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Internal Medicine EOR > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is stable angina?

A

predictable, relieved by rest and/or nitroglycerine

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2
Q

What is unstable angina?

A

previously stable and predictable symptoms of angina that are more frequent, increasing or present at rest

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3
Q

What is prinzmetal variant angina?

A

coronary artery vasospasms causing transient ST-segment elevations, not associated with clot

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4
Q

What are premature beats?

A
  • PVC: early wide bizarre QRS, no p wave seen
  • PAC: abnormally shaped P wave
  • PJC: narrow QRS complex, no p wave or inverted p wave
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5
Q

What is paroxysmal supraventricular tachycardia?

A

narrow, complex tachycardia, no discernible P waves

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6
Q

What is a-fib?

A

irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P wavws

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7
Q

What is a-flutter?

A

regular, sawtooth pattern, and narrow QRS complex

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8
Q

What is sick sinus syndrome?

A
  • Brady-tachy: arrhythmia in which bradycardia alternates with tachycardia
  • Sinus arrest: prolonged absence of sinus node activity (absent P waves) > 3 seconds
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9
Q

What is sinus arrhythmia?

A

normal, minimal variations in SA node’s pacing rate in association with the phases of respiration
-heart rate frequently increases with inspiration, decreased with expiration

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10
Q

What is premature ventricular contractions (PVCs)?

A

early wide “bizarre” QRS, no p wave seen

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11
Q

What is ventricular tachycardia?

A

three or more consecutive VPBs, displaying a broad QRS complex tachyarrhythmia

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12
Q

What is ventricular fibrillation?

A

erratic rhythm with no discernable waves (P, QRS, or T waves)

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13
Q

What is torsades de pointes?

A

polymorphic ventricular tachycardia that appears to be twisting around a baseline

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14
Q

What is dilated cardiomyopathy?

A

MC type; an index event or process (MI) damages myocardium, wakening heart muscle a decreased ventricular contraction strength + dilation left ventricle; systolic heart failure

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15
Q

What are the characteristics of dilated cardiomyopathy?

A
  • reduced contraction strength; large heart; caused by ischemia (CAD, MI, arrhythmia)
  • PE: dyspnea, S3 gallop, rales, JVD
  • Tx: no alcohol!!!; ACE-I, diuretic
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16
Q

What is hypertrophic obstructive (HOCM)?

A

hypertrophic portion of septum; LV outflow tract narrowed - worse with
-diastolic heart failure
-young athletes with positive family history sudden death of syncopal episode; inherited; SCREEN FAMILY
-

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17
Q

What is the PE of HOCM?

A

sustained PMI, bifid pulse, S4 gallop; high pitched mid-systolic murmur at LLSB increased with Valsalva and standing (less blood in the chamber); decreased with squatting

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18
Q

What is the tx of HOCM?

A

refrain from physical activity; BB or CCB; surgical or alcohol ablation of hypertrophied septum and defibrillator insertion

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19
Q

What is restrictive cardiomyopathy?

A

right heart failure; a history of infiltrative process; diastolic heart failure; still heart muscle
amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, cancer

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20
Q

What is the PE of restrictive cardiomyopathy?

A

pulmonary HTN; normal EF, normal heart size, large atria, normal LV wall, early diastolic filling

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21
Q

What is the tx of restrictive cardiomyopathy?

A

non-specific; diuretics, ACE-I, CCB

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22
Q

What are the MC cause of congestive heart failure?

A

CAD, HTN, MI, DM - LV remodeling = dilation, thinning, mitral valve incompetence, RV remodeling

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23
Q

What are the sx and signs of congestive heart failure?

A

sx: exertional dyspnea = rest, chronic nonproductive cough, fatigue, orthopnea, nocturnal dyspnea, nocturia
signs: Cheyne-stokes breathing, edema, rales, S4 (diastolic HF, preserved EF); S3 (systolic; reduced EF); JVC >8 cm, cyanosis, hepatomegaly, jaundice

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24
Q

What is the NY heart failure classification?

