Cardiology II

Question 1

Answer 1

Fibrinous Pericarditis

• Shows thin strands of fibrinous exudate that extend from epicardial surface to pericardal sac

Question 2

Answer 2

Fibrinous Pericarditis

Surface appears roughened from normal glistening appearance by strands of pink-tan fibrin

Question 3

Answer 3

Fibrinous Pericarditis

Epicardial surface of heary shows shaggy fibrous exudate. “Bread & butter” pericarditis.

Fibrin often results in finding on PE of friction rub as strands of fibrin on epi/pericardium rub against each other

Question 4

Answer 4

Microscopically, pericardial surface shows strands of pink fibrin extending outward w/ underlying inflammation.

Question 5

Answer 5

Hemorrhagic Pericarditis

Fibrous pericarditis + hemorrhage

W/o inflammation, blood in pericardial sac = hemopericardium

Question 6

Answer 6

Hemorrhagic pericarditis

Surface of heart with hemorrhagic pericarditis has roughened, red appearance

Most likely to occur with metastatic tumor & TB

Question 7

Answer 7

Suppurative/Purulent Pericarditis

Yellow exudate has pooled in lower pericardial sac. Usually implicates bacterial organism, and infection typically spreads from lungs.

Question 8

Answer 8

Purulent Pericarditis

Question 9

Answer 9

Xray of Dilated Cardiomyopathy (marked cardiomegaly)

Water bottle sign >1/2 chest width

Left heart edge appears far to the left

Question 10

Answer 10

Dilated Cardiomyopathy

Globoid shape because all chambers are dilated. Feels flabby & myocardium is poorly contractile.

Cardiomyopathy = poorly functioning myocardium and heart is large and dilated, but no specific histologic findings

Question 11

Answer 11

Dilated cardiomyopathy

Large, dilated LV

Question 12

Answer 12

Dilated Cardiomyopathy

Question 13

Answer 13

Dilated Cardiomyopathy

Question 14

Answer 14

Cardiomyopathy

Microscopically, heart demonstrates hypertrophy of myocardial fibers (prominent dark nuclei) + interstitial fibrosis

Question 15

Answer 15

Hypertrophic Cardiomyopathy

Marked LV hypertrophy w/ asymmetric bulging of large interventricular septum into LV

50% familial, though a variety of different genes may be responsible for the disease

Question 16

Answer 16

Hypertrophic Cardiomyopathy

Narrowing of outflow tract before aortic valve - subaortic stenosis

Question 17

Answer 17

Hypertrophic Cardiomyopathy

Question 18

Answer 18

Hypertrophic Cardiomyopathy

Myocardial disarray, not arranged parallel

Usually happens in fit, young adults and results fatally

Question 19

Answer 19

Hypertrophic cardiomyopathy

Myocardial disarray (not arranged in parallel)

Question 20

Answer 20

Hypertrophic Cardiomyopathy

Question 21

Answer 21

Cardiac Amyloidosis

Question 22

Answer 22

Cardiac Amyloidosis

Replacement of myocardium with amyloid (ECM, starch-like material)

>15 types of proteins that can result in amyloid deposition

Beta-pleated sheet configuration

Question 23

Answer 23

Cardiac Amyloidosis

Congo red stain on myocardium

Amyloid stain orange-red, but with polarized light, the amyloid has apple-green birefringence

Question 24

Answer 24

Cardiac Hemochromatosis

Excessive iron deposition can occur in heart, which leads to heart enlargement and failure similar to cardiomyopathy, making hemochromatosis a form of “restrictive” cardiomyopathy

Question 25

Answer 25

Acute Bacterial Endocarditis Aortic valve has large, irregular reddish tan vegetation Staph. aureus produces "acute" bacterial endocarditis, Strep. viridans produces "subacute"

Question 26

Answer 26

Acute Bacterial endocarditis More virulent bacteria cuasing acute bacterial endocarditis can lead to serious destruction Irregular reddish tan vegetations can overlie valve cusps that are being destroyed. Portions of vegetation can break off and become septic emboli.

