Vasculitis and Complications of MIs

Question 1

Two divisions of vasulitis

Answer 1

Infectious and non-infectious (primary)

Question 2

Predominant fungal cause of infectious vasculitls

Answer 2

Aspergillus

Question 3

Predominant bacterial cause of IV

Answer 3

Cytomegalovirus

Question 4

Predominant bacterial cause

Answer 4

Psuedomonas

Question 5

Pathophysiology of Primary Vasculitis

Answer 5

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.

Question 6

Major signs and symptoms

Answer 6

palpable purpura and fever

Question 7

Hypersensitivity angiitis

Answer 7

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

Question 8

Cutaneous hypersensitivity angiitis also referred to as?

Answer 8

Leukocytoclastic vasculitis

Question 9

10% of cases of hypersensitivity angiitis due to?

Answer 9

drugs

Question 10

What drugs?

Answer 10

Quinolones, penicillins, sulfonamides, Retinoids, etc…

Question 11

Microscopic polyangiitis is

Answer 11

hypersensitivity angiitis involving internal organs

Question 12

Pathogenesis of hypersensitivity angiitis?

Answer 12

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

Question 13

Pathology of hypersensitivity angiitis

Answer 13

infiltration of vessels by neutrophils, later lymphocytes

Question 14

Diagnosis requires?

Answer 14

biopsy

Question 15

Signs

Answer 15

palpable purpura

Question 16

Treatment

Answer 16

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

Question 17

Temporal arteritis

Answer 17

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

Question 18

Temporal arteritis common

Answer 18

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

Question 19

Temporal arteritis autoimmune?

Answer 19

yep

Question 20

Pathology of temporal arteritis

Answer 20

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

Question 21

Signs and symptoms

Answer 21

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

Question 22

Polymyalgia rheumatica

Answer 22

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

Question 23

Complcations of temporal arteritis

Answer 23

blindness, aortic aneurysm, arterial dissection, arterial rupture

Question 24

Temporal arteritis is diagnosed by

Answer 24

ESR and biopsy

Question 25

Treat temporal arteritis with

Answer 25

steroids

Question 26

Temporal arteritis

Answer 26

old white women

Question 27

Kawasaki disease

Answer 27

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

Question 28

kawasaki predominantly effects who>

Answer 28

children 1-2 yrs of age, males, japanese

Question 29

Kawasaki complications

Answer 29

arterial rupture, MI, death

Question 30

Pathogenesis

Answer 30

An immune reaction to an RNA virus

Question 31

Signs and symptoms

Answer 31

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

Question 32

Treat kawasaki with

Answer 32

Aspirin and IV Ig

Question 33

Seven most common MI complications

Answer 33

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)

Question 34

Cardiac arrhythmias complicate MI in what % of cases?

Answer 34

90%

Question 35

Most common arrhythmia

Answer 35

accelerated idioventricular rhythm

Question 36

What is an idioventricular rhythm

Answer 36

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.

Question 37

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

Answer 37

accelerated

Question 38

Accelerated idioventricular rhytm is often a sign of what

Answer 38

reperfusion, which can mean its a good thing

Question 39

supraventricular tacchycardia and sinus tacchycardia are only bad if:

Answer 39

they are too rapid

Question 40

Ventricular tachycardia

Answer 40

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

Question 41

AV block is most likely when?

Answer 41

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

Question 42

Heart failure

Answer 42

complicates 60% of MI

Question 43

Heart failure occurs when

Answer 43

20% or more of the LV is infarcted

Question 44

When 40% of the LV is infarcted,

Answer 44

the patient is in cardiogenic shock

Question 45

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

Answer 45

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

Question 46

Class II pts

Answer 46

Preserved CO but high left atrial pressure (over 18)

Question 47

Class III

Answer 47

Low cardiac output and high atrial pressure (over 18)

Question 48

Class IV

Answer 48

Low cardiac output and high left atrial pressure

Question 49

Class II treatment

Answer 49

diuretic

Question 50

Class III

Answer 50

Volume expansion

Question 51

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

Answer 51

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

Question 52

Mural thrombus

Answer 52

complicates MIs in 20% of cases

Question 53

Mural thrombi commony embolize where

Answer 53

brain or kidney in the 2nd or third week

Question 54

Cardiac rupture

Answer 54

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

Question 55

Pericarditis

Answer 55

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