Cardio Path

Front 1

Differentiate full-thickness infarcts from subendocardial infarcts, telling how each classically occurs. Also identify EKG with each.

Back 1

- full thickness = POOR collateral blood supply = STEMI
- subendocardial = arterial obstruction in heart with GOOD collateral blood supply = ST depression

Front 2

13. Differentiate dilated, restrictive, and hypertrophic cardiomyopathies, telling how the gross and microscopic pathology would appear.

Back 2

1

Front 3

14. List at least four causes of fibrinous pericarditis, and tell how it is clinically diagnosed.

Back 3

1

Front 4

Define pericardial tamponade, and give an example of a lesion that may cause this.

Back 4

1

Front 5

Trace the natural history of atherosclerosis from fatty streak through complicated plaque, mentioning vessels at risk, location of lesions.

Back 5

- Fatty streak (lipid--oxidized LDL--laden foam cells in intima) created by endothelial damage, leading LDL into subendothelial intima. => Intermediate Lesion => Atheroma => Fibrous Plaques (late lesions: overlying fibrous cap, proliferation of smooth muscle, dystrophic calcification) => Foam cells die, forming cholesterol clefts and grumous debris => possibility now of atheromatous plaque and 2ndary thrombosis => complicated rupture

Front 6

Complications of the plaques? (4 of them)

Back 6

1). THROMBOSIS of the lumen, secondary to damage of the plaque surface.
2). EMBOLIZATION of the grumous plaque contents secondary to cracking of the fibrous cap.
3). HEMORRHAGE into plaque, resulting in ballooning of the plaque against the opposite wall of the artery.
4). WEAKENING of the wall of the artery, with ballooning out (aneurysm), which may rupture and bleed.

Front 7

List at least six known or suspected risk factors for atherosclerosis, and briefly explain what is known about how each factor affects the disease process.

Back 7

1. AGE. Atherosclerosis is a progressive disease, beginning in childhood, but usually clinically manifest only in middle aged to elderly adults.
2. GENDER. Males are affected earlier and more severely. Premenopausal females are relatively protected by estrogen. After menopause, though, the disease progresses in females, so that by the seventh to eighth decade of life, the incidence is similar to men.
3. ELEVATED LDL cholesterol. This reflects your heredity, your diet, (both cholesterol-rich and saturated fat-rich diets elevate), and your exercise habits.
4. CIGARETTE SMOKING. This probably directly damages vascular intima and oxidizes LDL into an atherogenic form.
5. HYPERTENSION. Presumably damages the intima in some way.
6. DIABETES MELLITUS. Diabetes is associated with hypercholesterolemia, and glycosylated proteins may damage the intima, making it permeable to lipids.
7. NO EXERCISE. Exercise lowers LDL, raises HDL, lowers blood pressure, increases vascular anastomoses, and has other beneficial effects. However, fit athletes can and do still get atherosclerosis.
8. THROMBOTIC TENDENCIES, either hereditary or acquired.

Front 8

What is the prognosis of being diagnosed with Monckeberg’s medical calcific sclerosis.

Back 8

- "non-disease", common but clinically harmless lesion of the elderly
- does not shrink the lumen or weaken the wall!

Front 9

Describe hyaline arteriolar sclerosis, listing known risk factors.

Back 9

- hyaline arteriolar sclerosis = slow build up of extracellular basement membrane-like material
- risk = diabetics, hypertensives, or after radiation

Front 10

Describe intimal fibrosis, listing known risk factors.

Back 10

- intimal fibrosis = slow build up of fibrous tissue in the intima, without lipid
- risk = aging, hypertensives

Front 11

Describe hyperplastic arteriolar sclerosis, listing known risk factors.

Back 11

- hyperplastic arteriolar sclerosis = onion skin’ proliferation of smooth muscle cells with narrowing of the lumen
- risk = very bad (malignant) hypertension => may result in actual necrotizing arteriolitis with fibrinoid necrosis.

Front 12

Define varicose veins, and tell who is at risk for this disorder. Describe complications of this disorder.

Back 12

- self-perpetuating, dilated, tortuous veins from a LOSS OF COMPETENCY OF THE VALVES IN THE VEINS in the legs => POOLING

Risk:
- Obesity
- Pregnancy
- Prolonged Smoking

Complications:
- secondary stasis changes in the skin including pigmentation (stasis dermatitis)
- ulcers

Front 13

Polyarteritis Nodosa

describe it. associated with?

Back 13

- affects small to medium sized arteries which show acute necrotizing inflammation
- any organ can be affected, and infarcts typically occur.
- about a third have hepatitis B, most of the rest are idiopathic.

