with decreased hearing, increased hat size, and increased alk phos levels?
Paget's disease - pt is usually over 40 years. Often asymptomatic but when symptomatic, first symptom is crainial enlargement, associated hearing loss, and occasional headaches.
Basic pathophysiologic mechanism in Paget dz?
abnormal bone remodeling -excess osteoclastic bone resorption with increased numbers of larger than normal osteoclasts at the involved sites --> compensatory activation of the osteoblasts --> immature bone deposition with transformation of normal lamellar and woven bone into a chaotic "mosaic" pattern
What labs can accurately reflect the extent and activity of Paget's dz?
1) alkaline phosphatase - marker of bone formation - used to assess the activity of disease as well as response to treatment
2) urinary n telopeptide - most commonly used as a marker of bone resorption
2)
Pathogenesis of osteomalacia?
Vitamin D deficiency --> decreased intestinal calcium and phosphorus absorption --> hypocalcemia stimulates parathyroid glands --> 2dry hyperparathyroidism brings the serum calcium levels to normal or near normal BUT increases urinary phosphate excretion

Note: Look for greater hypophosphatemia than hypocalcemia, especially in the early stages of osteomalacia
Differential diagnosis of NORMOtensive patients with hypokalemia and metabolic alkalosis includes?
1) diuretic use
2) surreptitious vomiting
3) Bartter syndrome
4) Gitelman syndrome

Clue: Urine chloride level is MARKEDLY elevated (> 20 mEq/L and most often >40 mEq/L) in Bartter and Gitelman syndromes.
Classic presentation of Bartter syndrome?
polyuria, polydipsia, and growht and mental retardation that presents early in life but can occur later in life too.

Defect is in sodium and chloride reabsorption in the thick ASCENDing limb of the LOH, resulting in hypovolemia and consequent activation of the renin-angiotensin aldosterone system (RAAS). Activated RAAS causes an incr in potassium and hydrogen ion secretion, leading to hypokalemia and metabolic alkalosis. Sodium tends to be normal!

Note: Gitelman syndrome is a subset of Bartter syndrome with a defect in the distal convoluted tubule causing the same sequence of events.
Most common cause of hypokalemia?
diuretic use - can be diffeicult to identify
How to distinguish between primary hyperaldosteronism and renin-secreting tumors, both of which are characterized by HTN?
Plasma renin activity - HIGH in renin-secreting tumors and low in primary hyperaldosteronism. Plasma aldosterone will be high in BOTH conditions. Serum sodium tends to be high in both conditions too.
Preferred treatment for Graves disease and the contraindications of treatment?
Radioactive iodine ablative therapy - most patients achieve euthyroidism with a single dose of radioactive iodine. Approx 10-30% will become hypOthyroid during first 2 years and 5% per year therafter. Usual time for initial improvement is 6-8 weeks after administration of radioactive iodine

Contraindications: pregnancy and very severe ophthalmopathy.
Suspect what in a patient that presents with hypertension, muscle weakness, and numbness?
Primary hyperaldosteronism - usually (85% of pts) caused by an aldosterone-secreting adrenal tumor. The rest have adrenal hyperplasia. Excess aldosterone in the body causes increased renal sodium reabsorption with resultant hypertension. Aldosterone also increases renal potassium loss with resultant MUSCLE weakness/numbness.
Most specific lab value that indicates primary hyperaldosteronism?
increased early morning aldosterone/renin ratio (>30) bc increased aldosterone suppresses renin.
American Diabetes Association guidelines for the diagnosis of diabetes mellitus?
Any 1 of the following:
1) HbA1C - over 6.5%
2) fasting plasma glucose over 125 mg/dl
3) plasma glucose > 200 mg/dl after 2 hours into a 75 g glucose tolerance test
4) random plasma glucose > 200 mg/dL

Note: all tests should be repeated bc false positives are high. Recommended that repeat testing be performed using the SAME screening test that was initially abnormal.
Management of non-ketotic hyperglycemia?
First and most important step is fluid replacement with NORMAL saline. Because of large volumes of glucose induced osmotic diuresis, pateints may require up to 8-10 L of normal saline to reach a euvolemic state. Normal saline can then be changed to half-normal saline.

