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Nursing-Sem 1 > Pharm Section 4 > Flashcards

Pharm Section 4 Flashcards

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1
Q

functions of cholesterol

A

responsible for proper cell membrane synthesis and the formation of bile acids and steroid hormones

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2
Q

rate limiting step in cholesterol formation

A

mevalonate

formed by acetyl CoA and catalyzed to HMG-CoA reductase

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3
Q

cholesterol synthesis pathway

A

acetyl Coa > HMG CoA reductase > mevalonate > farnesyl pyrophosphate > squalene > cholesterol

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4
Q

cholesterol and transportation

A

hydrophobic, must be transported in blood by hydrophilic lipoproteins

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5
Q

most cholesterol in plasma normally carried in what form?

A

LDL; low density lipoproteins; “bad cholesterol” associated with increased risk of CAD

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6
Q

apoB

A

apolipoprotein B; apoB binds lipids to LDLs and acts as ligand to “unlock” cell membranes to allow LCL inside; it is responsible for carrying cholesterol to tissues

the more apoB, the more atherogenic

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7
Q

test for apoB amounts

A

“Berkeley” cholesterol test

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8
Q

HDL cholesterol

A

high density lipoprotein; “good cholesterol” because low HDL traditionally seen as strong risk factor for CAD. Recent data is challenging this.

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9
Q

triglycerides

A

carried in chylomicrons, VLDL (very low), and IDL (intermediate)

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10
Q

ATP IV guidelines (new 2013)

A

do away with specific goals (numbers) for LDL and instead categorize patients into four groups of primary and secondary prevention patients. Recommend “intensity” of tx for each prevention group in order to achieve desired LDL cholesterol reduction. No evidence to support specific target. May increase people on statins by 70 million in US (1/2 US pop 40-75).

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11
Q

ATP four new guideline documents include…

A
  1. tx of blood cholesterol in adults
  2. assessment of CV risk
  3. lifestyle management to reduce CV risk
  4. management of overweight and obesity in adults
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12
Q

ATP IV new risk categories for hyperlipidemia patients

A
  1. with CV disease; 40-75 years old; >=7.5% calculated risk for MI or stroke within 10 years
  2. with hx MI, stroke, angina, PAD, TIA, or revascularization
  3. 21 and older with LDL level of 190mg/dL or higher
  4. 40-75 years old with type 1 or 2 diabetes
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13
Q

ATP IV new guidelines for assessment of CV risk

A

focus on atherosclerosis as chronic disease that extends beyond the heart

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14
Q

ATP IV new guidelines for lightly management to reduce CV risk

A

recommendations cover evidence related to dietary patterns, nutrient intake, and levels/types of physical activity

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15
Q

ATP IV new guidelines for management of overweight/obese adults

A

BMI as quick, first screening step for wright loss counseling; waist circumference as indicator for T2 diabetes, CVD, all-cause mortality; new recommendations for BMI cutoff for treatment recommendations (was BMI30 or [25 +2comorbidities], now BMI25 and 1 comorbidity)

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16
Q

AACE response to ATP IV guidelines?

A

they reject the new guidelines and question their scientific basis. say certain at-risk populations will be underserved by new guidelines

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17
Q

Metabolic syndrome

A

–formerly syndrome X
–describes patients with three or more of: …obesity (waist circ >40in M/ >35in F)
…dyslipidemia (triglyceride >150; HDL <40 M/ <50 F)
…HTN (>135/85 mmHg)
…diabetes (FBG >110mg/dL)

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18
Q

HMG-CoA reductase inhibitors are also called…?

A

statins

most widely used drugs for dyslipidemia

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19
Q

first statin drug

A

lovastatin (Mevacor); 1987

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20
Q

how do statins work?

A

inhibit cholesterol synthesis

inhibit HMG-CoA reductase (rate-limiting step in cholesterol synthesis), which aids in removal of cholesterol from blood

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21
Q

how is ubiquinonse/coenzyme Q10 related to cholesterol? what might it be related to?

