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Pathology EX 2 > CV III > Flashcards

CV III Flashcards

1
Q

Mitral valve ________ is failure of a valve to open completely, obstructing forward flow.

A

Stenosis

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2
Q

Acute rheumatic fever (RF) is _____ disease, usually in ______, which follows a ___________

A

systemic

children

Group A beta hemolytic Streptoccocal pharyngitis

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3
Q

Myocarditis is characterized by _______ which are collections of mononuclear inflammatory cells and fibroblasts (essentially ________________)

A

Aschoff bodies

Granulomatous inflammation

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4
Q

Recurrent bouts of RF eventually lead to _______ and _______ of the mitral valve and possibly other heart valve diseases.

A

severe fibrosis

calcification

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5
Q

Valvular disease caused by severe RF is thought to be due to the production of _______ against the ______ bacteria which cross react with various antigens in the heart, joints and other sites

A

antibodies

streptococcal

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6
Q

Pericarditis - ______

Endocarditis - _______

A

fibrinous

sterile vegetations

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7
Q

MV ______ (insufficiency) refers to a valve that fails to close completely, allowing backflow of blood.

A

Regurgitation

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8
Q

MV regurgitation may be caused by _______ and ______

A

IHD

Endocarditis

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9
Q

MV ______ is a condition which the leaflets balloon into the left atrium during left ventricular contraction (systole).

A

Prolapse

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10
Q

Mild prolapse is _____ and occurs _____ of the general population and usually does not _____ to valvular regurgitation. ______ may be associated with valvular regurgitation.

A

common

5-10%

progress

severe prolapse

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11
Q

patients with severe prolapse may experience ______ and ______

A

chest pain

palpitations

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12
Q

Potential complications associated with sever prolapse are….. and only develop in about ____ of affected patients

A

Endocarditis

Mitral regurgitation

Thromboemboli

Sudden death

3%

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13
Q

MV prolapse is also known as ______

A

Floppy mitral valve

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14
Q

Floppy MV may be an isolated abnormality or part of a ___________ disorder such as ________

A

systemic CT disorder

Marfan syndrome

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15
Q

Aortic valve stenosis is caused by ______

A

fibrosis and calcification

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16
Q

Fibrosis and calcification reduce the ______

A

valve cusp mobility

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17
Q

Aortic valve stenosis can be due to ______ or may occur with advanced age (over ____ yrs)

A

Chronic rheumatic valvular disease

65 years

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18
Q

______ is a common congenital malformations and these valves are predisposed to calcification and fibrosis beginning at about ______ years of age

A

Biscuspid aortic valve

40-50

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19
Q

Aortic valve regurgitation is caused by ______, _______,and _______

A
  1. valve cusp destruction (endocarditis)
  2. Myxomatous degeneration: Marfan’s syndrome (weakended valve cusps)
  3. Dilation of the aortic root (degeneration of the media of the aorta)
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20
Q

Infective endocarditis is usually caused by ________

A

a bacterial infection in a heart valve

also by fungus or other unusual infections

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21
Q

Predisposing factors of IE include…

A

Intracardiac shutns

valvular disease

prosthetic valves (10-20% of all IE)

IV drug abuse

Immunosuppression

Diabetes

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22
Q

3 steps of pathogenesis

A
  1. Endocardial or endothelial injury due to abnormal blood flow
  2. fibrin thrombi
  3. organisms in the blood
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23
Q

Clinical manifestations of IE

A

Fever

Heart murmur

fatigue, anemia

arthralgia, myalgia

Splinter hemorrhages (nail bed)

Roth spots (retinal hemorrhages but not specific to IE)

24
Q

Complications of IE

A
  1. rupture of chordae tendineae
  2. spread of infection into myocardium or aorta
  3. thromboemboism with infarction
  4. septic thrombi with metastatic abscesses
  5. vavular dysfunction and CHF
25
Q

Characteristics of ACUTE Endocarditis

A

short duration

virulent organism

staphylococcus aureus

large friable vegetations

previously normal valve

prominent tissue destruction

26
Q

Characteristics of Subacute endocarditis

A

Longer duration

Low virulence

Streptococcus viridans

Small vegetations

previously abnormal valve

less tissue destruction

27
Q

Vascultis may be caused by ______

A

infection (usually by direct spread of an adjacent infection, some microorganisms infect cells and cause a vasculitis)

or

mechanical trauma, toxins, caustic substances, radiation and immune complexes

28
Q

Large vessel group?

A

Giant cell (temporal) arteritis

Takaysu arteritis

29
Q

Medium vessel group?

A

Polyarteritis nodosa (classic)

Kawasaki syndrome

30
Q

Small vessel group?

