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Family Med > CVD > Flashcards

CVD Flashcards

1
Q

Causes of 2ndry HTN

A

Renal/renovascular (e.g. stenosis) – most common cause
Endocrine –hyperaldo, thyroid, or parathyroid, Chusings, Pheo, acromegaly
Meds–OCPS, decongestants, estrogen, steroids, TCAs, NSAIDS
Coarctation of aorta
Cocaine/stimulants
Sleep apnea

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2
Q

Evaluation of pt with HTN

A
  • Look for 2ndry causes
  • Assess end organ damage (heart, kidneys, eyes, CNS)
  • Assess overall CV risk (Urinalysis, Cem, fasting glucose, lipid panel, ECG)
  • make therapeutic decisions
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3
Q

HTN thresholds

A 
BP >140/90 in general pop
BP > 130/80 in diabetes/renal disease
PreHTN: 120-139/80-89
Stage I: 140-159/90-99 (lifestyle, drug)
Stage II: >160/>100 (lifestyle, likely 2 drugs
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4
Q

Pregnancy and HTN

A
  • always get a hCG before initiating therapy
  • Thiazides, ACEis, CCBs, ARBs are bad
  • BBs and hydralazine are safe
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5
Q

General Tx HTN

A
  • Lifestyle: Salt, BMI (esp central obesity), Alcohol (pressor), Exercise, low saturated fat, unnecessary meds, stress management
  • Goal: ideal is 120/80, 135/85 minimum for diabetes/renal insuff, 140/90 general threshold
  • All agents are roughly equivalent, but ppl respond differently. Thiazides, CCBs, ACEis, ARBs used as initial monotherapy. BBs have adverse CV effects in the elderly
  • ACCOMPLISH trial: ACEi (benazepril) + CCB (amlodipine) > ACEi + diuretic
  • If one agent not successful, switch, then add a second if needed
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6
Q

Thiazides in HTN

A
  • “salt-sensitive” HTN more common in African Americans, so diuretic is good initial choice (unless comorbid diabetes –> ACEi)
  • Check K regularly (hypokalemia can be exacerbated by decreased salt intake)
  • SEs: hypokalemia, hyperuricemia, hyperglycemia, dyslipidemia, metabolic alkalosis, hypomagnesemia
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7
Q

BBs in HTN

A
  • Decrease HR and CO, decrease renin release
  • SEs: bradycardia, bronchospasm, insomnia, fatigue, may increase TGs and decrease HFL, depression, sedation.
  • not initial Tx in elderly bc of CV effects
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8
Q

ACEis in HTN

A

inhibit RAAS and bradykinin degradation

  • Preferred in diabetes because protective of kidney
  • SEs: acute renal failure, hyperkalemia, dry cough angioedema, skin rash, dysgusia, contraindicated in pregnancy
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9
Q

ARBs in HTN

A

similarly beneficial to kidneys as ACEis

Contraindicated in pregnancy

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10
Q

CCBs in HTN

A

cause vasodilation of arteriolar vasculature

Contraindicated in pregnancy

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11
Q

alpha blockers in HTN

A
  • decrease arteriolar resistance

- may benefit pts with BPH, but not first or second line agents

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12
Q

hydralazine minoxidil in HTN

A
  • Vasodilators

- Not typically given, but can be used with BBs and diuretics in pts with refractory HTN

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13
Q

Type I HLD

A
  • Exogenous
  • Chylomicrons
  • Tx: Diet
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14
Q

Type IIa HLD

A
  • Familial
  • LDL
  • Tx: Statins, Niacin, Cholestyramine
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15
Q

Type IIb HLD

A
  • Combined
  • LDL + VLDL
  • Tx: Tatins, Niacin, Gemfibrozil
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16
Q

Type III HLD

A
  • Familial dysbetalipoproteinemia
  • IDL
  • Tx: Gemfibrozil + Niacin
17
Q

Type IV HLD

A
  • Endogenous
  • VLDL
  • Tx: Niacin, Gemfibrozil Statins
18
Q

Type V HLD

A
  • Familial hyperTG
  • VLDL + chylomicrons
  • Tx: Niacin, Gemfibrozil
19
Q

2ndry causes of HLD

A
  • Endocrine: hypothyroid, DM, Chushing’s
  • Renal: nephrotic sydrome, uremia
  • Chronic liver disease
  • Meds: glucocorticoids, estrogen, thiazides, BBs
  • Pregnancy
20
Q

Threshold lvls for HLD (Total, LDL, TGs)

A

Total: Ideal: 240
LDL: Ideal 160
TGs: Ideal 250

21
Q

HDL and CAD risk

A
  • For every 10 inc, CAD risk decreases by 50%

- Low HDL 60) is a “negative” risk factor

22
Q

TGs and CAD risk

A

-elevated TGs are associated w/ risk, but uncertain whether lowering TG lvls reduces risk

23
Q

Total-to-HDL ratio and CAD

A

Desirable: <4.5
5 = avg
10 = double risk
20 = triple risk

24
Q

LDL goals/Tx thresholds

A

-DM + CAD: goal = 2 RFs: Goal <160, lifestyle at 160, drug Tx at 190.

25
Q

Xanthelesma

A

yellow plaques on eyelids from HLD

26
Q

Xanthoma

A

hard, yellowish masses on tendons from HLD

27
Q

Screening/workup for HLD

A
  • screen: total and HDL (nonfasting OK)
  • If abnormal, full lipid profile (TG and calculated LDL–fasting)
  • Workup for secondary causes: TSH, LFT, BUN, Cr, Glucose
28
Q

Risk factors for CAD in evaluation of HLD

A
  • Current cigarette smoking (dose dependent)
  • HTN
  • DM
  • Low HDL (60) is a negative RF
  • Male >45
  • Female >55
  • Male (don’t double-count with age)
  • FHx of premature CAD (first degree male relative MI/sudden death <65 yo)
29
Q

Statin Potencies

A
  • increasing order (cost increases too):
  • fluvastatin (Lescol) < lovastatin (Mevacor) and pravastatin (Pravachol) < simvastatin (Zocor) and atorvastatin (Lipitor).
30
Q

Lifestyle changes in HLD

A
  • Dietary: <300 mg/day cholesterol. Can reduce LDL by 10%

- Exercise and weight loss

31
Q

Tx elevated TGs

A
  • limited data
  • first line in lifestyle
  • Meds: fibrates, nictonic acid, fish oil
  • Statins should be considered (cardioprotective independent of LDL lowering)
32
Q

Lx in statins

A
  • monitor LFTs (monthly for 3 months, then every 3-6 months)

- harmless elevation in CPK can occur

33
Q

Niacin

A
  • lowers TG + LDL
  • Increases HDL
  • do not use in diabetics
  • Can cause flushing/pruritus.
  • Check LFTs/CPK
34
Q

Cholestyramine

A
  • Bile acid-binding resin
  • Lowers LDL, increases TGs
  • effective when combined with statins/niacin in high-risk pts
  • Adverse GI side effects
35
Q

Fibrates (gemfibrozil

A
  • Lowers VLDL and TG, increases HDL
  • Primarily for TG levels
  • GI side effects
  • abnormal LFTs, gynecomastia, gallstones, weight gain, myopathies

Family Med (8 decks)

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