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45 Cards in this Set

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What is the timeframe of hyperacute rejection?
Immediately or hours after transplant
What type of rejection?
Hemorrhage, edema, and platelet aggregates in blood vessels. With time, polys too.
Hyperacute rejection
What type of rejection?
Lymphocytes, macrophages, eos, no polys, no plasma cells.
Acute rejection
What type of rejection?
Capillary injury, endothelial swelling, intravascular macrophages, edema, hemorrhage, neutrophils near capillaries, thrombi and myocyte necrosis.
Acute antibody mediated rejection
What Acute Rejection Grade?
Interstitial and/or perivascular infiltrates with up to 1 focus of myocyte damage.
Grade 1 R, mild
What Acute Rejection Grade?
Two ore more foci of infiltrates with associated myocyte damage.
Grade 2 R, moderate
What Acute Rejection Grade?
Diffuse infiltrate with multifocal myocyte damage, +/- edema, +/- hemorrhage, +/- vasculitis
Grade 3, severe
What is the Quilty effect?
Dense lymphocytes (B and T) within the endocardium more commonly seen in the setting of cyclosporine. The lesion doesn't persist but may recur.

NOTE: Rejection is usually T cells only.
What is the size criteria for MI?
1 cm
Sequence of Changes in MI:
Grossly and microscopically normal
0-30 minutes
Sequence of Changes in MI:
Gross: No change
Micro: Thin wavy myofibers
30 minutes-4 hours
Sequence of Changes in MI:
Gross: Occasional dark mottling
Micro: Loss of striations, shrunken myocytes, loss of nucleus, hypereosinophilic cytoplasm
4-12 hours
Sequence of Changes in MI:
Gross: Dark mottling
Micro: Coagulation necrosis, many neutrophils
12-24 hours
Sequence of Changes in MI:
Gross: Pallor
Micro: Complete necrosis, heavy PMN
1-3 days
Sequence of Changes in MI:
Gross: Central pallor with hyperemia
Micro: Macrophages, granulation tissue at edges
3-7 days
Sequence of Changes in MI:
Gross: Maximal pallor
Micro: Phagocytosis and prominent granulation tissue
7-10 days
Sequence of Changes in MI:
Gross: red-gray depressed infarct
Micro: fibrosis
10-14 days
Sequence of Changes in MI:
Gross: Gray-white scar
Micro: increased collagen, acellular
2-8 weeks
Sequence of Changes in MI:
Gross: scar
Micro: dense collagenous scar, mummified "ghost-like" myocytes
> 2 months
Complications of MI:
Timeline for myocardial rupture
3-7 days post MI
Complications of MI:
Timeline for Dressler syndrome (fibrinous or fibrinohemorrhagic) pericarditis
2-3 days post MI
What are risk factors for myocardial rupture after MI? (3)
Females, hypertension, > 60 years old
What are the 3 most common viruses and parasites, and 2 bacteria causing myocarditis?
- Coxsackievirus A&B and other enteroviruses (most common)

- Trypanosoma cruzi
- Toxoplasmosis
- Trichinella

- Borrelia burgdorferi
- Corynebacterium diphtheriae (due to toxins)
This type of myocarditis is rapidly progressive, occurs in young adults, and is histologically characterized by multinucleated giant cells, lymphocytes, eos, necrosis. Transplant is the only treatment and there is a high chance of recurrence in the transplanted heart.
Giant cell myocarditis (AKA Fiedler's myocarditis)
This type of myocarditis is characterized by interstitial infiltrate of macrophages and eosinophils. There is little or no necrosis, no granulomas but multinucleated giant cells may be present.
Hypersenstiivty myocarditis

NOTE: classically associated with methyldopa
What are Aschoff nodules, Aschoff cells, and Anitschkow cells and what are they associated with?
They are associated with Rheumatic carditis.

Aschoff nodule: fibrinoid necrosis of the heart muscle
Aschoff cell: multinucleated giant cells in Aschoff nodules
Anitschkow cells: histiocytes with condensed chromatin give caterpiller or grooved appearance
What is mutated in idiopathic hypertrophic subaortic stenosis (or hypertrophic cardiomypathy)?
beta-myosin heavy chain (chromosome 14)
On EM this material is 10 nm non-branching extracellular fibrils.
What are AL, AA, ans AS amyloid?
AL: light chains (plasma cell neoplasms)
AA: chronic inflammatory diseases (rare in heart)
AS: transthyretin, senile amyloid
What is the most common heart tumor? What is the most common location?
Myxomas, left atrium (75%)
What are Carney's Complex (AKA Syndrome) and Carney's Triad?
Carney's Complex:
- Cutaneous and cardiac myxomas
- Blue nevi
- Endocrine overactivity (adrenal, testicular, thyroid, pituitary tumors)

Carney's Triad:
- Pulmonary chonndromas
- Extra-adrenal paragangliomas
What heart tumor can be seen in tuberous sclerosis?
This cardiac tumor occurs mostly in children or infants. Histologically, it is characterized by eosinophilic, polygonal cells with large glycogen-rich cytoplasmic vacuoles with stranding "spider cells".
Rheumatic heart disease can occur following what infection?
Streptococcus pyogenes pharyngitis
What organism caused this endocarditis?
S. aureus
What organism caused this endocarditis?
Prosthtic valves
S. epidermidis
What organism caused this endocarditis?
Damaged valves
What organism caused this endocarditis?
Colon cancer
S. bovis
What organism caused this endocarditis?
S. pneumoniae
Name the HACEK organisms. What other organisms can also cause culture negative endocarditis?
Haemophilus aphrophilus
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingii

Other causes: Intracellular Organisms
Coxiella burnetii (Q-fever)
Tropheryma whipplei (Whipple's disease)
What is Libman-Sacks endocarditis?
Vegetations on both sides of the heart valve in lupus patients.

NOTE: fibrinoid necrosis and inflammation
Large, medium, or small vessel vasculitis?
Giant cell arteritis
Takayasu arteritis
Large, medium, or small vessel vasculitis?
polyarteritis nodosa
Large, medium, or small vessel vasculitis?
Henoch-Schonlein purpura
Churg Strauss
This small vessel vasculiits presents with the triad of upper respiratory tract, lung, and kidney disease. Strong association with C-ANCA.
Wegener's granulomatosis