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106 Cards in this Set

  • Front
  • Back
R >> L shunt
blue babies
early cyanosis
ID'd early and require surgery/PDA to correct
The 5 T's of blue babies
Truncus Arteriosus (1 vessel)
Transposition (2 switched vessels)
Tricuspid Atresia (3 - Tri)
Tetratology of Fallot
TAPVR (5 letters)
**Tet, Transposition Truncus due to neural crest migration problems
Persistent Truncus Arteriosus
failure of truncus arteriosus to divide into pulm trunk and aorta >> most pts also have VSD.
Transposition of Great Vessels
Aorta leaves RV and pulmonary trunk leaves LV due to failure of aorticopulonary septum to spiral >> separation of systemic/pulmonary circuits.

**Must create shunt to allow survival until surgery. Give PGE to maintain PDA
**associated w/ maternal DM
Tricuspid Atresia
absence of tricuspid valve and hypoplastic RV; requires ASD and VSD for survival
Tetralogy of Fallot
Due to anterosuperior displacement of the infundibular septum. **most common cause of early childhood cyanosis

PROVe
Pulmonary stenosis
RVH (boot-shaped heart)
Overriding aorta
VSD
Tet sx
PS forces R >> L flow across VSD >> cyanotic spells. Squatting increases SVR and lessens shunt, improving cyanosis.
**amount of shunt depends on amount of stenosis
Total anomalous pulmonary venous return
Pulmonary veins drain into RH circulation; associated w/ ASD and PDA to allow R >> L shunt to maintain CO.
L >> R shunting
blue kids
late cyanosis
VSD > ASD > PDA
VSD
Most common congenital cardiac defect
Assoc w/ FAS
Asx at birth, may resolve or cause problems later on

Large lesion can lead to pulm HTN >> Eisenmenger
Eisenmenger Syndrome
Uncorrected L>>R shunt increases pulmonary blood flow >> pulm HTN >> RVH and shunt becomes R >> L. See late cyanosis, clubbing, polycythemia.
ASD
Loud S1, wide/fixed split S2.
Usually occurs in septum secundum
In Downs problem is in septum primum

Can cause paradoxical embolism
PDA
continuous machinelike murmur
maintained by PGE synthesis and low O2 tension
associated w/ congenital rubella

R >> L shunt in fetus becomes L >> R in newborn >> pulm HTN >> Eisenmenger >> cyanosis of lower extremities
Coarctation of the aorta
narrowing of the aorta assoc w/ bicuspid aortic valve
infantile coarctation of aorta
after the aortic arch, before the PDA
Associated w/ Turner's. Assoc w/ PDA. Can present as LE cyanosis.
adult coarctation of aorta
distal to the ductus; associated w/ notching of ribs due to collateral circulation, HTN in upper extremities and weak, delayed pulses in lower.
22q11

