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Goljan Path > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Jugular venous pulse

A

Usu. only R-side. C = S1. a wave = Right atrial contraction in LATE diastole. c wave = tricuspid billowing into the RA during systole. x descent = negative pressure b/c of blood going through pulmonary artery. v wave = filling up of RA right at the beginning of diastole. y wave = blood going down from RA to RV.

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2
Q

Tricuspid stenosis

A

GIANT A wave.

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3
Q

Tricuspid regurgitation.

A

GIANT Cv wave.

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4
Q

Turbidity of plasma?

A

Due to TG’s NOT cholesterol.

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5
Q

What carries the TG’s?

A

Chylomicrons (from gut). You don’t have to fast for cholesterol levels! But you do for accurate triglyceride levels. VLDL - what we make in liver from G3P from glucose. VLDL > chylomicron in density.

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6
Q

Xanthelasma

A

Cholesterol is high.

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7
Q

Familial hypercholesterolemia

A

AD. Absent LDL receptor. Tendon xanthoma. Type II hyperproteinlipoproteinemia.

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8
Q

Atherosclerosis

A

Injury to the endothelial cell lining elastic and muscular arteries. Cigarette (ammonium, CO). LDL esp. if oxidized. Infections (Chlamydia pneumoniae?). Homocysteine. Damaged endothelial cells = plt sticking. PDGF -> smooth muscle of media to proliferate (hyperplasia). Migrate to the subintimal level. Fatty streak 2/2 SMC + macrophages w/ LDL in them. Injury. Fibroblasts -> fibro-fatty plaque. Dystrophic calcification, fissuring, thrombosis.

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9
Q

Hyaline arteriosclerosis

A

Small vessel disease. DM and HTN. DM - non-enzymatic glycosylation (glucose attached to protein). E.g. HbA1C ~ 6-8 week of blood glucose levels + osmotic damage (lens, pericytes of the retina, schwann cells, have aldose reductase -> sorbitol = damage). Glycosylation of BM -> BM permeable to protein -> hyalinization of the vessels. In glomerulus –> proteinuria. HTN mechanism is protein driven by hydrostatic pressure through BM.

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10
Q

Hyperplastic arteriosclerosis

A

Seen in malignant hypertension.

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11
Q

Aneurysm

A

Area of out pouching of vessel 2/2 WEAKENING of vessel wall

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12
Q

Etio of vessel wall weakening?

A

Atherosclerosis

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13
Q

LaPlace law

A

Wall tension = pressure x radius / 2 x wall thickness

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14
Q

All aneurysms will rupture

A

B/c once you increase radius -> increase wall tension.

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15
Q

Why is aorta below renal arteries most common location for aneurysm?

A

No vaso vasorum. Peripheral areas are more susceptible to ischemia. Atherosclerosis -> weakening -> aneurysm

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16
Q

Ruptured AAA presentation?

A

LEFT flank pain, hypotension, pulsatile mass on physical exam = ruptured AAA

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17
Q

Aortic arch aneurysm?

A

Most common cause is tertiary syphilis. Pathology of syphilis is vasculitis of arterioles (plasma cell). Ischemic necrosis -> dead neurons -> painless chancre. Treponema infects the vaso vasorum (of the arch b/c it is very rich) = endarteritis obliterans. AR b/c of stretched ring or damaged valve. Will have increased SV b/c of increased volume in the LV (but dec. EF). Stretched recurrent laryngeal nerve = hoarseness.

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18
Q

Aortic dissection

A

HTN is the key factor. Weakening of the wall 2/2 elastic tissue fragmentation + cystic medial necrosis (glycosaminoglycans -> cystic pockets. Most of the tears are in the arch of the aorta. Loss of pulse. CP a tearing pain to the back. CXR is screening test - widening of aortic knob. Dx = angiography/TEE.

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19
Q

Predisposing to dissection

A

Marfan - chromosome 15, defect in fibrillin -> weakened elastic tissue (dislocated lens, MVP, dissection). Ehlers-Danlos syndrome. Pregnancy b/c of increased plasma volume.

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20
Q

SVC syndrome

A

Retinal vein engorgement. Usu. 2/2 to lung cancer.

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21
Q

Sturge Weber syndrome

A

In trigeminal nerve distribution - port-wine. AV malformation on the SAME side in the brain, which pre-disposes to bleeding.

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22
Q

Spider angioma

A

Normal in pregnant women. 2/2 hyperestrogenism. WILL blanch b/c it’s an AV fistula. Cirrhosis -> can’t metabolize estrogen. Petechiae will NOT blanch.

