Cardiac Ap

Front 1

What is the timeframe of hyperacute rejection?

Back 1

Immediately or hours after transplant

Front 2

What type of rejection?
Hemorrhage, edema, and platelet aggregates in blood vessels. With time, polys too.

Back 2

Hyperacute rejection

Front 3

What type of rejection?
Lymphocytes, macrophages, eos, no polys, no plasma cells.

Back 3

Acute rejection

Front 4

What type of rejection?
Capillary injury, endothelial swelling, intravascular macrophages, edema, hemorrhage, neutrophils near capillaries, thrombi and myocyte necrosis.

Back 4

Acute antibody mediated rejection

Front 5

What Acute Rejection Grade?
Interstitial and/or perivascular infiltrates with up to 1 focus of myocyte damage.

Back 5

Grade 1 R, mild

Front 6

What Acute Rejection Grade?
Two ore more foci of infiltrates with associated myocyte damage.

Back 6

Grade 2 R, moderate

Front 7

What Acute Rejection Grade?
Diffuse infiltrate with multifocal myocyte damage, +/- edema, +/- hemorrhage, +/- vasculitis

Back 7

Grade 3, severe

Front 8

What is the Quilty effect?

Back 8

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.

Front 9

What is the size criteria for MI?

Back 9

1 cm

Front 10

Sequence of Changes in MI:
Grossly and microscopically normal

Back 10

0-30 minutes

Front 11

Sequence of Changes in MI:
Gross: No change
Micro: Thin wavy myofibers

Back 11

30 minutes-4 hours

Front 12

Sequence of Changes in MI:
Gross: Occasional dark mottling
Micro: Loss of striations, shrunken myocytes, loss of nucleus, hypereosinophilic cytoplasm

Back 12

4-12 hours

Front 13

Sequence of Changes in MI:
Gross: Dark mottling
Micro: Coagulation necrosis, many neutrophils

Back 13

12-24 hours

Front 14

Sequence of Changes in MI:
Gross: Pallor
Micro: Complete necrosis, heavy PMN

Back 14

1-3 days

Front 15

Sequence of Changes in MI:
Gross: Central pallor with hyperemia
Micro: Macrophages, granulation tissue at edges

Back 15

3-7 days

Front 16

Sequence of Changes in MI:
Gross: Maximal pallor
Micro: Phagocytosis and prominent granulation tissue

Back 16

7-10 days

Front 17

Sequence of Changes in MI:
Gross: red-gray depressed infarct
Micro: fibrosis

Back 17

10-14 days

Front 18

Sequence of Changes in MI:
Gross: Gray-white scar
Micro: increased collagen, acellular

Back 18

2-8 weeks

Front 19

Sequence of Changes in MI:
Gross: scar
Micro: dense collagenous scar, mummified "ghost-like" myocytes

Back 19

> 2 months

Front 20

Complications of MI:
Timeline for myocardial rupture

Back 20

3-7 days post MI

Front 21

Complications of MI:
Timeline for Dressler syndrome (fibrinous or fibrinohemorrhagic) pericarditis

Back 21

2-3 days post MI

Front 22

What are risk factors for myocardial rupture after MI? (3)

Back 22

Females, hypertension, > 60 years old

Front 23

What are the 3 most common viruses and parasites, and 2 bacteria causing myocarditis?

Back 23

Virus:
- Coxsackievirus A&B and other enteroviruses (most common)
- CMV
- HIV

Parasites:
- Trypanosoma cruzi
- Toxoplasmosis
- Trichinella

Bacteria:
- Borrelia burgdorferi
- Corynebacterium diphtheriae (due to toxins)

Front 24

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.

Back 24

Giant cell myocarditis (AKA Fiedler's myocarditis)

Front 25

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.

Back 25

Hypersenstiivty myocarditis

NOTE: classically associated with methyldopa

Front 26

What are Aschoff nodules, Aschoff cells, and Anitschkow cells and what are they associated with?

Back 26

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

Front 27

What is mutated in idiopathic hypertrophic subaortic stenosis (or hypertrophic cardiomypathy)?

Back 27

beta-myosin heavy chain (chromosome 14)

Front 28

On EM this material is 10 nm non-branching extracellular fibrils.

Back 28

Amyoid

Front 29

What are AL, AA, ans AS amyloid?

Back 29

AL: light chains (plasma cell neoplasms)
AA: chronic inflammatory diseases (rare in heart)
AS: transthyretin, senile amyloid

Front 30

What is the most common heart tumor? What is the most common location?

Back 30

Myxomas, left atrium (75%)

Front 31

What are Carney's Complex (AKA Syndrome) and Carney's Triad?

Back 31

Carney's Complex:
- Cutaneous and cardiac myxomas
- Blue nevi
- Endocrine overactivity (adrenal, testicular, thyroid, pituitary tumors)

Carney's Triad:
- Pulmonary chonndromas
- GIST
- Extra-adrenal paragangliomas

Front 32

What heart tumor can be seen in tuberous sclerosis?

Back 32

Rhabdomyoma

Front 33

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".

Back 33

Rhabdomyoma

Front 34

Rheumatic heart disease can occur following what infection?

Back 34

Streptococcus pyogenes pharyngitis

Front 35

What organism caused this endocarditis?
IVDA

Back 35

S. aureus

Front 36

What organism caused this endocarditis?
Prosthtic valves

Back 36

S. epidermidis

Front 37

What organism caused this endocarditis?
Damaged valves

Back 37

Enterococcus

Front 38

What organism caused this endocarditis?
Colon cancer

Back 38

S. bovis

Front 39

What organism caused this endocarditis?
Alcoholics

Back 39

S. pneumoniae

Front 40

Name the HACEK organisms. What other organisms can also cause culture negative endocarditis?

Back 40

Haemophilus aphrophilus
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella kingii

Other causes: Intracellular Organisms
Rickettsia
Coxiella burnetii (Q-fever)
Tropheryma whipplei (Whipple's disease)

Front 41

What is Libman-Sacks endocarditis?

Back 41

Vegetations on both sides of the heart valve in lupus patients.

NOTE: fibrinoid necrosis and inflammation

Front 42

Large, medium, or small vessel vasculitis?
Giant cell arteritis
Takayasu arteritis

Back 42

Large

Front 43

Large, medium, or small vessel vasculitis?
polyarteritis nodosa

Back 43

Medium

Front 44

Large, medium, or small vessel vasculitis?
Henoch-Schonlein purpura
Lupus
Cryoglobulinemia
Goodpasture
Wegeners
Churg Strauss

Back 44

Small

Front 45

This small vessel vasculiits presents with the triad of upper respiratory tract, lung, and kidney disease. Strong association with C-ANCA.

Back 45

Wegener's granulomatosis