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UWorld Cardiology Flashcards

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USMLE® Step 1 flashcards
1
Q

“Please pray for me” in Emergent setting. Against your beliefs. What do you do?

A

Say “you are in my thoughts” Answer was NOT call a chaplain. Shifting responsibility is usu not correct in USMLE

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2
Q

MAP INC how much during exercise? What is this due to?

A

Usu only 20-40 mmHg. THis is due to massive vasodilation to muscles (can get up to 85% of bodies blood!)Constriction of venous INC blood flow return to the heart.

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3
Q

Most common endocarditis w/ dental work?

A

Strep Viridans/mutans

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4
Q

Culture Negative Endocarditis?

A

Bartonella, Coxiella, Mycoplasma, Histoplasma, Chlamydia, HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

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5
Q

When would you see enlarged intercostal arteries in young child?

A

Turners - Co-arctation - leads to poor flow to the

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6
Q

Familial Hypercholesterolemia inheritance pattern?>

A

AD

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7
Q

Knife wounnd to left sternal border, 4th intercostal space. Hits?

A

Right Ventricle. RV is majority of anterior surface of the heart.

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8
Q

Type 1 ErrorType 2 ErrorPower?

A

T1 Error - False Positive (seeing a different when there is no difference in reality)T2 Error - False Negative (seeing no different when there is a difference)Young scientist commit T1 error as they are trying to promote their career. Old scientist commit T2 error because they are stuck in their own ways. However, Old scientists have the power. Power = 1-T2 Error

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9
Q

Endocardial cushin defects lead to ?

A

Defects in AV septum - initially acyanotic, may form Left to right shunts that reverse due to pulmonary HTN (Eisenmernger syndrome) -> cyanotic

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10
Q

If they say, cyanotic since birth.. what do you think?

A

TranspositionTricuspid Atresia TetralogyTotal AnomalousTruncus ArteriosusEndocardial cushin defects (ASD, VSD) would not be cyanotic since birth

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11
Q

What are Tetralogy, Transposition, and Truncus Arteriosus due to?

A

Abnormal migration of neural crest cells through pirmitive truncus arteriosus and bulbus cordis

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12
Q

Mech of Doxorubicin, toxicity?

A

Formation of free radicals -> dialted CM. Dose dependant. Can get swelling of sarcoplasmic reticulum (early sign of txo) -> loss of myocytes (myofibrillar dropout) .Prevent doxorubicin CM w/ dexrazoxane (Iron chelating agent) that DEC oxygen free radicals.

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13
Q

Most reliable auscultatory indicator of severity of mitral stenosis? What indicates severity? What is clinical standard for diagnosis of MS?

A

A2/S2 to Opening snap time interval. Shorter the interval, MORE severe the stenosis. Think, the STENOSIS IS SO BAD, that the pressure INSTANTLY builds up and it HAS to snap openThe more thickened and fibrotic the MV, the earlier the tensing and snapping occurs. MS also assoc w/ INC mean transvalvular pressure on doppler.Therefore, the opening snap time is inversely related to transvalvular pressure.

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14
Q

Histology of acute cardiac rejection (2 weeks)Histo of chronic rejection?

A

Cell mediated - dense mononuclear lymphocytic infiltrates. (T lymphocytes sensitized against graft MHC antigens). Scant inflam cells and interstitial fibrosis

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15
Q

Acute hypersensitivty to cardiac transplant leads to?Compare to histo of hypersensitivity myocarditis?

A

Acute cessation of blood flow to organ due to preformed Ab. Perivascular infiltrate /w abundant Eos, often following new drug therapy -> atopipc response

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16
Q

Patchy necrosis w/ granulation tissue on heart?

A

Think ischemic damage. Atherosclerosis of MI

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17
Q

Hemolysis pattern of Group D strep. DifferentiateEnterococci, E. faeciumNonenterococci S. bovisAssoc for either one? When you see them?

