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Step 1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Right dominant configuration of the heart

A

SA and AV nodes supplied by RCA. RCA supplies inferior portion of LV via PD artery (most common. In left dominant the PD arises from the CFX)

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2
Q

Fick equation

A

CO = (rate of O2 consumption) / (arterial O2 content - venous O2 content)

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3
Q

What is the pulse pressure proportional to?

A

Stroke Volume

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4
Q

Name a classic venodilator and a classic vasodilator

A

Veno - nitroglycerin, Vaso - hydralazine

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5
Q

How does nitroglycerin help in angina?

A

Venodilation, decreased preload, decreased cardiac work, decreased demand for O2

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6
Q

Normal ejection fraction

A

Greater than or equal to 55 percent

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7
Q

Causes of increased blood viscosity (3)

A

Polycythemia, hyperproteinemic states (eg multiple myeloma), hereditary spherocytosis

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8
Q

Cardiac function curves - give the curve affected (CO or venous return) and direction the intersection moves in each of the following: pos inotropy, neg inotropy, inc blood vol, dec blood vol

A

Positive inotropy - CO, intersection moves up and left. Neg inotropy - CO, intersection moves down and right. Inc BV - venous return, intersection moves up and right. Dec BV - venous return, int moves down and left

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9
Q

On a cardiac cycle graph, the slope of what curve gives contractility?

A

A line from the origin to the top left portion (where aortic valve closes) of the curve

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10
Q

What causes an S3

A

Increased filling pressure (e.g. MR, CHF) and dilated ventricles. Normal in children and preggers

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11
Q

What causes an S4?

A

High atrial pressure. Due to ventricular hypertrophy and stiffness

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12
Q

What is going on in the right heart during each of the following: a wave, c wave, x descent, v wave, y descent

A

A wave - atrial contraction, c wave - RV contraction, x descent - atrial relaxation, v wave - RA filling, y descent - blood flow from RA to RV

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13
Q

What disorders lead to wide splitting of A2 and P2?

A

Pulmonic stenosis, RBBB

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14
Q

What condition leads to fixed splitting

A

ASD

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15
Q

What conditions lead to paradoxical splitting?

A

Aortic stenosis, LBBB

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16
Q

What kind of murmurs can be heard in an ASD?

A

Pulmonary flow murmur (inc flow through pul valve), and diastolic rumble (inc flow across tricuspid)

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17
Q

Between inspiration and expiration, which increases right heart findings and which increases left?

A

Inspiration increases right heart sounds, expiration increases left

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18
Q

What murmurs are louder on hand grip?

A

MR and VSD

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19
Q

What murmurs are louder on valsalva (decreased venous return)

A

MVP, HOCM. (most murmurs are quieter on valsalva)

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20
Q

Pulse associated with AS

A

Parvus and tardus

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21
Q

Murmur associated with VSD

A

Holosystolic, harsh sounding. Loudest at tricuspid area

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22
Q

Two common causes of PDA

A

Congenital rubella and prematurity

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23
Q

Give the main ions flowing across the cardiac ventricular muscle membrane during each of the phases of the cycle

A

Phase 0 - Na, Phase 1 - K starts, Na stops, Phase 2 - Ca, K, Phase 3 - K, Phase 4 - K

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24
Q

Why do CCBs work on heart but not on skeletal muscle?

A

Skeletal muscle has no dependence on extracellular calcium during an action potential (due to sarcoplasmic stores) unlike cardiac muscle

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25
Q

What causes rapid calcium decrease immediately before relaxation in cardiac muscle cells?

A

Na/Ca exchanger

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26
Q

Give the ions traversing the cardiac pacemaker cell membrane during each phase of the cardiac cycle

A

Phase 4 - Na (funny current, If), Phase 0 - Ca, Phase 1 and 2 absent, Phase 3 - K

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27
Q

What property of heart cell action potentials determines heart rate in normal individuals?

A

The slope of Phase 4 in SA nodal cells

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28
Q

How does symphathetic stimulation affect the AP in heart cells?

A

Increases the chance that If channels are open in pacemaker cells

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29
Q

Normal length of PR interval, QRS complex, and AV node delay

A

PR - less than 200 ms, QRS - less than 120 ms, AV node delay - around 100 ms

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30
Q

Torsades de pointes is related to what EKG abnormality?

