CV Pathology Flashcards Preview

Cardiovascular System > CV Pathology > Flashcards

Flashcards in CV Pathology Deck (132):
1

What cardiac markers are useful by bloodwork?

Troponin (T, I), CK-MB isoenzyme

2

What are the benefits of troponin markers over CK?

Very specific and more sensitive.

3

When does troponin appear?

Rises 4-8h after injury, may remain elevated for up to 2 weeks.

4

What injury other than cardiac can troponin indicate?

May be elevated with renal disease, poly/dermatomyositis.

5

What are the benefits of cardiac markers?

Provide prognostic information, elevation can be predictive of mortaily.

6

When does elevated CK-MB isoenzyme appear?

4-6h after injury, peak at 24h, remains elevated 36-48h.

7

What are the levels of CK/MB for a positive test?

>5% of total CK and 2x normal.

8

What are examples of false positives of CK-MB?

Exercise, trauma, muscle disease, DM, PE.

9

Graph of rise of troponin with mortality

10

What are the 3 types of Creatinine kinase isoenzyme fractions?

MM - Muscles cardiac & Skeletal, MB - exclusively in cardiac muscle. BB - Brain, Bowel & Bladder.

11

What are the tests that can be checked in the blood for an MI?

Creatinine Kinase; CK- Isoenzymes (Fractions), Troponins - I & T, LDH - 1-5, Myoglobin.

12

CK-MB levels corresponding to injury (graph)

Index is ratio to total CK

13

This epicardial coronary artery is almost completely occluded by atherosclerotic plaque. The plaque is heavily lipid laden and has ruptured, releasing thrombogenic substances into the narrow lumen. A thrombus has occluded the tiny lumen that remains.

14

This image shows an acute myocardial infarct in the free wall of the left ventricle, which also has an element of left ventricular hypertrophy. The infarct zone is pale tan, and it is surrounded by a hyperemic area that represents an inflammatory response. The infarct is about 5-7 days old. 

15

When can ultrastructural evidence of irreversible myocardial damage after occlusion of a major epicardial coronary artery be detected?

20-40mins after occlusion

16

When can wavy fiber change in occlusion of a major epicardial coronary artery occlusion be detected with a light microscope?

1-3 hours after occlusion

17

When are classic histologic features of necrosis established after major epicardial coronary artery occlusion?

4-12h.

18

Which is first, irreversible damage of subendocardial zones or classical features of necrosis?

Subendocardial zone damage.

19

When does progressive loss of myocardial zone occur?

Over 24h after necrosis begins, most of damage in first 4-6h.

20

There is a severe degree of narrowing in this coronary artery. It is "complex" in that there is a large area of calcification on the lower right, which appears bluish on this H&E stain. Complex atheroma have calcification, thrombosis, or hemorrhage. Such calcification would make coronary angioplasty difficult.

21

This distal portion of coronary artery shows significant narrowing. Such distal involvement is typical of severe coronary atherosclerosis, such as can appear with diabetes mellitus or familial hypercholesterolemia. This would make a coronary bypass operation difficult.

22

How do cholesterol clefts in thrombosis appear in the coronary artery?

Open, needle-like spaces in atheromatous plaque.

23

This high magnification of the atheroma shows numerous foam cells and an occasional cholesterol cleft. A few dark blue inflammatory cells are scattered within the atheroma.

24

Gross vs Microscopic changes in time progression of MI

0-18h | None | None
24-48h | Pale, edema | Edema, acute inflammation
2-3 days | Hemorrhage | Necrosis, granulation
1-3 weeks | Thin, yellow | Granulation--> fibrosis
3-6 weeks | Tough white | Dense fibrosis

25

Coronary atherosclerosis

26

MI in 2 wks v 3 days

27

What appears in MI after 18-24h?

Loss of nucleus and intercalated discs, contaction bands, coagulative necrosis.

28

What happens pathologically 3-4 days after an MI?

Hemorrhage, inflammation

29

What does a pathological slide look like 1-2 weeks after MI?

Granulation tissue

30

What happens in an MI 2-4 weeks after MI on a pathological slide?

Resorption, fibrosis.

31

What happens in a pathological slide 4-6 weeks after MI?

