Flashcards in Vasculitis and Complications of MIs Deck (55):
Two divisions of vasulitis
Infectious and non-infectious (primary)
Predominant fungal cause of infectious vasculitls
Predominant bacterial cause of IV
Predominant bacterial cause
Pathophysiology of Primary Vasculitis
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.
Major signs and symptoms
palpable purpura and fever
acute necrotizing inflammatory disease of the smallest vessels (arterioles, cappilaries, venuoles). Usually in the skin
Cutaneous hypersensitivity angiitis also referred to as?
10% of cases of hypersensitivity angiitis due to?
Quinolones, penicillins, sulfonamides, Retinoids, etc...
Microscopic polyangiitis is
hypersensitivity angiitis involving internal organs
Pathogenesis of hypersensitivity angiitis?
immune complex deposition and complement activation 7-10 days after exposure to an antigen (drug)
Pathology of hypersensitivity angiitis
infiltration of vessels by neutrophils, later lymphocytes
stop the drug, treat the infection, excise the tumor...etc...
If it infects the organs, treat with immunosuppresive therapy
Giant cell arteritis, granulomatous inflammatory disease of medium and larger arteries, esp in the head
Temporal arteritis common
Fairly...1 in 750 over the age of 50, female predominance, more common in whites
Temporal arteritis autoimmune?
Pathology of temporal arteritis
multinucleated giant cells destroy internal elastic lamina. Transmural granulomatous inflammation. Intimal thickening, cell proliferation and luminal stenosis
Signs and symptoms
headache, visual disturbance, jaw claudication, swollen tender artery.
Fever malaise and wt loss make blindness less likely
chronic autoimmune inflammatory disease of muscle. Temporal arteritis is associated with it in 40% of cases.
Complcations of temporal arteritis
blindness, aortic aneurysm, arterial dissection, arterial rupture
Temporal arteritis is diagnosed by
ESR and biopsy
Treat temporal arteritis with
old white women
mucocutaneous lymph node syndrome...vasculitis of medium arteries, especially coronaries.
kawasaki predominantly effects who>
children 1-2 yrs of age, males, japanese
arterial rupture, MI, death
An immune reaction to an RNA virus
Signs and symptoms
high fever, conjunctivitis, mucosal and skin erythema and edema, swollen strawberry tongue
Treat kawasaki with
Aspirin and IV Ig
Seven most common MI complications
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)
Cardiac arrhythmias complicate MI in what % of cases?
Most common arrhythmia
accelerated idioventricular rhythm
What is an idioventricular rhythm
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.
If the rate of an idioventricular rhythm is in the normal range it is called
Accelerated idioventricular rhytm is often a sign of what
reperfusion, which can mean its a good thing
supraventricular tacchycardia and sinus tacchycardia are only bad if:
they are too rapid
occurs in around 15% of cases. Always bad...can turn into ventricular fibrillation
AV block is most likely when?
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
complicates 60% of MI
Heart failure occurs when
20% or more of the LV is infarcted
When 40% of the LV is infarcted,
the patient is in cardiogenic shock
Heart failure due to MI are in four hemodynamic groups called forrester classes:
Class I patients have a preserved CO and low or normal left atrial pressure
Class II pts
Preserved CO but high left atrial pressure (over 18)
Low cardiac output and high atrial pressure (over 18)
Low cardiac output and high left atrial pressure
Class II treatment
Why is it important to differentiate class II from class III?
treatment is completely different because in class III the cardiac output is low
complicates MIs in 20% of cases
Mural thrombi commony embolize where
brain or kidney in the 2nd or third week
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