A

Gamma - no hemolysis of GDS.Enterococci, E faecium - grow in bile AND 6.5% NaGenitourinarny procedures (cystoscopy etc)Nonenterococci, S. bovis - grow in bile, NOT NaClColonic malignancies

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18
Q

Strep viridans/mutans - when do you get cardiac complications?

A

After dental work/dental caries

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19
Q

MAIN THERAPEUTIC EFFECT OF sublingual NITRATES (nitroglycerin)m IN DEC CHEST PAIN?

A

DEC in LV volume (DEC preload, buy promoting venodilation)have modest dilatory effect on cornoary arterioles and moest DEC in afterload through arteriolar vasodilation.

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20
Q

Formulas for.Volume DistributionHalf lifeLoading DoseMaintenance Dose

A

Volume Distribution = Dose/[Plasma]Half life = .7(VD)/CLLoading Dose = (VD)[PlasmaSS]\FMaintenance Dose = PlasmaSS(t)/F

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21
Q

How does AV shunt affect preload and afternload?

A

INC preload and DEC afterload. INC preload (as venous blood, big reservoir returns), and DEC afterload (because pressure is decreased w/ bypass into venous system.High volume AV shunts can lead to high output cardiac failure.

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22
Q

Why are skeletal muscles resistant to calcium channel blockers - compared to cadriac and smooth muscle?

A

Skeletal does NOT rely on extracellular Ca. Cardiac, smooth muscles do rely on extracellular Ca entering via voltage gated L type Ca channels. Skeletal muscle does have RyR1 - L type channel coupling in T tubule system - BUT does not require extracellular Ca. Ca from SR binds to troponin C.Cardiac muscle has T tubule but does not have L-RyR coupling. In this case you have L type Ca channels in plasma membrane that open and allow influx of extracellular Ca - this Ca binds to sarcoplasmic RyR2 channel (Calcium induced calcium release) -> moves Ca out of sarcoplasmic reticulum. Smooth muscle - similar to cardiac (no extracellular), but Smooth muscle does NOT have troponin, it is calmodulin.

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23
Q

What is the major mediator of autoregulation between little change in blood flow over INC in mean arterial pressure?

A

NO. Most important mediated for coronary vascular dilation in large ateries and pre-=arteriolar vessels. Causes smooth muscle relaxation via cGMP second messasnger. Adenosine also acts as a vasodilatory element in small coronary arterioles

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24
Q

Where does adenosine do most of its work?

A

AV node - slows conduction and DEC automaticity by hyperpolarizing cells. Also vasodilatory in cornoary arterioles. DOC for abolishing SVT.

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25
Q

Conduction speed of Ventricular, Atrial, Purkinje, AV node?

A

Fatest at Purkinge > Atrial> Ventricular> AVconduction speed of atrial is higher than ventricular muscle

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26
Q

Echocardiogram showing aorta lying anterior and to the right of pulmonary artery diagnostic for? What would year hear?

A

Transposition - Failure of septation. Life threatning cyanosis at birth. 2 circuits - incompatible w/ life unless PFO, Septal defect, PDA. Hence can hear any of these on auscultation. (Such as machine like murmur - dont let this throw you off!)

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27
Q

Wolff Parkinson White - 2 major findings on EKG?

A

Shortened PR (w/ early excitation, delta wave), and WIDENED QRS.

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28
Q

Where does mitral opening (OS) in mitral stenosis usually occur?

A

Early in diastole.

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29
Q

What are side effects of digoxin/digitalis ?

A

AV block, VTachyarrhythmias. Hyperkalemia found in acute digoxin toxicity.KNOW that hypokalemia INC susceptibility to toxic effects of digoxin tho!

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30
Q

Most common congenital malformation affecting hear in Turners syndrome? How does this present?Other buzzwords for turners?

A

Bicuspid aortic valve. Usually is asymptomatic in young pt. Can hear aortic ejection sound. As itprogressive valular dysfunction -> calcifies -> aortic stenosis, regurg. Susceptible to infectious endocarditis. Shortened fourth metacarpals, short stature, short thick/webbed neck, board chest. coarctation of preductal aorta.