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23
Q

Bacillary angiomatosis

A

Bartonella hensalae. Silver stain. Seen in AIDS. Tx with sulfa drug. Also causes cat-scratch disease

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24
Q

Angiosarcoma of the liver

A

VAT - vinyl chloride (plastics), Arsenic (pesticides), Thoratract?

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25
Q

Small vessel vasculitis

A

99% it will be type III HS = IC deposition. Activates complement, neutrophils = fibrinoid necrosis. PALPABLE PURPURA.

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26
Q

Medium vessel vasculitis (muscular)

A

INFARCTIONS.

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27
Q

Elastic artery vasculitis

A

Pulseless disease (Takayasu’s), strokes (carotids)

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28
Q

Temporal arteritis

A

Unilateral HA. Multinucleated giant cell = granuloma. Can cause blindness b/c of opthalmic. Screen for temporal arteritis with ESR! Tx = corticosteroids immediately x 1 year. Associated with polymyalgia rheumatica = NO CK elevation. But polymyositis will have increased CK.

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29
Q

Buerger disease (thromboangiitis obliterans)

A

Smokers. Digital vessel thrombosis = auto infarction of fingers and toes.

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30
Q

HSP

A

Most common vasculitis in children. Buttocks, legs. IC. Anti-IgA IC. RBC cast 2/2 glomerulonephritis (IgA nephropathy). Palpable purpura.

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31
Q

Wegener’s

A

Saddle nose (NOT congenital syphilis). Sinus, upper respi, glomerular. Granulomatosis + vasculitis. c-ANCA = Dx (highly specific). Tx = Cyclophosphamide. C and C. (Cyclo can cause hemorrhagic cystits - use mesna - and bladder cancer)

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32
Q

Polyarteritis nodosa

A

Male. Muscular arteries (infarctions). p-ANCA. Hepatitis B surface antigenemia.

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33
Q

RMSF

A

Spots are petechiae. Ricketssiae attack vasculature. Extremities to TRUNK. Vector = tick.

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34
Q

DKA with cerebral abscess. Fungus

A

Mucormycosis. Cribiform, frontal lobe, infarct.

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35
Q

Raynaud’s phenomenon

A

Different causes. Cold-reacting antibodies (IgM cold agglutinin, cryoglobulinemia = Hepatitis C). Vasculitis causes = scleroderma + CREST syndrome. Eventually will autoamputate fingers. Vasoconstriction causes - ergot derivatives

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36
Q

CREST

A

Calcinosis (dystrophic calcification) + Centromere antibody, Raynaud, Esophageal dysmotility, sclerodactyly, telangiectasia

37
Q

Hypertension

A

MI, Stroke, Renal failure are most common causes of death.

38
Q

Mechanism of salt-retaining HTN

A

Salt is retained in ECF. Plasma volume will be increased -> increased SV (systolic HTN). Salt likes to go into SMC (peripheral resistance arterioles) -> opens up Ca2+ channels -> increased vasoconstriction -> inc. diastolic pressure. Tx = HCTZ; But with HLD, then use ACEi. This is a low renin type of HTN.

39
Q

Complications of HTN

A

MI, stroke - hypertensive stroke (basal ganglia 2/2 lenticulostriate off of MCA form aneurysm called Charcot-Bouchard aneurysms that rupture 2/2 HTN). Renal failure - hyaline arteriosclerosis -> ischemia, atrophy of tubules, glomeruli destruction. LVH 2/2 afterload.

40
Q

Concentric hypertrophy vs. dilated hypertrophy

A

Afterload vs. preload problem

41
Q

S3

A

Usually pathologic if > 35. Volume overloaded chamber in early diastole -> turbulence.

42
Q

S4

A

Late-diastole = atrial kick. Compliance problem = stiff heart wall vibrating during atrial kick.

43
Q

Use breathing to determine which side the S3/S4 is coming from

A

Decreased thoracic pressure = sucked into RV.

44
Q

Aortic stenosis

A

Systole. Crescendo decrescendo. Ejection murmur. Radiate into carotid. Intensity increases on expiration. Probably hear a S4.

45
Q

Mitral stenosis

A

Diastolic. Atrial dilation - aFib, thrombus. Opening snap. Mid-diastolic rumble. Underfilling the LV. No hypertrophy of LV. Apex.

46
Q

Mitral regurgitation

A

Decreased SV, LA gets excess blood. Volume overload. Pan-Systolic murmur. S3 and S4.

