Cardiovascular

Question 1

Viral myocarditis

Answer 1

Interstitial lymphocytic infiltrates Common causes: coxsackie B, rubella, CMV

Question 2

Chagas myocarditis

Answer 2

Pseudocyts with amastigotes and interstitial lymphocytic infiltration

Question 3

Giant cell myocarditis

Answer 3

Idiopathic; mostly young pts Granulomas with myocyte necrosis

Question 4

What causes Janeway lesions in endocarditis?

Answer 4

Painless lesions in hands/feet Microabscesses of dermis surrounding septic emboli

Question 5

What causes Osler nodes in endocarditis?

Answer 5

Painful raised lesions on fingers/toe pads Immune complex deposition

Question 6

Aschoff nodules

Answer 6

Seen in rheumatic heart disease Perivascular collection of mononuclear inflammatory cells Contain Aschoff giant cells

Question 7

Anichkov myocyte

Answer 7

Long, thin cell with elongated nucleus seen in acute rheumatic carditis

Question 8

Arrhythmogenic right ventricular cardiomyopathy

Answer 8

Autosomal dominant mutation in genes for desmosomal proteins (i.e., plakoglobin) which affects gap junction med age onset 33 years Extensive fat replacement of RV myocardium Subendocardial layer is preserved

Question 9

Hypertrophic cardiomyopathy

Answer 9

Myofiber disarray with surrounding collagen Mutation in beta-myosin heavy chain most common Also associated with Friedrich ataxia (frataxin gene mutation causing spinocerebellar degeneration with hypertrophic cardiomyopathy, pes cavus and kyphoscoliosis)

Question 10

Endocardial fibroelastosis

Answer 10

Restrictive cardiomyopathy causing DIASTOLIC dysfunction Fibroelastic thickening of the left ventricle in children under 2 years old

Question 11

Concentric hypertrophy (sarcomeres added in…)

Answer 11

PARALLEL due to PRESSURE OVERLOAD

Question 12

Eccentric hypertrophy (sarcomeres added in…)

Answer 12

SERIES due to VOLUME OVERLOAD

Question 13

Cardiac myxoma

Answer 13

Benign mass most often in atria Bx - minimal cellularity, scattered thin spindle cells with scant pink cytoplasm within a loose myxoid stroma

Question 14

Rhabdomyoma

Answer 14

Most common primary cardiac tumor in infants and children Usually in LV wall or IV septum Half due to sporadic mutations; half due to TSC1 or TSC2 mutations in tuberus sclerosis Bx - prominany vacuolation and distinct cell borders, abundant glycogen with PAS, spider cells

Question 15

Spider cells

Answer 15

Seen in cardiac rhabdomyomas Centrally located nucleus with radial extensions to the cell wall; positive for ubiquitin (apoptotic pathway)

Question 16

Cardiac transplant rejection

Answer 16

Most are cell-mediated immunity Inflammation is mostly mononuclear and primarily perivascular

Question 17

3-7 day old MI

Answer 17

Gross - tan-yellow dead muscle with surrounding hyperemic border

Question 18

When is ventricular free wall rupture most likely to occur after an MI?

Answer 18

3-7 days after transmural infarction - necrotic muscle is soft and there hasn’t been reorganization with capillaries and fibroblasts

Question 19

Microscopic changes 4-12 hours after acute MI

Answer 19

Early coagulation necrosis, edema, hemorrhage, wavy fibers

Question 20

Microscopic changes 12-24 hours after acute MI

Answer 20

Coagulation necrosis and contraction band necrosis

Question 21

Microscopic changes 2-3 days after acute MI

Answer 21

Increased neutrophilic infiltrate Coagulative necrosis

Question 22

Microscopic changes 5-7 days after acute MI

Answer 22

Healing of MI begins Capillaries, fibroblasts and macrophages filled with hemosiderin

Question 23

When does granulation tissue become most prominent after acute MI?

Answer 23

2-3 weeks after infarction *granulation tissue is nonfunctional and noncontractile

Question 24

Monckeberg arteriosclerosis

Answer 24

Calcifications in the MEDIA Lumen is unaffected - no significant clinical consequences Involves muscular arteries

Question 25

Abdominal aortic aneurysm most commonly found where

Answer 25

Between renal arteries and aortic bifurcation at L4 Palpable pulsating abdominal mass

Question 26

Thoracic aortic aneurysms are associated with…

Answer 26

HYPERTENSION weakening of media usually asymptomatic but expansion can cause vague chest/back pain and can compress structures causing hoarseness and dysphagia when rupture - severe pain with hemodynamic instability

Question 27

Cystic medial degeneration of aorta

Answer 27

Associated with Marfan’s syndrome Mucin stain - pink elastic fibers disrupted by pools of blue mucinous ground substance Can lead to aortic dissection (blood dissects medial layers through longitudinal intimal tear)

Question 28

Nonbacterial thrombotic endocarditis (marantic endocarditis)

Answer 28

Vegetations are bland thrombus with strands of fibrin, immune complexes, and mononuclear cells

“platelet-rich” thrombi

**associated with hypercoaguable states

**ADVANCED MALIGNANCY (most common) and SLE (Libman-Sacks endocarditis)

Question 29

Malignant nephrosclerosis due to hypertensive emergency (2 histological patterns)

Answer 29

1) Fibrinoid necrosis - cell death and extensive fibrin deposition within arteriolar walls; circumferential, amphorphous, pink material with necrotic endothelial cells

2) Hyperplastic arteriolosclerosis - plts and injured cells release growth factors which induce concentric hyperplasia and layering of smooth muscle cells and collagen (onion skin)

can lead to miroangiopathic hemolyic anemia (schistocytes)

Question 30

Hypertensive nephrosclerosis is characterized by what? (3)

Answer 30

Interstitial fibrosis

Tubular atrophy

Degrees of glomerulosclerosis (focal or global)

Question 31

What are the major risk factors for abdominal aortic aneurysm?

Answer 31

> 65

Smoking ** 15x higher risk

Male

Question 32

0-4 hours after MI

Answer 32

minimal change

(uworld q)