Regular insulin should be administered.

Potassium should be administered in ALL cases once potassium reaches to the normal level. This is due to potential for hypOkalemia as K+ moves into the cells with administered insulin.

5% dextrse is given once blood glucose level has been lowered to 250 mg/dl by insulin therapy to prevent the development of cerebral edema.
Manifestations of hypercalcemia of malignancy due to prodxn of PTH related peptide?
Same effects that are seen with PTH secretion - including increased bone resorption, increased renal tubular calcium reabsorption, and phosphate secretion.
Suspect what in a patient that presents with symptoms of hypothyroidism despite elevated T3/T4 levels and a normal to elevated TSH level?
generalized resistance to thyroid hormones from receptor defects on the peripheral tissue. Patients usually present at an early age with growth and mental retardation; however pts with milder defects can present later in life.
What is sick euthyroid syndrome?
'Low T3 sydnrome' - any pt with an acute, severe, systemic illness may have abnormal thyroid function tests during the illness and while recovering from the illness. This is why TFTs are generally not performed unless there is a strong indication.

This condition is thought to be due to caloric deprivation and an increase in cytokine levels. Most common pattern is a fall in TOTAL and free T3 levels due to decreased peipheral conversion from T4 to T3. There is a rough correlation btn the severity of the underlying dz and fall in T3 levels. If illness continues for an extended period of time, serum T4 and TSH levels also decrease.

On recovery from non-thyroidal illness, pts often experience a modest, transient increase in serum TSH level, which is often misinterpreted as subclinical hypothyroidism.
Indications for treatment of Paget's disease:
1) bone pain
2) hypercalcemia of immobilization
3) neuro deficit
4) high output cardiac failure
5) preparation for orthopedic surgery
6) involvement of weight-bearing bones (to prevent deformities)

The initial goal is to establish which bones have been affected. Can be ascertained by full body bone scan, followed by radiologic confirmation in the documented areas of increased tracer uptake.

Symptomatic patients are best treated with oral or IV bisphosphonates. Calcium and vitamin D has NO effect on Paget's disease.
MEN II consists of?
1) virtually 100% will have C-cell hyperplasia or medullary thyroid carcinoma
2) 50% will have pheochrmocytoma
3) 20-30% have hyperparathyroidism
Best next step in a pt with suspected pheochromocytoma plus elevated serum calcium?
check serum calcitonin levels for possible medullary thyroid cancer (MEN II)
When is ACE-I therapy indicated in a diabetic?
when the patient has microalbuminuria, even if the blood pressure is normal. Microalbuminuria is a sensitive marker of renal microvascular damage.
Most helpful diagnostic test in a pt with suspected erectile dysfunction?
nocturnal penile tumescence - helps differentiate a psychogenic causes (these patients are eugonadal and still experience spontaneous erections during REM sleep and on waking up) VS. organic causes.
In patients with suspected MEN II syndrome, what is the recommended screening test?
genetic testing has replaced biochemical measurement of serum calcitonin. If genetic analysis is positive for a RET proto-oncogene (more than 95% of pts with MEN II have this mutation), total thyroidectomy is indicated.
What lab values can be expected in X-linked hypophosphatemic rickets?
Low serum phosphate due to RENAL phosphate wasting. There may also be a defect in 1-hydroxylase and as a result 1,25- dihydroxy vitamin D (calcitriol) may be low.