A
  • Class 1: no limitation of physical activity
  • Class 2: slight limitation physical activity; comfortable at rest
  • Class 3: marked physical limitation; comfortable at rest
  • Class 4: can’t carry on physical activity; anginal syndrome at rest
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25
Q

How is congestive heart failure dx?

A

BNP, EKG, CXR (Kerley B lines); echo = gold (best to assess size and function of chambers)

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26
Q

What is the tx of congestive heart failure?

A
  • Systolic: ACE-I + B-blocker + loop diuretic

- Diastolic: ACE-I + B-blocker or CCB

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27
Q

What is coronary vascular disease?

A

CAD is #1 killer in the USA and worldwide = Death rates decreased yearly since 1968 = MC cause of cardiovascular death and disability
-coronary artery disease can be due to either vasospastic disease (Prinzmetal angina) or atherosclerotic disease when a coronary artery narrows due to the build-up of atherosclerotic plaque - characterized by a type of chest pain called angina pectoris - it can be further divided into stable angina, unstable angina, and myocardial infarction

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28
Q

What are the risk factors of coronary vascular disease?

A

smoking, diabetes, dyslipidemia (increase LDL, decease HDL), hypertension, family hx, men >55, women >65

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29
Q

How is coronary vascular disease dx?

A

high-sensitivity, high CRP, lipids, triglycerides, carotid U/S

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30
Q

What is the tx of coronary vascular disease?

A

smoking cessation, lifestyle (BP, LDL/HDL, obesity)

  • primary prevention = platelet inhibitors (aspirin, etc.) = cornerstone
  • secondary prevention = aspirin, Beta-blockers, ACE-I/ARB, statins; nitro if symptomatic
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31
Q

What is the MOA of atherosclerotic disease?

A
  • foam cells are macrophages that gobble up lipids in the wall; it then dies off and stays there and becomes a foam cell; when it dies it releases cytokines that attract more macrophages to the area = plaque clot
  • fibrous plaque forms over lipid core: complete clot - ST -elevation MI; incomplete clot - unstable angina/NSTEMI
  • vulnerable plaque is easy to rupture; thick plaque is stable
  • adhesion, activation, aggregation, propagation of clot, platelet adherence
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32
Q

What is endocarditis?

A

inflammation of the lining or valves of the heart caused by the presence of bacteria in the bloodstream, typically introduced via dental or medical procedures in the mouth, intestinal tract or urinary tract

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33
Q

What are the characteristics of endocarditis?

A

fever and a new-onset heart murmur

  • acute bacterial endocarditis: infection of normal valves with a virulent organism (S. aureus)
  • subacute bacterial endocarditis: indolent infection of abnormal valves with less virulent organisms (S. viridans)
  • Endocarditis with intravenous drug users - staphylococcus aureus
  • Endocarditis with prosthetic valve - staphylococcus epidermidis
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34
Q

What is Duke’s Criteria?

A

-Definite: 2 major criteria, or 1 major and 3 minor criteria, or 5 minor criteria
-Possible: 1 major and 1 minor criterion, or 3 minor criteria
Major:
-Blood cultures: S. aureus, S. viridans, S. bovis or other typical species x 2, 12 hours apart
-drug users: staphylococcus, non-drug users: streptococcus
-echocardiogram: vegetations are seen (tricuspid-IV drug users, mitral-non drug users)
-New regurgitant murmur
Minor:
-Risk factors, fever 100.5, vascular phenomena (splinter hemorrhages, Janeway lesions: painless, palms and soles), immunologic phenomena (Osler node: raised painful tender; Roth spots: exudative lesions on the retina)

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35
Q

What are the classic signs of infective endocarditis?

A
  • Osler’s nodes - tender “ouchy” nodules
  • Janeway lesions - painless macules
  • Roth spots on the retina
  • Splinter hemorrhages on the nail bed
  • Clubbing
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36
Q

What is the tx of endocarditis?

A
  • empiric treatment: IV vancomycin or ampicillin/sulbactam PLUS aminoglycoside
  • Prosthetic valve: add rifampin
  • high-risk patients prophylaxis for procedures: Amoxicillin - 2 g 30-60 minutes before the procedures
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37
Q

What is aortic stenosis?

