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EOR Exam - Family Medicine > Cardiovascular Part 2 > Flashcards

Cardiovascular Part 2 Flashcards

1
Q

Define endocarditis.

A

Infection of endothelium/valves secondary to colonization during transient/persistent bacteremia

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2
Q

I what three circumstances does a patient most commonly develop endocarditis?

A

Direct inoculation during surgery
IV drug users
Late stage HIV

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3
Q

List the heart valves in order from most commonly affected by endocarditis to least commonly affected.

A

Mitral > Aortic > Tricuspid > Pulmonic

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4
Q

List 4 common generalized S/S seen in endocarditis.

A

Fever, ECG abnormalities, anorexia, weight loss.

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5
Q

List 5 specific peripheral sequelae that can result from endocarditis.

A
  1. Janeway lesions: painless erythematous macules on palms/soles
  2. Roth spots: retinal hemorrhage with pale center
  3. Osler nodes: tender nodules on pads of digits
  4. Splinter hemorrhages of proximal nail bed
  5. Septic emboli in CNS, kidneys, spleen, joints
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6
Q

What is the key diagnostic test that needs to be performed in evaluating for endocarditis and what is the timing/when should it be repeated?

A

Blood cultures obtained three times at least one hour apart from one another. Should be done before abx are administered.

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7
Q

What imaging study is best to evaluate for endocarditis?

A

Echo –> transthoracic first, but transesophageal is more sensitive.

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8
Q

What abnormalities will typically be seen in serum labs of an endocarditis patient?

A

Leukocytosis (increased WBCs)
Normocytic and normochromic anemia
Increased ESR and/or rheumatoid factor

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9
Q

What are the two major criteria used in the diagnosis of endocarditis?

A
  1. Two or more positive blood cultures

2. Echo showing new valvular regurgitation or vegetations/abscesses on endocardium

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10
Q

What are the six minor criteria used in the diagnosis of endocarditis?

A
  1. Predisposing condition (IV Drugs, Catheter)
  2. Fever > 100.4
  3. Vascular finding: janeways, septic emboli, etc.
  4. Immunologic findings: Osler’s, Roth, positive RF
  5. Single positive blood culture
  6. Positive echo not meeting major criteria
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11
Q

What major and minor findings are required to make a diagnosis of endocarditis?

A

2 major …or…
1 major and 3 minor …or…
5 minor

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12
Q

For patients undergoing high risk procedures, what prophylactic regimen against endocarditis is routinely administered?

A

Amoxicillin 2g 30-60m before procedure (Clindamycin 600mg if PCN allergy)

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13
Q

What routine, at home practice is recommended to protect against endocarditis?

A

Maintaining good oral hygiene

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14
Q

What abx are recommended in empiric treatment of endocarditis?

A

Native valve subacute endo: PCN/ampicillin plus Gentamicin –> Vancomycin in IV drug users
Prosthetic valves: vancomycin, gentamicin and rifampin
Fungal: ampho B –> caspofungin if severe

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15
Q

How long is abx therapy continued in the treatment of endocarditis?

A

4 - 6 weeks

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16
Q

What are the indications for surgical treatment of endocarditis?

A

Refractory CHF, persistent or refractory infection, invasive infection, prosthetic valve, recurrent systemic emboli, fungal infection.

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17
Q

What are the HACEK bacteria associated with vegetations resulting from endocarditis?

A 
H: H. flu
A: Antinobacillus
C: Cardiobacterium
E: Eikenella
K: Klingella
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18
Q

Differentiate acute from subacute endocarditis.

A

Acute develops quickly, subacute develops gradually over weeks to months

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19
Q

What pathogens are most commonly associated with endocarditis in IV drug users?

A

Staph aureus (MRSA), Pseudomonas, candida (especially in HIV)

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20
Q

Define a xanthoma and describe its association with hyperlipidemia.

A

Def: lipid buildup under the skin - most commonly at eyelids and achilles tendon.
Usually indicate a genetic cause when associated with hyperlipidemia. However, 2/3 with xanthelasmas (eyelids) have normal serum lipids.

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21
Q

Patients with hypertriglyceridemia are at increased risk of developing what digestive system disease?

A

Pancreatitis

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22
Q

Describe the USPSTF recommendations for lipid screening.

A

Screening should begin at age 35 for males and 45 for females if no evidence of CVD or other risk factors. High risk patients should start at 25 ad 35.

