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75 Cards in this Set

  • Front
  • Back
pathogenesis of Eisenmenger's syndrome
uncorrected VSD, ASD, or PDA (L to R shunt)
==>pulmonary HTN
==>shunt becomes R to L
==>late cyanosis: clubbing & polycythemia
Tetralogy of Fallot
-most imp determinant for prognosis?
-caused by what?
-most imp determinant for prognosis= degree of pulm sten
-caused by anterosuperior displacement of infundibular septum
boot-shaped heart
-what dz
-why does this dz create a boot-shape?

boot-shaped d/t RVH
in what congenital heart dz's do children tend to squat to improve Sx?
in the R to L shunts (TOF, Transposition of Great Vessels, and Truncus Arteriosis), kids squat
==>squatting compresses the femoral arteries
==>increases peripheral vascular resistance
==>decreases the R to L shunt
how Tx transposition of the great vessels
create shunts:

-patent foramen ovale
what causes transposition of the great vessels
failure of AorticoPulmonary septum to spiral
-notching of ribs
-HTN in upper extremities
-hypotension in lower extremitis


-more common in whom?
postductal coarctation of Ao

-more common in males (male:female = 3:1)
preductal coarctation of Ao d/t
d/t Turner's syndrome

(infantile tyle)
22q11 syndromes are assoc w what cardiac abnl
truncus arteriosus
Down sydnromes is assoc w what cardiac abnl
congenital rubella is assoc w what cardiac abnl
Turner's is assoc w what cardiac abnl
preductal coarctation of Ao
Marfan's is assoc w what cardiac abnl
Ao dissection
Ao insufficiency (AR)
offspring of diabetic mom is assoc w what cardiac abnl
transpos'n of great vessels
HTN defined as BP >140/90

MCC (90%)= Essential HTN (=primary HTN) d/t incr CO or incr TPR

2nd cause is chronic renal dz
plaques or nodules composed of lipid-laden histiocytes in the skin, esp the eyelids
-form in which part of artery?
fibrous plaques and atheromas form in INTIMA of arteries
ischemic heart dz- 4 types
1. Angina
2. MI
3. sudden cardiac death
4. chronic ischemic heart dz
MCC agina
CAD narrowing
what is crescendo angina?
=unstable angina
is there necrosis in unstable/crescendo angina?
no necrosis, but there is thrombosis
acute thrombosis d/t coronary artery atherosclerosis
MCC sudden cardiacv death
MCC=leathal arrythmia

(death within 1 hr of onset of Sx)
et of chronic ischemic heart dz
progressive onset of CHF over many years d/t chronic ischemic myocardial damage
How long post-MI:

grossly, heart has dark mottling; pale with tetrazolium stain
1 day
How long post-MI:

coag necrosis
1 day
How long post-MI:

contraction bands first visible`
4 hours
How long post-MI:

beginning of netrophil emigration
1 day
How long post-MI:

gross finding of hyperemia
2-4 days
what is pt at risk for in 2-4 days post-MI?
risk for arrythmia
what is pt at risk for in 5-10 days post-MI?
risk for free wall rupture (reperfusion injury)
what is pt at risk for in 7 weeks post-MI?
risk for ventricular aneurysm
how long post-MI:

tissue surroudnings infarct shows acute inflammation
2-4 days
how long post-MI:

dilated vessels (hyperemia)
2-4 days
how long post-MI:

neutrophil emigration
2-4 days

(starts at 1 day)
how long post-MI:

muscle shows extensive coag necrosis
2-4 days
how long post-MI:

grossly, heart has hyperemic border & central yellow-brown softening
5-10 days
how long post-MI:

ingrowth of granulation tissue
5-10 days
how long post-MI:

5-10 days
how long post-MI:

recanalized artery
7 weeks
how long post-MI:

grossly, heart has gray-white region where the infarct was
7 weeks
how long post-MI:

contracted scar complete
7 weeks
ST elevation
trasnmural infarct
pericarditis (Dr Moody)
ST depression
subendocardial infarct
pathological Q waves
transmural infarct
how long post-MI is there a risk for rupture of papillary muscle
4-10 days
friction rub
fibrinous pericarditis (3-5 days post-MI has risk for this)
how long post-MI is the risk for fibrinous pericarditis?
(=friction rub)

3-5 days post-MI
Dressler's syndrome
autoimmune phenomenon resulting in fibrinous pericarditis

several weeks post-MI
which cardiomyopathy causes systolic dysfxn?
dilated/congestive cardiomyopathy
which cardiomyopathy causes diastolic dysfxn?
hypertrophic cardiomyopathy
loud S4
apical impulses
systolic murmur

hypertrophic cardiomyopathy
Tx hypertrophic cardiomyopathy
Beta blocker
what can cause dilated/congestive cardiomyopathy
Alcohol (chronic)
Cocaine (chronic)
Coxackie B
Doxorubicin toxicity
DVT's predisposed by:
Virchow's triad:

1. stasis
2. hypercoagulability (ie OCP's)
3. endothelial damage (ie smoking)
inspiration==>decr pulse
incr JVD
Goljan: triad for pericardial effusion/ cardiac tamponade
Goljan: pathogenesis for pericardial effusion
pericarditis AKA cardiac tamponade:

there's fluid around the heart, so the heart cannot expand
==>incr JVD b/c not enough room in LA
==>when inspire, there's more blood in right side of heart, septum moves toward the left side of heart, so less ejection from left side of heart
==>hypotension & decr pulse (pulsus paradoxus)

triad (Goljan):
inspiration==>decr pulse
incr JVD

also, distant heart sounds
incr HR
ECG shows electrical alternans (beat-to-beat alterations of QRX complex height)
what causes non-bacterial endocarditis
-renal failure

(marantic/thrombotic endocarditis)
tender raised leasions on finger or toe pads

=Osler nodes

==>bacterial endocarditis
round white spots on retina surrounded by hemorrhage

=Roth's spots

==>bacterial endocarditis
splinter hemorrhages on nailbed

==>bacterial endocarditis
MC valve involved in bacterial endocarditis?
mitral valve (also for rheumatic heart dz)
MC valve involved in rheumatic heart dz
mitral (also for bact endocarditis)
vegetations develop on both sides of mitral valve, leading ot mitral stenosis, but do not embolize
=Libman-Sachs endocarditis (LSE)

-assoc w/lupus (mneum: SLE causes LSE)
friction rub
diffuse ST elevation in all leads
valves affected in Rheumatic heart dz
mitral > Ao > tricuspid (high pressure valves affected first)
-migratory polyarthritis
-erythema marginatum
-granuloma with giant cells
-activated histiocytes

Dx= rheumatic heart dz

-granuloma with giant cells=Aschoff nodule
-activated histiocytes=Anitschkow cells
pathogenesis of syphilitic heart dz
tertiary syphilis disrupts vasa vasora of Ao
==>dilation of Ao ring
==>incompetent Ao valve
==>aneurysm of Ascending Ao & AR
what causes calcification of Ao root and ascending Ao arch
tertiary syphilis
MC primary tumor in adults

cardiac myxoma

-location=LA ("ball-valve" obstruction in LA)
"ball-valve obstruction"
cardiac myxoma:

MC primary tumor in adults
-in LA
MC primary tumor in kids?

-assoc with what?

-assoc w/tuberous sclerosis
MC heart tumor
Kussmaul's sign

-suggests what?
Kussmaul's sign=incr systemic venous pressure on inspiration

-suggests cardiac tumor