A

Long QT

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31
Q

Jervell and Lange-Nielsen syndrome

A

Severe congenital sensorineural deafness and long QT (predisposes to torsades)

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32
Q

Order the following from fastest to slowest conduction: Atrial muscle, AV node, Purkinje system, Vent muscle

A

(fastest) Purkinje, Atrial muscle, Vent muscle, AV node (slowest)

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33
Q

Common precipitants of a-fib

A

Alcohol binge, increased cardiac sympathetic tone, pericarditis

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34
Q

Treatments for a-fib

A

B-blocker, CCB, digoxin. Also give warfarin

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35
Q

Treatment for a-flutter

A

Class Ia, Ic, or III antiarrhythmics or B-blockers

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36
Q

Treatment for third degree heart block

A

Pacemaker

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37
Q

What infectious disease can result in heart block and which type?

A

Lyme, third degree

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38
Q

Release of what may cause normal sodium levels even in hyperaldosterone hypertension?

A

Atrial natriuretic peptide

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39
Q

What effect does ANP have on renal vasculature?

A

Constricts efferent arterioles and dilates afferent arterioles (via cGMP)

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40
Q

Does the aortic arch baroreceptor respond to high pressure, low pressure, or both?

A

High pressure only

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41
Q

Where does the parasympathetic system exert its influence to slow heart rate?

A

By slowing conduction through the AV node

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42
Q

Give the factors that determine autoregulation in the brain and heart respectively

A

Brain - CO2 (via pH), Heart - CO2, adenosine, NO

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43
Q

Congenital right to left shunts (early cyanosis) (5)

A

Tetralogy of Fallot (most common), Transposition of great vessels, Truncus arteriosus, Tricuspid atresia, Total anomalous pulmonary venous return (TAPVR)

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44
Q

What is required for viability in tricuspid atresia?

A

ASD and VSD

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45
Q

Congenital left to right shunts (late cyanosis) (3)

A

VSD (most common), ASD, PDA

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46
Q

What effect does indomethacin have on a PDA?

A

Closes it

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47
Q

Eisenmenger syndrome

A

Reversal of L to R shunt (making it R to L), causing late cynaosis (clubbing and polycthemia)

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48
Q

4 features of tetralogy of Fallot

A

Pulmonary stenosis, RVH, Overiding aorta, VSD

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49
Q

In what congenital condition do patients typically squat to improve symptoms?

A

Tetralogy of Fallot (increased TPR reduces R-to-L shunt)

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50
Q

Where are infantile and adult type coarcations located respectively?

A

Infantile - preductal, Adult - postductal

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51
Q

Describe the cyanosis in each of the following conditions: aortic coarctation, PDA, septal defects and tetralogy of fallot

A

Coarctation - no cyanosis, PDA - late lower extremity cyanosis, Septal Defect and ToF - whole body cyanosis

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52
Q

What should you check first if you suspect aortic coarctation?

A

Upper and lower extremity pulses (upper will be strong, lower will be weak)

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53
Q

Cardiac defects associated with 22q11 syndromes (DiGeorge, velocardiofacial)

A

Truncus arteriosus, tetralogy of fallot

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54
Q

Cardiac defects associated with Down syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

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55
Q

Cardiac defects associated with congenital rubella

A

Septal defects, PDA, pulmonary artery stenosis

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56
Q

Cardiac defects associated with maternal diabetes

A

Transposition of great vessels

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57
Q

List the four signs of hyperlipidemia

A

Atheromas, xanthomas, tendinous xanthomas, and corneal arcus

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58
Q

In patients with visible signs of hyperlipidemia, what should you check for?

A

Cholestasis (eg primary or secondary biliary cirrhosis)

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59
Q

Which form of arteriosclerosis is calcific, where is it most commonly seen, and what is the prognosis.

A

Monckeberg. Radial and ulnar arteries especially. Benign

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60
Q

What are the keywords for arteriolosclerosis in essential hypertension, diabetes, and malignant hypertension respectively

A

Essential HTN and DM - hyaline, Malignant HTN - hyperplastic, onion skinning

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61
Q

In what conditions are fatty streaks seen?

A

EVERYONE over 10 years old

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62
Q

List the steps of atherosclerosis (7) in order

A

Endothelial cell dysfunction, Macrophage and LDL accumulation, Foam cells, Fatty streaks, SM migrational (PDGF and TGF-b), fibrous plaque, complex atheroma

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63
Q

Most common locations of atherosclerosis (in order starting with most common)

A

Abdominal aorta, coronary artery, popliteal artery, carotid artery

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64
Q

What decreases atherosclerotic plaque stability and thus increases chance of rupture

A

Metalloproteinases from macrophages

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65
Q

What are abdominal and thoracic aortic aneurysms respectively associated with?

