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IM EOR > Cardiology -- 20% of EOR > Flashcards

Cardiology -- 20% of EOR Flashcards

1
Q

Drugs used in the management of angina

A

ABC + nitro:

  • ASA
  • B-blocker (metoprolol, atenolol)
    - -> CCB only if BB CIx or if Prinzmetal angina
  • Cholesterol: statin

+ nitro PRN

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2
Q

What drugs lower mortality in CAD?

A

ASA and BB

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3
Q

When is CABG indicated for CAD?

A
  • L main artery stenosis
  • 3 vessel dz in diabetic patient
  • LV HFrEF <40%
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4
Q

Why is ASA used in patients with angina?

A

Prevents platelet activation/aggregation
– (via COX inhibition –> thromboxane A2 decrease –> prostaglandin inhibition)

Prevents disease progression by reducing likelihood of plaque rupture

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5
Q

Name AE of nitroglycerine

A
  • Flushing
  • HA
  • Hypotension
  • Peripheral edema
  • Tolerance/tachyphlyaxis after 24 hours (start a 48-hr nitro free period to avoid this)
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6
Q

What is the standard treatment for HF?

A

ACEi
B-blocker
Lasix + Na+ restriction
Consider defibrillator if EF <35%

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7
Q

Describe the pathology/lesion of a STEMI

A

Thrombosis + stenosis –> 100% occlusion

Transmural infarct –> ST elevation in 2+ anatomically contiguous leads

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8
Q

Describe the pathology/lesion of an NSTEMI

A

Thrombosis <100% occlusion causing ~ST changes but no elevation

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9
Q

You have a pt with CP that is present at rest, is not relieved by nitro. There are no ST elevations, but + troponins. What is the next step in management?

A

NSTEMI –> urgent (not emergent) cath lab

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10
Q

Pt presents with CP that is present at rest, is not relieved by nitro. There are no ST elevations or biomarkers present. What is the next step in management?

A

Admit and watch trops overnight - they may have not increased yet

  • If negative, stress test in the morning
  • —> ideally “elective” cath to r/o CAD (only way to decisively r/o)
  • If positive, go to cath lab non-urgently
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11
Q

Medications for managing acute CAD

A 
MONA-BASH-C
\+ morphine
\+ oxygen
\+ nitro
\+ ASA
\+ B-blocker (NOT if R-sided infarct b/c this is preload dependent, but these pts should be in cath lab anyway)
\+ ACEi
\+ Heparin (stabilizes thrombus)
\+/- Clopidogrel

If low risk (in process of r/o CAD), give prophylactic heparin and NO clopidogrel

If high risk, give therapeutic heparin + clopidogrel

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12
Q

Medical therapy for CHF (not exacerbation)

A
  • LSM (decrease Na+, restrict fluids)
  • ACEi/ARB
  • BB
  • Diuretic (loop or thiazide)

Step up: add MAR (BiDil [hydralizine], spiro)

Step up: add +inotrope (digoxin, dobutamine, milrinone)

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13
Q

Medical therapy for CHF exacerbation

A
  • O2 if <90% sat
  • Rapid volume reduction to decrease pulmonary congestion (IV lasix)

If hypotension is present + patient is HFrEF –> +inotrope (dobutamine is best in acute setting)
—— do not give inotrope for HFpEF

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14
Q

At what class of CHF are symptoms present at rest?

A

Class IV (most severe)

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15
Q

Describe the MOA of atherosclerosis

A

Foam cells (macrophages) consume lipids, stay on vessel walls. Then they die and release cytokines, which attract more macrophages, etc –> plaque

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16
Q

Tx for hypertensive emergency

A

Na+ nitroprusside + hydralazine (vaso- and arteriole dilators respectively)

Reduce slowly to prevent cerebral hypoperfusion (unless you’re treating something like aortic dissection)

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17
Q

Medical therapy for HTN

A

Non-Black:

  • ACEi/ARB
  • CCB or thiazide diuretic

Black:

  • Thiazide diuretic**
  • +/- CCB
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18
Q