A

harsh systolic ejection crescendo-decrescendo at the right upper sternal border with radiation to neck and apex

  • dyspnea, angina, syncope with exertion; squatting increases intensity; split S2
  • increased BNP, helmet cells (schistocytes); cardiomegaly
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38
Q

What is aortic regurgitation?

A

soft high pitched, blowing, crescendo-decrescendo along left sternal border; loud leaning forward/squatting

  • leaflets of aorta don’t close during diastole - blood regurgitates from the aorta into left ventricle - volume overload left ventricle
  • S3 or S4 with severe; water-hammer pulse (arterial pulse large and bounding)
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39
Q

What is mitral stenosis?

A

diastolic low pitched decrescendo rumbling with an opening snap heart best at the apex with pt. lying lateral decubitus position

  • leaflets of the mitral valve thicken, stiffen from rheumatic fever - valve doesn’t open well in diastolic; cause = rheumatic heart
  • left atrial hypertrophy, may also have mitral regurge
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40
Q

What is mitral regurgitation?

A

blowing holosystolic murmur at the apex with split S2 radiating to the left axilla

  • mitral valve doesn’t close fully in systole - blood regurge from LV to LA - murmur
  • caused by: CAD, HTN, MVP, rheumatic, heart valve infection; apical S3 = volume overload on the ventricle
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41
Q

What is mitral valve prolapse?

A

midsystolic ejection click heard best at the apex

-abnormal systolic ballooning in part of the mitral valve into the left atrium

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42
Q

What is tricuspid stenosis?

A

mid-diastolic rumbling murmur at LLSB with opening snap
-RARE! Leaflets of tricuspid valve = stiff/immobile - impaired RV filling from decreased tricuspid valve orifice = increased RA pressure - right and left heart failure

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43
Q

What is tricuspid regurgitation?

A

high pitched holosystolic murmur at LLSB radiates to the sternum and increases with inspiration
-tricuspid fails to close fully in systole, blood regurgitates from RV - RA = murmur

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44
Q

What is pulmonary stenosis?

A

harsh, loud, medium pitched systolic murmur heard best at 2nd/3rd left intercostal space that may increase inspiration

  • stenosis of pulmonic valve impairs flow across the valve; increases afterload on the ventricle
  • widely split S2, early pulmonic ejection sound; RVH
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45
Q

What is pulmonary regurgitation?

A

high pitched early diastolic decrescendo murmur at LUSB that increases with inspiration
-blood leaks abnormally backward from pulmonary artery though pulmonic valve - RV (RHF)

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46
Q

What are the screening guidelines for hyperlipidemia?

A
  • USPSTF recommends screening for patients with NO evidence of CVD and NO other risk factors should begin at 35 years of age
  • NCEP recommends screening all adults at age 20 years regardless of risk factors
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47
Q

What are the four groups that are most likely to benefit from statin therapy?

A
  • Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)
  • patients with primary LDL-C levels of 190 mg per dL or greater
  • patients WITH diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL
  • patients WITHOUT diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk >7.5%

Risk assessment for 10-year and lifetime risk is recommended using an updated ASCVD risk calculator

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48
Q

What are the treatment targets of hyperlipidemia?

A

there are no recommendations for or against specific target levels for LDL-C or non-HDL-C in the primary or secondary prevention of ASCVD

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49
Q

What are the lipid goals of LDL?

A

<100 optimal

  • 100-129 near-optimal
  • 130-159 borderline high
  • 160-189 high
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50
Q

What is the total lipid goal?

A

<200 desirable
-200-239 borderline high
>239 high

51
Q

What are the lipid goals of HDL?

A

> 60 protective
41-59 borderline
<40 at risk

52
Q

What is high intensity statin therapy?

A
  • daily dosage lowers LDL-C by approximately >50% on average
  • Atorvastatin (lipitor), 40 to 80 mg
  • Rosuvastatin (crestor), 20 (40) mg
53
Q

What is moderate intensity statin therapy?