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23
Q

Describe LDL level treatment goals in all patients, patients with CVD, and patients with no CVD but risk factors.

A

CVD: Start meds at LDL < 130. Goal is LDL < 100 but LDL < 70 is optimal.
RFs: Meds at LDL > 160, goal is LDL < 130
All others: Meds at LDL > 190, goal is LDL < 160

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24
Q

List risk factors for developing hyperlipidemia.

A

Diet high in saturated fats, lack of activity, smoking, obesity, HTN, family Hx

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25
Q

When screening what are the lipid level goals?

A

Total cholesterol < 200, HDL > 45, Triglycerides < 150, LDL < 160 (if no risk factors)

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26
Q

What meds are indicated for isolated increases in LDL, triglycerides, and to raise HDL.

A

LDL: statins, bile acid sequestering agents
Tri: fibrates, niacin
HDL: niacin, fibrates

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27
Q

What drug should not be used in DM patients and why? What other options would be used in its place?

A

Niacin causes hyperglycemia. Use fibrates and statins instead.

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28
Q

Name and describe the primary therapeutic method used to manage hyperlipidemia.

A

Lifestyle changes - weight reduction, exercise, reduce cholesterol, carbs, and trans fats in diet, increase fruits (antioxidants) and vegetables (fiber), smoke cessation.

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29
Q

What OTC medication is used as CAD prophylaxis in patients with hyperlipidemia?

A

ASA - 81 mg/day

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30
Q

What are the primary affects of statin medications?

A

Decrease LDL (best drug to dec LDL), increase HDL, decrease triglycerides.

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31
Q

Describe the MOA of statin medications.

A

HMGcoA reductase inhibitor - rate limiting step in cholesterol synthesis in the liver. Also increases LDL receptors which helps remove cholesterol from the blood.

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32
Q

What AEs are associated with statin drugs?

A

myositis, myalgias, rhabdo (rare), hepatitis

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33
Q

When should statin medications be taken?

A

At night when cholesterol synthesis is at its highest. Less important with newer statins - atorvastatin, pitavastatin, rosuvastatin.

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34
Q

Name and describe the newest method used to determine the need for statin drugs.

A

10-year and lifetime ASCVD risk calculator. Based on risk factors (age, race, smoking, BP, DM, serum cholesterol levels) rather than blood cholesterol alone.

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35
Q

In general what patients will score high on the ASCVD risk calculator and be given consideration for statin drugs?

A

Patients with known CVD, T1D or T2D older than 40, Any adult with LDL > 190, Anyone over 40 calculated to have a > 7.5% increased risk of stroke or MI within 10 years.

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36
Q

What is the best drug to increase HDL?

A

Niacin (aka nicotinic acid or vitamin B3)

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37
Q

What are the two primary affects of niacin?

A

Inc HDL and dec triglycerides –> mild dec in LDL

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38
Q

List AEs associated with niacin.

A

Hyperuricemia (gout), hyperglycemia, flushing, HA, warm sensation, pruritis.

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39
Q

What medication taken prior to niacin may reduce some of its AEs?

A

ASA or other NSAIDS may reduce flushing, pruritis, etc. –> no effect on hyperuricemia or hyperglycemia.

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40
Q

What are the effects of fibrate meds?

A

Primarily dec triglycerides –> minimal inc in HDL and dec in LDL.

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41
Q

What is the MOA of fibrates?

A

Inhibit peripheral lipolysis and reduce hepatic triglyceride production

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42
Q

What are the AEs associated with fibrates?

A

increased LFT’s, myositis, myalgias (esp combined with statines, gallstones

43
Q

What are the contraindications to fibrate use?

A

Severe hepatobiliary disease and renal disease.

44
Q

What are the affects of bile acid sequestering agents?

A

Dec LDL –> especially when combined with statins
May inc TGs –> Pt must have normal triglycerides
Mild inc HDL

45
Q

What is the MOA of bile acid sequestering agents?

A

Prevents intestinal absorption of bile acids which stimulates the liver to use cholesterol to make more bile acids.

46
Q

What is the only class of hyperlipidemia medications safe for use in pregnancy?

A

Bile acid sequestering agents.

47
Q

What are the AEs associated with bile acid sequestering agents?

A

GI –> N/V, bloating, abdominal pain.

Also, increased triglycerides and LFTs

48
Q

What is the best use of bile acid sequestering agents?

A

In combination with statins or niacin.

