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PATHO/PHARM II > Dyslipidemia & Agents > Flashcards

Dyslipidemia & Agents Flashcards

Kaplan Pharm

1
Q

Lipoproteins: What are there functions?

A

Lipid transport (not H2O soluble)

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2
Q

Classes of ”chylomicrons”

A

VLDL, LDL, HDL

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3
Q

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What are they made up of?

A

Lipid core = TGs

VLDL particles contain triglycerides as their major component, along with cholesterol and other lipids.

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4
Q

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What are they responsible for?

A

Responsible for transporting triglycerides synthesized in the liver to various tissues in the body for energy or storage.

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5
Q

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What is the risk with elevation of VLDL?

A

Increased VLDL ~ increase in TGs

Link to atherosclerosis not firmly established

> 500mg/dL ~ pancreatitis

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6
Q

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs

A

By-products of VLDL metabolism

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7
Q

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs:

What are they directly related to?

A

Directly related to ASCVD risk, target of TX

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8
Q

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs:

What are they directly related to?

A

Directly related to ASCVD risk, target of TX

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9
Q

Classes of ”chylomicrons”: High-Density Lipoproteins HDLs:

What are they directly related to?

A

Reduces ASCVD risk

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10
Q

Dyslipidemia: Complications

A

Atherosclerosis

HTN, CAD, PVD

Stroke

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11
Q

Dyslipidemia: Familial dyslipidemia

A

↑ liver production of cholesterol

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12
Q

Approach to Drug Therapy for Dyslipidemia:

A

Primary target ↓ LDL

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13
Q

Approach to Drug Therapy for Dyslipidemia:

Primary target ↓ LDL: What med is initiated first?

A

HMG-CoA reductase inhibitors initiated 1st

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14
Q

Approach to Drug Therapy for Dyslipidemia:

Primary target ↓ LDL: What med is an add on?

A

Add-on bile acid sequestrant

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15
Q

Approach to Drug Therapy for Dyslipidemia:

What are fibrates used for?

A

Fibrates primarily for TGs, not LDL

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16
Q

Drug Classes Used for Dyslipidemias & ASCVD PX include:

A

HMG-CoA Reductase Inhibitors (Statins)

Bile-Acid Sequestrants

Ezetimibe

Fibric Acid Derivatives (Fibrates)

PCSK 9 Inhibitors (Monoclonal Antibodies)

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17
Q

HMG-CoA Reductase Inhibitors end in?

A

(Statins)

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18
Q

HMG-CoA Reductase Inhibitors: What are they most effective for?

A

Most effective for ↓ LDL & total cholesterol

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19
Q

HMG-CoA Reductase Inhibitors: What can they aid in?

A

Evidence for possible benefits for osteoporosis

20
Q

HMG-CoA Reductase Inhibitors: When is cholesterol synthesis greatest in the day? What does this mean about when med should be taken?

A

increases Cholesterol synthesis @ night ~ QHS

21
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it inhibit?

A

Inhibition of HMG-CoA reductase (enzyme for cholesterol synthesis)

22
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it increase?

A

Increase hepatocyte production of LDL receptors

23
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it decrease?

A

↓ production of apolipoprotein B-100 ~  VLDL & TGs

24
Q

HMG-CoA Reductase Inhibitors (Statins)

ADEs:

A

Generally well tolerated-Transient HA, rash, GI disturbances

Hepatotoxicity

Cataracts

Myopathy

Rhabdomyolysis

Teratogenic

25
HMG-CoA Reductase Inhibitors (Statins) ADEs: Myopathy What is a sign of this?
Muscles aches, tenderness, weakness
26
HMG-CoA Reductase Inhibitors cont. ADEs: Rhabdomyolysis What are risk factors?
Advanced age, small body frame, frailty Multisystem DX ~ chronic renal insufficiency & DM High doses & rosuvastatin **Low vitamin D & coenzyme Q, supplement ** **Concurrent fibrates** Concurrent agents that  statins
27
HMG-CoA Reductase Inhibitors cont. Drug interactions:
Concurrent lipid-lowering drugs CYP-3A4 inhibitors
28
HMG-CoA Reductase Inhibitors cont. Drug interactions: CYP-3A4 inhibitors:
increase lovastatin & simvastatin increase atorvastatin
29
Bile-Acid Sequestrants: What do they do to LDLs? VLDL (what does this mean for people with very high VLDLs)?
decrease LDL ~ 20% Mild transient increases VLDL in some (Avoid if VLDL already high)
30
Bile-Acid Sequestrants: Mode of Action:
Bile acids --> intestine --> XX --> reabsorbed increases bile acid secretion excretion --> increase synthesis (requires cholesterol) increases LDL receptors on hepatocytes = increase LDL uptake from plasma
31
Bile-Acid Sequestrants ADE
Mainly issues w/ cholestyramine, colestipol Constipation decrease uptake of fat-soluble vitamins ADEK GI upset bloating, indigestion, nausea
32
Bile-Acid Sequestrants Interactions
Insoluble complex w/ PO meds
33
Bile-Acid Sequestrants Interactions: How should it be taken with thiazides, digoxin, warfarin, certain antibiotics?
Thiazides, digoxin, warfarin, certain ABX 1h before, 4h after
34
Ezetimibe: How is it used?
Used as add-on w/ statin, or monoTX
35
Ezetimibe: MOA: Actions on brush border cells (small intestine)
Inhibits dietary cholesterol absorption Inhibition of cholesterol reabsorption secreted in the bile
36
Ezetimibe: MOA: Lipoprotein effects
decrease total cholesterol, LDL, TGs, apolipoprotein B. Small increase in HDL No evidenced of decrease ASCVD
37
Ezetimibe: ADE: Who should it be avoided in?
Avoid in moderate-severe hepatic impairment
37
Ezetimibe: ADE:
Gallstones ~ increase bile cholesterol
38
Fibric Acid Derivatives (Fibrates) ~ -fibr Effects on lipoproteins?
Most effective for decreasing TG 40-55% Can increase HDL 6-10% Little or no effect on LDL (may actually increase) No evidenced of decreasing ASCVD
39
Fibric Acid Derivatives (Fibrates) ~ -fibr: When is it used?
Considered 3rd line
40
Fibric Acid Derivatives (Fibrates) ~ -fibr
Activation of PPAR-alpha receptor (liver & brown adipose tissue) Accelerated clearance of VLDLs ~ increases TGs Increase apolipoproteins A-I & A-II ~increasing HDL
41
Fibric Acid Derivatives (Fibrates) ~ -fibr ADEs:
Gallstones Myopathy Hepatotoxicity ~ periodic LFTs
42
Fibric Acid Derivatives (Fibrates) ~ -fibr Interactions
Displacement of warfarin from albumin
43
PCSK9 Inhibitors- end in what?
mab
44
PCSK9 Inhibitors- MOA:
Monoclonal antibodies that inhibit PCSK9 (protein) “Frees-up” receptor for LDL uptake ~ decrease in plasma LDL
45
Fish Oil & Omega-3 Agents
Contains omega-3 fatty acids ~ EPA & DHA Reduces risk of CAD progression & PX arrythmia
45
Contains omega-3 fatty acids ~ EPA & DHA: What is it not effective for?
OTC Fish oil is NOT effective for Lowering LDL Direct protection for ASCVD

PATHO/PHARM II (27 decks)

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