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Cardio Block > Vasculitis and Complications of MIs > Flashcards

Vasculitis and Complications of MIs Flashcards

1
Q

Two divisions of vasulitis

A

Infectious and non-infectious (primary)

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2
Q

Predominant fungal cause of infectious vasculitls

A

Aspergillus

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3
Q

Predominant bacterial cause of IV

A

Cytomegalovirus

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4
Q

Predominant bacterial cause

A

Psuedomonas

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5
Q

Pathophysiology of Primary Vasculitis

A

Dendritic cells int eh tunica adventitia go haywire and instead of disposing of self-recognizing immune cells they activate them. These immune cells then degrade the elastic lamina
Another mechanism…. Immune complex deposition. Inflammation mediated by complement, chemoattractants, neutrophils, lysosomal enzymes, free radicals.

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6
Q

Major signs and symptoms

A

palpable purpura and fever

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7
Q

Hypersensitivity angiitis

A

acute necrotizing inflammatory disease of the smallest vessels (arterioles, cappilaries, venuoles). Usually in the skin

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8
Q

Cutaneous hypersensitivity angiitis also referred to as?

A

Leukocytoclastic vasculitis

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9
Q

10% of cases of hypersensitivity angiitis due to?

A

drugs

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10
Q

What drugs?

A

Quinolones, penicillins, sulfonamides, Retinoids, etc…

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11
Q

Microscopic polyangiitis is

A

hypersensitivity angiitis involving internal organs

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12
Q

Pathogenesis of hypersensitivity angiitis?

A

immune complex deposition and complement activation 7-10 days after exposure to an antigen (drug)

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13
Q

Pathology of hypersensitivity angiitis

A

infiltration of vessels by neutrophils, later lymphocytes

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14
Q

Diagnosis requires?

A

biopsy

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15
Q

Signs

A

palpable purpura

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16
Q

Treatment

A

stop the drug, treat the infection, excise the tumor…etc…
If it infects the organs, treat with immunosuppresive therapy

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17
Q

Temporal arteritis

A

Giant cell arteritis, granulomatous inflammatory disease of medium and larger arteries, esp in the head

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18
Q

Temporal arteritis common

A

Fairly…1 in 750 over the age of 50, female predominance, more common in whites

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19
Q

Temporal arteritis autoimmune?

A

yep

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20
Q

Pathology of temporal arteritis

A

multinucleated giant cells destroy internal elastic lamina. Transmural granulomatous inflammation. Intimal thickening, cell proliferation and luminal stenosis

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21
Q

Signs and symptoms

A

headache, visual disturbance, jaw claudication, swollen tender artery.
Fever malaise and wt loss make blindness less likely

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22
Q

Polymyalgia rheumatica

A

chronic autoimmune inflammatory disease of muscle. Temporal arteritis is associated with it in 40% of cases.

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23
Q

Complcations of temporal arteritis

A

blindness, aortic aneurysm, arterial dissection, arterial rupture

24
Q

Temporal arteritis is diagnosed by

A

ESR and biopsy

25
Q

Treat temporal arteritis with

A

steroids

26
Q

Temporal arteritis

A

old white women

27
Q

Kawasaki disease

A

mucocutaneous lymph node syndrome…vasculitis of medium arteries, especially coronaries.

28
Q

kawasaki predominantly effects who>

A

children 1-2 yrs of age, males, japanese

29
Q

Kawasaki complications

A

arterial rupture, MI, death

30
Q

Pathogenesis

A

An immune reaction to an RNA virus

31
Q

Signs and symptoms

A

high fever, conjunctivitis, mucosal and skin erythema and edema, swollen strawberry tongue

32
Q

Treat kawasaki with

A

Aspirin and IV Ig

33
Q

Seven most common MI complications

A

cardiac arrhythmias, heart failure, mural thrombus formation, cardiac rupture, pericarditis, aneurysm formation, papillary muscle rupture

(A-rhhythmic heart forms murals that rupture peri form and then rupture)

34
Q

Cardiac arrhythmias complicate MI in what % of cases?

A

90%

35
Q

Most common arrhythmia

A

accelerated idioventricular rhythm

36
Q

What is an idioventricular rhythm

A

originates in the ventricle, from yocytes outside the conduction system. Spreads more slowly than a normal rhythm so the QRS is wider than normal and funny looking.

37
Q

If the rate of an idioventricular rhythm is in the normal range it is called

A

accelerated

38
Q

Accelerated idioventricular rhytm is often a sign of what

A

reperfusion, which can mean its a good thing

39
Q

supraventricular tacchycardia and sinus tacchycardia are only bad if:

A

they are too rapid

40
Q

Ventricular tachycardia

A

occurs in around 15% of cases. Always bad…can turn into ventricular fibrillation

41
Q

AV block is most likely when?

A

When the infarction is in right coronary artery territory b/c the AV node is more served by the right coronary artery than the left

42
Q

Heart failure

A

complicates 60% of MI

43
Q

Heart failure occurs when

A

20% or more of the LV is infarcted

44
Q

When 40% of the LV is infarcted,

A

the patient is in cardiogenic shock

45
Q

Heart failure due to MI are in four hemodynamic groups called forrester classes:

A

Class I patients have a preserved CO and low or normal left atrial pressure

46
Q

Class II pts

A

Preserved CO but high left atrial pressure (over 18)

47
Q

Class III

A

Low cardiac output and high atrial pressure (over 18)

48
Q

Class IV

A

Low cardiac output and high left atrial pressure

49
Q

Class II treatment

A

diuretic

50
Q

Class III

A

Volume expansion

51
Q

Why is it important to differentiate class II from class III?

A

treatment is completely different because in class III the cardiac output is low

52
Q

Mural thrombus

A

complicates MIs in 20% of cases

53
Q

Mural thrombi commony embolize where

A

brain or kidney in the 2nd or third week

54
Q

Cardiac rupture

A

5% of cases. Allows blood part of the systolic output to go into the pericardium causing a hemopericardium and cardiac tamponade. Typically around the fifth day

55
Q

Pericarditis

A

about 5% of cases…day 2-4 after MI or 2mths after due to Dressler syndrome.

Cardio Block (42 decks)

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