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Karboski's Pharmacology - UT AEMSN > Lipids > Flashcards

Lipids Flashcards

1
Q

What was the result of the “Mr. Fit” trial (ASCHD Mortality and Cholesterol)

A

Total cholesterol levels have a strong correlation to 10 year coronary heart disease

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2
Q

How can you tell the extent of CAD risk?

A

Calcification (CAC score) from a Heart Saver CT

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3
Q

Describe the overall process of atherosclerotic vessel changes/lesion development.

A
  • Infiltration into intima
  • Worsening build-up develops
  • Thrombus formation and increased calcification
  • Vessel rupture –> loosened thrombus
  • Embolism formed –> MI, CVA, PE
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4
Q

Describe how Bile Acid Resins (BARs) reduce LDL cholesterol.

A
  • BARs bind bile acids released that solubilize fats for absorption
  • Bile acids can’t be reabsorbed –> pooped out
  • Liver utilizes serum LDL to form new cholesterol –> ↓ serum level
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5
Q

↑↓ ≥ ≤

A

[symbols to copy/paste]

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6
Q

What are the BAR ADRs?

What % get SE? Why?

A

1) constipation, flatulence, bloating, epigastric fullness, nausea (not as much with newer)
2) 100% of ppl get SE. Because the SE are dose related and occur with every administration

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7
Q

How to manage SE of BARs?
What % of people d/c use? Why?
Suggestions to ↓ aversions to powdered formula?

A

1) Start w/ small doses and titrate up
2) ~40% d/c w/in a year b/c of GI ADRs
3) Suggestions:
- Mix powder with pulpy beverage and serve cold
- Do not mix w/ carbonated beverage (gas + gas)

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8
Q

What are some warnings associated with BARs?

A
  • A lot of Rx interactions (complexation interactions)
  • Fat soluble vitamins may not get absorbed (A,D,E,K)
  • Take vitamins/meds 4 hour before BARs
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9
Q

1) Describe Niacin’s MoA.
2) What is the immediate max dose/day?
3) What is the sustained release max dose/day?

A

1) ↓ liver production of VLDL –> ↓ LDL because of ↓ precursors
2) 4000 mg/day max for immediate release
3) 2000 mg/day max for sustained release

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10
Q

1) Which dosage form of Niacin has more common SE? Why?

2) Which of Niacin’s dosage forms is of more concern for serious ADRs? Why?

A

1) Immediate release; b/c higher max peak concentration
2) Sustained release
- Because longer DoA and larger area under curve = ↑ concentration over time and longer build-up
- –> Hepatotoxicity

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11
Q

1) What MoA occurs 100% of the time to some extent when taking Niacin? What SE does it cause?
2) Approx onset and duration of this SE?

A

1) vasodilation of vessels in skin; flushing

2) 15 min onset, 15-30 min duration

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12
Q

1) What are the common SE of Niacin?
2) What are the serious SE of Niacin?
3) Which serious SE occur only if certain conditions already present?

A

1) flushing, itching, rash, hives
2) liver toxicity, muscle damage, gastritis/GI bleed (ulceration)
3) Hyperglycemia and DM
- BGL may be harder to control or may ↑ if already ↑
Gout
- Symptoms may be worsened if ↑ uric acid levels already present

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13
Q

1) How can Niacin SE be prevented/reduced?

2) Which prevention method is not longer recommended? Why?

A

1) small doses and titrate ↑ (get used to slowly)
- take w/ food (slows absorption)
- XR –> ↓ SE (but concern for liver tox)
- avoid admin w/ hot fluids and EtOH (worsen Sx)
2) 325 mg ASA; not recomm d/t concerns w/ NSAID overuse

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14
Q

What is the definition of myalgia?

A

Muscle pain without ↑ in CK-MB

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15
Q

1) Define potency

2) If a drug is potent, what does that mean?

A

1) How much of a drug it takes to achieve a desired effect
2) If an extremely small dose of drug “A” –> desired effect versus and a large dose of drug “B” for the same effect, then drug “A” is more potent than “B”.