Collagen scar

32

Complications of MI

Arrhythmias and conduction defects,
Extension of infarction, or re-infarction
Congestive heart failure (pul edema)
Cardiogenic shock
Pericarditis
Mural thrombosis, - embolization
Myocardial wall rupture,  tamponade
Papillary muscle rupture, Ventricular aneurysm

33

Papillary muscle rupture/ventricular aneurysm

34

Major disorders of CVS

Atherosclerosis
Hypertension
Myocardial Infarction (MI)
Stroke
IHD -  Ischemic Heart Disease
VHD - Valvular Heart Disease
RHD – Rheumatic Heart Disease
CHD - Congenital Heart Disease

35

Atherosclerosis definition

Chronic inflammatory disorder of intima of large blood vessels characterised by formation of fibrofatty plaques called atheroma.

36

Arteriosclerosis definition

A type of atherosclerosis with hardening of arteries.

37

Nonmodifiable risk factors for atherosclerosis

Age – middle to late.
Sex – Males, complications
Genetic - Hyperchol.
Family history.

38

Potentially modifiable risk factors of atherosclerosis

Hyperlipidemia – HDL/LDL ratio.
Hypertension.
Smoking.
Diabetes
Life style, diet, excercise

39

How is an atheroma formed?

Initial intimal injury, inflammation, necrosis, Lipid accumulation, Fibrosis.

40

What does an atheroma lead to?

Atherosclerosis, obstruction or destruction of vessel. Organ damage d/t ischemia.

41

Complications of atherosclerosis

Thrombosis, embolism, aneurism, dissection & rupture.

42

Common sites of atherosclerosis

Aorta, Carotid & Iliac. (large vessels)
Major Vessels - Heart, Brain & Kidney.
Coronary
Renal
Abdominal
Limbs

43

Morphology of atherosclerosis

Fatty Dots
Fatty Streaks
Atheromatous – Soft Plaque
Fibrofatty – Hard Plaque
Complications
Ulceration, Rupture,Hemorrhage, Thrombosis
Atheroemboli or cholesterol emboli.

44

Stages of atheroma

6-3-2

45

Complications of atherosclerosis

Heart attack – Myocardial infarction.
Stroke – Cerebral infarction
Gangrene – tissue infarction.
Kidney failure – Kidney infarction.
Aneurysms
Rupture
Thromboembolism.

46

Risks of hyperlipidemia

Hypercholesterolemia – Risk
Hypertriglyceridemia - less significant
LDL – Increased risk
HDL – lowers the risk – Reverse transport
Mobilises the cholesterol from tissues to liver.

47

What is the hydrostatic pressure of the arterial vs venous capillary:?

+36/+16

48

How does oncotic pressure compare between arterial and venous capillaries?

-26 in both

49

What is the net filtration pressure between arterial and venous capillaries?

+10mmHg (leak out) vs -9mm Hg (reabsorb)

50

Edema definition

Increased interstitial fluid volume.

51

What are the 2 types of edema?

Local (inflammation), generalized (anasarca-systemic causes).

52

What is anasarca?

Liver or renal failure-generalized edema.

53

What are the mechanisms of edema

Leaky vessels (inflammation)- increased capillary hydrostatic pressure (venous obstructions, cardiac failure), decreased osmotic pressuer (hypoproteinemia from liver disease, anemia), lymphatic obstruction (elephantiasis)

54

A cross section through the heart reveals a ventricular aneurysm with a very thin wall at the arrow. Note how the aneurysm bulges out. The stasis in this aneurysm allows mural thrombus, which is present here, to form within the aneurysm.

55

Microscopically, the tear (arrow) in this aorta extends through the media, but blood also dissects along the media (asterisk). Aortic dissection may lead to hemopericardium, massive hemorrhage can lead to cardiac tamponade.

56

Dissection up vs dissection down

Aortic dissection went into the muscular wall. In any case, an aortic dissection is an extreme emergency and can lead to death in a matter of minutes. The blood can dissect up or down the aorta. Blood dissecting up around the great vessels can close off the carotids. Blood can dissect down to the coronaries and shut them off.

57

Marfan syndrom mitral valve.

The leaftlets of the mitral valve are redundant, and the one on the far left is ballooned upward. This is characteristic of floppy mitral valve with mitral valve prolapse. The chordae tendineae that hold the leaflets become long and thin. The characteristic finding on physical exam is a mid-systolic click. Same patient had an aortic dissection just above the aortic root leading to hemopericardium with tamponade within minutes.

58

What causes CT weakness in Marfan's syndrome that leads to aortic dissection?

Cystic medial degeneration/necrosis. Elastic fibers are disrupted by pools of blue mucinous ground substance.

59

What are the consequences of this condition?