A

Microscopic polyarteritis

Wegener’s granulomatosis

31
Q

Pathogenesis of immune-mediated vasculitis

A
  1. immune complex formation - reaction to drugs or viruses
  2. antineutrophilic cytoplasmic antibodies (ANCA)
    Anti-myeloperoxidase (anti-MPO) - perinuclear localization (Formeraly pANCA) - Microscopic polyarteritis

Anti-proteinase-3 (anti-PR3) - diffuse cytoplasmic distribution (formerly known as cANCA) - Wegener’s granulomatosis

  1. Anti-endothelial cell antibodies - Kawasaki disease
  2. Cell-mediated immunity
32
Q

Etiology of Giant cell (temporal) arteritis?

A

Unknown (T-cell mediated?)

33
Q

Clinical featrues of Giant cell arteritis..

A

Fever, weight loss, headache, visual problems, claudication of jaw, pain and tenderness over temporal artery, polymyalgia rheumatica. Rare under 50 years of age.

34
Q

Pathology giant cell arteritis?

A

Granulomatous inflammation with giant cells, fibrosis.

Eventually narrowing of vessel lumen, then less blood flow to affected tissues

35
Q

Takayasu Arteritis Etiology and Clinical features?

A

Etiology unkown

Thickening of the wall reduces blood flow in the major branches off the aortic arch. Usually affets young women.

Very similar to giant temporal arteritis but in younger patients (<40 yrs)

36
Q

Pathology of Takayasu arteritis?

A

Granulomatous inflammation with fibrosis involving (aortic arch + branches)

37
Q

Etiology of Polyarteritis nodosa?

A

Unknown in most cases.

Once ~30% had hep b surface antigen in the serum, now < 8% due to widespread immunizations

38
Q

Clinical features of Polyarteritis nodosa?

A

Fever, Weight loss, hematuria, renal failure, hypertension, ab pain, melena (blood in stool)

very confusing due to involvement of multiple organs

39
Q

Pathology of Polyarteritis nodosa?

A

Haphazard and segmental involvement of medium and small muscular arteries

Thrombosis, aneurysms

Heal by fibrosis

Kidney (85%)> Heart (75) > liver (65)> GI (50)

40
Q

Kawasaki disease is also known as…

A

Mucocutaneous lymph node syndrome

41
Q

Etiology of Kawasaki disease

A

Viral infection triggering a hypersensitivity reaction

42
Q

Clinical features of Kawasaki disease

A

Affects infants and young children (80% of patients 4 years old)

Skin rash, mucous membrane lesions, cervical lymphadenopathy

43
Q

Pathology of Kawasaki disease

A

Usually self-limited but 1-2% die with coronary artery vasculitis

44
Q

Etiology of Microscopic Polyangiitis

A

Antigen-antibody complexes

45
Q

Clinical features of Microscopic polyangiitis

A

Fever, rash, joint swelling, pleural effusion, pulmonary infiltrates, myocarditis, GI bleeding, renal failure, presence of circulating antineutrophilic cytoplasmic antibodies (MPO-ANCA). May be precipitated by drugs, microorganisms, foreign proteins or tumor proteins

46
Q

Pathology of Microscopic polyangiitis

A

Involves… Arterioles, capillaries, venules.

Fibrinoid necrosis, Karyoorhexis of PMN’s (leukocytoclatic vasculitis)

47
Q

Etiology of Wegener Granulomatosis?

A

Abnormal expression of PR3 on endothelial cell surface, followed by ANCA binding and neutrophil activation, resulting in damage to endothelium and vessel

48
Q

Clinical features of Wegener Granulomatosis?

A

Sinuses, Pneumonitis, renal failure, glomerulonephritis

49
Q

Pathology of Wegener granulomatosis?

A

Affects kidneys, upper and lower resp tract

Necrotizing granulomas

Vasculitis with fibrinoid necrosis

50
Q

Etiology of Thromboangiitis obliterans

A

AKA Buerger disease,

Endothelial injury from a substance in cigarette smoke

51
Q

Clinical features of Thromboangiitis obliterans?

A

Begins before age 35. Pain and ischemia in extremities, ischemic ulcers, gangrene

52
Q

Pathology of Thromboangiitis obliterans?

A

Vasculitis with thrombosis

53
Q

Pathology of Dissecting aortic hematoma?

A

Longitudinal tear of the aortic media (split between mid and outer 1/3) which begins in the ascending aorta and extends variable distance proximal (toward the heart) and distal to the descending aorta

Media may be normal or have degeneration

54
Q

Complications of Dissecting aortic hematoma?

A

Rupture -> severe hemorrhage, oran ischemia due to luminal compression by the expanding hematoma, branch obstruction

55
Q

Predisposing conditions of Dissecting aortic hematoma?

A

Hypertension, inherited CT disorder (Marfan syndrome) with medial degeneration

Pathology EX 2 (3 decks)

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