47
Q

AR

A

Austin-Flint murmur = significant leaflet.

48
Q

L heart failure

A

Etio - high afterload, volume overload, infarctions -> dec. contractility. EDV increased. Pulmonary congestion. “HF cells” = alveolar macrophages that have phagocytosed RBC. Main symptom = dyspnea. Pillow orthopnea, paroxysmal nocturnal dyspnea. You decrease Right heard return.

49
Q

R heart failure

A

Dx of signs. Back-up into systemic venous circulation. Neck vein distention. Hepatomegaly = “Nutmeg” liver.

50
Q

Treatment for HF

A

Restrict water and salt. ACEi = decreases preload (dec. aldo) AND afterload (dec. vasoconstrictive)

51
Q

High output failure etios

A

(Viscosity / r^4.) Septic shock, thiamine deficiency (ATP depletion -> SMC’s can’t vasoconstrict), Graves disease (thyroid hormone increases synthesis of Beta receptors in the heart), AV fistula (faster return).

52
Q

Fetal circulation

A

Oxygen comes from chorionic villi extracting blood from placenta. Req. high affinity Hb = HbF to get oxygen (left-shifted). Newborns have “polycythemia” to get around how HbF has such as high affinity for O2 (and doesn’t want to let it go). Syncytotrophoblast, cytotrophoblast -> myxomatous stroma of chorionic villus -> blood vessel. Coalesce to umbilical VEIN (highest oxygen) -> liver [hepatic sinusoids OR ductus venosus -> IVC] -> R heart -> mostly Foramen ovale -> LV -> aorta. Superior venal caval blood? SVC blood tends to go straight down into Tricuspid valve into the RV -> pulmonary circulation (high resistance) -> needs the patent ductus arteriosus (PGE2 made by placenta) -> R-L shunt -> aorta —> —> TWO umbilical arteries (LEAST oxygen)

53
Q

Birth = change in fetal circulation

A

When baby breathes, all the pulmonary vessels open. Sudden decrease of resistance.

54
Q

VSD

A

L to right shunt. Increased O2 in RV and Pulmonary artery. Volume overloaded R heart = pulmonary htn over time = Eisenmengers = cyanosis -> RVH -> reverse the shunt if R stronger than L.

55
Q

ASD

A

Left to right shunt. RA will have increased O2. RV increased O2. THEREFORE, an ASD has an increased O2 in RA! Volume overloaded Right side = risk for eisenmengers.

56
Q

Most common teratogen for ASD?

A

Fetal alcohol syndrome

57
Q

Patent ductus arteriosus

A

L to right shunt. Pulmonary a. higher O2. Machine-like murmur in supraclavicular region. Ductus empties DISTAL to the subclavian artery = pink and top and cyanotic and bond. Associated with congenital rubella. Tx = indomethacin

58
Q

Tetralogy of Fallot

A

Most common cyanotic congenital heart disease. Overriding aorta (straddles the septum), VSD, pulmonic stenosis BELOW the valve, RVH. The level of pulmonic stenosis = cyanosis b/c the greater the stenosis the more R to L shunt you have. What are the cardioprotective shunts in TOF? ASD and patent ductus arteriousus. ASD will L-R shunt. Patent ductus will also L-R shunt to oxygenate more blood via the pulmonary artery. Polycythemia, infective endocarditis risk.

59
Q

Transposition of great vessels

A

Not associated with Kartagener (normal heart on right side of chest). Transposed aorta and pulmonary artery. Spiral septum didn’t spiral. Always need shunts - patent ductus, foramen, atrial septal defect to get oxygenated blood into the right atrium to get to the RV and aorta.

60
Q

Aortic coarctation

A

Pre-ductal and post-ductal. Pre-ductal occurs in Turner’s syndrome. Post-ductal’s are found after birth. Systolic murmur between the shoulder blades. Increased risk for Berry aneurysm, SAH. Aortic regurgitation 2/2 stretching aortic ring. Dissecting aortic aneurysm. Distal to coarct = claudication, inc. RAS system -> HTN 2/2 renal a. stenosis. Rib notching 2/2 to intercostal artery collaterals.

61
Q

Most common cause of TRUE ventricular aneurysm?

A

HF. NOT free wall rupture.

62
Q

Mitral valve prolapse

A

Closer to S1 or S2? Increased volume –> click and murmur closer to S2. Decreased preload —> click and murmur closer to S1 b/c less time to do everything.

