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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
When screening what are the lipid level goals?
Total cholesterol < 200, HDL > 45, Triglycerides < 150, LDL < 160 (if no risk factors)
26
What meds are indicated for isolated increases in LDL, triglycerides, and to raise HDL.
LDL: statins, bile acid sequestering agents Tri: fibrates, niacin HDL: niacin, fibrates
27
What drug should not be used in DM patients and why? What other options would be used in its place?
Niacin causes hyperglycemia. Use fibrates and statins instead.
28
Name and describe the primary therapeutic method used to manage hyperlipidemia.
Lifestyle changes - weight reduction, exercise, reduce cholesterol, carbs, and trans fats in diet, increase fruits (antioxidants) and vegetables (fiber), smoke cessation.
29
What OTC medication is used as CAD prophylaxis in patients with hyperlipidemia?
ASA - 81 mg/day
30
What are the primary affects of statin medications?
Decrease LDL (best drug to dec LDL), increase HDL, decrease triglycerides.
31
Describe the MOA of statin medications.
HMGcoA reductase inhibitor - rate limiting step in cholesterol synthesis in the liver. Also increases LDL receptors which helps remove cholesterol from the blood.
32
What AEs are associated with statin drugs?
myositis, myalgias, rhabdo (rare), hepatitis
33
When should statin medications be taken?
At night when cholesterol synthesis is at its highest. Less important with newer statins - atorvastatin, pitavastatin, rosuvastatin.
34
Name and describe the newest method used to determine the need for statin drugs.
10-year and lifetime ASCVD risk calculator. Based on risk factors (age, race, smoking, BP, DM, serum cholesterol levels) rather than blood cholesterol alone.
35
In general what patients will score high on the ASCVD risk calculator and be given consideration for statin drugs?
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.
36
What is the best drug to increase HDL?
Niacin (aka nicotinic acid or vitamin B3)
37
What are the two primary affects of niacin?
Inc HDL and dec triglycerides --> mild dec in LDL
38
List AEs associated with niacin.
Hyperuricemia (gout), hyperglycemia, flushing, HA, warm sensation, pruritis.
39
What medication taken prior to niacin may reduce some of its AEs?
ASA or other NSAIDS may reduce flushing, pruritis, etc. --> no effect on hyperuricemia or hyperglycemia.
40
What are the effects of fibrate meds?
Primarily dec triglycerides --> minimal inc in HDL and dec in LDL.
41
What is the MOA of fibrates?
Inhibit peripheral lipolysis and reduce hepatic triglyceride production
42
What are the AEs associated with fibrates?
increased LFT’s, myositis, myalgias (esp combined with statines, gallstones
43
What are the contraindications to fibrate use?
Severe hepatobiliary disease and renal disease.
44
What are the affects of bile acid sequestering agents?
Dec LDL --> especially when combined with statins May inc TGs --> Pt must have normal triglycerides Mild inc HDL
45
What is the MOA of bile acid sequestering agents?
Prevents intestinal absorption of bile acids which stimulates the liver to use cholesterol to make more bile acids.
46
What is the only class of hyperlipidemia medications safe for use in pregnancy?
Bile acid sequestering agents.
47
What are the AEs associated with bile acid sequestering agents?
GI --> N/V, bloating, abdominal pain. | Also, increased triglycerides and LFTs
48
What is the best use of bile acid sequestering agents?
In combination with statins or niacin.
49
What drugs may bile acid sequestering agents interact with and what is the solution?
May impair absorption of warfarin, digoxin, and fat soluble vitamins. Solution is to space.
50
What is the MOA of ezetemibe?
Blocks cholesterol transporter which inhibits gastric absorption of cholesterol.
51
What is the best use of ezetemibe?
In combination with a statin to lower LDL.
52
What is the primary AE associated with ezetemibe?
Inc LFTs --> especially in combo with a statin.
53
When evaluating for HTN, what exam is more prognostic than even a single BP reading?
Papiledema seen on fundoscopic exam of the eye. Papiledema indicates advanced stage of HTN.
54
What signs on exam of the neck may be indicative of HTN?
Carotid artery bruits and/or JVD.
55
List potential complications of systemic HTN.
CAD, PVD, MI, HF, aortic aneurysms, stroke, brain aneurysm, renal disease, retinopathy, blindness.
56
T/F: HTN is the leading cause of chronic renal disease in the US.
False: It is the second leading cause of renal disease. DM is the leading cause of renal disease.
57
Describe the AHA's stages of HTN.
``` Normal: SBP < 120 / DBP < 80 Elevated: 120-129 / < 80 Stage 1: 130-139 / 80-89 Stage 2: > 140 / > 90 Stage 3: > 180 / > 120 ```
58
Which BP, systolic or diastolic, is more associated with risk of CAD?
Systolic > 140 indicates higher risk of CAD in patients older than 50.
59
What is required for a diagnosis of HTN?
2 elevated readings on 2 separate occasions.
60
What is the management goal in the average patient diagnosed with HTN? In patients with chronic kidney disease? In patients over age 65?
General: SBP < 130 / DBP < 80 CKD: < 140 / < 90 Over 65: < 150 / < 90
61
What is the most important prognostic factor for a patient with chronic HTN?