49
Q

What drugs may bile acid sequestering agents interact with and what is the solution?

A

May impair absorption of warfarin, digoxin, and fat soluble vitamins. Solution is to space.

50
Q

What is the MOA of ezetemibe?

A

Blocks cholesterol transporter which inhibits gastric absorption of cholesterol.

51
Q

What is the best use of ezetemibe?

A

In combination with a statin to lower LDL.

52
Q

What is the primary AE associated with ezetemibe?

A

Inc LFTs –> especially in combo with a statin.

53
Q

When evaluating for HTN, what exam is more prognostic than even a single BP reading?

A

Papiledema seen on fundoscopic exam of the eye. Papiledema indicates advanced stage of HTN.

54
Q

What signs on exam of the neck may be indicative of HTN?

A

Carotid artery bruits and/or JVD.

55
Q

List potential complications of systemic HTN.

A

CAD, PVD, MI, HF, aortic aneurysms, stroke, brain aneurysm, renal disease, retinopathy, blindness.

56
Q

T/F: HTN is the leading cause of chronic renal disease in the US.

A

False: It is the second leading cause of renal disease. DM is the leading cause of renal disease.

57
Q

Describe the AHA’s stages of HTN.

A 
Normal: SBP < 120 / DBP < 80
Elevated: 120-129 / < 80
Stage 1: 130-139 / 80-89
Stage 2: > 140 / > 90
Stage 3: > 180 / > 120
58
Q

Which BP, systolic or diastolic, is more associated with risk of CAD?

A

Systolic > 140 indicates higher risk of CAD in patients older than 50.

59
Q

What is required for a diagnosis of HTN?

A

2 elevated readings on 2 separate occasions.

60
Q

What is the management goal in the average patient diagnosed with HTN? In patients with chronic kidney disease? In patients over age 65?

A

General: SBP < 130 / DBP < 80
CKD: < 140 / < 90
Over 65: < 150 / < 90

61
Q

What is the most important prognostic factor for a patient with chronic HTN?

A

Presence of LVH

62
Q

What four durg classes can be used as first-line therapy in an uncomplicated, non-African Americn patient with a new diagnosis of HTN?

A

Thiazide diuretics, ACEIs, ARBs, CCB

63
Q

List some non-pharmacologic recommendations used in the management of HTN.

A

Salt restriction, weight loss, exercise, moderate or less alcohol consumption, DASH diet.

64
Q

What is a DASH diet?

A

DASH = dietary approaches to stop HTN. Recommends foods low in salt, high in K, Mg, and Ca. Generally avoid sweets and snacks.

65
Q

What is the most commonly used first-line medication in the treatment of chronic HTN?

A

HCTZ

66
Q

What two first line therapy options for treatment of HTN have a synergistic effect when given together?

A

ACEIs and thiazides –> decrease preload and afterload

67
Q

Which patients with HTN benefit most from ACEIs and why?

A

DM, nephropathy, CHF, prior MI –> ACEIs and both renal and cardio protective.

68
Q

What AEs are associated with ACEIs?

A

1st dose HypoTN, azotemia (inc BUN and SCr), renal insufficiency, HyperK, cough, angioedema

69
Q

What medications are best for use in African American patients with HTN?

A

CCBs and thiazides

70
Q

Which HTN medications are contraindicated in pregnancy?

A

ACEIs and ARBs

71
Q

What HTN medications are best for use in patients with CKD?

A

ACEIs and ARBs

72
Q

What patients would most commonly receive consideration for an ARB to treat HTN?

A

Patients unable to tolerate ACEIs or BBs or could be used as an adjunct with ACEIs.

73
Q

Which CCBs are the most potent vasodilators, and thus, best for use in HTN?

A

Dihydropyridines - nifedipine and amlodipine.

74
Q

What AEs are associated with CCBs?

A

HA, dizziness, flushing, non-cardiogenic peripheral edema.

75
Q

What HTN medication is also used to treat Raynaud’s syndrome?

A

CCBs

76
Q

What are the contraindications to use of CCBs?

A

2nd/3rd degree heart block, patients taking BBs

77
Q

What is the MOA of HCTZ?

A

Dec Na and H2O retention by limiting their reabsorption at the distal tubule.

78
Q

What are the AEs associated with HCTZ?

A

HypoNA, HypoK, hyperuricemia, hyperglycemia.

79
Q

What is the MOA of loop diuretics?

A

Inc excretion of Na, Cl, and K to inhibit water reabsorption at the loop of Henle.