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31
Q

VSD murmur sound/when?ASD Murmur sound/when?What accentuates either/both?

A

VSD - holosystolic, accentuated during hand grip (INC afterload)ASD - midsystolic - Loud S1, WIDE FIX SPLIT S2

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32
Q

What is cornoary sinus dilitation usualy due to?

A

Empties into right atrium (contains deox blood) - , so INC right side pressure.

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33
Q

Can a physician receive a gift that was given to a patient for free?

A

Basically no. Cant accept any sort of gift except cards, photos, cookies. Even if the pt was given free basketball tickets and is passing them on

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34
Q

What is dofetilide?

A

Class 3 antiarrhythmic - K channel blocker

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35
Q

Differentiate staph saprophyticus from staph epidermitis?

A

Staph epidermitis - novobiocin sensitiveStaph saprophyticus - novobiocin resistant

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36
Q

What calculation do you use for cohort study? For Case-control study?How do you calculate either?

A

Cohort - Relative Risk (risk of getting something)Case Control - Odds (there is no risk, you already have it or dont have it. what were the odds)Relative risk is a/(a+b) / (c/(c+d)Odds - ad/bc

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37
Q

What does glucagon treat and how does it do this?

A

Reverses beta blocker. It INC intracellular cAMP which INC Ca release and INC SA node firing.

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38
Q

When does coronary blood flow occur?

A

During diastole.

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39
Q

Which drugs have highest selectivty for ischemic myocardium compared to normal cardiac?

A

IB antiarrhythmic - Lidocaine -

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40
Q

What can digoxin be used for?

A

Slows conduction through AV node - Tx of atrial fibrillationOr CHF. INC contractility.

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41
Q

When do you see head bobbing and why?

A

Aortic regurg - bounding pulses - transfer of momentum of large left ventricular stroke volume to head and neck (bobbing = de Musset sign)

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42
Q

When does mitral valve stenosis opening snap occur?

A

Right at the beginning of diastole. Shorter the wait the worse it is.

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43
Q

Why would a baby momma have normal BP when standing and sitting, but DEC when supine?

A

Supine hypotension snydrome - compressionof IVC, DEC venous return, REDUCEd preload, DEC CO, hypotension.

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44
Q

When does myocyte loss of contractility occur? When does myocyte irreversible death occur?

A

After 60 seconds - loss of contractility.Irreversible death at 30 minutes

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45
Q

Wide fixed splitting of S2 think? What can this eventually lead to?

A

ASD - pulmonary vasculature resistance

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46
Q

What is a recombinant form of BNP? What does it do? How is BNP diff than ANP? What is the mech?

A

Nesiritide. It dilates arterioles and veins (DEC BP) and promotes diuresis. BNP is basically the same as ANP but BNP is from ventricles. Both ANP and BNP INC gMP.

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47
Q

What affect do B1 blockers have on cardiac, renal juxtaglomerular cells and vascular smooth muscle?

A

DEC cAMP in cardiac and renal. No change in vascular smooth muscles - they dont have B1 receptor

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48
Q

How do Diptheria and Shiga toxin differ in their approach? How does this differ from Clostridium perfringens? Pertussis toxin?

A

Diptheria - Exotoxin transfers ribose (ribosylates) EF2, a protein needed for peptide translocation. Shiga on the otehr hadn ACTUALLY INACTIVATES THE Ribosome (60s subunit)CLostridium - alpha atoxin - lecithinase - cleaves cell membranes/phospholipids. Pertussis toxin - stimulates intracellular G proteins -> INC cAMP -> INC insulin, lymphocytes and N! dysfunction. INC sensitivity to histamine.

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49
Q

How is NO created and what does it affect downstream? Total mech.

A

Arginite, O2, NADPH, + eNOS (enodthelial NO synthase) -> NO + citrulline.NO stims guanylate cyclase (GTP -> cGMP), which activates protein Kinase G, which DEC Ca levels and leads to relxation of vascular smooth muscle

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50
Q

Side effects of THiazide?