A
  • daily dosage lowers LDL-C by approximately 30 to 50% on average
  • Atorvastatin 10 (20) mg
  • Rosuvastatin (5), 10 mg
  • Simvastatin (Zocor) 20 to 40 mg
  • Pravastatin (Pravachol) 40 (80) mg
  • Lovastatin (Mevacor) 40 mg
  • Fluvastatin XL (Lescol XL), 80mg
  • Fluvastatin 40 mg twice daily
  • Pitavastatin (Livalo) 2 to 4 mg
54
Q

What is the low intensity statin therapy?

A
  • daily dosage lowers LDL-C by <30% average
  • simvastatin, 10 mg
  • pravastatin 10 to 20 mg
  • lovastatin, 20 mg
  • fluvastatin, 20 to 40 mg
  • pitavastatin, 1 mg
55
Q

What is primary hypertension?

A

resting systolic BP >130 or diastolic BP >80 on at least two readings on at least two separate visits with no identifiable cause

56
Q

What is the the ACC/AHA classification of BP?

A
  • normal: <120/80mmHg and <80mmHg
  • elevated: 120-129 mmHg and <80 mmHg
  • Stage 1: 130 to 139 mmHg or 80-89 mmHg
  • Stage 2: >140 mmHg or >90 mmHg

JNC 8 hypertension definitions not address but treatment threshold defined

57
Q

What is normal BP for children between 1 and 13 years of age?

A

both systolic BP (SBP) and diastolic BP (DBP) <90th percentile

58
Q

What is elevated BP for children between 1 and 13 years of age?

A

SBP and/or ABP >90th percentile but <95th percentile, or 120/80 mmHg to <95th percentile (whichever is lower)

59
Q

What is stage 1 hypertension for children between 1 and 13 years of age?

A

SBP and/or DBP >95th percentile to <95th percentile +12 mmHg, or 130/80 to 139/89 mmHg (whichever is lower)

60
Q

What is stage 2 hypertension for children between 1 and 13 years of age?

A

SBP and/or DBP >95th percentile +12 mmHg or >140/90mmHg (whichever is lower)

61
Q

What are ACC/AHA blood pressure targets?

A
  • target blood pressure: <130/80

- targets for patients with comorbidities: <130/80

62
Q

What are JNC 8 treatment targets?

A
  • reduce BP to <140/90 mmHg for everyone <60 including those with a kidney disorder or diabetes
  • reduce BP to <150/90 mmHg for everyone >60
63
Q

What are the treatment guidelines for normal bp for children between 1 and 13 years of age?

A

evaluate yearly and encourage healthy lifestyle changes

64
Q

What are the treatment guidelines for elevated bp for children between 1 and 13 years of age?

A

recommend healthy lifestyle changes and reassess in 3-6 months

65
Q

What are the treatment guidelines for stage 1 hypertension for children between 1 and 13 years of age?

A

assess ten-year risk using the ASCVD risk calculator

  • if risk <10% start healthy lifestyle management and reassess in 3-6 months
  • if risk >10% or CVD, DM, CKD - lifestyle mod + 1 medication - reassess in 1 month
  • if goal met after 1 month - reassess in 3-6 months
  • if goal not met after 1 month, consider different med or titrate
  • continue monthly follow-up until goal achieved
66
Q

What are the treatment guidelines for stage 2 hypertension for children between 1 and 13 years of age?

A

health lifestyle + 2 BP-lowering medications

  • if goal met after 1 month - reassess in 3-6 months
  • if goal not met after 1 month, consider different med or titrate
  • continue monthly follow-up until goal achieved
67
Q

For non-black patients, including those with diabetes what should initial treatment be?

A
  • ACE inhibitor or ARB
  • long-acting calcium channel blockers (most often a diydropyridine such as amlodipine)
  • or a thiazide-like diuretic (chlorthalidone or indapamide)
68
Q

For non-black patients, including those with diabetes what should initial treatment be for stage 2 htn?

A

the recommendation is”

-2 BP-lowering medications of different classes

69
Q

What is the recommendation for initial treatment for black adults?

A

2 or more medications are recommended to achieve a target of less than 130/80 mmHg
-thiazide-type diuretics and/or calcium channel blockers are more effective in black adults at lowering BP alone or in multidrug regimens

70
Q

What are the antihypertensives that are contraindicated or indicated in certain disorders?