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16
Q

1) Cholestyramine lipid average effects:

A

1) TRG ↑ and LDL-C ↓

- approx. 10-25%

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17
Q

1) Niacin lipid average effects:

A

1) TRG ↓ about double of HDL-C ↑ and LDL-C ↓ (15-25%)

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18
Q

1) Statin lipid effects (Atorvastatin):

A

1) TRG ↓ good and LDL-C ↓ great

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19
Q

Summary of Lipid Effects By Drug Class:

1) BARs (Cholestyramine)
2) Niacin
3) Statins
4) Fibric Acids (Gemfibrozil)
5) Omega-3 Fatty Acids (Lovaza)
6) Ezetimibe
7) PCSK9 Inhibitors

A

1) TRG ↑↑, LDL ↓↓
2) TRG ↓↓, HDL ↑↑, LDL ↓↓
3) TRG ↓↓, LDL ↓↓↓
4) TRG ↓↓↓, HDL ↑↑
5) TRG ↓↓, HDL ↑,
* may ↑↑ LDL in some
6) (solo or combo) LDL ↓↓
7) (solo or combo) LDL ↓↓↓

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20
Q

1) Fibric Acid lipid effects (Gemfibrozil):

A

1) TRG ↓ A lot and HDL-C ↑ some

21
Q

1) Omega-3 FA lipid effects (Lovaza):

A

1) TRG ↓ A lot and HDL-C ↑ 10%

- can LDL-C ↑ substantially, so check lipids at least once

22
Q

1) Ezetimibe lipid effects (Zetia):

A

1) LDL-C ↓ 15-20%

- monothpy or w/ statin

23
Q

1) PCSK9 Inhibitor lipid effects:

A

1) LDL-C ↓ 50-60% mono;

LDL-C ↓ 40% w/ statin

24
Q

Why are statins considered the drug of choice?

A
  • “Statin magic”

- ↓ LDL alone more than all other Rx

25
Q

Common statin ADRs

A
  • GI intol
  • Myalgia
  • Flu-like Sx
  • Fatigue
26
Q

Statin hepatotoxicity ADR three monitoring key points.

A
  • Watch for >3x upper limit of LFTs on 2 consecutive occasions
  • Routine LFT monitor no longer req’d b/c serious liver problems are now rare
  • ↓ dose or D/C until levels = nml then re-challenge
27
Q

What is the spectrum of statin-induced myopathy and CK levels?

A
  • Small ↑ in CK is nml
  • > 10x ↑ in CK = myopathy
  • > 10,000x ↑ in CK = Rhabdo
28
Q

What factors can ↑ incidence of myopathy with statins?

A

1) Higher statin doses
- r/t [statin] in blood
- ↓ incidence w/ ↑ potency
2) Renal impairment
3) Statin + Fibrate
4) Rx interfering w/ Statin metabolism
- Macrolide, cyclosporin, -azole’s

29
Q

Management of unexplained severe muscle Sx or fatigue in Statins?

A

1) D/C Statin
2) Address possible Rhabdo
- CK, SCr, UA for myoglobinuria

30
Q

Management of mild-moderate muscle symptoms in Statins?

A

1) D/C statin until Sx eval
- consider other causes (HoTSH, renal/hepatic, RA, steroid-induced)
2) If >2 mo and Sx not resolved or CK still ↑ = not Statin
3) Resume Statin if not cause

31
Q

1) How is Cognitive impairment different from Dementia?

2) What is the prognosis if a patient develops cognitive impairments on a Statin?

A

1) Cognitive impairment involves reduced cognitive functions (processing speed, etc..) while Dementia involves memory-based Sx
2) Risk goes away following D/C, fxn should return to nml after D/C

32
Q

1) What is the MoA for Fibric Acids?

2) What is its primary activity?

A

1) ↑ activity of lipoprotein lipase –> ↑ breakdown of VLDLs and chylomicrons
2) Lowers TRGs

33
Q

What are the Fibric Acid ADRs?

