UWorld 2017 Flashcards by Melissa Khalil

Digoxin indications

For ventricular rate control in Afib: increases parasymp vagal tone, decreases AV nodal conduction
For HF: inhibits Na/K ATPase, positive inotropic

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Causes of angioedema

Mast cell activation: HS I (IgE) or direct activation; ass w/ pruritus + urticaria
Excess bradykinin: ACE inh or C1 inh deficiency; No pruritus/urticaria

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Prinzmetal angina

Triggers: cigarette smoking, cocaine/amphetamines, dihydroergotamine/triptans
Dihydroergot (vasoconstriction by alpha-adren agon + serotonin agon)
Ttt: tobacco/drug cessation, vasodilator (nitrates, CCB)

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ECG changes in occlusion of different arteries

RCA: transmural isch of inf wall of LV, ST elev in II+III+aVF + sinus node dysfunction
Proximal LAD: anteroseptal transmural isch, ST elev in V1-V4
LCX: transmural isch of lat wall of LV, ST elev in V5-V6 +/- I and aVL

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Severity of Mitral regurgitation

Holosystolic murmur
Audible left S3: high regurgitant volume (severity) + LV overload
Intensity of murmur does not correlate w/ severity

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Beta1-adrenergic receptors

In cardiac tissue + juxtaglomerular cells
Not in vascular smooth muscle
Selective B1-recept blockade: decreased cAMP in cardiac+renal tissue

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Daily long-acting nitrates

Need to have nitrate-fee period every day

Avoid tolerance to the drug

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Mitral valve prolapse

Midsystolic click + mid-late systolic murmur of MR

Defect in mitral valve connective tissue proteins that predispose to degen of leaflets + chordae tendineae

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Pressures in RA, RV, PA

Diastolic RV = RA = central venous pressure = 1-6 mmHg

Diastolic Pulm Art press = 6-12 mmHg

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Major risk factors for Ao dissection + Ao aneurysm

Hypertension: intimal tear leading to Ao diss

HTN, db, hypercholest: major risk factors for atherosclerosis that predisposes to Ao aneurysm

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Drug interaction of Nitrates + PDE inhibitors

PDE inh (tadalafil): erectile dysfct, pulm HTN
Nitrates+PDEinh: increased intracellular cGMP, vasodilation, profound hypotension
Absolutely CI together

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Nonvalvular heart failure

Congestive HF: dilated CM or chronic ischemic H ds; dilation of 1-2 V + systolic dysfct
Diastolic dysfct: HTN H ds w/ concentric V hypertrophy, hypertrophic CM w/ asymmetric septal hypertrophy

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Atherosclerotic plaque rupture

Rupture related to plaque instability rather than size or degree of luminal narrowing
Stability depends on mechanical strength of fibrous cap
Inflammatory macrophages in intima secrete metalloproteinases so reduce stability

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Cause of symptoms/signs in AR

By abnormally large (wide) pulse pressure

Nocturnal palpitations, head pounding w/ exertion

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Cough secondary to ACE inh

Dry, nonproductive, persistent

Accumulation of bradykinin, substance P, prostaglandins

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Circulation in heart vs other organs

Heart perfused during diastole
Myocardial oxygen extraction very high (60-75% at rest): blood in coronary sinus is most deoxygenated
Myocardial oxygen demand + coronary blood flow: tightly coupled; O2 use increased several-fold during exercise by increased coronary blood flow

Left atrial enlargement

Left recurrent laryngeal nerve impigement

Neurapraxia: left vocal cord paresis + hoarseness

ACEinh + ARBs in systolic HF

Improve hemodynamics
Inhibit chronic AngII-mediated cardiac remodeling
Reduce mortality

Indicated + CI medications in Hypertrophic CM

Indicated: negative inotropic agents (beta blockers, nondihydro CCBs, disopyramide) reduce LVOT obstruction and symptoms
Avoid: vasodilators (dihydro CCBs, nitrogl, ACE inh) decrease SVR then afterload + LV volumes
Avoid: diuretics decrease preload so greater obstruction

Congenital QT prolongation syndrome

Unprovoked syncope in asymptomatic young person
Romano-Ward sd or Jervell+Lange-Nielsen sd
Mutation in K+ channel protein: delayed rectifier current of action pot

Atherosclerotic plaques dev

#1 large elastic arteries (Ao, carotid, iliac)
#2 large or medium musc arteries (coronary, popliteal)
In body: abdo Ao > coronary art > popliteal art > internal carotid art > circle of Willis

Beta blockers and AMI

Reduce HR, CO and myocardial O2 demand
Non-cardioselective BB: bronchospasm if asthma/COPD
Cardioselective BB: esp on B1 recept (Metoprolol)

Nitrates function

Venodilators: increase periph venous capacitance, reduce preload + LVED volume and pressure
Arteriolar dilation (modest effect): decrease SVR + afterload

Nitroprusside function

Short-acting balanced venous + arterial vasodilator

Decrease preload + afterload: so stroke volume maintained

Causes of angina

Asymptomatic: atherosclerotic plaque obstr <75% Stable: fixed atherosclerotic plaque obstr >=75% ACS (unstable, MI, sudden cardiac death): acute plaque change w/ superimposed thrombosis Unstable or subendocardial infarction: ulcerated atherosclerotic plaque w/ partially obstr thrombus Transmural MI: ruptured atherosclerotic plaque w/ fully obstr thrombus

Intracellular changes of nitrates

Nitrates to NO then activate guanylate cyclase, increase intracellular cGMP Myosin light-chain dephosphorylation Vascular smooth relaxation

Abciximab MOA

Blocker of GP IIb/IIIa receptor (platelet to fibrinogen) | Glanzmann thrombasthenia: deficiency/defective GP IIb/IIIa

Ttt when AFib w/ rapid ventricular response

``` #1: CCBs and Beta blockers #2: digoxin (esp when systolic dysfct) ```

Digoxin toxicity

``` Cardiac arrhythmias GI (N/V) Neuro (confusion, weakness) Visual symptoms, color vision alterations Hyperkalemia ```

Chronic aortic stenosis + concentric LV hypertrophy

Atrial contractions contributes to LV filling | If AFib, reduced LV preload and CO: systemic hypotension + acute pulm edema

Synthesis of NO

From arginine by nitric oxide synthase | Arginine supplementation: role in ttt to improve vasodilation (stable angina)

Non-dihydro CCB + Beta blocker

Additive negative chronotropic effect | Severe bradycardia + hypotension

Carotid sinus massage

Increase in parasympathetic tone Temporary inh of SA node, slow conduction in AV node, prolongation of AV node refractory period For termination of paroxysmal SVT

Isoproterenol

Beta-1 and beta-2 adr recept agonist Increased myocardial contractility Decreased systemic vascular resistance

ACE inhibitors cause hypotension

If volume depletion of HF: first-dose hypotension | Avoid this by initiating at low dosages

Ventricular hypertrophy

Concentric: due to increased afterload (chronic HTN, Ao stenosis) Eccenctric: due to volume overload

Restrictive cardiomyopathy

By infiltrative ds (amyloidosis, sarcoidosis, hemochromatosis) Ventric hypertrophy + impaired filling: Diastolic HF

Dobutamine

Beta-adren agonist: B1 > B2 and a1 B1: increased cAMP and cytosolic Ca So increased myocardial contractility