Serum calcium, PTH, alk phos, and 25-hydroxy vitamin D are all normal.
What lab values can be expected in psuedohypoparathyroidism?
low serum calcium, high serum phosphate, and high serum PTH. Alk phos and Vit D levels are WNL.
What effects on calcium metabolism, phophate, PTH, and vitamin D does renal failure have?
low serum calcium, high serum phophate, high PTH, and low 1,25 dihydroxy vitamin D.
Osteomalacia due to Vitamin D deficiency shows what lab values?
LOW 25-OH Vitamin D, low calcium, low phosphate, high PTH (secondary hyperparathyrodisim). 2dry increase in PTH brings calcium closer to normal values but makes hypophosphatemia worse.
What lab value indicates that microalbuminuria has progressed to macroproteinuria?
urine protein excretion of more than 300 mg/d - this is accompanied by progressive decline in GFR. Intensive blood pressure control is the most beneficial therapy to slow progression of diabetic nephropathy.
Immediate cessation of antithyroid drugs (propilthiouracil or methimazole) is indicated when?
any pt taking antithyroid drugs develops fever and sore throat suspicious of agranulocytosis caused by immune destruction of granulocytes (most cases occur wi 90 days of treatment). After stopping drug, measure WBC count. WBC < 1,000/cubic mm warrants permanent discontinuation whereas WBC count > 1,500/cubic mm makes antithyroid drug toxicity the unlikely source of fever/sore throat.
How does PARTIAL deficiency of 21-hydroxylase present?
in ADULThood as hyperandrogenism but NO salt wasting (therefore normal blood pressure).
What is the next best step in a male pt with suscpected secondary (central) hypogonadism indicated by low testosterone and low or INNAPPOPriately normal levels of gonadatropin levels?
prolactin levels - high serum prolactin inhibits release of GnRH thereby resulting in hypogonadism.
glycosylated hemoglobin is an excellent way to monitor CHRONIC glycemic control bc?
it is reflective of the pt's average glucose levels over the preceding 100-120 days (which correlates with RBC survival time). Generally a 1% increase in HbA1c corresponds with a 35 mg/dL increase in the mean plasma glucose level.
The most reliable indicator of metabolic recovery in a pt with diabetic ketoacidosis?
serum anion gap or arterial pH
Drugs of choice in diabetic neuropathy?
tricyclic antidepressants BUT TCAs can worsen urinary symptoms (due to cystopathy) and orthostatic hypotension (due to cardiovascular autonomic neuropathy). Gabapentin is an alternative for these patients.
Pathophysiologic mechanism of Addison's disease?
autoimmune! aka autoimmune adrenalitis. Pts with autoimmune adrenalitis also have autoimmune damage of other endocrine glands such as thyroid, parathyroid, and ovaries. Other non-endocrine autoimmune conditions such as pernicious anemia and vitiligo are also common.
How should patients with PID be managed?
1) Appropriate abx (ceftriaxone for gonorrhea and azithromycin for chlamydia)
2) Counseled on safe sex practices
3) encouraged to inform sexual partners in the past 60 days of their condition
4) Screened for HIV, syphillis, hepatitis B, cervical cancer (pap smear), and (if they have a hx of IV drug abuse) hepatitis C.
A PPD test is positive when?
1) induration > 5 mm in:
HIV-positive pts, with recent TB contact, signs of TB on CXR, or immunosuppressed.

2) Induration > 10 mm in:
Recent immigrants, IV drug abusers, exposure to high-risk settings (prisons, homeless shelters), or hx of DM or chronic kidney disease or malignancy or fibrotic lung disease.

Also children less than 4 years or teens exposed to high risk adults.

3) induration > 15 in:
healthy individuals with no risk factors
Treatment for a positive PPD test?
Isoniazid for chemoprophylaxis for 9 months PLUS pyridoxine to prevent isoniazid-induced neuropathy.

Isoniazid-induced hepatitis is still possible, so check LFTs periodically.
What is the gardener's disease?
Sporotrichosis from Sporothrix schenckii - initial lesion is a reddish nodule that later ulcerates, at the site of the thorn pick or skin injury. From this site of inoculation, the fungus spreads along lymphatics forming subQ nodules and ulcers.
Esophagitis in HIV usually occurs when the CD4 count is?
< 50/microL. Pts complain of swalloing and substernal burning. The most common agent is Candida. Start treating with oral fuconazole for 3-5 days. Failure to respond warrants further investigation with endoscopy, biopsy, and culture.
How to distinguish between a primary HIV infection and infectious mononucleosis?
1) Rash (unless antibiotics have been administered) and diarrhea are less likely in infectious mono.