A

other side of the pathway for cholesterol production

deals with muscle properties, so may be related to myopathy side effects of statins

may be helpful to give statins with CoQ10 supplement

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22
Q

statin impact on LDL, HDL, total cholesterol and triglyceride concentrations

A

lower plasma concentration of LDL
lower total cholesterol
reduce levels of triglycerides
increase levels of HDL

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23
Q

statins must be taken for how long?

A

indefinitely. if stopped, cholesterol will return to baseline within a few weeks

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24
Q

statins may be beneficial for what non-CV conditions?

A

improved endothelial function
decreased platelet aggregation
reduced inflammation

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25
Q

seven statin drugs available include…?

A 
lovastatin (Mevacor)
simvastatin (Zocor)
Pravastatin (Pravachol)
Fluvastatin (Lescol)
Atorvastatin (Lipitor)
Rosuvastatin (Crestor)
Pitavastatin (Livalo)
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26
Q

statin combo drugs include…?

A

Vytorin (simvastatin and ezetimibe)
Liptruzet (atorvastatin and ezetimibe)
Simcor (simvastatin and ER Niacin) no more
Caduet (atorvastatin and amlodipine)

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27
Q

comparison between statin drugs…

which to choose?

A
  • -rosuvastatin a little more potent
  • -simvastatin don’t use more than 40 mg
  • -if fail to achieve cholesterol goals with less potent statin, switch to more potent drug
  • -CAD pts with hard LDL goals, max dose of atorvastatin
  • -pravastatin totally hydrophilic, not metabolized or excreted @liver (may have fewer interactions, side effects)
  • -Asian descent, 2 fold inc in concentrations of rosuvastatin–use in lower dose in asians
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28
Q

effect of doubling dose of statin?

A

only increases LDL reduction by 5-7%, but probably doubles the side effects

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29
Q

statins and pediatrics

A

most statins approved in kids

recommended screening beginning at 2 and tx for kids over 8

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30
Q

statins and pregnancy

A

statins are contraindicated in pregnancy

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31
Q

which statins should you take in the evening?

A

those with shorter 1/2 lives

lovastatin (2hr 1/2 life); fluvastatin (<3hrs); simvastatin (<5hrs)

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32
Q

which statins should you take in the morning?

A

those with longer 1/2 lives

atorvastatin (14hrs); rosuvastatin (19 hrs); pravastatin (22hrs)

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33
Q

all statins except _______ can be taken without regard to meals

A

lovastatin (should be taken with dinner)

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34
Q

adverse effects of statins?

A

all are contraindicated in pregnancy
liver monitoring no longer required
primary concern: myopathy
other concerns: myalgia, myositis, rhabdomyolysis

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35
Q

statins and myopathy

A

considered in any pts with diffuse myalgia, muscle tenderness, weakness, increase in CPK/CK,

> 10 ULN levels indicate myopathy

symptoms usually resolve apron 2 mo after discontinuing statin, can restart same statin at lower dose or try new one

can also be due to hypothyroidism, low CoQ10 levels, vitamin D

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36
Q

FDA recommendations in relation to inc risk of muscle damage with statins?

A

providers should restrict prescribing max dose of a statin

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37
Q

drug interactions and myopathies related to statins

A

protease inhibitors for HIV and hep C and statins may cause renal failure assoc with rhabdo

greater risk if administered with P450 inhibitors like azole antifungals, amiodarone, and fabric acid derivatives

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38
Q

statins and rhabdomyolysis

A

breakdown of skeletal muscle protein myoglobin with leakage of muscle contents into the circulation. can infiltrate kidneys and cause toxic reaction, obstruction (block O2 supply).

characterized by tea-colored urine, flu-like symptoms, and muscle pain
15% acute renal failure
8% mortality
<0.001% cases annually with statins
also crush injuries, overexertion, alcohol abuse

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39
Q

statins and diabetes

A

statins may cause small inc in risk of raising blood glucose levels

ADA still recommends mod-high dose statins. Risk shouldn’t stop diabetics from taking statins.