Presence of LVH
62
What four durg classes can be used as first-line therapy in an uncomplicated, non-African Americn patient with a new diagnosis of HTN?
Thiazide diuretics, ACEIs, ARBs, CCB
63
List some non-pharmacologic recommendations used in the management of HTN.
Salt restriction, weight loss, exercise, moderate or less alcohol consumption, DASH diet.
64
What is a DASH diet?
DASH = dietary approaches to stop HTN. Recommends foods low in salt, high in K, Mg, and Ca. Generally avoid sweets and snacks.
65
What is the most commonly used first-line medication in the treatment of chronic HTN?
HCTZ
66
What two first line therapy options for treatment of HTN have a synergistic effect when given together?
ACEIs and thiazides --> decrease preload and afterload
67
Which patients with HTN benefit most from ACEIs and why?
DM, nephropathy, CHF, prior MI --> ACEIs and both renal and cardio protective.
68
What AEs are associated with ACEIs?
1st dose HypoTN, azotemia (inc BUN and SCr), renal insufficiency, HyperK, cough, angioedema
69
What medications are best for use in African American patients with HTN?
CCBs and thiazides
70
Which HTN medications are contraindicated in pregnancy?
ACEIs and ARBs
71
What HTN medications are best for use in patients with CKD?
ACEIs and ARBs
72
What patients would most commonly receive consideration for an ARB to treat HTN?
Patients unable to tolerate ACEIs or BBs or could be used as an adjunct with ACEIs.
73
Which CCBs are the most potent vasodilators, and thus, best for use in HTN?
Dihydropyridines - nifedipine and amlodipine.
74
What AEs are associated with CCBs?
HA, dizziness, flushing, non-cardiogenic peripheral edema.
75
What HTN medication is also used to treat Raynaud's syndrome?
CCBs
76
What are the contraindications to use of CCBs?
2nd/3rd degree heart block, patients taking BBs
77
What is the MOA of HCTZ?
Dec Na and H2O retention by limiting their reabsorption at the distal tubule.
78
What are the AEs associated with HCTZ?
HypoNA, HypoK, hyperuricemia, hyperglycemia.
79
What is the MOA of loop diuretics?
Inc excretion of Na, Cl, and K to inhibit water reabsorption at the loop of Henle.
80
What are the AEs associated with loop diuretics?
HypoK, hyperuricemia, HypoCl, metabolic alkalosis, hyperglycemia
81
What diuretics are contraindicated in patients that have a sulfa allergy?
HCTZ and loop diuretics.
82
Which diuretics do not decrease serum potassium?
Spironolactone, amiloride, eplernone
83
What is the MOA of potassium sparing diuretics?
Inhibit aldosterone mediated Na and H2O reabsorption at the distal tubule.
84
List the AEs associated with potassium sparing diuretics.
Hyperkalemia, gynecomastia specific to spironolactone.
85
When would BB medications be considered for use in management of HTN?
No longer first line --> more common in patients with CAD HX, especially prior MI or tachycardia.
86
What are the contraindications to use of BBs.
High degree heart block, decompensated HF, asthma/COPD (nonselective only), worsen Raynaud's and other PVDs.
87
Identify BBs that are nonselective, B1 selective, and both alpha and beta.
Non-sel: propranolol most common B1 sel: atenolol, metoprolol, esmolol A & B: labetalol, carvedilol
88
Identify three alpha-1 antagonists and state what they are used for?
Prazosin, terazosin, doxazosin --> 1at line in patients with HTN and BPH
89
Define secondary HTN and state some common causes.
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
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
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
What triglyceride level is required for diagnosis of hypertriglyceridemia?
> 150
92
What medications is best for reduction of triglyceride levels?
Fibrates
93
Describe the S/S associated with peripheral artery disease.
Intermittent claudication (pain brought on by exercise - most common), ED, weak/absent distal pulses, bruits, dependent rubor (erythema), pallor
94
What S/S are associated with a more severe/advanced state of peripheral artery disease?
Cool skin with dependent rubor
95
What are the 6 P's of acute arterial embolism?
Pain, pulseless, pallor, paresthesia, poiklothermia (cool skin), paralysis.
96
What diagnostic tests are used to evaluate for peripheral artery disease?
Arteriography (only done when intervention planned), doppler US, ankle-brachial index (normal = 1 - 1.2)
97
What lifestyle changes are recommended in the management of peripheral artery disease?
Smoke cessation, control of DM, HTN, and hyperlipidemia. exercise until pain induced
98
What medication is the mainstay of therapy for peripheral artery disease?
Cilostazol - anti-platelet and vasodilator
99
What vessel is most likely to become a varicose vein?
Saphenous
100
What is recommended in the management of varicose veins?
compression stockings, weight loss, weight loss, exercise, elevation
101
Differentiate between S/S of superficial and deep phlebitis.
Sup: dull pain, erythema, induration Deep: swollen, warm, red, calf pain with foot in dorsiflexion (Homan's Sign)
102
What is used in the management of phlebitis?
Sup: rest, local heat, elevation, NSAIDs Deep: anticoagulation (prevention is key)
103
Describe S/S of chronic venous insufficiency.
progressive edema, itching, dull pain, ulcerations, shiny and thin atrophic skin

EOR Exam - Family Medicine (15 decks)

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