Describe some of the CIx for common drugs used to lower BP

A
  • Don’t use ACEi/ARB in setting of proteinurea/AKI
  • Don’t use ACEi in pregnancy
  • Don’t use ACEi in hyperkalemia
  • Don’t use spironolactone in hyperkalemia or poor kidney fxn
  • Don’t use BB with asthma
  • Hydralyzine can cause lupus-like syndrome
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19
Q

Describe the symptoms of pericarditis, and compare them to myocarditis

A

Pericarditis: 4 Ps:

  • Pleuritic pain
  • Persistent pain
  • Postural pain (may radiate)
  • Pericardial friction rub

Myocarditis has more vague symptoms: fatigue, fever, CP/discomfort, palpitations, and hallmark is tachycardia disproportionate to fever/level of discomfort

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20
Q

What is a hallmark EKG finding in a patient with pleuritic chest pain + pericardial friction rub?

A

(Pericarditis)

Diffuse ST changes and PR depression in V2-V6

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21
Q

Tx for pericarditis?

A

NSAIDs, ASA x 7-14 days – use colchicine 2nd line

DO NOT use NSAIDs if this occurs 2-6 weeks after MI (or heart surgery) = Dressler Syndrome; NSAIDs impair myocardial scar formation. ASA and colchicine is okay.

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22
Q

Describe Duke’s Criteria:

  • What are they?
  • What does it diagnose?
  • How is it treated?
A

Diagnoses endocarditis

2 major + 1 minor OR
1 major + 3 minor OR
5 minor

Major:

  • Positive blood cultures of:
      • S aureus, S viridans, S bovis or other typical species
  • Echo showing vegetation
  • New regurgitant murmur

Minor:

  • Risk factors present
  • Fever 100.5+
  • Vascular phenomena
  • Immunologic phenomena
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23
Q

Endocarditis with S bovis

A

Highly ass’d with colon cancer, wins you a colonoscopy

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24
Q

What is the MC location for vegetation in endocarditis?

A

Mitral valve MC

Tricuspid in IV drug users

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25
Q

IV drug user presents with fever, new regurgitant murmur, splinter hemorrhages, JVD, and SOB. Where do you look and what is the most likely cause and treatment?

A

Endocarditis of tricuspid valve
Likely S aureus
Empiric coverage is Naficillin + Ceftriaxone; cover MRSA with Vanc

26
Q

What is the treatment for a patient with endocarditis of a prosthetic valve?

A

Vanc + gent + rifampin

27
Q

What is the likely etiological agent of a patient with suspected endocarditis who had a prosthetic valve placed 2 weeks ago?

A

S epi

28
Q

What is the empiric treatment for suspected endocarditis?

A

Naficillin + ceftriaxone

29
Q

What are AAA screening protocol?

A

One time abdominal US for men 65-75 who have ever smoked

30
Q

What are AAA monitoring parameters?

A

Via US:
3-4 cm = q/year
4-4.5 cm = q/6 month
>4.5 cm = refer to vascular surgery

For anything 5.5+ cm OR anything with rapid expansion (>0.5 cm/yr) = immediate surgical repair

31
Q

How is an aortic dissection diagnosed?

A

CT angiogram

32
Q

How is an aortic dissection treated?

A

Surgical, with pre-op BP control:

  • Rapidly lower BP to SBP 100-120 within 20 minutes
  • Use labetalol, sodium nitroprusside, and nicardipine
33
Q

What is the MC site for an AAA?

A

Infrarenal

34
Q

A patient complaining of joint pain in the hips and shoulders, HA, vision disturbances, and intense scalp pain when brushing her hair is suspicious for what?

A

Temporal arteritis – associated with polymyalgia rheumatica

35
Q

Pt develops dull pain, erythema, and indurated vein with palpable cord at IV site. What is the dx and tx?

A

Superficial phlebitis, dx via US.

Tx with elevation, NSAIDs, warm compress

36
Q

Pt with brawny, atrophic, shiny skin of the BLE is concerning for what diagnosis? How is it diagnosed and what is the treatment?

A
  • Venous insufficiency
  • Diagnosed w/ABI measurement
  • if <0.4, immediate surgical consult
37
Q

What is Virchow’s triad, how do you definitively diagnose the associated condition, and how is it treated?