2) Tonsillar exudates are uncommon in HIV.
What is Kaposi sarcoma?
Cutaneous lesions caused by human hersvirus 8 - lesions begin as papules and later develop into plaques or nodules. The color typically changes from light brown to violet. No associated necrosis of the skin or underlying structures.
Management of a healthcare worker that is exposed to HIV?
HIV serology and immediate initiation of aniretroviral therapy with 2-3 drugs.
Management of mucormycosis most often caused by the fungus, Rhizopus?
aggressive surgical debridement plus early systemic chemotherapy with amphotericin B.
Management of disseminated histoplasmosis in HIV pts?
Initial treatment with IV amphotericin B decreases the fungal load, and lifelong treatment with itraconazole prevents relapse.
Classic signs of secondary syphillis?
Bilateral symmetrical maculopapular rash involving the entire trunk and extremities (including palms and soles)! Also condylomata lata - broad exophythic formations which develop on the anogenital region or upper thighs and ulcerate subsequently. sSecond stage lesions may resolve spontaeously or even, never appear.
What is indicated in a pt suspected to have infectious mononucleosis with a negative heterophile test?
EBV-specific antibody test
Treatment for primary syphillis in a penicillin allergic patient?
single dose of oral azithromycin or a 2-week course of doxycycline
Treatment of Pneumocystis pneumonia (an AIDS defining illness when CD4 counts are < 200)?
TMP-SMX is the DOC.

Add oral prednisolone when PaO2 < 70 mmHg.
Clinical features of Pneumocystis pneumonia?
fever, DRY cough, exertional dyspnea, imaging that shows diffuse bilat intersititial infiltrates.
Most likely organism in osteomyelitis from a nail puncture wound?
Pseudomonas aeruginosa - treat with oral or parenteral quinolones and aggressive surgical debridement
What should be considered in the differential when a pt with mononucleosis-like symptoms and atypical lymphocytes have a negative monospot test?
CMV - usually presents withOUT pharyngitis and lymphadenopathy unlike EBV.
Suspect what organism with nausea and vomiting 1-6 hours after eating rice?
Bacillus cereus - from a PREformed, heat stable toxin.
Most common cause of pneumonia in HIV pts?
encapsulated bacteriadue to impaired humoral immunity, especially Pneumococcus
Streptococcus bovis endocarditis whould prompt investigation for?
colorectal or upper GI cancer
A tick bite infection that is indemic to the northeastern United States and causes hemolyis?
Babesiosis caused by Babesia. Unlike other tick-borne illnesses, rash is NOT a feature except in severe infection with thrombocytopenia which may cause a secondary petechial or purpuric rash.

Dx is made from Giemsa-stained blood smear. Tx is with either quinine-clindamycin OR atovaquone-azithromycin.
The characteristic rash of rubella starts where?
On the FACE and progresses to trunk and extremities. Prodromal symptoms include fever and occipital/posterior cervical lymphadenopathy. Adult women usually have associated arthritis!

Note: these patients usually have an unknown or not up to date vaccination status.

Also, measles (rubeola) can present with a similar rash that starts on the face but will have Koplik's spots and NO arthritis.
Most appropriate management for a pt suspected to have HSV encephalitis?
PCR for herpes simplex virus DNA from a CSF sample (not viral culture!). Start IV acyclovir without delay!
When can influenza virus be treated with more than bed rest and simple analgesics such as acetaminophen?
Antivirals are only effective within 48 hours of onset of illness.

Influenza A - amantadine and rimantadine

Influenza A & B - neuraminidase inhibitors zanamivir or oseltamivir are effective.

Note: treatment with antivirals shortens duration of symptoms by 2-3 days. Typical duration is usually 1-7 days. Most common in the fall and winter months.
Treatment of choice for CNS cryptococcal infection in AIDS pt?
IV amphotericin plus flucytosine.