A

Abdominal - atherosclerosis (men, smokers, over 50), Thoracic - HTN, cystic medial necrosis (Marfan)

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66
Q

What are aortic dissections associated with?

A

HTN and cystic medial necrosis (Marfan). Same risk factors as THORACIC aortic aneurysms

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67
Q

What is the precursor lesion in aortic aneurysm and aortic dissection respectively?

A

Aneurysm - intimal streak (atherosclerosis), Dissection - intimal tear

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68
Q

Where do we typically harvest vessel from for CABG?

A

Great saphenous vein just below the pubic tubercle

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69
Q

Give the pathology associated with each of the following precursor lesions: intimal streak, intimal tear, medial degeneration, medial inflammation, vasa vasorum obliteration

A

Intimal streak - atherosclerosis, intimal tear - aortic dissection, medial degeneration - aortic dissection (eg Marfan), medial inflammation - takayasu, GCA, vasa vasorum obliteration - syphillis

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70
Q

How much narrowing has to occur in coronary arteries to get angina?

A

75 percent or greater

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71
Q

What is seen on EKG with prinzmetals angina?

A

ST elevation (note that ST DEPRESSION is seen in stable and unstable angina)

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72
Q

What kills you in sudden cardiac death?

A

Arrhythmia (usually V-fib)

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73
Q

What prevents or slows the development of pulmonary edema in pts with MR?

A

Increased left atrial compliance (holds more blood in the LA rather than refluxing it to the lungs)

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74
Q

Give the light microscopy findings at various points after an MI

A

0-4 hrs - normal, 4-12 hrs - edema, hemorrhage, wavy fibers, 12-24 hours - contraction bands, neutrophils arrive, 2-4 days - coag necr, neutrophils leave, 5-10 days - neovascularization, gran tissue, 7 weeks - scar

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75
Q

Give the main complications post MI and the time window for each

A

0-4 days - Arrhythmia. 3-5 days - pericarditis and friction rub. 5-10 days - Ruptures (free wall, papillary muscle, IV septum) and tamponade. After 10 days - ventricular aneurysm. Several weeks - Desslers

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76
Q

Which cardiac enzyme peaks first?

A

Troponin

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77
Q

CK-MB is not the first cardiac enzyme to peak (troponin is) and is less specific. What is the value of CK-MB in addition to troponin?

A

CK-MB goes away sooner, so you can use it diagnose reinfarction

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78
Q

What finding would you have in a patient with pulmonary edema post-MI

A

S3 (also crackles from the edema). Its due to LV failure

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79
Q

Which type of cardiomyopathy is most common?

A

Dilated

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80
Q

Which type of dysfunction (systolic or diastolic) is each type of cardiomypoathy associated with?

A

Dilated - systolic, Hypertrophic - diastolic, Restrictive/Obliterative - diastolic

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81
Q

Which cardiomyopathy is concentric hypertrophy and which is eccentric?

A

Dilated - eccentric, Hypertrophic - concentric

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82
Q

Causes of dilated cardiomyopathy (8)

A

ABCCD plus 2. Alcohol, wet Beriberi, Coxsackie B, Cocaine, Chagas, Doxorubicin, hemochromatosis, peripartum cardiomyopathy

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83
Q

What is the most common cause of hypertrophic cardiomyopathy?

A

Familial (AD)

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84
Q

What cardiac problem is associated with Friedreichs ataxia?

A

Hypertrophic cardiomyopathy

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85
Q

Treatment for hypertrophic cardiomyopathy

A

Beta blockers or non-dihydropyridine CCBs (eg verapamil)

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86
Q

Findings in hypertrophic cardiomyopathy

A

Systolic murmur and syncopal episodes

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87
Q

Causes of restrictive cardiomyopathy (6)

A

Sarcoidosis, amyloidosis, postradiation, endocardial fibroelastosis (kids), Lofflers (eosinophils), hemochromatosis (also dilated CM)

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88
Q

What drugs reduce mortality in CHF and what are just used for symptomatic relief?

