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Pathology Exam 2 > Lecture 15 - CV III (Cardiac Valvular Disease and Vasculitis) > Flashcards

Lecture 15 - CV III (Cardiac Valvular Disease and Vasculitis) Flashcards

1
Q

What is mitral valve stenosis?

A

Acquired stenosis (failure of a valve to open completely, obstructing forward flow) is usually due to chronic (recurrent) rheumatic valvular disease)

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2
Q

What disease is described:
Systemic disease, usually in children
-follows a group A beta-hemolytic streptococcal pharyngitis

A

acute rheumatic fever

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3
Q

What are some manifestations that acute rheumatic fever (RF) produces?

A
  • myocarditis
  • pericarditis
  • arthralgia
  • arthritis
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4
Q

The myocarditis associated with mitral valve stenosis is characterized microscopically by what?

A

Aschoff bodies

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5
Q

What are Aschoff bodies?

A
  • collections of mononuclear inflammatory cells and fibroblasts (essentially granulomatous inflammation)
  • Found in myocarditis
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6
Q

Recurrent bouts of rheumatic fever eventually lead to what?

A

-severe fibrosis and calcification of the mitral valve and possibly other heart valves

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7
Q

acute rheumatic fever is thought to be due to what?

A

production of antibodies against the streptococcal bacteria which cross react with various antigens in the heart, joints, and other sites

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8
Q

In terms of the heart what is meant by regurgitation?

A
  • insufficiency

- a valve that fails to close completely, allowing backflow of blood

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9
Q

What two conditions specifically can cause mitral valve regurgitation?

A

IHD (ischemic heart disease)

endocarditis

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10
Q

What is mitral valve prolapse?

A

a condition in which the leaflets ballon into the left atrium during left ventricular contraction (systole)

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11
Q

If mild prolapse common and what percent of the general population does it occur?

A

mild prolapse is VERY common and occurs in 5-10% of the general population

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12
Q

True/ False: Mild prolapse usually progresses to valvular regurgitation

A

False:

Mild prolapse usually does NOT progress to valvular regurgitation

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13
Q

Severe prolapse may be associated with what?

A

valvular regurgitation

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14
Q

What are two side effects that patients with mitral valve regurgitation may experience?

A

chest pain and palpitations

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15
Q

What are some potential complications of mitral valve regurgitation?

A
  • endocarditis
  • mitral regurgitation
  • thromboemboli
  • sudden death (rare)
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16
Q

what is another name for severe prolapse?

A

floppy mitral valve

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17
Q

what is found in severe prolapse?

A

the valve cusps are large and microscopically show fragmentation, separation and loss of collagen (myxomatous degeneration)

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18
Q

Floppy mitral valve (or severe prolapse) may be an isolated abnormality or part of a systemic connective tissue disorder such as what?

A

Marfan syndrome

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19
Q

in aortic valve stenosis, what two things specifically can reduce the valve cusp mobility?

A

fibrosis and calcification

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20
Q

What are causes of aortic valve stenosis?

A
  1. chronic rheumatic valvular disease

2. advanced age (over 65 years)

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21
Q

when a patient has chronic rheumatic valvular disease the mitral valve is almost always _____

A

stenotic

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22
Q

What is described: common congenital malformation and these valves are predisposed to calcification and fibrosis beginning at about 40 years of age

A

bicuspid aortic valve

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23
Q

What are the three mechanisms of aortic valve regurgitation?

A
  • valve cusp destruction (endocarditis)
  • myxomatous degeneration
  • dilation of the aortic root
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24
Q

infective endocarditis is usually cause by what?

A

BACTERIAL infection in a heart valve

*Although it may also be cause by fungus or other unusual infections

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25
Q

What are the predisposing factors of infective endocarditis? (6 of them)

A
  1. abnormal heart valves
  2. prosthetic valves
  3. intravenous drug use
  4. intracardiac shunts
  5. diabetes
  6. immunosuppression
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26
Q

The three factors that have been identified as having importance in the pathogenesis of infective endocarditis include:

A
  1. endocardial or endothelial injury due to abnormalities in blood flow
  2. Fibrin thrombi
  3. organisms in the blood
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27
Q

What are the clinical manifestations of infective endocarditis?