Infective endocarditis. The more virulent bacteria causing the acute bacterial form of infective endocarditis can lead to serious destruction, as shown here in the aortic valve. Irregular reddish tan vegetations overlie valve cusps that are being destroyed. Portions of the vegetation can break off and become septic emboli.

60

What are the vegetations in infective endocarditis made of?

Fibrin and platelets mixed with inflammatory cells and bacterial colonies. Friable-explains embolism.

61

What is this and when does it most often occur?

Chronic Rheumatic scarring.The heart has been sectioned to reveal the mitral valve as seen from above in the left atrium. The mitral valve demonstrates the typical "fish mouth" shape with chronic rheumatic scarring. Mitral valve is most often affected with rheumatic heart disease, followed by mitral and aortic together, then aortic alone, then mitral, aortic, and tricuspid together.

62

When is fibrinous pericarditis typical?

Uremia with renal failure, underlying myocardial infarction, and acute rheumatic carditis. 

63

What is a typical feature of fibrinous pericarditis?

Strands of fibrin/fibrinous exudate within fluid from epicardial surface can be seen.

64

What are Aschoff nodules?

Granulomatous inflammation centered in iinterstitium around vessels in the myocardium during acute rheumatic carditis. The myocarditis may be severe enough to cause congestive heart failure. The most characteristic component is the Aschoff giant cell. Several appear here as large cells with two or more nuclei that have prominent nucleoli. Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.

65

Another peculiar cell seen with acute rheumatic carditis. This is a long, thin cell with an elongated nucleus.

66

67

What is the most common type of myocarditis?

Viral

68

What is a typical characteristic of viral myocarditis?

Interstitial lymphocytic infiltrates.

69

What is the most common viral agent of viral myocarditis?

Coxsackie B.

70

What is the clinical presentation of viral myocarditis?

Usually sublinical, cause for sudden death in young persons. Little necrosis.

71

What is a rhabdomyoma?

A rare primary tumor of the heart.

72

What is the most common primary cardiac neoplasm?

Atrial myxoma

73

What is an atrial myxoma?

Benign mass (minimal cellularity) often attached to atrial wall, but can arise on a valve or in a ventricle. They can produce a "ball valve" effect by intermittently occluding the atrioventricular valve orifice. Embolization of fragments of tumor may also occur.

74

How are myxomas usually diagnosed?

Echocardiography.

75

What is the rate of cardiac metastases?

5-10% of malignancies

76

What is a consequence of cardiac metastasis?

Hemorrhagic pericarditis. Seen over the surface of the epicardium are pale white-tan nodules.

77

What is the neoplasm with the greatest propensity to metastasize to the heart?

Melanoma.

78

What is a characteristic of melanoma?

Brown/black pigment.

79

What are the types of congenital heart disease?

VSD, ASD, PDA, Tetrology of Fallot, Transposition of Great Vessels, Truncus Arteriosus, Hypoplastic Left Heart Syndrome, Coarctation of Aorta, Total Anomalous Pulmonary Venous Return

80

Causes of endocarditis

Rheumatic Fever, Infection, Non infective (Nonbacterial thrombotic endocarditis, SLE), Carcinoid heart disease

81

Definition of infective endocarditis

The infection of the endocardium (esp. heart valves) by a microbiological agent, with the formation of thrombotic debris and organisms known as vegetations.

82

Causes of infective endocarditis

Bacteria (most common), fungi, Rickettsiae (Q fever), Chlamydia

83

Cocci causes of bacterial endocartidis

Alpha-hemolytic streptococci: esp. with damaged or otherwise abnormal native valves (often subacute). Staphylococcus aureus: healthy or deformed valves, esp. in intravenous drug abusers (often acute). Coagulase-negative staphylococci: esp. with prosthetic valves.

84

What is the HACEK group of bacterial endocarditis?

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, & Kingella (commensals of oral cavity)

85

What are the common causes of bacterial endocarditis?

Strep, Staph, HACEK, Gram-negative bacilli

86

Predisposing valvular factors for infective endocarditis

Rheumatic heart disease, Myxomatous mitral valve, Calcific valvular stenosis, Bicuspid aortic valve, Artificial (prosthetic) valve (but may develop on previously normal valve).

87

Other predisposing factors for endocarditis?

Neutropenia, Immunodeficiency, Therapeutic immunosuppression, Diabetes mellitus, Alcohol or IV drug abuse, Sepsis, Invasive procedures.