A

Reduce mortality - ACEi, B-blocker, ARBs, Spironolactone. Symptomatic relief - Thiazides, Loop diuretics, Nitrates

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89
Q

Presentation of bacterial endocarditis

A

Fever, Roths spots (retinal white spots), Oslers nodes (fingers, toes), new Murmur, Janeway lesions (palm or sole), anemia, splinter hemorrhages

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90
Q

Most common causes of acute and subacute bacterial endocarditis respectively

A

Acute - s aureus. Subacute - viridans strep (dental procedures)

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91
Q

Most common causes of nonbacterial endocarditis

A

Malignancy, hypercoagulability, lupus, colon cancer (strep bovis), prosthetic valve (staph epidermis)

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92
Q

Most common agents in tricuspid endocarditis due to IV drug use

A

S aureus, pseudomonas, candida

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93
Q

What organisms cause rheumatic fever?

A

Group A beta hemolytic strep

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94
Q

Early death in rheumatic fever

A

Myocarditis

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95
Q

Early and late valvular lesions of rheumatic fever

A

Early - MVP, late - MS

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96
Q

Aschoff bodies and anitschkow cells

A

Aschoff - Granuloma with giant cells, associated with rheumatic fever, Anitschkow - activated histiocytes also associated with rheumatic fever

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97
Q

What type of hypersensitivity is rheumatic fever

A

Type 2 (antibodies are to M protein)

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98
Q

Presentation of rheumatic fever

A

FEVERSS. Fever, Erythema marginatum, Valvular damage, ESR inc, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, St Vitus dance (chorea)

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99
Q

Pulses paradoxus

A

Associated with cardiac tamponade, asthma, OSAS, pericarditis, and croup. Decreased amplitude in sys BP by 10 or more during inspiration.

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100
Q

Most frequent cardiac tumor in children and what condition its associated with

A

Rhabdomyosarcoma, tuberous sclerosis

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101
Q

Complications of varicose veins

A

Poor wound healing and ulcers. Rarely throws emboli (as opposed to stasis in DEEP veins)

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102
Q

Causes of Raynauds phenomenon (3)

A

Mixed connective tissue disease, SLE, CREST

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103
Q

What vascular condition is associated with a hepatitis and which hepatitis?

A

Hep B with PAN

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104
Q

Fever, weight loss, malaise, headache, abdominal pain, melena, HTN, neurologic dysfunction, cutaneous eruptions

A

PAN

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105
Q

What vessels are typically involved in PAN?

A

Renal and visceral vessels. DOES NOT involve pulmonary arteries

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106
Q

Treatment for PAN

A

Corticosteroids, cyclophosphamide

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107
Q

Fever, lymphadenitis, conjunctivitis, oral mucosa changes, hand-foot erythema, desquamation

A

Kawasaki

108
Q

Treatment for Kawaski

A

IVIG and aspirin

109
Q

What finding is unique to Buergers disease?

A

Hypersensitivity to tobacco extract antigen

110
Q

Give the ANCA associated with each of the following: microscopic polyangiitis, Wegners, Churg-Strauss

A

MP - p-ANCA, Wegener - c-ANCA, Churg-Strauss - p-ANCA

111
Q

What is found in the kidney with Wegeners?

A

Necrotizing (crescentic) glomerulonephritis

112
Q

Treatment for Wegeners

A

Cyclophosphamide, corticosteroids

113
Q

Microscopy of Churg-Strauss

A

Granulomatous vasculitis with eosinophilia

114
Q

Asthma, sinusitis, palpable purpura, peripheral neuropathy

A

Churg-Strauss (may also involve heart, GI, kidneys)

115
Q

What does Henoch-Schonlein purpura typically follow?

A

Upper Respiratory Tract Infection

116
Q

What type of immune complexes are seen in Henoch-Schonlein purpura?

A

IgA immune complexes

117
Q

Palpable purpura of buttocks and legs, arthralgia, abdominal pain, melena

A

Henoch-Schonlein

118
Q

What is an important difference between the lesions of PAN and Henoch-Schonlein

A

PAN the lesions are of different ages, Henoch-Schonlein they are all the same age

119
Q

What size blood vessels are affected by Sturge-Weber

A

Capillary size

120
Q

Findings with Sturge-Weber other than port-wine stain

A

Ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early onset glaucoma

121
Q

Best way to differentiate a strawberry from a cherry hemangioma

A

Strawberry in little kids (also they regress), Cherry in elderly (also they do not regress)

122
Q

What are pyogenic granulomas associated with and what is the main complication?

A

Can ulcerate and bleed. Associated with trauma and preggers

123
Q

What are cystic hygromas associated with, where are they found, and what do they look like on microscopy?