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40
Q

statins and confusion (cognitive decline)

A

2012-statin use could affect memory, attention span, etc.
2015- meta-analysis says no significant worsening of cognitive capacity
2015-statin and non-statin LDL meds associated with acute memory loss within 30 days, but confounded by fact that they see MD more, more likely to detect memory loss

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41
Q

statins and cataracts

A

risk of developing cataracts increased by 27% in those taking statins (2013)

other studies did not find association

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42
Q

efficacy of statins

A

average about 1/3 reduction in incidence of cardiovascular events (coronary heart disease)

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43
Q

statins after heart surgery

A

anti-inflammatory effects of statins may mitigate inflammation and other risks (fib in CABG) associated with extended time under anesthesia

benefits outweigh risks

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44
Q

statins effect on serious vascular events

A

they reduce serious vascular events by 20% regardless of heart disease status

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45
Q

statin recommendations for elderly (esp men)

A

97% between 65 and 77 and 100% of men in that age group should consider taking statins to reduce risk of heart attack and stroke

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46
Q

statin recommendations for adults under 75 with risk factors

A

low-moderate dose statins for those 40-75 with CVD risks

no evidence to suggest whether or not those younger than 20 should be screened for lipid disorders

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47
Q

PCSK9 inhibitors

A

proprotein convertase subtilisin/kexin type 9 inhibitors

monoclonal antibodies that target specific protein (PCSK9), which works by reducing the number of receptors in liver that remove LDL from the blood. By blocking these receptors, increase the number of receptors available to remove LDL from blood…and thus lower LDL cholesterol in blood.

“promote modulation of a receptor that clears LDL in blood”

48
Q

PCSK9 inhibitor drugs

A

alirocumab (Praluent): 1st approved. biweekly subQ injection of 75 or 150mg or monthly of 420mg

evolocumab (Repatha):biweekly 140 mg injection or monthly 420 mg subQ

49
Q

PCSK9 inhibitors are approved for use in what populations

A

in addition to diet modification and statin therapy in people with heterozygous familial hypercholesterolemia (HeFH) OR in patients with clinical atherosclerotic CVD (MI, strokes) who need additional lowering of LDL

50
Q

PCSK9 inhibitors and % LDL reduction

A

average reduction of 36-59%

51
Q

side effects of PCSK9 inhibitors

A

no myopathies (yet)!

itching, swelling, pain, bruising at injection site, nasopharyngitis, cold/flu symptoms

52
Q

bile acid resins (sequestering agents)…how do they work?

A

bind to and sequester bile acids, decreasing cholesterol return from intestines to liver and stimulating liver to produce more bile acids, “draining” liver of cholesterol and excreting it via GI tract

53
Q

major side effect of bile acid resins/dequestering agents?

A

increase triglyceride levels.

54
Q

contraindication for bile acid resins?

A

triglyceride levels >400mg/dL

55
Q

bile acid resins and % reduction of LDL

A

bile acid resins reduce LDL by 20% and increase HDL by 8%

if patients can’t take statins, they should take these…next best.

56
Q

bile acid resin agents

A

cholestyramine (Questran, Prevalite): many drug interactions, reduces their bioavailability, requires adjustment of other drugs; powder mix with liquid

colesevelam (Welchol): more potent, fewer side effects, used as absorbent in tx of c.diff

57
Q

first and only medication approved for tx of diabetes AND hyperlipidemia?

A

bile acid resin, colesevelam (Welchol)

58
Q

adverse side effects of bile acid resins

A

not absorbed systematically, no severe effects. mostly GI (constipation, heartburn, nausea)

59
Q

cholesterol absorption inhibitor drug

A

Ezetimibe (Zetia)

available as combination therapy with simvastatin (Vytorin) or atorvastatin (Liptruzet), which 2014 study shows is beneficial for lowering LDL

60
Q

cholesterol absorption inhibitor mechanism

A

inhibits intestinal absorption of cholesterol, does not affect absorption of fat soluble vitamins, triglycerides, or bile acids

different from bile acids that bind cholesterol in small intestine

makes it complementary to statins which work in the liver

61
Q

how well does Ezetimibe (Zetia) work? (% dec in LCL)

A

reduces LDL levels by 15-25%

62
Q

niacin (what it is and mechanism)

A

naturally occurring B vitamin (B3) that in large doses (100-300x the recommended daily dose as a vitamin) increases HDL and lowers LDL and triglyceride levels

mechanism unknown. thought to inhibit VLDL production, thus dec LDL

63
Q

adverse effects of niacin?