A

HYPERcA,URICEMIA, GLYCEMIA, LIPIDEMIAHYPOkalemia, tension.

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51
Q

What do you see 0-4 hours4-12 hours12-24 hours1-5 days5-10 days10-14 days2 weeks to 2 months

A

0-4 hours - no change4-12 hours - wavy fibers, early coag necrosis12-24 hours coag necrosis + contraction band nec1-5 days coag necrosis + N!5-10 days M!10-14 days - granulation tissue + neovascularization2 weeks to 2 months - collagen/scar

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52
Q

INC cell size in transiet MI (less than 30 minutes) is due to what 2 solute accumulations?

A

Na and Ca.NCX is Na flowing in to tower Ca flowing out.

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53
Q

What drugs can prolong QT. What does this usually lead to. What drug is atypical?

A

IA and Class 3 drugs prolong QT by DEC K effect in phase 3. This precipitates Torsade de pointes. HOWEVER, Amiodarone DEC risk of torsades for whatever reason even tho it prolonges QT.

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54
Q

What drug prolonges QT, but does not INC risk of Torsades?

A

Amiodarone

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55
Q

Aging patient w/ yellowish brown intracytoplasmic granules. (in myocardial cells). Most likely due to?

A

Lipid peroxidation - this is lipofuscin.

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56
Q

Most common site of aortic rupture in MVA?

A

Aortic isthmus - connection between ascending and descending - distal to left subclavian artery branch.

57
Q

Most common cause of endocarditis in IVDU? Second most common?

A

S AureusP. aeruginosa

58
Q

Do you tell wife of pts heart attack?

A

No. HIPAA. Unless they have explcit consent of patietn. even from loved ones and family members.

59
Q

How does vagal massage or valsalva affect conduction?

A

Parasympathetic tone slows conduction through AV node.

60
Q

How does the carotid sinus massage work?

A

Carotid sinus innervated by CN 9 (glossopharyngeal) - constantly firing. If pressure INC, impulses to CNS INC -> INC parasymaphetic tone to heart and vessels. Prolonges AV refractory period. Stops AV re-entrant tachycardias.

61
Q

Nitroglycerin - works primary where?

A

Large veins - venodilator.

62
Q

Best auscultaory indicator for Mitral Regurgitation?

A

S3 gallop - due to INC left ventricular filling due to LARGE VOLUME of regurgitant flow reentering ventricle during middistole.

63
Q

How does constrictive pericarditis appear on CT?Etiology?

A

Thickening and calcification (white) of pericardium. Normally 1-2 mm thick4-20 mm thick in constrictive pericarditis.Present w/ slowly preogressive dyspnea, chronci edema, ascites Can be from radiation therapy to chest, cardiac surgery, TB.

64
Q

Nitroprusside - affect on pressure-volume curve?

A

Short acting balanced venous and arterial vasodilator.DEC preoload and DEC afterload.left shift w/ low pressure and low volume

65
Q

Nitrates major side effects?

A

Headaches (throbbing) and Facial flushing. Due to vasodilation of meninges and skin.More common at higher doses when nitrates can produce some arteriolar dilation - BUT PRIMARY ACTION OF ALL NITRATES IS VENODILATION (INC nitroprusside)

66
Q

Pressures in RA, RV, Pulmonary A, LA, LV

A

RA - less than 5RV - 25/5PA - 25/10RV - less than 12RV - 130/10There is an INC from RV to PA diastolic pressure.

67
Q

Differenate ab seen in DILE from SLE

A

All have change for ANA, Anti-histone, and anti-dsDNAANA frequent in bothAnithistone more frequent in DILEAntidsDNA more frequent in SLE

68
Q

qHow does an INC ejection fraction look on a ventricular pressure volume loop?

A

Widening of the graph w/ a left shift. Smaller End Systolic Volume because more was pumped out.

