2nd Exam: Vavular and Endocardial Heart Disease Flashcards
Trauma valves experience:
mechanical, shearing, friction
Changes per minute of valves under mech stress:
60-80 times per minute
Shearing forces of the valve come from:
blood flow
Friction of valves occurs here:
points of coaptation (where they come together)
Aging changes to aortic valve:
fibrosis, thickening of leaflets, loss of elasticity, lipid deposition, aortic root/ ring/ anulus dilates
Consequences of age changes of heart valves:
murmurs, stenosis, insufficiency, endocarditis, calcification
This leads to aortic insufficiency:
loss of elasticity of valves
Root/ ring/ anulus:
where leaflets attach, dilate
Do these aging changes to the valves happen to valves throughout the body?
yes
Calcification of aortic valve is seen in:
aortic stenosis
Valve thickening can lead to:
benign murmor, or more severe disease
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
Cross reactions, antistrep Ab’s and heart muscle:
vegetations, Aschoff body (only RF), fibrinous pericarditis
How long after GAS infection does RF present as immune mediated carditis?
1-4wks
Site of infection for RF:
pharyngitis, usually not skin or other sites
Common M types of acute RF:
1, 3, 5, 6,18, 24
What bind, leading to RF?
Ag’s in heart bind M protein epitopes on bacteria that are shared with myosin, tropomyosin
Contributing factors to the prevalence of acute RF:
poverty, crowding, cold climate
Why we are we at lower RF risk in U.S.:
less virulent organisms, earlier dx, tx, and rx
Antibodies w this cross react with heart Ag’s, producing heart disease (?) rf (?):
M proteins
disorder of kidneys, occurs after infection w some strains of strep bacteria:
poststreptococcal nephritis
Test to determine if pt has strep infection:
If they are producing Abs to streptolysin secreted by strep
streptolysin is an:
exotoxin
Substances secreted by strep:
Streptolysin, streptokinase, strepteornases, pyrogenic exotoxins, DNAase, Hyaluronidase
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:
IE
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:
RF
Variable size vegetations in endocarditis are assoc w:
IE
Large vegetations in endocarditis are assoc w:
NBTE
line of closure is assoc w:
RF
Destruction is assoc w:
IE
“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