A

Associated with Turner. Found in neck. Appear as cystic spaces with connective tissue and lymph aggregates (they are cavernous lymphangiomas)

124
Q

Where are glomus tumors found, what do they arise from, and what is the prognosis?

A

They are red-blue tumors under the fingernails, arising from smooth muscle cells of the glomus body. They are benign

125
Q

What does a bacillary angiomatosis look like, what causes it, and what patients get them? What is the prognosis?

A

Look like Kaposi. Found in AIDS pts. Caused by bartonella henselae. Benign.

126
Q

Where are angiosarcomas found, what causes them, what is their marker, and what is the prognosis?

A

Liver, vinyl chloride, arsenic, and thorotrast exposure, CD31 (endothelial marker), and they are highly lethal malignant

127
Q

What are lymphangiosarcomas associated with?

A

Lymphedema (eg post-radical mastectomy)

128
Q

Causal agent of Kaposi sarcoma

A

HHV-8

129
Q

Hydralazine

A

Directly relaxes SM cells via increased cGMP. Vasodilates arterioles more than veins. Use in HTN, CHF (esp in pregnancy). AE - compensatory tachycardia, lupus like syndrome

130
Q

What is the first line treatment for isolated systolic hypertension?

A

Thiazides and calcium channel blockers

131
Q

Calcium channel blockers (4)

A

Nifedipine, verapamil, diltiazem, amlodipine

132
Q

Which CCBs work mostly only vascular smooth muscle?

A

(most) Nifedipine, Diltiazem, Verapamil (least)

133
Q

Which CCBs work most on heart muscle?

A

(most) Verapamil, Diltiazem, Nifedipine (least)

134
Q

What agents are used to treat Prinzmetals angina and Raynauds disease?

A

CCBs

135
Q

Nifedipine class

A

CCB (more SM than heart)

136
Q

Verapamil class

A

CCB (more heart than SM)

137
Q

Diltiazem class

A

CCB

138
Q

Amlodipine class

A

CCB

139
Q

Nitroprusside

A

Increases cGMP via NO release. Can cause cyanide toxicity. Decreases preload AND afterload

140
Q

What do you give in a nitroprusside overdose?

A

Sulfur thiosulfate (prevents cyanide toxicity)

141
Q

Fenoldopam

A

Dopamine D1 agonist. Relaxes renal vascular smooth muscle, use in malignant HTN

142
Q

Diazoxide

A

K channel opener (hyperpolarizes vascular SM). Use in malignant HTN. AE - hyperglycemia (reduces insulin release)

143
Q

Malignant HTN drugs (3)

A

Nitroprusside, fenoldopam, diazoxide

144
Q

What drug works essentially the same as nitroglycerin?

A

Isosorbide dinitrate

145
Q

Does nitroglycerine work more on arteries or veins

A

Much more on veins

146
Q

Nitroglycerine is sublingual. If you wanted to give it PO, what would you give instead?

A

Isomononitrate

147
Q

Symptoms of Monday morning disease (on monday morning) and what chemical it is due to.

A

Due to nitroglycerin. Will have tachycardia, hypotension, flushing, headache

148
Q

What should you give when you want to lower BP and raise HR?

A

Nifedipine (causes vasodilation and reflex tachycardia)

149
Q

What is it important for patients to do when taking nitrates

A

Have a nitrate free period every day to avoid developing tolerance

150
Q

Nifedipine and verapamil are both CCBs but are somewhat different. For each, which other class of drugs is it most similar to?

A

Nifedipine is like nitrates, Verapamil is like B-blockers

151
Q

Which beta blockers are contraindicated in angina and why?

A

Pindolol and Acebutolol because they are partial agonists

152
Q

Effects of statins on lipids

A

LDL down, HDL up (a little), TGs down (a little)

153
Q

Side effects of statins

A

Hepatotoxicity (inc LFTs), rhabdomylosis

154
Q

Effects of niacin on blood lipids

A

LDL down, HDL up (quite a bit), TGs down (so all the good things)

155
Q

What is the mechanism of niacin relative to lipids?

A

Inhibits lipolysis in adipose, reduces hepatic VLDL secretion

156
Q

Side effects of niacin

A

Flushing (give aspirin), Hyperglycemia and acanthosis nigricans, Hyperuricemia (hope your patient doesnt have gout)

157
Q

What mediates flushing when niacin is given?