A

“niacin flushes out toxins from the body”
“I feel like I’m on fire”
primary effects are flushing and pruritus (itching). others are: nausea, GI distress, glucose intolerance, hyperuricemia, hepatic toxicity (mostly with sustained release)

64
Q

niacin and flushing (cause, management)

A

cause: mediated by prostaglandin PGD2 (vasodilation @ skin)
management: “start low and go slow; antiprostaglandins (NSAIDs) may help, avoid hot beverages and alcohol, pretreat with 325mg aspirin or 200mg ibuprofen.

65
Q

niacin and liver damage

A

more damage with SR, and OTC niacin products

Niaspan ER may be better bc its ER and not SR formulation, but its costly.

66
Q

niacin and diabetes

A

not contraindicated, but use caution! can cause a loss in glucose control, but helps lower triglycerides which are problematic in diabetic patients

67
Q

Niaspan vs. others?

A

stick with Niaspan. slower than immediate release Niacor, but faster than long acting Slo-Niacin. Long acting niacins run risk of toxic buildup from slow metabolism. others not as effective or not effective at all.

68
Q

niacin and illicit drug users

A

may try to take niacin to conceal illicit drug use. doesn’t work, but get flushing side effects and could end up with liver failure.

69
Q

HDL controversy and niacin

A

framingham study and others suggest inc HDL to lower CV risk. HPS2-THRIVE and AIM-HIGH studies show no benefit and some harm to use niacin to inc HDL levels

so, niacin should not be used routinely, only in patients with very high CV risks with contraindications for taking statins. 4th line therapy after lifestyle modification, fabric acid derivatives, pharm fish oil preparations).

bottom line: reducing HDL in isolation probably not overly beneficial

70
Q

niacin combinations, new FDA decisions?

A

in 2016, FDA pulled approval for combos of niacin ER and fenofibric acid with statins

Niaspan, Trilipix, Advicor, Simcor all affected

71
Q

fibric acid derivatives

A

decrease triglycerides and increase HDL

esp beneficial for pts with atherogenic dyslipidemia

they enhance oxidation of fatty acids in the liver and muscle to reduce the rate of lipogenesis, thus reducing VLDL triglycerides

72
Q

triglyceride levels in serum…normal/abnormal?

A

normal = 10-70mg/dL
abnormal = >150mg/dL
very high = >500mg/dL inc risk of pancreatitis

73
Q

fibric acid derivatives…drugs?

A

gemfibrozil (Lopid): GI, liver side effects. interact w/ statins to inc risk of rhabdo

fenofibrate (Tricor): many different branded generics to improve absorption

fenofibric acid (TriLipix): active metabolite of fenofibrate in SR form, lower trigly, inc HDL, lower total cholesterol (not as well as statins tho)

74
Q

omega 3 fatty acids “fish oil” (what are they used for?)

A

FDA has approved 3 of these meds to treat hypertriglyceridemia (levels >500mg/dL)

may also inc HDL and lower apoB. Lp-PLA2, and hs-CRP.

75
Q

FDA approved formulations of omega3 FAs?

A

omega-3 acid ethyl ester (Lovaza, Omtryg): DHA and EPA

icosapent (Vascepa): EPA only

omega-3 carboxylic acids (Epanova): free fatty acid form

76
Q

other tx for cholesterol?

A
  • -high soluble fiber diet
  • -garlic (0-6% dec in LDL)
  • -Policosanol (waxy substance, unclear evidence)
  • -red yeast rice/ cholestin (really works, but side effect is myopathies, if pt takes both statin and RYR, may inc chance of developing)
  • -phytosterols (prevent cholesterol absorption @ gut, no sig pharm effectS)
77
Q

how to determine if someone is in heart failure?

A

LVEF <40% is considered HF and assessment, tx should be initiated

BNP levels <100pg/ml can be used to rule out HF

78
Q

who generally gets HF?

A

those 60 years and older (75%)

blacks more at risk than whites

79
Q

first line therapy for HF?