69
Q

Amyloid composition of Senile cardiac amyloidosis vs Familial amyloid cardiomyopathy

A

Senile cardiac amyloidosis - misfolded ANPFamilial amyloid cardiomyopathy - mutated serum transthyretin

70
Q

Scattered cells w/in mucopolysaccahrdie stroma. Histo for what?

A

Left atria myxoma

71
Q

Nitrate with greatest oral abs(PO/swallow).What drugs are IV only? Tox?

A

Isosorbide MONO-nitrate - 100% bioavailable PO.Nitroglycerin and Isosorbide DI-nitrate - significant first pass metabolism. Therefore are given SUBLINGUAL. Nitroprusside is IV only. Used in HTN emergency. Can cause cyanide toxicity/.

72
Q

Trousseau syndrome. Relation to valvular destruction?

A

Sign of malignancy - migratory thrombophlebitis - hypercoag state induced by disseminated CA.Can get sterile nondestructive vegtations on valves w/ CA. Realted to wasting of tissue “marasmus -> marantic” - endocarditis, tumor associated procoagulation similar to Trousseau syndrome

73
Q

What causes mitral stenosis?

A

Acute/chronic rheumatic fever - 99% of all cases.

74
Q

What is the effect of a chronic AV shunt on heart output? And TPR, Venous REturn?

A

INC Cardiac Output. DEC TPR. INC venous return.

75
Q

What drugs DEC slope 4 of Nodes?

A

Adenosine and ACh

76
Q

What does “coffee ground emesis” suggest?

A

Presence of blood in vomitus that has been exposed to gastric acid. Due tot he oxidation of heme. Can be upper GI bleed.

77
Q

What is Milrinone and what are its effects? How is it administered?

A

Phosphodiesterase inhibitors. INC cardiac contractility and DCE preload AND afterload. is IV only.

78
Q

What drugs have been show to slow progression of CHF and DEC mortality in pt w/ HF?

A

Beta blockerse. Carvedilol in particular. These slow ventricular rate and DEC afterload

79
Q

DEC LV cavity size and sigmoid shaped ventricualr septum.Light microscopy shows collagenized connective tissue in ventricular wall, and some cells have brownish perinuclear cytoplasmic inclusions. Change in 78 year old. What are these?

A

Normal aging. Aging shows DEC in LV chamber size, due to basal ventricular septum to bulge into LV outflow tract (sigmopid septum) Lipofuscin

80
Q

Most affective treatment option in pt w/ HTN and Chronic ishemic MI?

A

Ace inhibitors. Inhibit myocardial remodeling and DEC blood pressure. Prevents the chronic AT2 mediate LV hypertrophy and modeling assoc w/ MIBeta blocker owuld also be beneficial to pt.

81
Q

When do you use B blocker, when do you use Thiazide, when do you use Ace inhibitor?

A

B blcoker and ACE for pt w/ HTN and MI/ischemic myocardial failure.Thiazide for pt w/ HTN WITHOUT CHF OF DIABETES. ACE esp if they have diabetes.

82
Q

Biventricular pacemaker - hwere are the leads?

A

Usu requires 2 or 3 leadsIf 3,one in the RA,one in the RV,one in the LV, via the coronary sinus -> atrioventricular groove (posterior aspect of heart)-> LV

83
Q

What medication could cause QRS segments to be prolonged?

A

Sodium channel blockers. PARTICULARLY IC antiarrhythmics. ESP during exercise/higher heart rates.

84
Q

Family history of sudden death w/ QT interval prolongation. What accompanies this condition?

A

Jervell and Lange NIelsen syndrome - common congenital long QT syndromes. AR. Seen w/ congenital neurosensory deafness. Long QT predisposes to syncopal events as well as torsades -> sudden cardiac death

85
Q

Most likely cause of death in acute rheumatic fever?

A

Sever myocarditis. Mitral stenosis afte rARF takes years/decades tod evo

86
Q

Early and late valvular defects w/ RF?