63
Q

Aortic stenosis

A

Radiates into neck. Increased intensity with INC preload. This is what distinguishing this murmur from HOCM. Diminished pulse. Low SV. Syncope with exercise. Angina with exercise possible.

64
Q

Mitral stenosis

A

Diastole. OS + rumble. Most common etio = rheumatic fever

65
Q

Rheumatic fever

A

ARF 2/2 GAS (strep pyogenes). Usu. post-pharyngitis. Post-strep glomerulonephritis can be either pharyngitis or skin infection. Blood cx negative in rheumatic fever. M-protein? pathogenic of GAS. Molecular mimicry. Vegetations around the opening of the valve. Polyarthritis is the most common symptom. ACUTE valvular problem = MR NOT MS. MS takes time to develop. Erythema marginatum. SQ nodules. ASO.

66
Q

LA enlargement signs

A

Ortner’s syndrome (hoarseness b/c of recurrent). AF. Dysphagia b/c onto esophagus.

67
Q

Two genetic syndromes with MVP

A

Marfan’s and Ehler-Danlos syndrome

68
Q

Sudden death in Marfans?

A

Not dissection b/c not quick enough. Serious MVP with conduction defects.

69
Q

Tricuspid regurgitation

A

IV drug abuse with infective endocarditis

70
Q

Carcinoid syndrome

A

REQUIRES METASTASES to the liver. 5-Ht -> venous blood -> bathes right heart and produces fibrosis of the valves. Tricuspid insufficiency and Pulmonic stenosis. TIPS.

71
Q

Infective endocarditis

A

Most common organisms = Viridians strep. 2nd = staph aureus, which can infect both normal and damaged valves. Most common valve involved = Mitral. 2nd = aortic. IV drug abuser -> tricuspid valve (TR), aortic valve (AR). Colon cancer or ulcerative colitis -> strep bovis (group D strep). Associated VSD -> aortic regurg

72
Q

Osler node vs. Janeway’s lesions

A

Painful vs. not

73
Q

Koplik spot of the eye

A

Red with white center = Roth spots

74
Q

ARF

A

IC-vasculitis.

75
Q

Libman-Sack’s endocarditis

A

SLE. Pericarditis is most common heart manifestations. VEGETATIONS EVERYWHERE>

76
Q

Merantic vegetations

A

Paraneoplastic syndrome. Vegetations around the margins of the valve.

77
Q

Coxsackie B

A

Myocarditis and pericarditis. Viral meningitis. Hand-foot-mouth disease. Herpangina.

78
Q

Coxsackie B Myocarditis

A

Path - lymphocytic infiltrates. Endomyocardial bx.

79
Q

Dilated cardiomyopathy

A

Disease of the cardiac muscle. Etios - postpartum (~6 wk), Coxsackie myocarditis, doxorubicin, TCA’s, EtOH -> thiamine deficiency,

80
Q

HOCM

A

VERY thick septum. Asymmetric hypertrophy. Anterior leaflet of the mitral valve against septum obstructs blood flow. Obstruction in the LVOT 2/2 Venturi phenomenon (neg pressure). Increased preload will pull away the leaflet and lead to LESS obstruction/murmur. NO DIGITALIS. Beta-blocker or CCB can slow down -> increased preload.

81
Q

HOCM histology

A

Septum has muscle all over the place. BAD CONDUCTION defects -> risk of V-tach.

82
Q

Endocardial fibroelastosis

A

Most common restrictive cardiomyopathy in children.

83
Q

Restrictive Cardiomyopathies

A

Pompe, Fe overload, amyloid

84
Q

Cardiac myxoma

A

85% in LA. 15% in right. Benign tumors. Attached by stalk and can move -> blockage of valve -> syncope or embolization.

85
Q

Tumor in the heart of the kid?

A

Rhabdomyoma 2/2 tuberous sclerosis.

86
Q

Water bottle configuration

A

Muffled heart sounds, Kussmaul’s sign (neck veins distend on inspiration), >10 mmHg drop in Bp on inspiration (Pulsus paradoxus). Beck’s triad. Pericardial effusion. Most common etio is pericarditis.

87
Q

Young woman with unexplained pleural effusion or pericardial effusion?

A

SLE.

88
Q

Constrictive pericarditis

A

TB in 3rd world. Previous cardiac surgery. Can’t fill up. Once it hits the pericardium = Pericardial RUB! Dystrophic calcifications would see on X-ray. RESP is next.

Goljan Path (9 decks)

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