88

Pathology of infective endocarditis

Vegetations of fibrin, inflammatory cells, & bacteria or other organisms. Located most commonly on heart valves, esp. aortic & mitral. May erode & perforate valve, & may erode into underlying myocardium to produce an abscess (ring abscess). May produce emboli that produce septic infarcts in brain, kidney, myocardium, & other organs.

89

Clinical presentation of infective endocarditis

Fever, chills, fatigue, weight loss, flu-like syndrome, Murmur (may change as vegetation/damage to valve changes), petechiae.

90

Complications of infective endocarditis

Valvular insufficiency or stenosis with resulting congestive heart failure.

91

Definition of nonbacterial thrombotic endocarditis (NBTE)

The deposition of sterile vegetations on the leaflets of cardiac valves, also called MARANTIC ENDOCARDITIS.

92

Pathology of NBTE

Vegetations of fibrin, platelets, & other blood elements (i.e.. a thrombus). Sterile, nondestructive, noninflammatory & small (1-5mm). Occur singly or multiply along the lines of closure of heart valves. Local effect on vavle unimportant but may produce emboli-->infarcts. May eventually organize leaving delicate strands of fibrous tissue.

93

Pathogenesis

Probably occurs as a consequence of a hypercoagulable state. Seem with concomitant venous thrombosis &/or pulmonary embolism. May be seen with hyperestrogenic state, extensive burns, or endocardial trauma from indwelling catheters.

94

Endocarditis of SLE definition

Also known as Libman-Sacks endocarditis. Small sterile vegetations on mitral & tricuspid valves or fibrous thickenings occurring with the antiphospholipid syndrome. Circulating antiphospholipid antibodies also associated with venous or arterial thrombosis, recurrent pregnancy loss, and thrombocytopenia.

95

Pathology of SLE endocarditis

Vegetations are small (1-4 mm), single or multiple, sterile, granular, and pink. Frequently located on the undersurfaces of AV valves, but may be elsewhere on valves or even on mural endocardium of atria or ventricles. Consist of finely granular fibrinous eosinophilic material. May have valvulitis, characterized by fibrinous necrosis, contiguous with vegetation. Can result in fibrosis and valve deformity that can resemble chronic rheumatic heart disease.

96

Carcinoid Heart Disease (CarHD) definition

Seen in one half of patients with carcinoid syndrome (episodic skin flushing, cramps, nausea, vomiting, and diarrhea). Involves endocardium and valves of the right side of the heart.

97

Pathology of CarHD

Intimal thickenings on the inside surfaces of the cardiac chambers & valvular leaflets, mainly on the right side of the heart. Thickenings consist of smooth muscle cells & sparse collagen fibers embedded in an acid mucopolysaccharide – rich matrix that expands the endocardium. Underlying structure of the heart intact.

98

Pathophysiology of CarHD

Produce a variety of bioactive products including serotonin, kallikrein, bradykinin, histamine, prostaglandins, & tachykinins. Serotonin appears to induce the cardiac lesions.

99

Why are CarHDs preferential to the right side?

Serotonin inactivated by pulmonary vascular endothelial monoamine oxidase. Can see left sided lesions if have high levels of serotonin not completely inactivated by lungs, pulmonary carcinoid, or right to left cardiac shunts.

100

When can carcinoid-like heart lesions be seen on the left side?

Methysergide or ergotamine treatment for migraine headache since these serotonin analogs are metabolized to serotonin by lungs. Fenfluramine & phemtermine (fen-phen) appetite suppressants since they affect serotonin metabolism.

101

Definition of myocarditis

Inflammatory processes of the myocardium that result in injury to the cardiac myocytes.

102

Infective causes of Myocarditis

Viruses (e.g., coxsackie, ECHO, HIV), Chlamydia (e.g., C. psittaci), Rickettsiae (e.g., R. typhi), Bacteria (e.g., C. diphtheria), Fungi (e.g., Candida), Protozoa (e.g., toxoplasmosis), Helminths (e.g., trichinosis).

103

immune-mediated causes of myocarditis.

Postviral, Poststreptococcal (rheumatic fever), Systemic lupus erythematosus, Drug hypersensitivity (e.g., methyldopa, sulfonamides), Transplant rejection.

104

Other causes of myocarditis

Sarcoidosis, giant cell myocarditis

105

Gross pathology of myocarditis

Heart may appear normal or dilated, some hypertrophy may be present. Ventricular myocardium may be flabby and mottled by pale foci and/or minute hemorrhage foci. May have mural thrombi.