Question 27

Answer 27

Acute bacterial endocarditis of AV valve

Question 28

Answer 28

Acute bacterial endocarditis of aortic valve

Question 29

Answer 29

Subacute bacterial endocarditis

Question 30

Answer 30

Acute bacterial endocarditis with a perforation

Question 31

Answer 31

Vegetations of bacterial endocarditis

Question 32

Answer 32

Vegetations of Bacterial Endocarditis

Question 33

Answer 33

Vegetations of Bacterial Endocarditis

Question 34

Answer 34

Vegetations of Bacterial Endocarditis PMNS mixed with a lot of fibrous material

Question 35

Answer 35

Vegetations fragment easily, enter circulation & enter different organs A: Splinter hemorrhages B: Conjunctival Petechiae C: Osler's Nodes (tender, sub-cut. nodules in pulp of digits or thenar eminence) D:Janeway's lesions (non-tender erythematous, hemorrhagic, or pustular lesions on palms/soles)

Question 36

Answer 36

Clinical Manifestation of Bacterial Endocarditis Janeway Lesion

Question 37

Answer 37

Clinical Manifestation of Bacterial Endocarditis (Roth Spot)

Question 38

Answer 38

Endocarditis of Rheumatic Fever Small verrucous vegetations seen along closure line of mitral valve Warty vegetations average only a few mm and form along the line of valve closure over areas of endocardial inflammation. These verrucae too small to cause serious cardiac problems

Question 39

Answer 39

Aschoff Nodule Microscopically, acute rheumatic carditis marked by granulomatous inflammation with Aschoff Nodules seen best in myocardium. Centered in interstitium around vessels. Myocarditis may be severe enough to cause congestive heart failure.

Question 40

Answer 40

Anitschkow Cells Discrete collection of activated macrophages that turn into Anitschkow Cells Anitschkow cells collect and form Aschoff nodules Contains "Caterpillar nuclei" which is pathonomonic for this disease

Question 41

Answer 41

Aschoff Nodule

Question 42

Answer 42

Aschoff nodule at high magnification Most characteristic component is Aschoff giant cell Have prominent nucleoli, scattered inflamatory cells

Question 43

Answer 43

Chronic Rheumatic Heart Disease Usually can't identify Aschoff bodies due to fibrosis Dominated by endocardial (valve) damage, not myocardial damage (as in acute RHD)

Question 44

Answer 44

Chronic Rheumatic Heart Disease Mitral valve demonstrates typical "fish mouth" associated with chronic rheumatic scarring Mitral valve most commonly affected with RHD, followed by Mitral+Aortic; Aortic; Mitral+Aortic+Tricuspid

Question 45

Answer 45

Chronic Rheumatic Heart Disease

Question 46

Answer 46

Chronic Rheumatic Heart Disease

Question 47

Answer 47

Chronic RHD

Question 48

Answer 48

Chronic RHD

Question 49

Answer 49

Non-bacterial Thrombotic Endocarditis ("Marantic endocarditis") Small pink vegetation on rightmost cusp margin = typical finding Tends to occur in people with hypercoagulable state (Trousseau's syndrome) and very ill persons

Question 50

Answer 50

Non-infective Thrombotic Endocarditis on leftmost cusp Vegetations rarely over 0.5 cm, but they are friable (can fragment) and prone to embolization

Question 51

Answer 51

Non-infective thrombotic endocarditis

Question 52

Answer 52

Non-infective thrombotic endocarditis

Question 53

Answer 53

Non-infective Bacterial endocarditis Pink because made of fibrin & platelets. Displays about as much morphologic variation as a brown paper bag (Bland!!) such vegetations are typical of non-infective forms. NO inflammatory cells because no infection

Question 54

Answer 54

Non-infective Thrombotic Endocarditis Valve seen on left and bland vegetation seen on right. Pink bc made of fibrin + platelets. BLAND. No inflammatory cells.

Question 55

Answer 55

Flat, pale, tan spreading vegetations over mitral valve surface & even on chordae tendinae Patient has systemic lupus erythematosus, so vegetations can be on any valve or endocardial surface. These vegetations appear on 4% of of SLE patients and rarely cause problems because not large and rarely embolize. Also, note thickened, shortened, & fused chordae tendinae that represent remote rheumatic heart disease.