A
  • CCB’s for angina pectoris
  • ACEI or ARB for diabetes with proteinuria
  • ACE inhibitors are associated with cough, angioedema and can cause hyperkalemia, they are contraindicated in pregnancy
  • spironolactone can cause hyperkalemia
  • Betablockers contraindicated in Asthma and may cause impotence
  • CCB cause leg edema
  • Verapamil and diltiazem are rate control CCBs
  • alpha-blockers treat HTN and BPH
  • hydralazine may cause lupus-like syndrome and can cause pericarditis
71
Q

What is hypertensive emergency?

A

BP usually >180/120 WITH impending or progressing end-organ damage

72
Q

What is hypertensive urgency?

A

BP usually >180/120 WITHOUT signs of end-organ damage

73
Q

What is malignant HTN?

A

diastolic reading >140 associated with papilledema and either encephalopathy or nephropathy

74
Q

What is the tx for hypertensive emergency?

A

sodium nitroprusside (drug of choice)

75
Q

What is the tx for hypertensive urgency?

A

clonidine (drug of choice)

76
Q

What is the tx for malignant hypertension?

A

hydralazine

77
Q

What is a STEMI?

A

myocardial necrosis with acute STE or q waves; coronary artery completely blocked; full thickness of myocardial wall involved; elevated troponin I, troponin T, CK, CK-MB (serial troponins 3 in 24 hours)

78
Q

What leads is an anterior wall STEMI seen in?

A

STE in leads I, AVL, V2-V6

79
Q

What leads is an inferior wall STEMI seen in?

A

II, III, AFV

80
Q

What leads is a lateral wall STEMI seen in?

A

lateral leads - I, AVL, V4-6 and reciprocal STD in inferior leads

81
Q

What leads is a posterior wall STEMI seen in?

A

ST depression in V1-3

82
Q

What is the tx for STEMI?

A

beta-blocker + NTG + aspirin and plavix + heparin + statins + reperfusion

  • door to balloon time = 90 minutes; thrombolytic therapy in first 3 hours if PCI not available
  • CI fibrinolytic: intracranial hemorrhage, ischemic stroke 3 months, suspected dissection, active bleeding
83
Q

What is a NSTEMI?

A

myocardial necrosis but coronary artery not completely blocked - rise in cardiac markers without STE or q wave

84
Q

What are the labs for a NSTEMI?

A
  • troponin at 2-4 hours, peaks 12-24 hours, lasts 7-10 days
  • CK/CK-MB: appears at 4-6 hours, peaks 12-24 returns normal 48-72 hours
  • Myoglobin: appears at 1-4 hours, peak at 12 hours, returns to baseline within 24 hours
85
Q

What is the tx for NSTEMI?

A

beta-blocker + NTG + aspirin and plavix + heparin + ACE-I + stain +reperfusion (less time-sensitive than STEMI)

86
Q

What is myocarditis?

A

a disease that causes inflammation of the heart muscle (myocardium)

87
Q

What is myocarditis caused by and what are the etiologies?

A
  • myocarditis is usually caused by a viral infection

- etiologies: bacterial, parasitic, cardiotoxin, systemic disorder, radiation, hypersensitivity

88
Q

What are the symptoms of myocarditis?

A

fatigue, fever, chest discomfort, dyspnea, palpitations, tachycardia disproportionate to fever or discomfort
-a severe case can weaken the heart, which can lead to heart failure, abnormal heartbeat, and sudden death

89
Q

How is myocarditis dx?

A

endomyocardial biopsy = gold standard; clinical presentation, cardiovascular MRI; echo = decreased ventricular EF with hypokinesis

90
Q

What is the tx for myocarditis?

A

supportive, heart failure treatment prn, antidysrhythmic prn

91
Q

What are the causes of pericarditis?

A

SLE, uremia, coxsackievirus, TB, RA, neoplasm, drug, radiation, scleroderma, MI, open-heart surgery, radiothearpy

92
Q

What is the MOA of pericarditis?

A

inflammation of pericardial sac; often = pericardial effusion

93
Q

What are the symptoms of pericarditis?