A

Prostaglandins

158
Q

What can you give when administering niacin to reduce pain associated with niacin?

A

Capsaicin (will decrease substance P levels)

159
Q

List the bile acid resins (3)

A

Cholestyramine, Colestipol, Colesevelam

160
Q

Effects of bile acid resins (cholestyramine, colestipol, colesevelam) on blood lipids

A

LDL down, HDL up (slightly), TGs up slightly

161
Q

Mechanism and side effects of bile acid resins (cholestyramine, colestipol, colesevelam)

A

Prevent intestinal reabsorption of bile acids (liver must use cholesterol to make more). SEs - pts hate it, GI discomfort, GALLSTONES.

162
Q

Ezetimibe

A

Cholesterol absorption blocker. Prevents cholesterol reabsorption at small intestine brush border

163
Q

Effects of ezetimibe on blood lipids and side effects of ezetimibe

A

Decreases LDL, does not affect HDL or TGs. Rarely increases LFTs

164
Q

List the fibrates (4)

A

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

165
Q

Effects of fibrates on blood lipids

A

LDL down, HDL up, TGs way down (all the good things)

166
Q

Mechanism of fibrates and side effects

A

Upregulate LPL leading to increased TG clearance. AEs - myositis, hepatoxocity (inc LFTs), cholesterol GALLSTONES

167
Q

Which lipid lowering agents lead to cholesterol gallstones?

A

Niacin and fibrates (also the two that do all the good things)

168
Q

What combination of lipid lower agents gives a high risk of myopathy?

A

Statins and fibrates

169
Q

What enzyme do fibrates inhibit

A

7a-hydroxylase (converts cholesterol to bile acid)

170
Q

What effect does digoxin have on HR and how?

A

Slows it. Positive inotropy stimulates vagus nerve. This slows conduction at AV node and depresses SA node

171
Q

Uses of digoxin

A

CHF and a-fib

172
Q

What increases digoxin toxicity?

A

Renal failure, hypokalemia, quinidine

173
Q

Digoxin non-EKG toxicity

A

Blurry yellow vision, cholinergic effects (n/v/d)

174
Q

Digoxin EKG toxicity

A

Increased PR, short QT, scooping, T-wave inversion, arrhythmias, hyperkalemia

175
Q

Antidote for digoxin

A

Lidocaine, anti-dig Fab, Mg, normal K, cardiac pacing

176
Q

Nesiritide

A

Recombinant B-type natriuretic peptide (increases cGMP and vasodilates). Acute decompensated heart failure. AE - hypotension

177
Q

Give the mechanism of each class of antiarrhytmic

A

1 - Na channel blockers, 2 - B blockers, 3 - K channel blockers, 4 - Ca channel blockers

178
Q

List the class Ia antiarrhythmics

A

Quinidine, Procainamide, Disopyramide

179
Q

Class Ic antiarrhythmics

A

Flecainide, propafenone, moricizine

180
Q

What effect does each of the Class I subclasses have on AP duration?

A

Ia - longer, Ib - shorter, Ic - no effect

181
Q

What is the mnemonic for class I antiarrhythmics?

A

Double Quarter Pounder. Lettuce Tomato Mayo. More Fries Please

182
Q

Which antiarrythmics increase the risk of TdP?

A

Class Ia, and Sotalol (III)

183
Q

Brief summary of the uses of class I antiarrhythmics

A

Ia - Reentrant and ectopic rhythms, Ib - Ventricular arrhytmias post-MI and digitalis toxicity arrhythmias, Ic - last resort in tachyarrhythmias

184
Q

What increases the toxicity of all class I antiarrhythmic drugs?

A

Hyperkalemia

185
Q

Class II antiarrhytmics

A

Beta blockers. Propanolol, esmolol, metoprolol, atenolol, timolol

186
Q

What part of the EKG do beta blockers (class II antiarrhythmics) affect primarily?

A

P wave and PR interval

187
Q

Uses of Class II antiarrhythmics

A

V-tach, SVT, slowing ventricular rate in a-fib and a-flutter

188
Q

What do you treat overdose of Class II antiarrhythmics (b-blockers) with?

A

Glucagon

189
Q

What class of antiarrhythmics may mask signs of hypoglycemia?

A

Class II (Beta blockers)

190
Q

Class III antiarrhythmics

A

K blockers. Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide

191
Q

What drug increases the QT interval but does not increase risk of TdP?