Down's
DiGeorge; characterized by truncus arteriosus, tet of fallot

Down's: ASD, VSD, AV septal defect
Marfan
characterized by MVP, thoracic aortic aneurysm, AR
Infant of diabetic mother
characterized by transposition of great vessels
HTN etiology
90% primary in adults; related to increased CO or TPR. Rest is secondary due to renal dz like fibromuscular dysplasia.
Signs of hyperlipidemia
Xanthomas: skin plaques composed of lipid-laden histiocytes
Tendinous Xanthomas: lipid deposits in achilles or other tendons.
Corneal arcus: pale lipid ring in cornea seen early w/ hypercholesterolemia, common in elderly.
Monckeberg
rare calcification of the media of radial or ulnar arteries. Does not obstruct blood flow. Usually benign. No involvement of the intima. Pipestem arteries on xray.
Arteriolosclerosis.
hyaline thickening of small arteries in essential HTN or DM or hyperplastic onionskinning in severe HTN.
progression of atherosclerosis
Endothelial cell dysfunction >> macrophage and LDL accumulation >> foam cell formation >> fatty streaks >> SM cell migration, prolif and ECM deposition >> fibrous plaque > complex atheroma
**SM cells play a key role in hyperplasia/fibrosis
**metalloproteases from macrophages degrade collagen and predispose to rupture.
atherosclerosis locations
abd aorta > coronary artery > popliteal > carotid
aortic aneurysm
localized pathologic dilation of the aorta. Pain a sign of leak, dissection or imminent rupture
Abd aortic aneurysm
associated w/ atherosclerosis; more frequent in male hypertensive smokers 50+
thoracic aortic aneurysm
Associated w/ cystic medial degeneration due to HTN (older) or Marfan (younger) and tertiary syph.
aortic dissection
Longitudinal intraluminal tear forms a false lumen. Associated w/ HTN, bicuspid valve, Marfan.
-presents w/ tearing chest pain that radiates to back, +/- unequal BP in arms.
-Mediastinal widening on CXR
Angina
Chest pain due to inadequate O2 supply to heart. No necrosis. Reversible injury; subendocardium is most at risk.
stable angina
Pattern of predictable transient chest discomfort during exertion secondary to fixed plaque and inappropriate vasoconstriction due to endothelial cell dysfunction.
-ST depression on EKG
-treated by decreasing O2 demand w/ rest or nitroglycerin
-reversible damage to myocytes
-70% stenosis
unstable angina
Sudden increase in tempo/severity of angina, occurring w/ less exertion or at rest.
-due to plaque rupture and incomplete obstruction.
-reversible injury to myocytes
-ST depression on EKG
-need to restore supply w/ drugs or stent
variant angina
Prizmetal
-seen at rest due to CA spasm
-transient ST elevation on EKG
-triggers are tobacco, cocaine, triptans
-tx is Ca blocker, nitrate, smoking cessation
MI
Severe crushing chest pain that radiates to jaw, arm
Acute thrombosis >> complete obstruction >> necrosis.
-ST elevation if transmural
-ST dep if subendocardial
-biomarkers are dx
LAD > RCA > LCX
Sudden cardiac death
Death w/in 1 hour of cardiac sx
-lethal arrhythmia is top cause
-assoc w/ CAD, cardiomyopathy, long QT
Chronic ischemic HD
progressive onset CHF over many years due to chronic ischemic myocardial damage
MI on ECG
ECG is gold standard in first 6 hours
-STEMI (transmural)
-ST depression (subendocardial)
-pathologic Q waves (evolving or old infarct)
troponin
rises after 4 hours, peaks at 24 stays high for 7-10 days. Most specific protein marker
CK-MB
in myocardium and also Skeletal muscle; rises 4-6 hours, peaks at 24, returns in 48
**helpful for diagnosing reinfarction following acute MI.
transmural infarct
necrosis affecting entire wall
See STEMI, Q waves
subendocardial infarct
ischemic necrosis of <50% of ventricular wall
See ST depression
MI first 4 hrs
No gross or microscopic changes;
cardiogenic shock, CHF and arrhythmia
MI 4-24hrs
dark mottling; nuclei disappear
coagulative necrosis
arrhythmia
MI 1-3 days
yellow pallor
PMN's
fibrinous pericarditis presents w/ chest pain and friction rub
MI 4-7 days
yellow pallor
macrophages
Rupture of ventricular free wall >> cardiac tamponade risk is highest day 6-14
MI 1-3wks
red border of dead tissue
granulation tissue w/ fibroblasts
MI months
white scar, type I collagen
fibrosis
aneurysm, Dressler syndrome
Dressler syndrome
AI phenomenon resulting in fibrinous pericarditis 6-8wks after MI; make autoAB for pericardium
diagnosing MI location: anterior wall
LAD, V1-V4
diagnosing MI location: anteroseptal
LAD; V1-V2
diagnosing MI location: anterolateral
LAD or LCX; V4-V6
diagnosing MI location: lateral wall
LCX; I, AVL
diagnosing MI location: inferior wall
RCA, II, III, AVF
MI complication
**arrhythmia (early complication, esp before reaching hospital)
cardiogenic shock
ventricular free wall rupture
friction rub day 1-3
dressler syndrome (after weeks/months)
DCM
-Most common type
-Causes ABCCCD: alcohol, wet beriberi, coxsackie B, cocaine, chagas, doxorubicin
also pregnancy
Dilated cardiomyopathy dx and tx
Findings: HF, S3, dilated heart w/ balloon appearance on EKG, eccentric hypertrophy and systolic dysfunction