A
  • chest pain that is relieved by sitting and/or leaning forward
  • pericardial friction rub heard best with patient upright and leaning forward
  • Dressler’s syndrome is pericarditis 2-5 days after an acute myocardial infarctions
  • Maneuver: sitting learning forward
  • Position: Erb’s-point (middle left sternal border)
  • Chest Piece: Diaphragm
94
Q

How is pericarditis dx?

A

EKG will demonstrate diffuse, ST-segment elevations in the precordial leads
-echo may show pericardial effusion/tamponade

95
Q

What is the tx for pericarditis?

A

Treat underlying disease

  • NSAIDs 7-14 days; steroids if sx >48 hrs, abx to treat bacterial endocarditis; pericardiocentesis; head at 45 degrees
  • Dressler’s syndrome: pericarditis 2-5 days after acute MI
96
Q

What is peripheral vascular disease?

A

atherosclerotic disease of the lower extremities (and vessels outside the heart and brain)

97
Q

What are the sx of peripheral vascular disease?

A

intermittent claudication = MC presentation; reproducible pain/discomfort in lower extremity brought on by exercise with exercise and relieved with rest; erectile dysfunction

98
Q

What are the symptoms of peripheral vascular disease?

A
  • aortic bifurcation common iliac = buttock, hip ground claudication
  • Leriche syndrome refers to a buildup of plaque in the iliac arteries - claudiction, impotence, decreased femoral pulses
  • femoral artery: thigh/upper calf claudication (MC)
  • popliteal artery: lower calf claudication
  • signs: weak or absent distal pulses, arterial bruits, loss of hair, shiny atrophic skin, pallor with dependent rubor
  • The 6 P’s caused by acute arterial embolism: pain, pulselessness, pallow, paresthesias, poikilothermia (inability to regular temperature), paralysis
99
Q

How is peripheral vascular disease dx?

A

arteriography is the gold standard (clinically only done if revascularization is planned); Doppler ultrasonography; ankle-brachial-index (ABI) <0.9 (normal = 1-1.2)
-a falsely high index may indicate severely hardened, non-compressible leg vessels

100
Q

What is the tx of peripheral vascular disease?

A

risk factor modification: discontinue tobacco, control diabetes, hypertension, hyperlipidemia

  • medications: B-blocker, ACE-I, satins
  • Platelet inhibitors:
  • cilostazol = mainstay of treatment (helpful for intermittent claudication)
  • aspirin
  • clopidogrel (Plavix)
  • Revascularization: Angioplasty - Fem-pop bypass - Endarterectomy
  • Aspirin, cilostazol, rosuvastatin, smoking cessation, structured exercise
101
Q

What is Varicose Veins?

A
  • sx: asymptomatic; aching and fatigue
  • signs: dilated, tortuous veins; greater saphenous = MC; flat, reticular veins; telangiectasia; spider veins
  • Diagnostics: duplex ultrasonography
  • Management: weight loss, control risk factors; graduated compression stockings
  • Interventions: exercise programs, elevation, radiofrequency or laser ablation, compression, sclerotherapy, surgical stripping
102
Q

What is phlebitis?

A
  • sx: superficial = dull pain, erythema; deep = swelling, heat, redness
  • signs: superficial = erythema, tenderness, induration; deep = heat, edema, Homan’s sign (calf pain with foot dorsiflexion)
  • diagnostics: duplex ultrasonogrpahy, venography, D-dimer
  • Management: superficial: bed rest, local heat, elevation, NSAIDs; deep = anticoagulation (prevention is key)
  • Interventions: surgery
103
Q

What is Chronic Venous Insufficiency?

A
  • Symptoms: progressive edema, itching, dull pain, ulcerations
  • Signs: shiny, thin, atrophic skin
  • Severe disease: ulceration (stasis ulcer, dermatitis) - PAINLESS
  • Diagnostics: clinical; duplex ultrasonography
  • Management: prevention, elevation, avoid extended standing or sitting, compression hose
  • Interventions: wet compresses, compression boots or stockings, skin grafting
104
Q

What is rheumatic fever?