A

Virchow’s Triad - venous thrombosis:

  • Stasis
  • Trauma
  • Hypercoaguability (OCPs, Factor V Leiden, immobilization)

First line is duplex US but gold standard is venography

Tx w/ heparin –> coumadin bridge

38
Q

Electrical alternans is associated with what condition, and what is the treatment?

A

Pericardial effusion (diagnosed via echo)

  • Tx via pericardiocentesis
  • Small or stable, can monitor closely
  • Pericardiotomy in worst case
39
Q

What are the leads and the artery associated with the heart’s anterior and septal portions?

A
  • V1-V4

- LAD

40
Q

What are the leads and the artery associated with the heart’s inferior portion?

A
  • II, III, aVF

- RCA (mc) or LCx

41
Q

What are the leads and the artery associated with the heart’s lateral portions?

A
  • I, V5-V6, aVL

- LCx and the diagonal of LAD

42
Q

Name 4 systolic murmurs

A

Mitral regurg
Aortic stenosis
Tricuspid regurg
Pulmonic stenosis

43
Q

Name 4 diastolic murmurs

A

Mitral stenosis
Aortic regurg
Tricuspid stenosis
Pulmonic regurg

44
Q

What is the MC valvulopathy that occurs as a results of rheumatic heart disease?

A

Mitral regurgitation, but also mitral stenosis and aortic stenosis

Rheumatic fever is the MC cause of mitral stenosis

45
Q

What are two valvulopathies that are likely be associated with endocarditis?

A

Mitral regurgitation, aortic regurgitation

46
Q

Describe the murmur of mitral valve prolapse and some potential etiologies

A

Early-mid systolic click with the murmur occurring during late systole, heard at the LLSB

Congenital defect MC etiology

47
Q

Describe the murmur of mitral regurgitation and some potential etiologies

A

Loud holosystolic murmur with radiation to the base that is heard best at the apex

Acute murmurs ass’d with endocarditis, MI, or trauma; chronic murmurs associated with rheumatic heart disease

48
Q

Describe the murmur of mitral stenosis and some potential etiologies

A

Low-pitched, rumbling diastolic murmur with a loud S1, rumbling, and an opening snap, best heard at the apex

Often ass’d with rheumatic heart disease

49
Q

Describe the murmur of aortic stenosis and some potential etiologies

A

Crescendo-decrescendo systolic murmur with radiation to the neck, best heard at the RUSB

MC murmur, often seen in older pts, ass’d with calcification and degeneration of the valve. Also ass’d with congenital bicuspid aortic valves.

50
Q

Describe the murmur of pulmonic stenosis and some potential etiologies

A

Harsh mid-systolic ejection crescendo-decrescendo murmur with widely-split S2, best heard at LSB with radiation to L shoulder and neck
- This is the murmur associated with Tetralogy of Fallot)

51
Q

Describe the murmur of tricuspid regurgitation and some potential etiologies

A

High-pitched, holosystolic murmur best heard at the LSB.

Will increase with increased venous return (leg raising, hepatic compression).

Small amount is normal in most people, increased/2ndry often due to RA dilation

52
Q

Differentiate between early and mid/late diastolic murmurs

A

Early are regurgitative (usually aortic)

Mid/late are stenotic, usually mitral

53
Q

How does the murmur ass’d with mitral stenosis change with preload?

A
  • Becomes later (closer to S2) with increased preload

- Becomes earlier with decreased preload (standing)

54
Q

What is the indication for statins?

A

Decrease LDL

Decrease CV complications

55
Q

What is the indication for niacin?

A

Increasing HDL

56
Q

What is the indication for fibrates?

A

Decreasing triglycerides

Fenofibrate is the only fibrate approved for use with statins

57
Q

What is the indication for bile acid sequestrants?

A

Can be added to statin to further reduce LDL

May also see mild-mod increase in HDL

  • Safe in pregnancy (intrahepatic cholecystitis of pregnancy or pruritis of biliary obstruction)
58
Q

What is the indication for ezetimibe?

A

Decreases LDL, without significant changes to HDL or triglycerides

59
Q

What is an important AE ass’d with fibrate use?

A

Gallstone formation

60
Q

What are three important CIx to using statins?

A

Active hepatic disease evidenced by persistently elevated LFTs

Pregnancy/breastfeeding
Concurrent use of amlodipine

IM EOR (8 decks)

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