Note: Cryptococcus grows as an "encapsulated" yeast on CSF cultures.
What can cause pulmonary cavitation in an HIV-infected patient?
many organisms: Mycobacterium tuberculosis, atypical mycobacteria, Nocardia, gram-negative rods, and anaerobes.
How to diagnose Nocardia related pulmonary cavitation if suspected?
A presumptive diagnosis can be made if sputum exam shows partially acid-fast, filamentous, branching rods.

DOC is TMP-SMX.

The lung is the most frequently involved organ and infection can manifest as nodules, reticulonodular pattern, diffuse pulmonary infiltrate, abscess, or cavity formation.
When should Doxycycline be avoided as first-line treatment for early Lyme disease and possible simultaneous ehrlichiosis (spread by the same vector)?
Children and pregnant/lactating mothers bc of possible skeletal and dental problems.

Amoxicillin is the preferred tx in these cases.
What other organ beside the liver (hydatid cysts) is commonly affected by echinococcosis?
lungs in 25% - transmitted in areas with sheep and dogs.
Poorly controlled diabetes predisposes patients to _______ which causes a bloody, necrotic infection of the nasal cavities and often involves chemosis, proptosis, and diplopia of the eyes?
mucormycosis caused by Rhizopus.
HIV pts should be on MAC prophylaxis at what point?
CD4 < 50/microL
How is disseminated histoplasmosis (occurs in immunocompromised pts) characterized?
Non-specific symptoms plus pancytopenia, hepatosplenomegaly, and PALATAL ulcers.
Suspect what in an AIDS pt with multiple ring-enhancing lesions on CT of the CNS?
toxoplasmosis - TMP-SMX for prophylaxis and empirical sulfadiazine and pyrimethamine is BOTH diagnostic and therapeutic.
Suspect what with a bright red, firm, friable, exophytic nodule in an HIV pt?
Bacillary angiomatosis caused by Bartonella - oral erythromycin is the ABX of choice.
Definition of febrile neutropenia?
absolute neutrophil count < 1500/microL PLUS a single temp reading of 100.9 OR a sustained temp of 100.4 for over an hour.

This is a medical emergency! Cover for Pseudomonas aeruginosa and treat with monotherapy or combination therapy!

monotherapy: cefepime, ceftazidime, imipenem, or meropenem.

Combo therapy: aminoglycoside plus an anti-pseudomonal beta-lactam.
What form of MS is characterized by well-defined acute episodes with NO significant disease progression btn episodes.
relapsing-remitting form of MS - several well defined clinical trials have proven that INTERFERON-BETA decreases the frequency of relapse and reduces disability in pts with relapsing-remitting form of MS.
An important complication of subarachnoid hemorrhage?
hyponatremia from "cerebral salt-wasting syndrome" - pathology involves (1) inappropriate secretion of vasopressin, which causes wter retention and (2) an increased secretion of atrial/brain natriuretic peptide, which causes cerebral salt wasting. Resolves wi 1-2 weeks.

Any intracranial hemorrhage can also cause SIADH leading to hyponatremia. Tx is water restriction.
Classic triad of normal pressure hydrocephalus?
abnormal gait, incontinence, and dementia - due to increased VENTRICULAR size withOUT persistent elevations in intracranial pressure.
Pathophysiology of normal pressure hydrocephalus?
TRANSIENT increase in intracranial pressure that causes ventricular enlargement. After ventricles enlarge, the pressure returns to normal. Initial increase in pressure is due to DIMINished CSF absorption at the arachnoid villi OR obstructive hydrocephalus.
Features of NML age-related cognitive changes?
tiredness, occasional forgetfulness, occasional word finding difficulty, and trouble falling asleep. Dementia canNOT be diagnosed unless there are functional impairments!
Best way to determine if a Guillain-Barry patient is at high-risk for developing respiratory failure?
SERIAL measurements of bedside vital capacity. VC below 15 mL/kg, especially with a clear downward trend indicates a significantly INCR risk for ventilatory failure.