A

minimum, both an ACEI and/or beta blocker (unless contraindicated). IF cannot tolerate ACEI, try ARB.

80
Q

second line therapy for HF?

A

aldosterone agents and combo therapy with hydralazine and a nitrate (possibly digoxin too, see sub specialist)

81
Q

drugs that exacerbate HF?

A

nondihydro CCBs, NSAIDs, thiazolidinediones

82
Q

classifications and stages for HF?

A 
Classes:
I: asymptomatic
II: symptomatic with moderate exertion
III: symptomatic with minimal exertion
IV: symptomatic at rest

Stages:
A: at risk because of CV probs
B: no symptoms but recent MI or heart damage
C:structural heart disease plus symptoms
D: refractory symptoms of HF, even @ rest

83
Q

digoxin (Digitek, Lanoxin) for HF

A

used for both heart failure and a fib

avoid at first line therapy; don’t give more than 0.125mg/day for any indication

actions: cardio-tonic (more contraction), bradycardia, anti-arrhythmic, increased cardiac output

84
Q

digoxin is a classic example of what?

A

NTI (narrow therapeutic index) drug

today’s recommendations: 0.5-0.8ug/L, don’t exceed 1.0 ug/L esp in women

85
Q

side effects of digoxin

A

bradycardia
anorexia, nausea, vomiting
yellow/green halos around lights
EKG changes (arrhythmia)
hypokalemia (doesn’t cause it, but if have it, inc risk for digoxin toxicity)
dec cardiac output (fluid, dec. K+ levels)

86
Q

how to treat digoxin toxicity?

A

hold, DC digoxin
supplement K+ if needed
treat arrhythmia
Digibind for acute toxicity (also possibly Question or Welchol)

87
Q

ACEIs for HF

A

first line therapy

improve symptoms within days, 4-12 weeks

88
Q

ARBs for HF

A

can be used alone or with Bblocker

use in patients with persistent problems even on ACEIs

89
Q

Diuretics and HF

A

loop diuretics generally more effective than thiazides for HF patients

most HF patients have fluid retention, req these

Spironolactone (inc K+) and Eplerenone (SARA) for aldosterone inhibition

90
Q

vasodilators for HF

A

concurrent use of hydralazine and ISDN (isosorbide dinitrate) improves EF

combo drug = BiDil for Af Am pop removed from market

91
Q

Beta blockers for HF

A

1st line drugs, use with ACEI or ARB if not contraindications

metoprolol succinate ER, bisoprolol, carvedilol (Best)

92
Q

antidysrhythmic agents for HF

A

arrhythmias common in HF pts

amiodarone = most positive results

93
Q

antidysrhytmic drugs for HF?

A

ivabradine (Corlanor)niche drug, blocks pacemaker channel slows rate w/ no effect on vent depolarization or contractility

Sacubitril/Valsartan (Entresto) game changer combo neprilysin inhibitor and A-II agonist given FDA priority approval. neprilysin inhibition inc. conc. on natriuretic (sodium excretion) peptides (natriuretic and vasodilatory properties)

94
Q

Entresto (sacubitril and valsartan)

A

game changer) combo drug inc. natriuretic peptides

new AHA guidelines list it as 1st line therapy instead of ACEIs and ARBs.

side effects: hypotension, hyperkalemia, renal impairment, angioedema

95
Q

drugs used for acute cardiac failure and shock include…?

A

vasopressors (change muscle contractility) and inotropic drugs (alter contractility)

dopamine (Inotropin) first line tx hotn/shock
dobutamine (Dobutrex) no norepi release
norepinephrine (Levophed) septic shock
phenylephrine (Neo-Synephrine) anesthesia
epinephrine anaphylactic shock
atropine not for asystole
milrinone (Primarcor) danger low BP
vasopressin/ADH (Pitressin) severe septic shock or afib
hBNPs (Nesiritide) doesn’t hurt, doesn’t help

96
Q

medications that worsen/exacerbate HF?