A
  • Fever
  • Heart murmur
  • Fatigue
  • Anemia
  • Arthralgia
  • Myalgia
  • Splinter hemorrhages (nail bed)
  • Roth spots (retinal hemorrhages, not absolutely specific to IE)
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28
Q

what are the complications of infective endocarditis? (5 of them)

A
  1. rupture of chordae tendinaea
  2. Spread of infection into myocardium or aorta
  3. Thromboembolism with infarction
  4. Septic thrombi with metastatic abscesses
  5. valvular dysfunction and CHF
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29
Q

which has a longer duration, acute or subacute endocarditis?

A

Subacute endocarditis has a longer duration

Acute endocarditis has a short duration

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30
Q

is virulent organism associated with acute or subacute endocarditis?

A

acute

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31
Q

what is the virulent organisms for acute endocarditis and what is the low virulent organism of subacute endocarditis?

A

acute endocarditis: staphylococcus aureus

subacute endocarditis: streptococcus viridans

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32
Q

Does acute endocarditis have large friable or small vegetations?

A

acute: large friable vegetations
subacute: small vegetations

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33
Q

There was a previously normal valve in acute or subacute endocardidits?

A

acute endocardidits has a previously normal valve

34
Q

(T/F) Subacute endocarditis has a previously normal valve

A

FALSE - subacute endocarditis had a previously ABnormal valve

35
Q

Does acute or subacute endocarditis has more prominent tissue destruction?

A

acute endocarditis has more prominent tissue destruction

36
Q

What is the main cause of vasculitis?

A

-Infection (usually due to direct spread of an adjacent infection; some microorganisms infect endothelial cells and cause vasculitis)

37
Q

What are some other causes of vasculitis?

A
  1. mechanical trauma
  2. toxins
  3. caustic substances
  4. radiation
  5. immune complexes
38
Q

what are two examples of large vessel vasculitis?

A
  1. giant cell (temporal) arteritis

2. Takayasu arteritis

39
Q

what are two examples of medium vessel vasculitis?

A
  1. Polyarteritis nodosa (classic)

2. Kawaski syndrome

40
Q

what are two examples of small vessel vasculitis?

A
  1. microscopic polyarteritis

2. Wegener’s granulomatosis

41
Q

in the pathogenesis of immune mediated vasculitis, the immune complex formation is from reaction to what?

A

drugs or viruses

42
Q

in the pathogenesis of immune mediated vasculitis, antineutrophilic cytoplasmic antibodies (ANCA) what are the two subtypes?

A
  • Anti-myeloperoxidase (anti-MPO) - perinuclear localization (formerly known as pANCA) - microscopic polyarteritis
  • Anti-proteinase-3 (anti-PR3) - diffuse cytoplasmic distribution (formerly known as cANCA) - Wegener’s granulomatosis
43
Q

in the pathogenesis of immune mediated vasculitis, anti-endothelial cell antibodies are associated wth what disease?

A

Kawasaki disease

44
Q

____ - mediated immunity is associated with pathogenesis of immune mediated vasculitis

A

cell-mediated immunity

45
Q

What is the etiology of giant cell (temporal) arteritis?

A

unknown

maybe T cell mediated

46
Q

what are the clinical findings of giant cell (temporal) arteritis?

A
  • Fever
  • Weight loss
  • headache
  • visual problems (including blindness)
  • claudication of jaw (weakness when chewing due to decreased blood supply)
  • pain and tenderness over temporal artery
  • polymyalgia rheumatica (inflammatory disorder that causes muscle pain and stiffness)
47
Q

(T/F) giant cell (temporal) arteritis is typially seen in younger individuals

A 
FALSE
giant cell (temporal) arteritis is rare under the age of 50 years
48
Q

what is the pathology of giant cell (temporal) arteritis?

A

granulomatous inflammation with giant cells, fibrosis

*Eventually causes narrowing of vessel lumen, with decreased blood flow to affected tissues

49
Q

what is the etiology of Takayasu arteritis?

A

unknown

50
Q

what are the clinical findings in Takayasu arteritis?

A

Thickening of the wall reduced blood flow in the major branches off the aortic arch

51
Q

what condition is also known as “pulseless disease” due to weak pulses in the arms

A

Takayasu arteritis

52
Q

Takayasu arteritis usually affects what population?

A

young women

may be the same disease as temporal arteritis, but in a younger patient

53
Q

what is the pathology of Takayasu arteritis?

A

granulomatous inflammation with fibrosis involving the aortic arch and the arch branches

54
Q

What disease is unknown in most cases, once up to 30% has hepatitis B surface antigen in the serum, now less than 8% due to widespread immuniations

A

polyarteritis nodosa

55
Q

what are some clinical manifestations of polyarteritis nodosa?