106

Microscopic pathology of myocarditis

Interstitial inflammatory infiltrate, may be patchy, most commonly have mononuclear cell infiltrate, predominantly lymphocytes. Focal necrosis. Healing myocarditis results in fibrosis.

107

Microscopic pathology of hypersensitivity myocarditis.

Lymphocytes, macrophages, & eosinophils. Giant cell myocarditis has multinucleated giant cells with lymphocytes, eosinophils, plasma cells, & macrophages with necrosis.

108

Pathology of Chagas disease myocarditis

Parasitization of myofibers by Trypanosomes with neutrophils, lymphocytes, macrophages, and eosinophils.

109

Clinical presentation of myocarditis

Fatigue, dyspnea, palpitations, precordial chest pain, fever. Heart failure, dilated cardiomyopathy, Arrhythmias, Mitral regurgitation. Can be asymptomatic or result in sudden death.

110

What are the types of pericardial diseases?

Pericardial effusion, hemorrhage, pericarditis.

111

What is pericardial effusion?

Distention of pericardial sac by transudate.

112

Causes of pericardial effusion

Infection, autoimmune disease, congestive heart failure, renal failure, malignancy, myocardial infarction, drugs, and radiation.

113

Clinical presentation of pericardial effusion

Low blood pressure, dyspnea, dizziness, and chest pain.

114

Pericardial hemorrhage

Bleeding into pericardial sac. May produce compressino of heart resulting in cardiac tamponade.

115

What are causes of pericardial hemorrhage?

Cardiac rupture from myocardial infarction or perforating trauma and ruptured aortic dissection.

116

Types of pericarditis

Serous pericarditis, Fibrinous & serofibrinous pericarditis, Purulent or suppurative pericarditis, Hemorrhagic pericarditis, Caseous pericarditis, Adhesive mediastinopericarditis, Constrictive pericarditis.

117

Causes of pericarditis

Infections, Rheumatic fever, Autoimmune disease, Drug reaction, Myocardial infarction, Uremia, Malignancy, Radiation.

118

What are the causes of serous pericarditis?

Noninfectious inflammations (rheumatic fever, SLE, scleroderma, tumors, uremia), adjacent infection (bacterial pleuritis).

119

Microscopic pathology of serous pericarditis

Inflammatory reaction in epicardium and pericardium with PMNs, lymphocytes, and histiocytes. Slow leakage of fluid of high specific gravity & rich protein content into pericardial sac, (about 50-200 ml).

120

What is the most frequent type of pericarditis?

Fibrinous and serofibrinous.

121

Definition of serofibrinous pericarditis

Serous fluid mixed with fibrinous exudate. Inflammation leads to leakage of fluid & inflammatory cells into pericardial sac in addition to fibrin. Fibrin may be digested or organized.

122

Common causes of fibrinous and serofibrinous pericarditis

Acute myocardial infarction, uremia, radiation, rheumatic fever, SLE, trauma, & postinfarction syndrome.

123

Definition of fibrinous pericarditis

Finely granular pericardial surface & may produce a pericardial friction rub.

124

Definition of purulent or suppurative Pericarditis

Pus in pericardial sac usually from infective organisms. Acute inflammatory reaction involving pericardium with purulent exudate. If survive usually organizes, may produce constrictive pericarditis.

125

Definition of hemorrhagic pericarditis

Blood mixed with fibrin or pus. Can be seen with tuberculosis and other bacterial infections, malignancy, and following cardiac surgery.

126

What is the usual involvement of caseous pericarditis?

Granulomatous inflammation involving pericardium

127

What is the usual cause of caseous pericarditis?

Tuberculosis

128

What is a consequence of caseous pericarditis?

Fibrocalcific chronic constrictive pericarditis.

129

What often precedes adhesive mediastinopericarditis?

Suppurative or caseous pericarditis, cardiac surgery or mediastinal radiation.

130

What is adhesive mediastinopericarditis.

Pericardial sac obliterated & adherence of the outer portion of the parietal pericardium to surrounding structures produces great stain on cardiac function. Increased work of heart leads to cardiac hypertrophy and dilatation.

131

What often precedes constrictive pericarditis?

Suppurative, hemorrhagic or caseous pericarditis.

132

What is constrictive pericarditis?

Pericardial sac obliterated & heart surrounded by dense adherent layer of scar tissue with or without calcification (if extreme encasement called concretio cordis). Encasing scar limits diastolic expansion of heart leading to decreased cardiac output.