A

although rheumatic fever follows a streptococcal throat infection (strep throat), it is NOT an infection

  • rather, it is an inflammatory reaction to the infection
  • rheumatic fever (RF) is caused by an acute inflammatory immune response to Group A Strep with the formation of antistreptolysin antibodies which react with proteins on the synovium, heart muscle and heart valves
105
Q

What is the Modified Jones Criteria?

A

diagnosis of the first episode of acute rheumatic fever is based on the modified Jones criteria: 2 major criteria or 1 major and 2 minor criteria are required, along with evidence of preceding GAS infection

Major:

  • carditis
  • chorea
  • erythema marginatum
  • polyarthritis
  • subcutaneous nodules

Minor:

  • arthralgia
  • elevated ESR or C-reactive protein
  • fever
  • prolonged PR interval on ECG
106
Q

What is the tx for rheumatic fever?

A

aspirin/NSAID, steroid, abx

  • antistreptococcal prophylaxis should be maintained continuously after the initial episode of ARF to prevent recurrences - PENICILLIN G
  • children without carditis should receive prophylaxis for 5 yr up to age 21 (if the patient turns 21 before 5 yr of prophylaxis is completed)
  • children with carditis without evidence of residual heart damage receive prophylaxis for 10 yr
  • children with carditis and evidence of residual heart damage should receive prophylaxis for > 10 yr; many experts recommend that such patients continue prophylaxis indefinitely
107
Q

What is Rheumatic heart disease?

A

a consequence of rheumatic fever characterized by inflammation and scarring of the heart valves

108
Q

what are the etiology of rheumatic heart disease?

A
  • most commonly affects the mitral valve > aortic valve > tricuspid valve
  • at least 1 episode of acute rheumatic fever from group A streptococci
  • molecular mimicry between streptococcal M protein and cardiac proteins
  • cross-reaction of antibodies to streptococcal M protein with self-antigens
  • immune-mediated (type II) hypersensitivity
109
Q

What is rheumatic fever disease characterized by?

A

the disease is characterized by valve regurgitation (early stage), most commonly of the mitral vale and valve stenosis (late stage)

  • the early-stage may last for years and may be asymptomatic
  • the onset of symptoms usually occurs 10-20 years after acute rheumatic fever
110
Q

What are the sx of rheumatic fever disease?

A

palpitations, dyspnea, mitral regurgitation, mitral stenosis, aortic regurgitation, or aortic stenosis

111
Q

How is rheumatic fever disease dx?

A

making the diagnosis: based on clinical presentation and confirmed with echocardiography

  • echocardiography - valvular abnormalities, including regurgitation or stenosis
  • labs: increased anti-streptolysin O (ASO) titers
  • histology: Aschoff bodies (granulomas with giant cells) on heart valves
112
Q

What is the tx of rheumatic fever disease?

A

prophylaxis to prevent recurrence or worsening of rheumatic heart disease

  • all patients with rheumatic heart disease should undergo prophylaxis with penicillin for the specified time period below
  • no evidence of carditis = 5 years or until age 21 (whichever is longer)
  • evidence of carditis without valvular abnormalities = 10 years or until age 21 (whichever is longer)
  • evidence of carditis and valvular abnormalities = 10 years or until age 40 (whichever is longer)
  • Medical
  • penicillins for all patients in need of prophylaxis
  • sulfadizine for all patients in need of prophylaxis if patients are allergic to penicillin
  • Operative
  • valve repair or replacement depending on type and severity of valve pathology
  • surgical repair
  • percutaneous intervention
113
Q

What is a diastolic murmur?

A

almost always mean heart disease

  • early = regurgitative flow through an incompetent valve (usually aortic)
  • rumbling = mild/late diastole suggests stenosis of AV valve (usually mitral)
  • aortic regurgitation: soft, high pitched, blowing diastolic along LSB with pt sitting, leaning forward after exhaling
  • mitral stenosis: diastolic low pitched decrescendo and rumbling with opening snap at apex
  • Pulmonary regurgitation: high pitch, decrescendo murmur at LUSB, increases with inspiration
  • Tricuspid stenosis: mid-diastolic rumbling at LLSB with opening snap
114
Q

What are midsystolic murmurs?

