Cardiac Immune Disorders- Barrington Flashcards
pathogenesis of rheumatic fever
post GAS sequellae;
molecular mimicry where auto-Ab’s against GAS M protein that looks like cardiac myosin and our own body will attack the myosin and cause cardiac damage
recurrent ARF leads to what
rheumatic heart disease
GAS infection can be treated with what
Penicillin
where is ARF and RHD most prominent
in underdeveloped countries
R: Beta hemolytic
L: gram + cocci in chains
(GAS)
common sites of GAS infection
throat and skin
untreated GAS can lead to what
ARF
GAS is aka
S. pyogenes
what specific cells are activated with ARF
B cells
most important sign of ARF
carditis
what is targeted in carditis
mitral valve
mitral valve
Aschoff nodules seen in carditis; ARF
another sign of ARF involving joints
polyarthritis
migrating arthritis from joint to joint
polyarthritis
another sign of ARF (jerky movements)
Sydenham’s chorea
painless rash on torso (sign of ARF)
Erythema marginatum
common when carditis is present
subcutaneous nodules (formed from Ashcoff bodies)
hard to diagnose ARF w/ testing why
b/c it takes 2-5 wks after GAS infection to show up
minor signs of ARF
fever, arthralgia
labs done for ARF
anti-streptolysin O titer
throat swab
to Rx ARF:
penicillin to GAS
bed rest; Rx sx’s
likelihood of graft rejection is high in what graft
allograft
how to donor match for heart since limited time frame
ABO and PRA (checking for reactive Ab’s)
post op drugs for heart transplant
cyclosporin
corticosteroids
azathioprine
-mab
what has to be done to endocardium frequently after heart transplant
biopsy
worst grades
2 and 4 (graft rejection)
rejection that happens within min-hours of transplant; pre-existing Ab’s
hyperacute
rejection that happens w/in first 1-2 months of tranplant; alloreactive T cells
acute rejection
rejection that is harder to control and causes vasculopathies
chronic rejection
pig heart transplant
xenotransplantation
problem w/ xenotransplantation
hyperacute rejection
solution to xenotransplantation
genetically modify pigs to make it where human T cells won’t recognize and not attack
ischemia/MI reperfusion injury in a nut shell
damage to heart due to some kind of immune response (B or T cells); complement activation
mouse to use for best outcome for ischemia/MI reperfusion injury
RAG deficient mouse (unable to make B and T cells)
MoA for cyclosporine
blocks calcineurin; inhibits IL-2 (therefore stopping T cell expansion)
success of xenotranplantation meaning
lack of hyperacute rejection