A
  • Dyspepsia, ABD pain
  • Myopathy (↑ w/ renal impairment and concurrent statin)
  • ↑ hypoglycemic effect w/ sulfonylureas
34
Q

What are the indications for Omega-3 Fatty Acids?

A

Adjunct to diet to ↓ TRG if severe ( >500)

35
Q

What are the common ADRs for Omega-3 FAs?

A
  • eructation (burping)
  • flu-like Sx
  • dyspepsia
  • taste sensation changes
36
Q

What are some warnings to know about Omega-3 FAs?

A
  • Possible hepatic impair
  • May ↑↑ LDL in some
  • Seafood allergy
  • May ↑ bleeding risk on anticoags
37
Q

Ezetimibe:

1) MoA
2) Indications
3) ADRs

A

1) Inhibits chol absorption
2) Monothpy or w/ Statin to ↓ LDL
3) No diff from placebo GASP

38
Q

PCSK9 Inhibitors:

1) MoA
2) Route
3) Efficacy
4) Other important notes

A

1) inhibits enzyme that bkdwn LDL receptors
2) Subcut, can be self-admin
3) Mono ↓ LDL 50-60%; w/ Statin ↓ LDL 40%
4) Puts a price tag on life $$$$ and QAYL; great additive but not proven to ↓ M/M, esp w/ familial HLD

39
Q

PCSK9 Inhibitor ADRs

A
  • Injection site swelling/rash
  • Limb/back pain
  • fatigue, cold/flu-like Sx
  • Neurocognitive (conf, memory impair, diff focus)
40
Q

Overall message of “Old Way”, ATP 3?

A
  • optimal LDL approx 40 mg/dL

- At this level, showed same risk as ppl w/out LDL issues

41
Q

Overall message of “New Way”, AHA/ACC?

A

1) HDL : LDL more important
- –> No LDL goal
2) ↑ Statin –> ↑ benefits
- –> No Statin –> No proven risk reduction in ASCVD

42
Q

What are the 4 Statin Benefit Groups?

A

1) Individ w/ ASCVD: ACS + Hx
2) ≥ 21 yo w/ LDL ≥ 190
3) DM, 40-75 yo, LDL 70-189
4) No DM, 40-75, LDL 70-189, ASCVD risk ≥ 7.5%

43
Q

Statin Therapy Intensity for High, Mod, and Low:

  • % LDL ↓
  • One of the Drugs + Dose
A

1) High: ↓ LDL by ~50%; Atorvastatin 40-80 mg
2) Moderate: ↓ LDL by 30-50%; Atorvastatin 10-20 mg
3) Low: ↓ LDL by < 30%; Simvastatin 10 mg

44
Q

When is one of the only instances when Low-Intensity Statin Thpy is indicated?

A

When SE at High and Moderate levels not tolerated

45
Q

How does a patient meet Very-High Risk criteria for Secondary Prevention?

A

2 major ASCVD events
or
1 major ASCVD event + 2 High Risk Conditions

46
Q

What are the major ASCVD events for Secondary Prevention?

A

1) ACS w/in past 12 mo
2) Hx of MI, CVA
3) Hx/Sx of PAD
- ABI < 0.85 w/ claudication
- prev revascularization
- arthroplasty
- amputation

47
Q

What are the Very High RIsk Conditions for Secondary Prevention?

A

1) ≥ 65 yo
2) HLD family Hx
3) Hx of PCI
4) DM
5) HTN
6) CKD
7) Current smoking
8) Persistent LDL ≥ 100 despite Statin and ezetimibe
8) Hx of CHF

48
Q

What to do if goals not met?

A

1) eval adherence to statin thpy and efforts at lifestyle changes
2) ↑ statin dose if possible
3) Add ezetimibe and/or PCSK9
4) Address other risk factors
- Tobacco, DM, HTN

Karboski's Pharmacology - UT AEMSN (11 decks)

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