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HLST220: Pharmacology > Chapter 53: Cholesterol and Triglyceride Levels > Flashcards

Chapter 53: Cholesterol and Triglyceride Levels Flashcards

1
Q

cholesterol is manufactured by cells primarily in the

A

liver

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2
Q

cholesterol comes from

A

dietary sources

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3
Q

cholesterol is required for

A

synthesis of certain hormones and bile salts
e.g. estrogen, progesterone, testosterone

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4
Q

lipoproteins function

A

transports lipids in the blood

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5
Q

Very-low-density lipoproteins (VLDLs)

A
  • trglycerides
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6
Q

Low-density lipoproteins (LDLs)

A
  • cholesterol is the primary core lipid
  • greatest contributor to coronary artery disease
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7
Q

High density lipoproteins (HDLs)

A
  • cholesterol primary core lipid
  • carry cholesterol from peripheral tissues back to the liver thereby promoting cholesterol removal
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8
Q

what intitiates the development of atherosclerosis

A

LDL

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9
Q

Framingham Risk score

A
  • risk level
  • treatment recommendation
  • therapeutic target
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10
Q

who is most susceptible to coronary artery disease

A
  • older adults
  • women
  • diabetes
  • unhealthy eating problems
  • people exposed to air polution
  • physically inactive
  • stress
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11
Q

Lifestyle interventions

A
  • smoking cessation
  • mediterranean diet
  • weight loss, diabetes treatment
  • stress, alcohol
  • exercise
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12
Q

drug classes

A
  • HMG-CoA reductase inhibitors (statins)
  • Bile acid sequestrants (resins)
  • nicotinic acid [niacin]
  • fibrates
  • ezetimibe [Ezetrol]
  • Monoclonal antibody inhibitors (evolocumab and alirocumab)
  • Icosapent ethyl (Vascepa)
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13
Q

Metabolic abnormalities include

A
  • high blood glucose
  • high triglycerides
  • waist circumference (large)
  • hypertension
  • prothrombotic state
  • proinflammatory state
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14
Q

metabolic syndrome treatment goals

A
  • reduce risk for atherosclerotic disease
  • reduce risk for type 2 diabetes
  • increase physical activity
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15
Q

HMG-CoA Reductase Inhibitors (Statins) is

A

most effective drug for lowering LDL

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16
Q

HMG-CoA Reductase Inhibitors (Statins) is used to

A
  • reduce LDL cholesterol
  • elevate HDL cholesterol
  • reduce triglyceride levels
  • promote plaque stability
  • reduce risk for cardiovascular events
  • increased bone formation (reduced osteoporosis, fractures)
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17
Q

HMG-CoA Reductase Inhibitors therapeutic uses

A
  • hypercholesterolemia
  • primarily and secondary prevention of cardivascular events
  • Post MI therapy
  • cardiovascular risk reduction in diabetes
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18
Q

does HMG-CoA Reductase Inhibitors have first pass effect

A

yes

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19
Q

which ethnicity is reccomonded lower doeses of HMG-Co-A reductase inhibitors

A

east asians

20
Q

HMG-CoA Reductase Inhibitors adverse effects

A
  • headache, rash, Gi disturbance, dyspepsia, constipation, abdominal pain
  • myopathy/rhabdomyolysis, hepatotxicity, new onset diabetes
21
Q

HMG- CoA Reducatase Inhibitors drug and food interactions

A
  • drugs that inhibit CYP3A4
  • grapefruit juice
22
Q

HMG-CoA Reducatase Inhibitors dosing

A

once daily in the evenings

23
Q

Examples of HMG-CoA Reductase Inhibitors (Statins)

A

Atorvastatin [Lipitor]
- Fluvastatin [Lescor]
- Pravastatin [Mevacor]
- rosuvastatin [Crestor]
- Simvastatin [Zocor]

24
Q

Nicotinic Acid [Niacin] efffects on lipids

A
  • reduces LDL and TG levels
  • raises HDL levels better than other drugs
25
Q

Nicotinic Acid [Niacin] adverse effects

A
  • flushing and itching skin
  • gastrointestinal upset
  • hepatotxicity
  • hyperglycemia
  • gouty arthritis
26
Q

Nicotinic Acid [Niacin} contradicitions

A

severe peptic ulcer disease, chronic liver disease

27
Q

Bile acid Sequestrants are used

A

as adjuncts to statims to reduce LDL; can minimally increase HDL

28
Q

Bile Acid Sequestrants examples

A

Cholestyramine [Questran]
- colestipol [colestid]

29
Q

Bile Acid Sequestrants adverse effects

A
  • consipation
  • bloating
  • indigestion
  • decreased absorption of fat soluable vitamins
30
Q

Bile Acid Sequestrants drug interaction

A
  • Warfarin (antibiotics, Diuretics)
    ** space 2 hours apart from other meds
31
Q

Ezetimibe [Ezetrol] therapeutic use

A
  • reduces total cholesterol, LDL cholesterol, and apolipoprotein B
  • approved for monotherapy and combined use with stains
32
Q

Ezetimibe [Ezetrol] should be used cautiously in

A

liver dysfunction

33
Q

Ezetimibe [ezetrol] adverse effects

A
  • myopathy
  • rhabdomyolysis
  • hepatitis
  • thrombocytopenia
  • pancreatitis
34
Q

what is the most effective available for lowering TG levels

A

Fibric Acid Derivative [Fibrates]

35
Q

Fibric Acid Derivative [Fibrates] effect on HDL

A

can raise cholesterol

36
Q

Fibric Acid Derivative [Fibrates] available drugs

A

Gemfibrozil [lopid]
- fenofibrate
- bezafibrate

37
Q

Fibric Acid Derivative [Fibrates] can increase risk for bleeding in patients taking

A

warfarin

38
Q

Fibric Acid Derivative [Fibrates] can increase the risk for rhabdomyolysis is patient taking

A

statins

39
Q

Gemfibrozil effects on plasma lipoproteins

A
  • decreases plasma TG content
  • lowers VLDL levels
  • can raise HDL cholesterol
40
Q

Gemfibrozil drug interactions

A
  • displaces warfarin from plasma albumin
41
Q

Gemfibrozil adverse effects

A

rashes, gastrointestinal disturbances (abdominal pain, GI upset), gallstones, myopathy, liver injury (hepatotoxic)

42
Q

Gemfibrozil contradictions

A

Hepatic or renal disease

43
Q

Monoclonal Antibodies examples

A

Alirocumab [Praluent], Evolocumab [Repatha], Inclisiran [Leqvio]

44
Q

monoclonal Antibodies are used for

A

patients with high LDL

45
Q

Icosapent Ethyl [Vascepa] indication

A

decreasing risk of ASCVD events in clients with:
- diabetes and additional risk factors
- known CVD on a stain with high TG’s

46
Q

Icosapent Ethyl [Vascepa] adverse effects

A

prolonged bleeding time

47
Q

Icosapent Ethyl [Vascepa] dose

A

2g BID

HLST220: Pharmacology (46 decks)

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