A

Early = MRLate - MS

87
Q

In what position is AR best heard and hwere?

A

Pt leaning forward, end of expiration left sternal boarder.

88
Q

What murmurs are best heard at the left sternal boarder? (E) area

A

Aortic regurg. Pulmonic regurg. Hypertrophic cardiomyopathy

89
Q

Prophylactic first line tx for cluster headaches?

A

Verapamil

90
Q

When do you see atrialization of RV, apical displacement of tricuspid valve leaflets in infant?

A

Bipolar - Lithium in mom -> Ebstein abnormality

91
Q

Weight loss drugs, appetite suppressants, what major side effects?

A

Fenfluramine, dexfenfluramine, phentermine -> secondary pulmonary HTN. Can lead to RV hypertrophy. Corpulmonale. Sudden death

92
Q

Dextran producing think?!

A

Viridans. Dental aries. Subacute bacerial endocarditis. PROPHYLAX THOSE W/ VALVULAR ABNORMALITIES PRIOR TO DENTAL WORK

93
Q

What does reliable mean?

A

Same thing as precise!

94
Q

Becks triad?

A

Hypotension, JVD, Distant/muffled heart sounds… + tachycardia -> TAMPONADE

95
Q

Difference in presentatsion ofAcute fibrinous pericarditis vsConstrictive Pericarditis vsCardiac tamponade?

A

Acute fibrinous pericarditis - pleuritic chest pain and pericardial friction rubConstrictive Pericarditis - chronic process - takes years to produce. Cardiac tamponade - acute - distant muffled hart sounds, tachy, hypotension JVD. MI - vs Tamponade - MI may have pulmonay edema + rales. Vs Tamponade, whihc usu has clear lung sounds.

96
Q

What does pulmonary cap wedge pressure (PCWP) measure?

A

LA End Diastolic pressure

97
Q

Irregular rhythm, Heart rate 120 - narrow QRS, no Pwaves. What is this?

A

A fib. QRS narrow due to tachy

98
Q

IN Afib - what is the mechanism. What are the average atrial rate? Average Atrial fibrillation rate?

A

Atrial - 300-500 beats/minVentricular - 90-170 bpmEach time AV is excited -> REFRACTORY period -> tehrefore atrial impulses cannot be transmitted - AV serves as the BOTTLENECK during afib

99
Q

In pt w/ MR, what is one way to INC forward regurgitant volume?

A

DEC LV Afterload.

100
Q

What may may B blockers mask?

A

Hypoglycemia.This is why HTN w/ DM first go to is ACE. However B blockers may still be used as the benefits may outweight th emasked hypoglycemia costs

101
Q

Berkson’s bias

A

Bias created by selecting hospitalized pt as a control group

102
Q

What i a concern of around the clock nitrate administration?

A

Tolerance devo

103
Q

EKG findings in ST eleevation of MI in LAD vsRight Coronary?

A

LAD - V1-V4Right cornoary Leads 2,3, aVF, possible sinus node dysfunction

104
Q

Etiology of Stable and Unstable

A

Less than 70% obstruction - asymptomatic usuStable - more than 70% obstruction - pain/dyspnea w/ exerciseUnstable - thrombosis w/ incomplete cornonary artery occlusionBoth have ST depression.

105
Q

What are the first and late ECK signs of MI?

A

Peaked T waves -> first ECG sign -reflect local hyperkalemia - death of cells. Deep Q waves - appear within hours or days

106
Q

U wave. Think?

A

Hypokalemia. most common.Inverted U wave may be MI

107
Q

Histological change in 0 to 4 fours post MI/death

A

Minimal Change on light microscopyEarly coag edema, heomrrage, wavy occurs in 4-12 hours

108
Q

What are these and when are they seen?Pulsus alternansDicrotic pulsePulsus Parvus (et tardus)Hyperkinetic pulse

A

Pulsus alternans - LV dysfunction - beat to beat variations in magnitude of pulse w/ regular rhythmDicrotic pulse - 2 distinct peaks (one in diastole one in systole) - can be palpaed at carotid arteries - suggests SEVERE systolic dysfunctionPulsus Parvus et tardus - Aortic Stenosis - low magnitude w/ delayed peakHyperkinetic pulse - large stroke volume agaisnt DEC afterload. PDA or AV fistual

109
Q

Hypertrophic cardiomyopathy -what is dynamic outflow obstruction caused by?

