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17 Cards in this Set

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Name the dz:
altered blood flow across **two-cusp** but otherwise normal AV predisposes to degeneration.

Is this a congential or a degenerative process?
Bicuspid Aortic Valve

both - congenital abnormality predisposes to valve calcification.
What are the three major components Rheumatic Heart Dz?

Two stages?

Globally, it accounts for >__% of all childhood ht dz.

USA?

microorganism associated with?
infectious, immunologic, degenerative

Acute rheumatic fever
Chronic: rheumatic ht. dz.

50%

rare dz

Group A Streptococcus
Is heart dz related to GAS due to direct bacterial injury?

What is *THE* defining inflammatory lesion in ARF? Characteristics (where, what, etc.)?
No; rather, due to indirect immunological attack against valve.

Aschoff Body
- myo/endo-cardium
- macrophages & multinucleated Giant Cells
- central collagen degen. w/ fibrinoid necrosis
- chronic nodular focus of scar formation
Carditis, Polyarthritis
Chorea
Erythema marginatum
subcut. nodules

Arthralgia
Fever
Elevated acute phase reactants
- erythrocyte sedimentation rate
- C-reactive protein
Prolonged PR interval

Top group is what? Bottom?
Major manifestations of Acute rheumatic fever.

Minor manifestations.
What are three characteristic things found in ARF myocardium?

**Are these cells singe/multinucleated myocytes?
Aschoff Body

Anitschkow cell
- macrophage w/ catipillar or owl-eye chromatin pattern

Aschoff myocyte
- multinucleated macrophage

NO!! Dammit. They are mono/multinuclear histiocytes.
What do we call fine, nodular fibrin depositis at the line of valve closure concurrant with fibrinoid degeneration, inflamm., ulceration, and neovascularization?

Does ACF contribue to the development of valve degeneration and chronicity?
Endocarditis related to ARF

Yes.
What occurs w/ ARF that is described as:
- fibrinous exudation: shaggy deposition of fibrin on visceral and parietal pericardium
- loss of "smooth, moist lining"
- can hear friction rub on ascultation

What is this reflective of?
Pericarditis

reflection of multisystem immunologic injury.
In which pts does this heart take on an ovoid shape?
kids with ARF that --> heart failure... --> dilation (eccentric hypertrophy)
What do the arrows point to?
Aschoff bodies (note that the whole big conglomeration is an Aschoff body)
What are these slides focused on? What are the cells the arrows are pointing at?
Aschoff bodies

Anitschkow cells (owl's eyes - caterpillar)
What are the two valves most common involved in Rheumatic Ht dz?

Can these be present:
thickening of cusps (fibrosis, neovas, calcification)
fusion of commissures of cusps
narrowed valvular opening
inability of cusps to fully oppose

****what accounts for this variance of clinical presentation?
mitral & aortic

All can be present w/ aortic valve pathology in RHD.

variations in location and extent of valve involvement; years of lesion evolution
What is also known as non-bacterial thrombotic endocarditis?

Associated with?
Valve most freq involved?

Is it inflammatory? infective? destructive?
Marantic endocarditis

cancer and other wasting dz; due to hypercoag. state
MV

No, none of them.
What is the liklihood of embolization of marantic endocarditis vegetations?
high; presenting findings might actually be the CVA results of embolization.
Which etiology are these patterns associated with?
Left to right, top to bottom:
ARF, bacterial, Marantic, Libman Sacks (SLE)
What is the most classic Collagen vascular dz associated with cardiac involvement?

Sx?

Other collagen vascular dz?

*** Immunological injury can lead to ....
Systemic Lupus Erythematosus (SLE) aka Libman-sacks endocarditis.

asymp. or mitral regurg.

Rheumatoid arthritis
ankylosing spondylitis
etc.

valve pathology.
In what dz do circulating serotonin and other bioactive products contact endocardium (especially tricuspid valve).... causing fibrosis on the right side of the heart & tricuspid fibrosis/stenosis/regurg?

What must a bioactive substance-producing tumor do in order to cause this?

Why is the left heart often spared?
Carcinoid heart dz

met to the liver so that the substances can be released into the systemic venous return to the heart w/o having gone thru hepatic deactivation.

Metabolic deactivation occurs i/ lungs, sparing the L Ht.
Pros and Cons of Mechanical valves vs bioprosthetic valves (major problems)?

Which are better?
Mechanical:
- ***provides a thrombogenic surface
-*** poten. site of infec.
- surg. issue = discontinuity at seat of valve
- mechanical failure (disc embolization = oh shit!)

Bioprosthetic valves:
- initial good functionality
- ***late degeneration w/ calcification
- 20-30% failure @ 10y

Trade-off b/t pros and cons, tailor choice to the clinical setting of the pt for best results.