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Pharmacology > DRUGS FOR LIPID DISORDERS > Flashcards

DRUGS FOR LIPID DISORDERS Flashcards

1
Q

what are the three main types of lipids?

A
  • triglycerides
  • phospholipids
  • steroids (eg, cholesterol)
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2
Q

what are triglycerides?

A
  • account for 90% of total lipids in the body
  • important source of energy (fuel in times of energy need)
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3
Q

what are phospholipids?

A

essential for the formation of plasma membranes

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4
Q

what are steroids (cholesterol)

A
  • essential component of plasma membranes
  • building block for bile acids, vitamin D, cortisol, estrogen & testosterone
  • liver can synthesize cholesterol; no need for source from diet
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5
Q

what are lipoproteins?

A

lipids are not soluble in plasma and require “special packaging” to be distributed to body tissues
- complex of triglycerides, cholesterol and phospholipids with a protein carrier (apoprotein)

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6
Q

what are the 3 major types of lipoproteins?

A
  • high density lipoprotein (HDL)
  • low density lipoprotein (LDL)
  • very low density lipoprotein (VLDL)
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7
Q

what is LDL?

A
  • bad cholesterol
  • transports cholesterol from the liver to tissues; used to create plasma membranes and other steroids; cholesterol can be stored for later use
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8
Q

what is VLDL?

A

primary carrier of triglycerides, converted into LDL; reduced to LDL

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9
Q

what is HDL?

A
  • good cholesterol
  • transports cholesterol from tissues back to the liver “reverse cholesterol transport”
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10
Q

what is dyslipidemia?

A
  • increases risk of atherosclerosis and coronary artery disease
  • occurs predominantly in men compared to non-menopausal women
  • after menopause (>50 years of age), risk becomes higher in women
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11
Q

what are the non pharmacological managements for lipid disorders?

A
  • smoking cessation
  • abstaining from alcohol
  • maintain weight an waist circumference
  • regular exercise and stress reduction
  • reduce dietary saturated fat, trans fat and cholesterol (cholesterol intake should not exceed 300mg/day)
  • increased consumption of plant sterols/stanols & soluble fibre
  • nuts, olive oil, corn, rye, oats, rice an wheat
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12
Q

what are statins?

A
  • HMG-CoA reductase inhibitors (atorvastatin)
  • inhibits activity of HMG-CoA reductase, blocking cholesterol synthesis
  • increases the # of LDL receptors in the liver and stimulates removal of LDL from the blood
  • high efficacy
  • significant reduction in LDL, lower VLDL, increases HDL levels
  • slows progression of CAD and reduces CVD associated mortality
  • effects are reversible, may take up to a month to achieve
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13
Q

what is the first line therapy in treatment of lipid disorders?

A

statins

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14
Q

what can statins be combined with?

A

may be combined with other cholesterol lowering medications and antihypertensive medications

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15
Q

what are cautions of statins?

A

contraindicated in people who are pregnant or may become pregnant; contraceptive coverage recommended
- therapy must be discontinued during pregnancy; treatment can resumed after breastfeeding
- some statins are more hydrophilic (pravastatin), should be considered in pregnant people

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16
Q

what are adverse effects of statins?

A

headache, heart burn, GI upset (take with evening meal)

17
Q

drug-drug interactions with statins?

A
  • clients should avoid alcohol an grapefruit juice
  • small but significant risk of rhabdomyolysis, especially in elderly clients
  • waste products cause acute renal failure, associated with significant muscle pain
  • risk increased with higher doses or co-administration of drugs (macrolides, anti-fungal agents) that inhibit CYP 450 enzymes or drugs that increase the bioavailability of statin drugs (PPIs an H2RAs)
  • statins potentiate the effects of warfarin
18
Q

what is the selective cholesterol absorption inhibitor?

A

ezetimibe

19
Q

what is ezetimibe?

A
  • inhibits intestinal cholesterol absorption; first line “add-on therapy”
  • blocks absorption by as much as 50%
  • can be used as mono therapy in clients with complete statin intolerance for LDL lowering
20
Q

what is the most common adverse effect of ezetimibe?

A

Gi distress

21
Q

when is statin therapy co administered with ezetimibe?

A

for clients that fail to reach their LDL targets with statin therapy alone
- reduces LDL levels 20% in addition to statin
- act to synergistically to inhibit cholesterol absorption (ezetimibe) and cholesterol synthesis (statin)

22
Q

what happens to bile acid?

A

gets recycled

23
Q

where are bile acid sequestrants?

A

non absorbed, bind to bile acids and impede enterohepatic circulation, increasing the excretion of cholesterol (via the feces)
- ultimately reduce blood cholesterol levels and reduce risk of major cardiovascular events
- 2-% drop in LDL cholesterol events

24
Q

what happens when cholesterol levels are reduced?

A

induces the formation of additional LDL receptors in the liver, increasing the rate at which LDL is removed from the blood an promoting the conversion of cholesterol to bile acids

25
Q

what effect occurs when when bile acid sequestrants are co prescribed with statins?

A
  • additive effect
  • considered an alternative to ezetimibe as an “add on” to statin therapy
26
Q

what are adverse effects to bile acid sequestrants (eg. colesevelam)?

A
  • GI upset, may induce abdominal pain, bloating, diarrhea, steatorrhea, constipation
27
Q

what drugs does bile acid sequestrants interfere with absorption?

A

thiazide diuretics, warfarin, thyroid hormones, corticosteroids
- take other medications 1 hour before, or 4 hours after
- also may induce vitamin deficiency (vitamin A,D,K
- vitamin K deficiency leads to increased bleeding times

28
Q

what are the PCSK9 inhibitors?

A

evolocumab (repatha) & alirocumab (praluent)

29
Q

what are the function of PCSK9 inhibitors?

A
  • inhibit PCSK9 proteins that target liver LDL receptors for degradation
  • lower LDL levels by 50-70% in addition to statin
  • inject subcutaneously every 2 weeks or a month
  • significant reduction in clinical outcomes (50%) associated with atherosclerotic cardiovascular disease
30
Q

what is the function of monoclonal antibodies?

A

bind to PCSK9, preventing it from binding to LDL receptors

Pharmacology (20 decks)

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