80
Q

What are the AEs associated with loop diuretics?

A

HypoK, hyperuricemia, HypoCl, metabolic alkalosis, hyperglycemia

81
Q

What diuretics are contraindicated in patients that have a sulfa allergy?

A

HCTZ and loop diuretics.

82
Q

Which diuretics do not decrease serum potassium?

A

Spironolactone, amiloride, eplernone

83
Q

What is the MOA of potassium sparing diuretics?

A

Inhibit aldosterone mediated Na and H2O reabsorption at the distal tubule.

84
Q

List the AEs associated with potassium sparing diuretics.

A

Hyperkalemia, gynecomastia specific to spironolactone.

85
Q

When would BB medications be considered for use in management of HTN?

A

No longer first line –> more common in patients with CAD HX, especially prior MI or tachycardia.

86
Q

What are the contraindications to use of BBs.

A

High degree heart block, decompensated HF, asthma/COPD (nonselective only), worsen Raynaud’s and other PVDs.

87
Q

Identify BBs that are nonselective, B1 selective, and both alpha and beta.

A

Non-sel: propranolol most common
B1 sel: atenolol, metoprolol, esmolol
A & B: labetalol, carvedilol

88
Q

Identify three alpha-1 antagonists and state what they are used for?

A

Prazosin, terazosin, doxazosin –> 1at line in patients with HTN and BPH

89
Q

Define secondary HTN and state some common causes.

A

HTN caused by identifiable and correctable cause –> suspect in severe HTN or a patient refractory to HTN meds. Causes include: renal disease (most common), hyperaldosteronism, pheochromocytoma, sleep apnea, OCPs, coarctation of the aorta.

90
Q

State the preferred anti-HTN meds for each of the following: systolic HF, post-MI, CKD, angina, A-fib/flutter, BPH, essential tremor, hyperthyroid, migraine, osteoporosis, Raynaud’s

A

Systolic HF: ACEI/ARB, BB, diuretic, aldosterone ag
Post-MI: ACEI/ARB, BB, diuretic, aldosterone ag
CKD: ACEI and/or ARB
Angina: BB, CCB (amlodipine/nifedipine)
A-Fib/Flutter: BB, CCB (diltiazem, verapamil)
BPH: Alpha blocker
Tremor: BB (propranolol)
Hyperthyroid: BB
Migraine: BB (propranolol), CCB
Osteoporosis: Thiazide diuretic
Raynaud’s: CCB (amlodipine, nifedipine)

91
Q

What triglyceride level is required for diagnosis of hypertriglyceridemia?

A

> 150

92
Q

What medications is best for reduction of triglyceride levels?

A

Fibrates

93
Q

Describe the S/S associated with peripheral artery disease.

A

Intermittent claudication (pain brought on by exercise - most common), ED, weak/absent distal pulses, bruits, dependent rubor (erythema), pallor

94
Q

What S/S are associated with a more severe/advanced state of peripheral artery disease?

A

Cool skin with dependent rubor

95
Q

What are the 6 P’s of acute arterial embolism?

A

Pain, pulseless, pallor, paresthesia, poiklothermia (cool skin), paralysis.

96
Q

What diagnostic tests are used to evaluate for peripheral artery disease?

A

Arteriography (only done when intervention planned), doppler US, ankle-brachial index (normal = 1 - 1.2)

97
Q

What lifestyle changes are recommended in the management of peripheral artery disease?

A

Smoke cessation, control of DM, HTN, and hyperlipidemia. exercise until pain induced

98
Q

What medication is the mainstay of therapy for peripheral artery disease?

A

Cilostazol - anti-platelet and vasodilator

99
Q

What vessel is most likely to become a varicose vein?

A

Saphenous

100
Q

What is recommended in the management of varicose veins?

A

compression stockings, weight loss, weight loss, exercise, elevation

101
Q

Differentiate between S/S of superficial and deep phlebitis.

A

Sup: dull pain, erythema, induration
Deep: swollen, warm, red, calf pain with foot in dorsiflexion (Homan’s Sign)

102
Q

What is used in the management of phlebitis?

A

Sup: rest, local heat, elevation, NSAIDs
Deep: anticoagulation (prevention is key)

103
Q

Describe S/S of chronic venous insufficiency.

A

progressive edema, itching, dull pain, ulcerations, shiny and thin atrophic skin

EOR Exam - Family Medicine (15 decks)

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