- associated with p-ANCA (perinuclear anti-neutrophil cytoplasmic antibodies)

Front 14

Are advanced plaques reversible?

Back 14

Yes! Just improve your lifestyle, decrease risk factors.

Front 15

Microscopic Polyarteritis
(Leukocytoclastic Vasculitis)

describe it.

Back 15

- affects small vessels, often venules
- often a manifestation of a drug reaction
- involvement of skin results in palpable purpura (a bruise you can palpate)

Front 16

Wegener’s granulomatosis

describe it. associated with?

Back 16

- affects the lungs, kidneys, and upper respiratory tract, with granulomatous vasculitis.

- strong association with c-ANCA (cytoplasmic anti-neutrophil cytoplasmic antibodies)

Front 17

Thromboangiitis Obliterans (Buerger’s disease)

describe it.

Back 17

- DISTINCT vasculitis disease affects young SMOKERS
- inflammation and thrombosis of the tibial or radial arteries
- they often get GANGRENE!, and have bad pain

Front 18

Describe histologic and clinical findings in temporal (giant cell) arteritis. Any associated diseases?

Back 18

- histologically: SEGMENTAL INFLAMMATION
- lymphoid and macrophage type cells attacking the internal elastic lamina of cranial arteries

Clinical Presentation:
- common disease of the elderly
- HEADACHE WITH JAW CLAUDICATION
- elevated sedimentation rate

- 1/2 the pts associated with POLYMYLGIA RHEUMATIC (flu-like pain and weakness of muscles)

Front 19

Tell what complications Temporal or Giant Cell Arteritis has.

Back 19

- BLINDNESS! (from involvement of ophthalmic artery)

Front 20

Describe the role and limitations of clinical lab tests and biopsy findings in diagnosis of GCA.

Tx with?

Back 20

- diagnose with MULTIPLE SECTIONS OF BIOPSY (or may miss the lesion)

- tx with prednisone.

Front 21

congenital (berry) aneurysm

cause? where is it likely to occur? clinical presentation? complications? risk factors?

Back 21

Cause:
- HTN of any kind

Location:
- cerebral arteries (Circle of Willis)

Clinical Presentation:
- SUBARACHNOID HEMORRHAGE (worst headache of life, CNS deficits)

Complications:
- may burst causing SAH => quick death, strokes

Risk Factors:
- POLYCYSTIC KIDNEY DISEASE => simply because they have HTN

Front 22

atherosclerotic (abdominal aortic) aneurysm

where is it likely to occur? clinical presentation?complications?

Back 22

Location:
- aorta, below renal arteries (aorta lacks vasa vasorum below the renal arteries)

Clinical Presentation:
- usually ASYMPTOMATIC
- ruptured = triad = sudden FLANK pain, hypotension, palpable pulsatile mass

Complications:
- ruptured = LIFE THREATENING hemorrhage INTO RETROPERITONEUM

Front 23

syphilitic aneurysm aneurysm

where is it likely to occur? clinical presentation? complications?

Back 23

Location:
- ascending aorta, with dilation of aorta and aortic valve ring

Clinical Presentation:
- aortic regurgitation, cough/rough voice (recurrent laryngeal n)
- “tree bark” appearance grossly, plasma cells histologically

Complications:
- tertiary syphilis => ENDARTERITIS OBLITERANS (obliteration of vasa vasorum)

Front 24

dissecting aneurysm

where is it likely to occur? clinical presentation? complications? risk factors?

Back 24

Location:
- commonly ascending or descending thoracic aorta

Clinical Presentation:
- acute RETROSTERNAL TEARING PAIN, radiating to back
- aortic regurgitation = aortic valve ring dilation
- widened mediastinum & double barrel (2 lumens) aorta seen on imaging

Complications:
- CARDIAC TAMPONADE (retrograde extension of dissection into pericardium)
- blockage of aortic artery branches => subclavian arteries (loss of pulse in upper extremity) & coronary arteries, Spinal arteries, etc

Risk Factors:
- MARFANS & EHLERS DANLOS
- CYSTIC MEDIAL NECROSIS/DEGEN OF ERDHEIM (misnomer = no cysts, or necrosis)

Front 25

What is a hemangioma? What is it's micro/gross appearance? What are 2 types, and their prognosis?

Back 25

- benign vascular tumors

- micro: increased density of vessels
- gross: granulation tissue

- strawberry = congenitally, regress with time
- cherry = tiny ones in adults, do NOT regress with time

Front 26

mycotic aneurysm

what is this? what is a subcategory of this?

