2nd Exam: Vavular and Endocardial Heart Disease Flashcards by Tedman McMahon

Trauma valves experience:

mechanical, shearing, friction

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Changes per minute of valves under mech stress:

60-80 times per minute

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Shearing forces of the valve come from:

blood flow

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Friction of valves occurs here:

points of coaptation (where they come together)

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Aging changes to aortic valve:

fibrosis, thickening of leaflets, loss of elasticity, lipid deposition, aortic root/ ring/ anulus dilates

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Consequences of age changes of heart valves:

murmurs, stenosis, insufficiency, endocarditis, calcification

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This leads to aortic insufficiency:

loss of elasticity of valves

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Root/ ring/ anulus:

where leaflets attach, dilate

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Do these aging changes to the valves happen to valves throughout the body?

yes

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Calcification of aortic valve is seen in:

aortic stenosis

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Valve thickening can lead to:

benign murmor, or more severe disease

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Acute rheumatic fever:

kids 5-15yo, no organism, AI, hypersensitivity d., Ab response, indirectly related to Group A strp infection (GAS, B-hemolytic), can lead to heart infection, inflammation of myocardium, valves and pericardium

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Cross reactions, antistrep Ab’s and heart muscle:

vegetations, Aschoff body (only RF), fibrinous pericarditis

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How long after GAS infection does RF present as immune mediated carditis?

1-4wks

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Site of infection for RF:

pharyngitis, usually not skin or other sites

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Common M types of acute RF:

1, 3, 5, 6,18, 24

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What bind, leading to RF?

Ag’s in heart bind M protein epitopes on bacteria that are shared with myosin, tropomyosin

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Contributing factors to the prevalence of acute RF:

poverty, crowding, cold climate

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Why we are we at lower RF risk in U.S.:

less virulent organisms, earlier dx, tx, and rx

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Antibodies w this cross react with heart Ag’s, producing heart disease (?) rf (?):

M proteins

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disorder of kidneys, occurs after infection w some strains of strep bacteria:

poststreptococcal nephritis

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Test to determine if pt has strep infection:

If they are producing Abs to streptolysin secreted by strep

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streptolysin is an:

exotoxin

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Substances secreted by strep:

Streptolysin, streptokinase, strepteornases, pyrogenic exotoxins, DNAase, Hyaluronidase

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m protein projects directly out of:

the cell mem

Cx dx of acute RF:

Jones criteria: evidence of inflammation w a rheumatic (joint) component, polyarthritis, evidence of HD, recent GAS infection, skin lesions, carditis

acute RF affects what parts of the heart?

all

arthritis, part of acute or chronic rf?

acute

Most severe long term disease in rheumatic fever

heart disease

Polyarthritis:

transient, migratory joint pain and swelling, many joints affected, nonsuppurative, usually no residual disability

Erythema marginatum:

serpiginous(wavy margin), erythematous, non-pruritic (not itchy), on trunk/ extremities, circular, thin line of hyperemia, small % of pts with acuter RF get this

Erythema marginatum is assoc w:

acute RF

Cx dx of rheumatic pericarditis:

friction rubbing sounds in stethoscope

Parts of heart invovled in Rheumatic pericarditis

peri-, myo- , endo-, epicardium

This disorder has a bread and butter appearance w fibrinous exudate:

Rheumatic Pericarditis

This disorder has a bread and butter appearance w fibrinous exudate:

Rheumatic Pericarditis

Aschoff bodies are usually seen in:

acute RF, occasionally in old d.

Aschoff body:

acute RF, usually only in h., granuloma-like lesion, multifocal, chronic inflammatory rxn, possible necrosis T cells, macs (antischkow "myocytes", Aschoff (giant) cells)

Giant cells are aka:

Aschoff cells

TF? Aschoff bodies are granulomatous lesions.

F. granuloma-like

Multinucleated Aschoff/giant cells:

linear, fusiform, fused macs in Aschoff body (looks like a fibroblast)

Antischkow myocyte:

linear chromatin, "caterpillar cells"

acute RF valvulitis:

most important long term consequence of the d., affects valves preferentially, stenosis and/or regurgitation later on

Valves affected by ARF valvulitis, greatest to least:

mitral, aortic, tricuspid, pulmonary

most important aspect of ARF in the long run:

ARF valvulitis

acute ARF valvulitis:

verrucae (small wart) at line of closure of valve leaflets, inflammation, edema and fibrinoid necrosis, may dissipate

If valve is damaged by ARF valvulitis you will get:

chronic valve disease

Valves on this side of heart are more commonly affected by ARF valvulitis:

L, bc higher pressure = more damage, maybe

wart like lesions:

veruci

Acute RF valvulitis causes:

acute rheumatic endocarditis, tiny lesion at line of closure

Acute rheumatic endocardiits:

tiny lesion at line of closure, tiny white bumps, ai inflammation

Valve fluid from necrosis and edema during acute valvulitis can lead to:

scarring of valve, stiffer, thicker, now more prone to chronic rheumatic valve disease

Chronic rheumatic valve disease:

yrs after ARF, turbulence adds to original damage, deformed, thickened, fibrotic, stenotic and/or insufficient

Disease pt most likely has if heart valve won't open:

chronic RF

This will appear white on a valve leaflet w chronic RH disease:

necrosis

Signature lesion of RF:

mitral stenosis

mitral stenosis:

classic murmurs (snap open), inc L atrial P, atrial dilation/ hypertrophy, atrial thrombi, arrhythmias (atrial fibrillation), IE is secondary

This results in fish mouth valve:

mitral stenosis

IE is secondary to:

acute RF and mitral stenosis

Is a damaged valve due to mitral stenosis from ARF more like to bc IE because the damage has created a good host environment for the bacteria?

ask

sequela of damaged tissue:

calcification, calcific valve disease, dystrophic calcification, heart murmurs, valve opening narrowing leading to inc L atrial P

Is valve damage slight or severe from RF?

severe

2 types of IE:

bacterial, fungal

Which type of IE is further broken down to acute and subacute?

bacterial

Ppl prone to fungal IE:

IV drug users, IC pts, i.e. HIV

Types of non-rheumatic endocarditis:

infective and non-infective

More common, bacterial or fungal infective endocarditis?

bacterial

Most common organism to cause acute bacterial endocarditis (ABE):

staph a., virulent = acute

Infective endocarditis is infection of:

heart valve, prosthetic valve or catheter

ABE:

virulent organisms like Staph A., valve not damaged, more destructive than Subacute BE (SBE)

SBE:

lower virulence like Strep viridans, valve already damaged, may incur more

This is like a revolving door:

endocarditis, contaminated blood goes to heart, heart valves sheds organism into blood

Sx and Dx of endocarditis:

fever, chills, pos blood culture

Source of infection for endocarditis:

IV lines, IV drugs, dental procedures, unknown

dental procedures that can lead to endocarditis:

AGE: abscess, gum disease, extraction

1st step in pathogenesis of endocarditis:

altered or damaged endo

steps in pathogenesis of edocarditis:

altered or damaged endo, exposure of collagen and matrix substances, platelet aggregation, and fibrin deposits (nidus)

This is the nidus for endocarditis:

fibrin deposits

Pws to endo damage:

normal/ abnormal valve, previously injured valve, endo MAY already be damage, turbulence and stasis put platelets at the endo

What can put platelets at the endothelium?

turbulence and stasis

This can lead to endo damage:

mitral stenosis

Each vegetation from IE and CRF contains:

inflammatory cells and bacteria

Types of non-infective/ non-rheumatic endocarditis:

NBTE ("marantic"), atypical verrucous endocarditis (Libman-Sacks)

"marantic" is assoc with:

NBTE

Libman-Sacks is assoc w:

Atypical verrucous endocarditis (Libmann-Sacks)

This is characterized by large vegetations that can embolize, shower into brain, kidney, etc. producing infarcts:

NBTE vegetation

shown destroying the valve, seen in endocarditis-cotran:

NBTE "marantic":

pancreatic cancer, emboli, infarct (check)

When does NBTE often occur?

hypercoagulabe state (60%)

NBTE is often assoc w:

mal d. such as adenocarcinomas-pancreas, GI, lung

NBTE freq affects normal:

valve

This disease often does not change the valve:

NBTE

This often gives rise to emboli:

NBTE

'Marantic" endocarditis:

bulky, more frialbe lesions tha IE

These are vegetations in row, not damaging valve, but can embolize no inflammation, no bacteria:

"marantic" endocardiits

Characteristics of NBTE in slides:

friable (easily crumbled), fibrin, sterile deposits

Tiny vegetations in endocarditis are assoc w:

Variable size vegetations in endocarditis are assoc w:

Large vegetations in endocarditis are assoc w:

NBTE

line of closure is assoc w:

Destruction is assoc w:

"Friable" is assoc w:

NBTE

Friable:

easily pulverized or crumbled

Vegetations in endocarditis that can lead to emboli:

IE, NBTE

Specific valve lesions:

aortic stenosis, myxomatous (benign ct tumor containing gelatinous or mucous material) degeneration, mitral valve prolapse, mitral valve ring calcification, carcinoid valve disease

Aortic stenosis means:

less blood can flow through valve

Causes of aortic stenosis:

RF, age

Complications of aortic stenosis:

L ven hypertrophy, agina, sudden death