Note: 20-30% will develop respiratory failure.
Antecedent to Guillain-Barre?
respiratory tract or GI (especially with Campylobacter infection) infection.
What is internuclear ophthalmoplegia?
A disorder of conjugate lateral gaze - eye shows impairment of ADDuction during gaze to the CONTRAlateral side. The opposite (contralateral) eye ABducts but with nystagumus. Same thing happens when gaze is changed to the other direction.

Convergence remains intact. Due to dysfunction in the MEDIAL LONGITUDINAL FASCICULUS, a characteristic finding in multiple sclerosis.
Exacerbationof neuro deficits by hot weather or exercise are a useful clue to what dx?
MS
Suspect what in a pt with rapid onset of severe pain and vision impairment with an effected that appears injected with a NON-reactive DILated pupil?
acute angle closure glaucoma - when a preexisting narrow anterior chamber angle is closed in response to pupillary dilation from medications (anticholinergics or sympathomimetics) or other stimuli (such as dime light). If untreated, can lead to severe and permanent vision loss in 2-5 hours after onset.
Typical presenting features of Huntington's?
mood disturbances (depression, apathy), dementia, anc chorea (facial grimacing, ataxia, dystonia, tongue protrusion, writhing movements of the extremities), and a family hx of similar symptoms.

Note: affects BOTH sexes equally. Age of presentation typically btn 30-50 years.
Approved treatment for amyotrophic lateral sclerosis that prolongs survival and time to tracheostomy?
riluzole - a glutamate inhibitor. Does not arrest underlying pathological process.

note: this is a neurodegenerative disorder NOT immunologically-mediated so corticosteroids and IVIG have no role in mgmt.
Most appropriate management for pt suspected to have an acute ISCHEMIC stroke?
1) First a NON-contrast head CT to confirm that stroke is ischemic and not hemorrhagic.
2) Confirmed ischemic stroke should be treated with fibrinolytics such as intravenous alteplase (tPA) within 3-4.5 hours of symptom onset.

Note: Anticoagulation with heparin is not recommended for acute ischemic stroke even if etiology is CARDIOembolic bc of increased risk for intracranial hemorrhage. However, warfarin anticoagulation should be started 2 wks after an acute CARDIOembolic stroke to prevent recurrence.
Pronator drift is a relatively sensitive and specific physical exam finding for?
upper motor neuron damage affecting the upper extremities. The supinator muscles are naturally weaker than the pronators so when pts close their eyes with arm extension and palms facing upward, an AFFECTED arm will tend to pronate. However, a pt that is faking will "drop" the affected arm withOUT pronating. Pt with strokes my demonstrate pronator drift.
Hemi-neglect syndrome affects what part of the brain?
the NON-dominant (usually right side) PARIETAL lobe, which is responsible for spatial organization.
Manifestation of a lesion to the POSTERIOR limb of internal capsule (typically from a lacunar infarct)?
UNIlateral motor hemiparesis of the face, arm, and leg withOUT loss of higher cortical function and NO visual field abnormalities.
Manifestation of middle cerebral artery occlusion?
CONTRAlateral hemiplegia, conjugate eye deviation TOWARD side of injury, and homonoymous hemianopia. Aphasia if the DOMinant hemisphere is involved OR hemi-neglect if the NON-dominant side is involved.
Manifestation of anterior cerebral artery occlusion?
CONTRAlateral weakness that affects predominantly lower extremities.
Manifestation of a lesion to the vertebrobasilar system (supplying the brain stem)?
"alternate" syndrome - CONTRAlateral hemiplegia BUT IPSIlateral cranial nerve involvement.
Suspect what in a pt that presents with Parkinsonism symptoms, plus orthostatic hypotension, impotence, incontinence, or other autonomic symptoms?
Shy-Drager syndrome aka multiple system atrophy, a degenerative dz characterized by:
1) Parkinsonism
2) Autonomic dysfunction (postural hypotension, abnormal sweating, bowl or bladder dysfunction, abnormal salivation/lacrimation, impotence, gastroparesis, etc.)
3) Widespread neuro deficits (cerebellar, pyramidal or lower motor neuron).