Back 26

- "INFECTIVE" Aneurysm

- SYPHLITIC is a subcategory of mycotic

Front 27

What is an angiosarcoma? What is it's micro appearance? What is the prognosis?

Back 27

- very agressive vascular malignancy seen as a brown-red growth

- endothelial cells bulge into vessel lumens

- rare, but HIGHLY FATAL

Front 28

What is Kaposi’s sarcoma? What is the progression like? Who is at risk? Associated with what virus?

Back 28

- raised red-purple discoloration

- flat lesion => plaque => nodule => ulceration

- AIDS PATIENTS AT RISK!
- elderly men of mediterranean descent

- Association with herpes virus 8 (HHV8)

Front 29

Stable angina pectoris

Pathogenesis? Causes? Clinical Presentation?

Back 29

Pathogenesis:
- decreased oxygenation affects SUBENDOCARDIUM (furthest from supply)

Causes:
- atherosclerosis of coronaries (decrease flow), LVH (increased requirements)

Clinical Signs:
- Exercise induced substernal chest discomfort, lasting less than 30 minutes
- Relieved by rest or nitro
- Exercise stress test shows ST depression (non-STEMI) on EKG

Front 30

UnStable angina pectoris

Pathogenesis? Clinical Presentation? What do you never do with them? What can it progress to?

Back 30

Pathogenesis:
- severe disease with clot on a pre-existing ruptured plaque

Clinical Signs:
- Frequent pain, onset with minimal exertion or at rest
- NOT relieved by rest or nitro
- May be a non-STEMI or STEMI

- NEVER DO A STRESS TEST on these patients
- Can PROGRESS TO A MYOCARDIAL INFARCTION (need immediate evaluation and treatment)

Front 31

Printzmetal’s variant angina

Pathogenesis? Clinical Presentation? (+, EKG?)

Back 31

Pathogenesis:
- VASOSPASM of coronary arteries

Clinical Presentation:
- comes on randomly, not always associated with activity
- EKG shows ST elevation (the ENTIRE vessel constricts => thus ENTIRE heart affected)

Front 32

Myocardial Infarction.

Pathogenesis? Causes?

Back 32

Pathogenesis:
- severe block of flow results in ischemic death of cardiac tissue

Causes:
- ATHEROSCLEROSIS (MCC)
- embolism
- vasculitis
- cocaine

Front 33

Myocardial Infarction

Describe the process in terms of thrombus formation.

Back 33

- rupture of atherosclerotic plaque => platelet aggregation and thrombus formation => blockage of flow & vasoconstriction (thromboxane A2 released by platelets)

Front 34

Myocardial Infarction

What property of a plaque makes it more vulnerable to rupture? What makes it less vulnerable?

Back 34

- Soft => can easily rupture and form clot
- Thick fibrous cap => less likely to form acute thrombus (thin = ruptures!)

Front 35

Myocardial Infarction

What is the main cause of problems in a plaque rupture?

Back 35

Plaque rupture => INFLAMMATION is key
- Inflammation leads to monocyte attraction and production of matrix metalloproteinases which digest collagen
- Inflammation also produces free radicals => oxidze LDL => more inflammation

Front 36

Clinical Presentation of MI?

Back 36

Clinical Presentation:
- Severe RETROSTERNAL CHEST PAIN, lasting over 30-45 minutes; not relieved by nitro
- PAIN RADIATES to left arm, shoulder, jaw, or epigastrum
- DIAPHORESIS (sweating), ANXIETY, S.O.B (shortness of breath)
- Note: Elderly and diabetics often have NO pain

Front 37

List the major complications of MI, noting when they are likely to occur. What is heard on auscultation?

Back 37

Complications:
- CARDIAC ARRHYTHMIAS: hours to days; MCC cause of death from MI is V-fib
- CHF (congestive heart failure) with cardiogenic shock: within first day
- RUPTURE: 3-7 days, weak granulation tissue replaces infarcted myocardium
(- Ventricle rupture => cardiac tamponade
- Papillary muscle rupture => mitral insufficiency
- Interventricular septum rupture => L to R shunt)
- FIBROUS PERICARDITIS: 1-7 days

- Chest pain relieved by leaning forward; FRICTION RUB heard on auscultation

Front 38

Can you use thrombolytics to fix an MI?

Back 38

- ONLY IF EARLY!!!
- if too late, then damage already done, and you cause REPERFUSION INJURY!

Front 39

Describe the use of serum enzyme creatine kinase in the diagnosis of myocardial infarction, including the relative sensitivity and specificity of these markers in diagnosis.

(? - Tell how thrombolytic therapies might affect these markers.)