Tx: Na restriction, ACE inhib, beta blocker, diuretic, digoxin, ICD, transplant
HCM
most are familial, AD defect of beta myosin heavy chain (sarcomere problem)
-Can be assoc w/ Friedrich ataxia (rarely)
-Sudden cardiac death in athletes
HCM dx and tx
findings: S4, systolic murmur, myofibrillar disarray and fibrosis on path, concentric hypertrophy, diastolic dysfunction
Tx: Stop high-intensity athletics, use beta blocker or Ca blocker, ICD if high risk.
obstructive HCM
subset w/ hypertrophied septum too close to anterior mitral leaflet >> outflow obstruction >> dyspnea, syncope
-functional AS
RCM
Major causes are sarcoid, amyloid, post-RT fibrosis, hemochromatosis, Loffler syndrome (endomyocardial fibrosis w/ Eos)
RCM presentation
diastolic dysfunction, low-voltage EKG despite thick myocardium
HF
cardiac pump dysfunction
LHF
can be due to ischemia, HTN, DCM, MI, RCM

Sx include dyspnea, orthopnea, fatigue, rales, JVD, pitting edema, RAS activation
Systolic dysfunction
low EF, poor CTY, often secondary to ischemic HD or DCM
diastolic dysfunction
normal EF and CTY, impaired relaxation, decreased CPL.
RHF
most often results from LHF. Isolated RHF usually due to cor pulmonale

Sx include JVD, HSM, nutmeg liver, pitting edema
decreasing mortality w/ HF
ACE inhib, beta blockers, ARB, spironolactone decrease mortality
-thiazides/loop diuretics relieve sx
-hydralazine + nitrates can improve sx and mortality in some
cardiac dilation
due to greater EDV
dyspnea on exertion
due to failure of CO to increase w/ exercise
presentation of bacterial endocarditis
bacteria FROM JANE
fever, roth spots, osler nodes, murmur, janeway lesions, anemia, nail-bed hemorrhage, emboli
bacterial endocarditis location
Mitral valve is most common; tricuspid in drug user. can cause chordae rupture, glomerulonephritis, pericarditis, emboli
acute bacterial endocarditis
staph aureus; see vegetations on previously normal valves. Rapid onset, large vegetations that destroy valves.
subacute bacterial endocarditis
strep viridans; see smaller vegetations on already abnormal valve. Thrombotic vegetations trap transient bacteria after dental procedure.

low virulence org can only infect abnormal valves
other causes
-staph epidermis on prosthetic valve
-strep bovis in colon cancer pts
-coxiella burnettii or bartonella if neg culture
rheumatic fever
consequent to pharyngeal infection w/ GAS
Death due to myocarditis or late-developing valve lesion mitral > aortic >> tricuspid. MR then MS
rheumatic fever mechanism
Type II hypersensitivity rxn, not a direct effect of bacteria. AB for M protein cross react w/ self.
**molecular mimicry
rheumatic fever signs and sx
Evidence of prior GAS infection: ASO or anti-DNase B titer, fever, high ESR, major criteria