A

Abnormal systolic ANTERIOR motion of ANTERIOR leaflet of MITRAL VALVE towards hypertrophied inerventricualr septum

110
Q

How to differentiate cardiac tamponade from tension pneumothorax?BOth have JVD, hypotension muffled heartsounds (more tamponade), tachycardia and pulsus paradoxus,

A

Lung examination is normal w/ cardiac tamponadeBronchial and VESICULAR breathing are normal. Just is diff places.

111
Q

Kussmaul Sign - what is it and when is it seen?

A

INC in JVP upon inspiration. JVP usually DEC on inspiration.Seen in constrictive pericarditis.

112
Q

What are signs of constrictive pericarditis?

A

INC JVP, Kussmaul Sign (INC JVP w/ inspiration - also seen in cardiac tamponade), Pulsus paradoxus, Pericardial knock (diastolic - before s3)

113
Q

How do phosphodiesterase inhibitors work on the heart?

A

INC cAMP, which INC intracellular Ca in cardiac myosites. INC cAMP INC conductanse of Ca channels in SR -> more Ca can enter the cell. INCREASES CONTRACTILITY.In vascular smooth muscle, INC cAMP causes vasodilation.

114
Q

What is the fastest firing nodal generator in the heart?

A

SA node (60-100 beats per minute)AV is 45-55 beats per minuteVentrilces is 20-40

115
Q

Complete dissociation between P and QRS complexes - with bradycardia w/ regular rhythm and narrow QRS? What is pacing the ventricles?

A

Dissociation is 3rd degree block - AV block. This mean sthat the SA nodes are controlling the atrial and AV nodes are controlling the ventricle.

116
Q

Digoxin completes w what for binding?

A

K.So hypokalemia is a major risk factor for toxicity - the Digoxin will go crazy and bind too muchAlso hyperkalemia can result from digoxin - it cant get into cells.

117
Q

How does No effect change on mascular smooth muscles. More than the first downstream affect.

A

NO -> INC cGMP -> DEC intracellular Ca -> DEC myosin light chain kinase and leads to myosin DEPHOSPHORYLATION -> smooth muscle relaxation

118
Q

When can you see angioedema w/ heart failure meds?

A

Ace inhibitors. Diff mech than cough. Not explained. but its edema of lips and larynx.

119
Q

Common complication for digoxin?

A

V tachy/dysrhythmias

120
Q

Diptheria toxin - what is it how does it work - immune response to prevent it?

A

AB exotoxin. B - binding, A - active.These inhibit ribosome function. Immunization induces circulating IgG against exotoxin B subunit - preventing disease. Toxin is major mediator of damage. Deactivates EF-2 (via ribosylation), a protein needed for ribosome function.

121
Q

What is common cause of death in bicuspid aortic valve? Live until?

A

Aortic stenosis in sixties. premature calcific aortic stenosis. Without defect - senile calcific aortic stenosis comes in the 80s or 90s.

122
Q

Where are you most likely to see an atherosclerotic plaque? Top 4 places in order.

A

Large and medium/muscualr sized vessels. Abdominal aorta, followed by coronary arteries, then internal carotid, then circle of Willis.

123
Q

How do you treat coag negative gram positive cocci in heart valve pt?

A

Empirically w/ Vanc. With or without rifampin/gentamicin due to widespread antibiotic resistance S. epidermidis

124
Q

During transesophageal echocardigraphy - what is directly anterior, psterior?