Note: Anti-Parkinson drugs are INeffective. Tx is aimed at intravascular volume expansion with fudrocortisone, salt supplements, alpha-adrenergic agonists, and application of contrictive garments to the lower body.
How is Riley-Day syndrome aka familial dysautonomia characterized?
seen predominantly in Ashkenazi Jewish children - gross dysfunction of the autonomic nervous system with severe orthostatic hypotension.
How doesa thalamic stroke present?
aka Dejerine-Roussy syndrome - caused by a stroke involving the ventral postero-lateral (VPL) nucleus of the thalamus, which ransmits sensory information from the contralateral side of the body.

Classic presentatin involves CONTRAlateral hemiANESthesia with accompanied TRANSient hemiparesis, athetosis, or ballistic movements. Severe DYSESTHesia (hypersensitivity to all kinds of stimuli inducing severe pain) of the affected area is also typical.
Most common causative organisms of brain abscesses?
aerobic and ANaerobic streptococci and Bacteroides species (ANaerobe).
An ISOLATED, round, smooth-bordered, ring-enhancing intracranial lesion on contrast CT scan of the brain in an immunoCOMPETENT pt is suspicious for?
brain abscess especially if there is a known extracranial infection. Streptococcus and Bacteroides (anaerobe) are the most common causes.
Suspect what in a pt with cafe-au-lait spots, axillary freckles, Lisch nodules of the iris, neurofibromas, and bony lesions?
Type 1 neurofibroma.

Note: Neurofibromatosis is a neurocutaneous syndrome with a tendency to form tumors in the CNS, PNS, skin and viscera.
Suspect what in a pt with brain tumors, especially bilateral acoustic neuromas?
Type 2 neurofibramatosis.

Note: Neurofibromatosis is a neurocutaneous syndrome with a tendency to form tumors in the CNS, PNS, skin and viscera.
Suspect what in a pt with ash leaf hypOpigmentation, cardiac rhabdomyomas, kidney angioleimyomas, mental retardation, and seizures?
Tuberous sclerosis: a neurocutaneous syndrome
Suspect what in a pt with port wine stains in the V1 cranial nerve distribution, angomatous malformations of the brain, seizures, and hemiparesis?
Sturge-Weber syndrome: a neurocutaneous syndrome
CSF analysis reveals what findings in Guillain-Barre?
INCR protein with remaining factors being NML (including glucose levels, WBC, and RBC counts).
How does anticholinergic excess present?
Red as a beet, dry as a bone, hot as a hare, blind as a bat, mad as a hater, and full as a flask which describes:
flushing, anhidrosis/dry mouth, hyperthermia, mydriasis/vision changes, delirium/confusion, and urinary retention/constipation.

Headache, dizziness and tachycardia can also be present: headache and retro-orbital pain is attributed to precipitation of acute glaucoma by anticholinergics!!!!!!

ex of anticholinergics: trihexyphenidyl, benztropine
Suspect what in a pt with hx of INTERmittent, painLESS vision loss (lasting a few seconds) with no other complaints and no hx of trauma to the eye BUT a medical hx significant for cardiac risk factors?
Amaurosis fugax - painLESS loss of vision from emboli, which is a warning sign for impending stroke. Most emobli occur from the carotid bifurcation. Hence a duplex ultrasound of the neck is often done to identify plaques that may be present.
Suspect what in a pt that presents with inability to move one-half of the face for 24 hours and absence of forehead furrows?
Bell's palsy (peripheral 7th nerve palsy). A central facial paresis can be ruled out bc patients with central lesions STILL HAVE forehead furrows due to intact contralateral MOTOR innervation.

So forehead muscles SHOULD be paralyzed in Bell's palsy whereas the forehead muscles are not paralyzed in a central lesion.
Suspect what type of lesion with a patient that has Broca's aphasia with right-sided weakness?
a left MCA infarct of the FRONTAL lobe, likely from a CARDIAC embolic source!

Note: Broca's area is in the left frontal lobe.