A

Amiodarone

192
Q

Effects of class III antiarrhytmics on EKG

A

Incrased AP duration, Increased ERP, increased QT interval

193
Q

What do you need to check when using amiodarone?

A

PFTs, LFTs, and TFTs

194
Q

Amiodarone toxicities

A

Pulmonary fibrosis, hepatotoxicity, hypo or hyper thyroidism, corneal deposits, skin deposits (blue or gray), photodermatitis, neurologic effects, constipation, CV effects

195
Q

Amiodarone

A

A class III antiarrhythmic that has class 1, 2, 3 and 4 effects because it alters the lipid membrane

196
Q

Class IV antiarrhythmics

A

Ca channel blockers. Verapamil and diltiazem

197
Q

EKG effects of class IV antiarrhythmics

A

Increased ERP, Increased PR interval, decreased conduction velocity

198
Q

What is the main use of Class IV antiarrhythmics?

A

Nodal arrhythmias (eg SVT)

199
Q

What is the drug of choice in SVT?

A

Adenosine (for diagnosing or treating)

200
Q

What blocks the effects of adenosine?

A

Theophylline

201
Q

What arrhythmias is magnesium used to treat?

A

Torsades de pointes and digoxin toxicity

202
Q

Why is the most common site of aortic aneurysm below the renal arteries?

A

Because in this section there is no vasa vasorum on the aorta

203
Q

Signs and symptoms of abdominal aortic aneurysm

A

Severe left flank pain, hypotension, pulsatile mass

204
Q

Most common cause of aneurysm in the arch of the aorta

A

Tertiary syphilis

205
Q

Water hammer pulse

A

AR

206
Q

Absent pulse on the left

A

Dissecting aneurysm of the aortic arch (has closed off the lumen of the subclavian)

207
Q

Test of choice for a dissecting aortic aneurysm

A

Chest x-ray (look for widening of the proximal aortic knob)

208
Q

Conditions predisposing to aortic dissection (3)

A

Marfan, Ehlers Danlos, Pregnancy

209
Q

What are spider angiomas usually due to?

A

Hyperestrogenism

210
Q

Typically what type of hypersensitivity is involved in all small vessel vasculitis?

A

Type 3

211
Q

How can you tell polymyalgia rheumatic (eg with GCA) apart from polymyositis?

A

No elevation of serum CK in polymyalgia rheumatic (but will have aches and pains in muscles and joints)

212
Q

A cause of saddle nose besides congenital syphillis

A

Wegners granulomatosis

213
Q

What infection includes a rash that starts on the extremities and goes to the trunk?

A

Rocky Mountain Spotted Fever

214
Q

CREST syndrome

A

Calcinosis (also Centromere Ab), Raynauds, Esophageal dysmotility, Sclerodactyly, Telangiectasia

215
Q

What class of drugs can cause Raynauds?

A

Ergot derivatives

216
Q

In the case of what heart murmur should you get an immediate surgical consult?

A

Austin flint murmur. The AR has gotten so bad that the valve needs to be replaced fairly soon

217
Q

What is paroxysmal nocturnal dyspnea a sign of?

A

Left heart failure

218
Q

Best nonpharmacologic treatment for heart failure

A

Restrict water and salt

219
Q

Why are ACE inhibitors the treatment of choice in CHF

A

They decrease preload (decreased sodium reabsorption) and afterload (vasodilation)

220
Q

How does thiamine deficiency lead to high output heart failure?

A

ATP depletion causes vascular smooth muscle to fail and dilate, causing your BP to tank

221
Q

What impact does chronic hyperthyroidism have on the heart?

A

Increases synthesis of beta receptors, leading to increased force of contraction (high systolic pressure, high output heart failure eventually)

222
Q

Brenhams sign

A

Heart rate slows when you press on the proximal part of an AV fistula

223
Q

What vessels in the fetus have the highest and lowest O2 concentration respectively?

A

Highest - umbilical vein, Lowest - umbilical arteries (2)

224
Q

Most common cause of a congenital ASD?

A

Fetal Alcohol Syndrome

225
Q

Where is the murmur of a PDA heard best?

A

Between the shoulder blades

226
Q

What is the most common cause of PDA?

A

Congenital rubella

227
Q

Why are the junctions of the communicating arteries and main cerebral arteries common points for aneurysms (berry aneurysm)?