Aschoff bodies (granuloma w/ giant cells)
rheumatic fever major criteria
JONES
joint polyarthritis, endocarditis, subq nodules, erythema marginatum, sydenham chorea
acute pericarditis
sharp pain worse w/ inspiration, relieved by sitting up/forward. Friction rub.
ECG: widespread STE, PR depression
fibrinous type
dressler syndrome, uremia, radiation. see loud friction rub
serous
viral; resolves spontaneously often
suppurative
bacterial like strep pneumo. rare w/ AB
cardiac tamponade
heart compressed by fluid in pericardium >> decreased CO.
-see equal diastolic pressure in all chambers
-Beck triad of hypotension, distended neck veins, distant heart sounds
-increased HR, pulsus paradoxus, Kussmaul sign
-low-voltage EKG, electrical alternans
pulsus paradoxus
decrease in aplitude of SBP by 10+mm during inspiration. seen in cardiac tamponade, asthma, OSA, croup, pericarditis
syphilitic heart dz
tertiary syph disrupts the vasa vasorum of the aorta >> atrophy of vessel wall, aortic dilation.
-calcifications of aorti root and ascending arch >> tree bark appearance.
-aneurysm of ascending aorta/arch
most common cardiac tumor
met
come from breast, lung, melanoma, lymphoma
myxoma
most common primary cardiac tumor; pedunculated valve obstruction in LA associated w/ syncopal episodes

arises from mesenchyme
rhabdomyoma
most common primary cardiac tumor in kids; assoc w/ TSC

benign hamartoma that arises in vents
Kussmaul sign
paradoxical increase in JPV on inspiration seen w/ constrictive pericarditis, RCM, RH tumors

insp >> negative intrathoracic pressure not transmitted to heart >> impaired RV filling >> blood backs up into VC >> JVD.
Raynaud phenomenon
decreased blood flow in skin due to arteriolar vasospasm in response to cold temp or stress.
-Raynaud dz is idipathic
-syndrome when secondary to a CT dz, SLE
strawberry hemangioma
benign capillary tumor of infancy that grows rapidly and spontaneously regresses at 5-8yrs
cherry hemangioma
benign cap tumor of elderly that does not regress.
cystic hygroma
cavernous lymphangioma of neck. assoc w/ turner's
bacillary angiomatosis
benign capillary skin papules in AIDS pts due to bartonella. Mistaken often for kaposi's
angiosarcoma
rare blood vessel malignancy in head, neck, breast. Seen in elderly, sun-exposed areas. Assoc w/ RT, arsenic. aggressive and tough to resect.
lymphangiosarcoma
lymphatic malignancy assoc w/ persistent lymphedema, like post mastectomy. See persistent arm swelling 10 years after mastectomy
Kaposi sarcoma
endothelial malignancy of skin or mouth, assoc w/ HHV8 and HIV.
-older eastern european men, AIDS pt, transplant recipients
temporal arteritis
affects branches of carotid; see unilateral headache, jaw pain in elderly females.
-can cause blindness
-granulomatous inflammation and high ESR
-corticosteroids prior to temporal artery biopsy
Takayasu arteritis
granulomatous thickening/narrowing of aortic arch in Asian females under 40
-weak UE pulses, fever, arthralgia, night sweats
-corticosteroids
Polyarteritis nodosa
immune-complex mediated vasculitis of renal and visceral vessels in in yount adults, esp HB+
-fever, wt loss, abd pain, melena, HTN
-corticosteroids
-spares the lung
Kawasaki Dz
vasculitis in asian kids <4 yrs
-fever, cervical lymph, strawberry tongue
-may dev CA aneruysm >> MI
-Tx is IVIG and aspirin
Buerger dz
segmental thrombosing vasculitis in heavy smokers male 40+
-gangrene of digits, raynaud
-quit smoking
Wegeners
C disease: affects nasopharynx, lungs, kidney. C-ANCA positive; tx is cyclophosphamide, corticosteroids
-large nodules on CXR
-C-ANCA: cytplasmic anti-neutrophil cytoplasmic AB
Microscopic polyangitis
Similar to Wegeners but no nasopharyngeal involvement
same tx
-P-ANCA - perinuclear staining
Churg-Strauss
asthma, peripheral neuropathy, granulomatous necrotizing vasculitis w/ eos.
P-ANCA
Henoch-Schonlein purpura
most common childhood systemic vasculitis; often follows URI
-palpable purpura, arthralgia, abd pain
-Secondary to IgA complex deposition
-assoc w/ IgA nephropathy