A

aka ejection murmurs; MC kind of heart murmur; peak near mid systole and stop before S2; gap between murmur and S2

  • pathologic - secondary to structural cardiovascular abnormalities
  • physiologic - secondary to physiologic alteration in body
  • innocent - not associated with detectible physiologic/structural abnormality
  • aortic stenosis: systolic ejection crescendo-decrescendo RUSB
  • pulmonic stenosis: hard midsystolic ejection crescendo-decrescendo murmur with widely split S2 at LSB that radiates to left shoulder and neck
  • HCOM: medium-pitched, mid-systolic murmur that decreases with squatting and increases with straining
  • S4 gallop and apical lift with a thick, stiff left ventricle
  • Mitral valve prolapse: midsystolic ejection click at the apex
115
Q

What are pansystolic (holosystolic) murmurs?

A

pathologic; heard when blood flows from high to low-pressure chamber; begins immediately with S1 and continues up to S2

  • mitral regurgitation: blowing holosystolic murmur at the apex with a split S2
  • Tricuspid regurgitation: high pitched holosystolic murmur at mid-LSB
  • ventricular septal defect: harsh holosystolic murmur heard at LSB with wide radiation and fixed, split S2
116
Q

What is an aortic aneurysm?

A

flank pain, hypotension, pulsatile abdominal mass; screen if male >65 and hx of smoking
-tx: immediate surgical repair if >5.5 cm or expands >0.5 cm per year; monitor annual if >3cm, q6mo >4 cm; beta-blocker

117
Q

What is an aortic dissection?

A

sudden onset tearing chest pain between scapula; diminished pulses; widened mediatstinum; unequal blood pressures on the arm
-tx: ascending aorta = surgical emergency; descending: beta-blocker

118
Q

What is an arterial embolism/thrombosis?

A

sudden arterial occlusion

  • pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia
  • angiography = gold standard
  • Tx: IV heparin if not limb-threatening call vascular surgeon for angioplasty, graft or endarterectomy
119
Q

What is giant cell arteritis?

A

inflammation of large and medium vessels - jaw claudication and HA, thickened temporal artery scalp pain elicited by touching scalp/hairbrush; acute vision disturbances; associated with polymyalgia rheumatica

  • amaurosis fugax (temporary monocular blindness) secondary to anterior ischemic optic neuritis
  • dx: ESR >100, temporal artery biopsy
  • Tx: high dose prednisone URGENTLY - don’t wait for biopsy results
120
Q

What is peripheral artery disease?

A

intermittent claudication, ABI <0.9

  • s/s: lower extremity hair loss, brittle nails, pallor, cyanosis, hypothermia, ulcers pale to black, PAINFUL, lateral/distal
  • arteriography = gold standard
  • tx: definitive = arterial bypass; medical; antiplatelet, anti-lipid, manage r/f, cilostazol, aspirin, plavix
121
Q

What is phlebitis/thrombophlebitis?

A

spontaneous/after trauma or IV/PICC lines - dull pain, erythema, induration of vein, palpable cord

  • dx: duplex U/S = gold standard
  • tx: symptomatic: NSAIDs, warm compress
122
Q

What is varicose veins?

A

dilated tortuous superficial veins, venous stasis ulcers, ankle edema, LE pain after sitting/standing
-tx: leg elevation, compression stockings, vein stripping

123
Q

What is venous insufficiency?

A

edema, atrophic shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, ulcers above the medial malleolus

  • dx: ABI, Trendelenburg tests, U/S
  • tx: sclerotherapy, vein strippling, compression hose
124
Q

What is venous thrombosis?

A

unilateral (asymmetrical) swelling of lower extremity

  • Virchow’s triad: stasis, trauma, hypercoagulability (OCP, cancer, surgery, factor V Leiden)
  • dx: d-dimer, venous duplex U/S = 1st line; venography = gold standard; Homan sign = discomfort behind knee on forced foot dorsiflexion
  • tx: heparin to coumadin bridge

Internal Medicine EOR (10 decks)

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