Back 39

6h – 3d
Best for diagnosing re-infarction (troponins will still be elevated, which would give a false positive)

Front 40

Describe the use of myoglobin in the diagnosis of myocardial infarction, including the relative sensitivity and specificity of these markers in diagnosis.

Back 40

4h – 1d
Sensitive, but very non-specific

Front 41

Describe the use of troponin in the diagnosis of myocardial infarction, including the relative sensitivity and specificity of these markers in diagnosis.

Back 41

8h – 1wk
Gold Standard for diagnosis – sensitive & specific

Front 42

Define "shunt"

Back 42

abnormal blood flow through somewhere other than the usual channel

Front 43

Define "atresia"

Back 43

opening fails to develop or closes during development

Front 44

Define "jet lesion"

Back 44

high-velocity stream emerging from stenotic lesion => dilatation distal to stenosis

Front 45

Tell what the consequences of a left-to-right shunt within the heart are, and of a right-to-left shunt.

Back 45

left-to-right shunt = LATE cyanosis

right-to-left shunt = EARLY cyanosis

Front 46

Diagram Tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia, tracing the flow of blood through the heart.

Tell what additional lesions must be present in kids with transposition of the great vessels and tricuspid atresia to allow survival after birth.

Back 46

- Imagine it!

- ASD and PDA?

Front 47

Diagram ventricular septal defect, atrial septal defect, and patent ductus arteriosus, tracing the flow of blood through the heart.

Tell what additional lesions must be present in kids with transposition of the great vessels and tricuspid atresia to allow survival after birth.

Back 47

- Imagine it!

- Cyanosis?

Front 48

List common causes of aortic stenosis.

Back 48

Calcification
Chronic rheumatic fever

Front 49

List common causes of aortic insufficiency.

Back 49

Aortic root dilation
Endocarditis
Rheumatic fever
Chronic HTN
Coarctation

Front 50

Tell why patients with aortic stenosis are at risk of sudden death.

Back 50

ARRHYTHMIAS, secondary to inadequate blood flow through the narrowed aortic valve into the coronary arteries of the heart.

Front 51

Describe the pathogenesis of rheumatic fever.

Back 51

- type II hypersensitivity rxn to Group A Strep pharyngitis (Strep throat)
- Mimicry: M protein of GAS elicits antibodies that cross react with human tissue (myocardium, valves, pericardium, skin, joints)

Front 52

What are the most important complications of rheumatic fever?

Back 52

Aortic and Mitral Stenosis

Front 53

Describe clinical and pathologic findings in mitral valve prolapse (Barlows or floppy valve syndrome)... recognizing how common this disorder is, and what its natural history is.

Back 53

asymptomatic; may have mitral insufficiency; unusual murmur


- ***“Click-murmur”***: Valve leaflets balloon up during systole, but chordae provide sudden restraint resulting in a ***mid-systolic click => mid to late-systolic murmur*** occurs due to mitral regurgitation
- ↓preload: click-murmur moves closer to S1 (ie anxiety, standing, valsalva)
- ↑preload: click-murmur moves closer to S2 (reclining, squatting)

Front 54

Define aortic coarctation.

Back 54

Fibrous narrowing of aorta; can be infantile (associated with Turner’s) or adult type

Front 55

Tell how the common post-ductal type can be clinically diagnosed.

Back 55

It is associated with NOTCHING OF THE RIBS (because of collateral circulation), hypertension in the upper extremities, and weak pulses in the lower extremities.

Front 56

Tell why infective endocarditis is so dangerous.

Back 56

Early symptoms are often very subtle and non-specific.

(flu-like symptoms with a high temperature that lasts for longer than a week)

Front 57

Differentiate acute from subacute endocarditis, telling typical organisms associated with each, patients at risk and what valves are usually affected.

Back 57

Acute Endocarditis = S.Aureus, mostly in IV drug abusers
SBE = S.Viridans

In general, Mitral > Aortic
IVDA, Tricuspid > Aortic

Front 58

Describe complications of bacterial endocarditis, and clues to its diagnosis.

Back 58

 Splinter hemorrhages in nail beds
 Janeway lesions –painless lesions on palms and feet
 Osler nodes—painful lesions on pads of fingers and toes

o Changing cardiac murmurs (new regurgitation… chronic stenosis)
o Splenomegaly
o Immunocomplex vasculitis  Roth spots on retina, glomerulonephritis

Front 59

Describe pathologic and clinical findings in viral myocarditis, naming the virus.

Back 59

- pathology: lymphoid inflammation (viral – Coxsackie Virus)
• Presentation: asymptomatic to flu symptoms, EKG abnormalities, & rapidly fatal CHF