A

Because there is no internal elastic lamina or smooth muscle there

228
Q

2 main ways to get around an aortic obstruction (such as a coarctation)

A

1) Superficial epigastric artery with internal mammary artery. 2) Intercostals (which is why you have notching of the ribs in coarctation)

229
Q

CAD risk factors

A

Age (most important), Family History, Cigarette Smoking, HTN, Diabetes, LDL, HDL (negative risk factor)

230
Q

Is tPA more effective on arterial or venous clots and why?

A

Arterial, they have less fibrin than venous clots

231
Q

Thrombosis of what artery can cause MR?

A

RCA. It supplies the papillary muscles of the mitral valve

232
Q

What type of an MI can present with epigastric pain?

A

An RCA MI

233
Q

What type of MI is the most common antecedent to IV septum rupture?

A

LAD MI

234
Q

If the patient had an LAD MI, what do you need to be sure to give to prevent a particular complication?

A

Warfarin or Heparin to prevent a mural thrombus from forming (most common after an LAD MI)

235
Q

How would a post MI ventricular aneurysm present?

A

Massive pectoralis major which bulges with the pulse

236
Q

What is the most common cause of death in ventricular aneurysm?

A

Heart failure (they generally do not rupture)

237
Q

What is the best predictor of survival at time of discharge from an MI?

A

Ejection fraction

238
Q

Reinfarction is defined by CK-MB that is still elevated after how long?

A

3 days

239
Q

What is seen with LDH in MI?

A

LDH1 becomes higher than LDH2 (called the flip)

240
Q

What is the pathology of MVP?

A

Myxomatous degeneration

241
Q

What GAG makes up the mitral valve?

A

Dermatan sulfate. Too much of it becomes redundant and you get MVP

242
Q

Which way do the murmur and click in MVP move when you increase and decrease preload respectively?

A

Increased preload - moves towards S2 (takes longer for all blood to get out), Decreased preload - moves towards S1

243
Q

Does the murmur of MVP move closer to S1 or S2 when one is anxious?

A

Closer to S1 (ventricles have less time to fill due to higher HR)

244
Q

In AS and HOCM respectively, does increased blood volume in the LV increase or decrease the intensity of the murmur?

A

AS - increases it, HOCM - decreases it

245
Q

Most common symptom in rheumatic fever

A

Polyarthritis

246
Q

Differential for polyarthritis

A

Juvenile rheumatic arthritis, Henoch Schonlein, rubella, rheumatic fever

247
Q

2 genetic diseases associated with MVP

A

Marfans and Ehler Danlos

248
Q

Most common cause of sudden death in the Marfan

A

MVP and conduction defect

249
Q

Valvular lesions associated with carcinoid syndrome

A

Tricuspid insufficiency and pulmonic stenosis (TIPS)

250
Q

Top two most common causes of infective endocarditis

A

1) Strep viridians, 2) Staph

251
Q

What defect predisposes patients to getting infective endocarditis on the aortic valve?

A

VSD (because membranous portion of septum is right next to the valve)

252
Q

What actually causes the visible findings in infective endocarditis (splinter hemorrhages, oslers nodes, janeway lesions, roth spots, and glomerulonephritis)?

A

Type 3 hypersensitivity (immune complex vasculitis)

253
Q

Most common lesion of the heart in lupus

A

Pericarditis. Libman-Sacks endocarditis is associated with SLE but is less common

254
Q

Most common cause of myocarditis and pericarditis

A

Coxsackie virus

255
Q

Most common cause of viral menigitis

A

Coxsackie virus

256
Q

Cause of hand, foot, and mouth disease

A

Coxsackie virus

257
Q

Cause of herpangina (painful mouth blisters)

A

Coxsackie

258
Q

What is contraindicated in HOCM?

A

Digitalis (as are all positive inotropic agents)

259
Q

Treatment for HOCM

A

Beta blocker, Ca channel blocker

260
Q

Most common cause of restrictive cardiomyopathy in children

A

Endocardial fibroelastosis

261
Q

What heart defect does Pompes disease cause?

A

Restrictive cardiomyopathy (as does Fe overload, and amyloidosis)

262
Q

First step in management of a suspected pericardial effusion

A

Echocardiogram (then call the surgeon to do a pericardiocentesis)

263
Q

Most common cause of pericardial effusion

A

Pericarditis (the most common cause of which is Coxsackie)

264
Q

Most common cause of constrictive pericarditis

A

Worldwide - TB, US - previous cardiac surgery

265
Q

Auscultatory finding in constrictive pericarditis

A

Pericardial knock (important because no knock present in pericardial effusion)

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