A

negative inotropics (dysarrhythmics)
cardiotoxic agents (CCBs)
Thiazolidinediones
Na/H2o retention (corticosteroids, NSAIDs)

97
Q

antianginal drugs

A

low-dose aspirin (reduce MI risk by 1/3)
CCBs (if Bblockers don’t work, can’t use)
Bblockers (initial therapy unless contraindic)
nitrates (improve exercise tolerance)
cholesterol-lowering drugs (prevent MI)
Ranolazine (Ranexa) chronic angina, prolongs QT interval

all clients should have sublingual nitroglycerin for immediate relief

98
Q

nitrate-type vasodilators

A

nitric oxide relaxes vascular smooth muscle, inhibits platelet aggregation

potent vasodilators, arterial dilators @ high doses, reduce LV wall stress, which dec. myocardial O2 demand

dosage forms: sublingual, ointment, patches, IV, aerosol, buccal

ISDN and ISMN

99
Q

ISDN vs ISMN (isosorbide dinitrate vs mononitrate)

A

ISMN preferred for management of angina

ISDN more evidence for heart failure

100
Q

side effects of nitrates?

A

flushing, headache, hypotension (monitor BP)

DONT TAKE WITH 5PDE inhibitors (viagra, cliais) b/c BP will bottom out.

101
Q

tolerance and nitrates

A

can develop tolerance over time, so make sure to use in intervals. nitrate free intervals now recommended @ least 14 hours (only wear for 8 hours)

102
Q

nitrates storage

A

they are volatile
store in close containers, check expiration dates often
newer tablets less volatile than old ones

103
Q

how many nitro tablets to take before calling 911?

A

call 911 if don’t get relief within 5 minutes of taking 1 tablet. can take up to two more (total = 3) while EMS on the way if need to.

104
Q

Ranolazine (Ranexa)

A

“metabolic modifier” for chronic angina tx
inhibits fatty acid oxidation, improves exercise performance/tolerance

prolongs QT interval

105
Q

antiarrhythmic drugs

A 
class I: Na2+ channel blockers
class II: beta blockers-inhibit catecholamines
class III: K+ channel blockers 
class IV: Ca2+ channel blockers
misc: digoxin, adenosine
106
Q

vaughn-williams classifications

A 
class I: Na2+ channel blockers
a--rarely used, frequent toxicity
b--
c--proarryhthmics, no structural HD
class II: beta blockers-inhibit catecholamines
class III: K+ channel blockers 
class IV: Ca2+ channel blockers
107
Q

arrhythmia should be called?

A

dysarrhythmia (connotes tachyarrhythmia)

108
Q

most commonly encountered arrhythmia and common recommendation for it?

A

a fib

warfarin or NOAC daily to prevent complications of fib (clots, stroke)

109
Q

initial therapy for a fib?

second-line therapy?

A

control ventricular rate with nodihydro CCB, BBlocker, or digoxin

restore sinus rhythm w/ electrical cardioversion

110
Q

Class IA anthiarrhythmic agents

A

quinidine (Quinagulate, Quinidex)
Procainamide (Pronestyl)
disopyramide (Norpace)

111
Q

Class IB anthiarrhythmic agents

A

lidocaine (Xylocaine) *losing to amiodarone, may cause seizures, short acting)

fosphenytoin (Cerebyx) prodrug to dilantin, mostly with digitalis-induced tachyarrhythmia

Mexiletine (Mexitil): “oral lidocaine”

112
Q

Class IC anthiarrhythmic agents

A

proarrhythmic, only use in pts without structural heart disease

boxed warning: use only for life-threatening refractory arrhythmias

includes felcainide (Tambocor) and propafenone (rythmol)

113
Q

Class II anthiarrhythmic agents

A

beta blockers

includes: 
propranolol (Inderal)
acebutolol (Sectral)
Timuolol (Blocadren)
Esmolol (Brevibloc) *rapid
Sotalol (Betapace) *rapid, also K+ blcoker*
114
Q

Class III anthiarrhythmic agents

A

K+ channel blockers

sotalol
ibutilide
dofetilide
AMIODARONE complete VW classifications

115
Q

Class IV anthiarrhythmic agents

A

verapamil

diltiazem

Nursing-Sem 1 (13 decks)

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