Question 56

Answer 56

From Left to Right: Rheumatic heart disease (viruchae) Infective endocarditis Non-bacterial thrombotic endocarditis (medium size, few) Libmann-Sacks Endocarditis (found anywhere)

Question 57

What are the different types of pericarditis? Describe each

Answer 57

Fibrinous (most common), Serous, purulent, and hemorrhagic Fibrinous: "bread & butter", composed of pink, fibrinous material and inflammatory cells Purulent: Bacterial/fungal infections Hemorrhagic: Malignancy, tuberculosis (granulomatous inflammation)

Question 58

What are the types of Cardiomyopathies? Describe.

Answer 58

Dilated (Congestive): Main problem is systolic dysfunctino with all 4 chambers dilated (w/ some hypertrophy). Associations-genetic abnormalities, chronic alcoholism/toxins, prior viral myocarditis, pregnancy, or idiopathic Hypertrophic: Most common form, idiopathic hypertrophic subaortic stenosis, due to asymmetric interventricular septal hypertrophy, resulting in LV outflow obstruction and impaired diastolic filling due to massive myocardial hypertrophy. Restrictive: myocardium infiltrated or replaced with material that results in decreased ventricular compliance and impaired ventricular filling (classic example: cardiac amyloidosis)

Question 59

What type of mutations (and non-genetic etiologies) cause dilated cardiomyopathy?

Answer 59

1. Sarcomere (actin, B-myosin heavy chain, tropomyosin, troponin T) 2. Cytoskeleton (sarcoglycan, dystrophin, desmin) 3. Nuclear envelope (Lamin A/C) 4. Mitochondria 5. Non-genetic (Myocarditis, peri partum, toxic, idiopathic)

Question 60

What is the phenotype of dilated cardiomyopathy?

Answer 60

Hypertrophy, dilation, fibrosis (interstitial), and intracardiac thrombi Caused by defect in force generation or transmission

Question 61

What causes hypertrophic cardiomyopathy?

Answer 61

100% genetic causes * Mutations in sarcomere (actin, myosin, tropomyosin, troponin, titin)

Question 62

What is the phenotype of hypertrophic cardiomyopathy?

Answer 62

Caused by defect in force generation * Hypertrophy, marked * Assymetrical septal hypertrophy * Myofiber disarray * Fibrosis (interstitial & replacement) * LV outflow tract plaque * Thickened septal vessels

Question 63

What are the 3 main complications of bacterial endocarditis?

Answer 63

1. Valve destruction w/ valvular incompetence 2. Myocardial ring abscess, or myocarditis & perforation 3. Septic emboli with consequent infarct/abscess

Question 64

What are clinical manifestations of bacterial endocarditis?

Answer 64

Roth spots: retinal hemorrhage with pale/white areas Splinter hemorrhages: hemorrhagic lesions, typically linear, beneath nails Janeway lesions: small, flat, painless erythematous to hemorrhagic lesions on palms & soles Osler's nodes: small, tender, transient nodules in pads of fingers/toes

Question 65

Rheumatic Heart Disease: what effect does it have on the heart?

Answer 65

Acute rheumatic carditis = "Pancarditis" (peri, myo, and endocarditis) Endocarditis: multiple, small inconspicuous vegetations on valve leaflets Myocarditis: Aschoff bodies/nodules; focus of fibrinoid material & aggregates of histiocytes (Anitschkow "caterpillar" cells) - seen ONLY in acute rheumatic fever; may be present in myocardium, pericardium or valve leaflets

Question 66

What's the difference between Acute rheumatic heart disease and chronic?

Answer 66

Acute: chamber dilation & conduction abnormalities Chronic: Scarring & calcificatino of valves (fish mouth mitral valve), atrial dilation

Question 67

What are 3 complications of rheumatic heart disease?

Answer 67

Bacterial endocarditis, mural thrombi, congestive heart failure

Question 68

Describe non-bacterial thrombotic endocarditis Are the vegetations destructive?

Answer 68

Small non-infectious vegetations seen in association with certain disorders (malignancy, hypercoagulable states, or severely ill persons) Bland vegetations are non-destructive, but may embolize

Question 69

Libman-Sacks Endocarditis Associated with? Are the vegetations destructive?

Answer 69

Associated with systemic lupus erythematosus Non-destructive vegetations, but commonly embolize