Cardiovascular Flashcards
Viral myocarditis
Interstitial lymphocytic infiltrates Common causes: coxsackie B, rubella, CMV
Chagas myocarditis
Pseudocyts with amastigotes and interstitial lymphocytic infiltration
Giant cell myocarditis
Idiopathic; mostly young pts Granulomas with myocyte necrosis
What causes Janeway lesions in endocarditis?
Painless lesions in hands/feet Microabscesses of dermis surrounding septic emboli
What causes Osler nodes in endocarditis?
Painful raised lesions on fingers/toe pads Immune complex deposition
Aschoff nodules
Seen in rheumatic heart disease Perivascular collection of mononuclear inflammatory cells Contain Aschoff giant cells
Anichkov myocyte
Long, thin cell with elongated nucleus seen in acute rheumatic carditis
Arrhythmogenic right ventricular cardiomyopathy
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
Hypertrophic cardiomyopathy
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)
Endocardial fibroelastosis
Restrictive cardiomyopathy causing DIASTOLIC dysfunction Fibroelastic thickening of the left ventricle in children under 2 years old
Concentric hypertrophy (sarcomeres added in…)
PARALLEL due to PRESSURE OVERLOAD
Eccentric hypertrophy (sarcomeres added in…)
SERIES due to VOLUME OVERLOAD
Cardiac myxoma
Benign mass most often in atria Bx - minimal cellularity, scattered thin spindle cells with scant pink cytoplasm within a loose myxoid stroma
Rhabdomyoma
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
Spider cells
Seen in cardiac rhabdomyomas Centrally located nucleus with radial extensions to the cell wall; positive for ubiquitin (apoptotic pathway)
Cardiac transplant rejection
Most are cell-mediated immunity Inflammation is mostly mononuclear and primarily perivascular
3-7 day old MI
Gross - tan-yellow dead muscle with surrounding hyperemic border
When is ventricular free wall rupture most likely to occur after an MI?
3-7 days after transmural infarction - necrotic muscle is soft and there hasn’t been reorganization with capillaries and fibroblasts
Microscopic changes 4-12 hours after acute MI
Early coagulation necrosis, edema, hemorrhage, wavy fibers
Microscopic changes 12-24 hours after acute MI
Coagulation necrosis and contraction band necrosis
Microscopic changes 2-3 days after acute MI
Increased neutrophilic infiltrate Coagulative necrosis
Microscopic changes 5-7 days after acute MI
Healing of MI begins Capillaries, fibroblasts and macrophages filled with hemosiderin
When does granulation tissue become most prominent after acute MI?
2-3 weeks after infarction *granulation tissue is nonfunctional and noncontractile
Monckeberg arteriosclerosis
Calcifications in the MEDIA Lumen is unaffected - no significant clinical consequences Involves muscular arteries
Abdominal aortic aneurysm most commonly found where
Between renal arteries and aortic bifurcation at L4 Palpable pulsating abdominal mass
Thoracic aortic aneurysms are associated with…
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
Cystic medial degeneration of aorta
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)
Nonbacterial thrombotic endocarditis (marantic endocarditis)
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)
Malignant nephrosclerosis due to hypertensive emergency (2 histological patterns)
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)
Hypertensive nephrosclerosis is characterized by what? (3)
Interstitial fibrosis
Tubular atrophy
Degrees of glomerulosclerosis (focal or global)
What are the major risk factors for abdominal aortic aneurysm?
> 65
Smoking ** 15x higher risk
Male
0-4 hours after MI
minimal change
(uworld q)