A

Anterior - left atrium, posterior, descending aorta

125
Q

Cardiac output = ? not the Sv xHR one

A

O2 consumption/AV O2 diffAKA O2 consumption = COxDiff

126
Q

What are 2 major (1 minor) drugs that cause coronary steal. What is the mech?

A

Adenosine and Dipyridamole - selective vasodilators of cornoary vessels -> cornonary steal. Blood flow to ishemic areas is DEC due to arteriolar vasodilation in NONISCHEMIC areas. Can lead to hypoperfusion and WORSENING of existing ischemia.

127
Q

What holosystolic murmurs INC w/ inspiration. What would not?

A

Tricuspid Regurg INC Mitral Regurg, VSD would not. This is due to DEC thoractic pressure causes INC return to right heart, as well as vasodilation of pulmonary vessels (leading to DEC venous return to LV). DEC return on left side means less murmur sounds

128
Q

3 common causes of Aortic Stenosis?

A

Congenital abnormal valve w/ calcification (bicuspid valve), calcified normal valve, Rhuematic heart disease. Rheumatic more common worldwideClacified oartic vales (eitehr bicuspid or tricuspid is more common in US)

129
Q

Sign of cardiac myocyte irreversible death not related to nuclear falling apart?

A

Mitochondrial vacuolization - vaculose and phospholipid containing amorphous densitites within mito signify irreversible injury, as there is a permanent inability to gernerate furtehr ATP via ox phosph. Dissaggregation of nuclear granules and clumping of nuiclear chromatic are reversible?!However picnosis, karyolysis, karyhorrhesis are irreversible

130
Q

Where does Aortic stenosis have the loudest murmur?

A

The point at which the magnitude of LV to aorta pressure gradient is highest.

131
Q

Someone has exertional chest pain (angina pectoris) (not MI) and is allergic to aspirin. What should be used instead for prophylaxis?

A

Clopidogrel. Antiplatelet agent to that inhibits ADP receptor.

132
Q

Why is liver not very susceptible to infarction secondary to arterial occlusion?

A

It has a dual supply - hepatic artery and portal vein. Whcih drain via hepatic vein. Also a lot of accessory stuff. However, a transplant liver is susceptible as it does not have all the collateral and has severed connections

133
Q

What are three common drugs used to treat MRSA? Side effects of each?

A

Vanc -blocks polymerization of glycopeptide - 1 red manm, neprhotoxDaptomycin - myopathy, CPK elevation, inactivated by pulmonary surfactant.Linezolid - inbhits bacterial protein synth at 50s - thrombocytopenia, optic neuritis, risk for serotonin syndrome

134
Q

What can trgiger prinzmetal vasospams (aids diagnosis). How do you treat Prinzmenta?

A

Ergonovine can trigger it. (constricts vascular smooth muscle by stimulating alpha adrenergic and serotonergic receptors). Tx w/ vasodilating nitrates and Calcium channel blockers.

135
Q

What congenital heart findings is considered a normal variant?

A

Patent formaen ovale (20-30% of normal adults) patent! Suspect in DVT + stroke pt.

136
Q

What drugs put you at risk for ttorsades?

A

TCA antidepressants, phenothiazine, antiarrhythmics - esp those that INC QT interval aka Class 3 K blockers and Class1A drugs (quinidine, procainamide, disopyramide, ibutilide, dofetilide, SOTALOL)

137
Q

What agents better allow Staph A to cause bacterial endocarditis?

A

Coagulase + , forms fibrin clot around self.

138
Q

Name congenital long QT syndrome. What are the mutations in congenital long QT sndrome. What is a diff in presentation?

A

Both are K channel defects.lRomano Ward - AD - no deafnessJervell Lange Nielsen - AR - deafness

139
Q

Common findings in lightening strike injuries?

A

Superficial burns (dep is rare due to flashover quick duration - discharges to ground) - Lichtenberg figures - erythematous cutaneous marks in fern leaf pattern - Death via arrhythmias is most common. 25% fatal after stroke.

USMLE (16 decks)

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