A
  • Fever
  • Weight loss
  • Hematuria
  • Renal failure
  • Hypertension
  • Abdominal pain
  • Melana (bloody diarrhea)

*Clinical presentation may be very confusing due to involvement of multiple organ systems

56
Q

What pathology is described: Haphazard and segmental involvement of medium and small muscular arteries. Acute lesions show fibrinoid necrosis, thrombosis, neutrophils, aneurysms.

A

polyarteritis nodosa

57
Q

with healing of polyarteritis nodosa there is predominance of what and progressive fibrous _____?

A

macrophages and plasma cells and progressive fibrous scarring

58
Q

in the order of most sites of involvement to least what are the most usual sites of involvement in polyarteritis nodosa?

A

Kidneys (85%)
Heart (75%)
Liver (65%)
GI tract (50%)

59
Q

what is the etiology of Kawasaki disease?

A

viral infection triggers a hypersensitive reaction

AKA: mucocutaneous lymph node syndrome

60
Q

Kawasaki disease normally affects what population and 80% of patient are less than what age?

A

African infants and young children

80% of patients are less than 4 years

61
Q

what are some of the clinical manifestations of Kawasaki disease?

A
  • skin rash
  • mucous membrane lesions
  • cervical lymphadenopathy
62
Q

Kawasaki disease is usually self limited, but 1-2% die with because of what?

A

coronary artery vasculitis

63
Q

what is the etiology of microscopic polyangitis?

A

often due to antigen-antibody complexes

64
Q

what are the clinical manifestations of microscopic polyangitis?

A
  • fever
  • rash
  • joint swelling
  • pleural effusion
  • pulmonary infilitrates
  • myocarditis
  • GI bledding
  • renal failure
  • presence of circulating anti-neutrophilic cytoplasmia antibodies (MPO-ANCA)
65
Q

microscopic polyangitis may be precipitated by what?

A
  • Drugs
  • Microorganisms
  • Foreign proteins
  • Tumor proteins
66
Q

what is the pathology of microscopic polyangitis?

A

involves arterioles, capillaries, venules

Fibrinoid necrosis, neutrophils (leukocytoclasic vasculitis)

67
Q

What etiology is described: abnormal expression of proteinase 3 on endothelial cell surface, followed by ANCA binding and neutrophil activation, resulting in damage to endothelium and vessel

A

Wegener granulomatosis

68
Q

what are the clinical manifestations of Wegener granulomatosis?

A
  • involves sinuses

- lungs and kidneys (glomerulonephritis)

69
Q

Wegener granulomatosis is - Associated with the presence of what?

A

anti-neutrophilic cytoplasmic antibodies direct against proteinase 3 (PR3-ANCA)

70
Q

what vasculitis condition has the pathology of necrotizing granulomas with vasculitis

A

wegener granulomatosis

71
Q

thromboangiitis obliterans as also known as what?

A

Buerger disease

72
Q

in thromboangiitis obliterans (Buerger disease) it results from ENDOthelial injury from a substance in what?

A

cigarette smoke

73
Q

What are the clinical findings of thromboangiitis?

A

pain and ischemia in extremities

74
Q

thromboangiitis usually begins around what age

A

before age 35

75
Q

what is the pathology of thromboangiitis obliterans?

A

segmental acute and chronic vasculitis mainly in extremities with thrombosis

76
Q

in an aortic hematoma (aneurysn) it begins in the ______ ______ and extends variable distance proximal (toward the heart) and distal to the ____ _____

A

begins in ASCENDING AORTA and extends variable distance proximal (toward the heart) and distal to the DESCENDING AORTA

77
Q

what are some complications of a dissecting aortic hematoma (aneurysm)

A
  • severe hemorrhage from rupture

- organ ischemia due to luminal compression by the expanding hematoma

78
Q

what are the predisposing factors of dissecting aortic hematoma (aneurysm)?

A
  • hypertension

- inherited connective tissue (i.e. Marfan’s syndrome) with medial degeneration

79
Q

Repeated episodes of acute rheumatic fever can cause what?

A

mitral valve fibrosis and calcification with valvular stenosis

80
Q

what is the histopathologic feature of severe mitral valve prolapse (floppy mitral valve)?

A

myxomatous degeneration

81
Q

what are the ANCA-positive forms of vasculitis?

A

Wegener’s granulomatosis and microscopic polyarteritis

82
Q

what are the complications of dissecting hematoma (split (hematoma) in the media)?

A

-hemorrhage and branch obstruction

Pathology Exam 2 (8 decks)

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