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🄼💊 CARDIO PATH/RX > pharm: 9-29 Hyperlipidemia drugs > Flashcards

pharm: 9-29 Hyperlipidemia drugs Flashcards

1
Q

Statins

Indications

A

High LDL

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2
Q

Statins

  • Effect On [Serum Lipids]*
  • -LDL*
  • -TriAcylGlycerides*
  • -HDL*
A
  • DEC LDL by 20-60%
  • DEC TriAcylGlycerides by 10-20%
  • INC HDL by 5-10%
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3
Q

Statins

A: Adverse Effects (4)

A2: Which 2 Adverse Effects are Dose Dependent?

B: Contraindications (3)

A

A:

  1. Muscle myopathy —-> myalgia (Dose Dependent)
  2. RHABDOMYOLYSIS (Dose Dependent)
  3. Hepatitis
  4. small risk of [Type2DM] development

B: Contraindications

“Don’t give Statins to Pregnant Lady Girls “

(x) Pt with Severe Liver Dz
(x) Pt taking Gemfibrozil
(x) Pregnant Women

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4
Q

Statins

  • Drug Interactions:*
  • A: Name the compounds that inhibit* [CYP3A4] (7)
  • B: How does this affect Statins?*
  • C: Which Statins specifically does it affect? (3)*
A

A: “CYP3A4 is inhibited by a CHECK WIG”

1) Erythromycin / Cyclosporin / Ketaconazole / Itraconazole [HIV protease inhibitors] / Warfarin / [Ca+ channel blockers] / Grapefruit Juice

B: THESE INC RISK OF ADVERSE EFFECTS FROM STATINS

C: “S A L is easily affected by CYP3A4 inhibition”

( Simvastatin- Atorvastatin- Lovastatin )

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5
Q

Statins

Mechanism of Action

A

[HMG-CoA Reductase analogs] that Competitively Inhibit [HMG-CoA Reductase] once they bind—> and as a result DEC Endogenous Cholesterol–>triggers [S-REB-P tx factor] —–>

*INC [Hepatic LDL receptors]

*INC [LDL Clearance from Blood]

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6
Q

Statins

  • Drug Interactions:*
  • A: Name the compounds that inhibits* [CYP2C9] (2)
  • B: Which Statins specifically do they affect? (2)*
A

A:

1) Ketaconazole and Metronidazole

B: INCREASES (Fluvastatin-Rosuvastatin)

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7
Q

Statins

  • Drug Interactions:*
  • A: Name the compounds that stimulate* [CYP3A4] (3)
  • B: How does this affect Statins?*
  • C: Which Statins specifically does it affect? (3)*
A

A:

1) Phenytoin / Rifambin / Phenobarbital - PRP

B: THESE DEC CLINICAL EFFICACY OF STATINS

C: DECREASES in (Lovastatin-Simvastatin-Atorvastatin)

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8
Q

Statins

Drug Interactions:

A: How does Gemfibrozil affect Statins? (2)

B: What serious condition can this lead to?

A

A: Gemfibrozil [Inhibits (Hepatic OATP2 Transporter)] –> [DEC Glucoronidation] AND [DEC (Hepatic UGTA1/3)] ———> INC ALL STATIN BIOAVAILABILITY

B: Rhabdomyolysis!!

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9
Q

[Bile Acid Binding Resins - BABR]

A: Name the 3 drugs in this class

B: Indications (5)

C: Mechanism of Action:

CATION tht Binds up _____ and prevents _____ ReAbsorption —> [INC _____]—-> [DEC Hepatic Cholesterol] —-> [INC _____] —> [DEC​ ______ by ___%]

A

A:

Cholestryramine / Colestipol / Colescelam

B: LA COP

[LDL elevated in Pregnant women and children]

[Adjunct tx with Statin]

  • [Crohn’s Dz iLeal Resection Diarrhea - CDiRD]
  • OD tx for Digoxin and Levothyroxine
  • Pruritus 2º to Liver failure

C:

CATION tht Binds up [Anion Bile Acids] and prevents Intestinal ReAbsorption —> [INC Cholesterol 7alpha hydroxylase]—-> [DEC Hepatic Cholesterol] —-> [INC LDL Receptors] —> [DEC LDL in blood by 10-25%]

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10
Q

[Bile Acid Binding Resins]

  • A: Adverse Effects (2)*
  • B: Contraindications*
A

A:

(x) Can INC [TriAcylGlyceride] during hyperTriglyceridemia
(x) [Cholestyramine and Colestipol] at HIGH levels–> [DEC Vitamin DEKA absorption]

B: Contraindicated in [Type 3 Dysbetalipoproteinemia pts with TAG > 400 mg/dL]. BABR INC [HMG-CoA Reductase] which can cause VLDL levels to further INC

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11
Q

Niacin

Adverse Effects (5)

A

Dying Pigeons Should Help Hide Germs

  1. [DMType2 relative contraindication] (Niacin causes INC glucose)
  2. Skin Flushing that requires NSAID Tx (prostaglandin mediated)
  3. Gout Risk by Inhibiting [Uric Acid Secretion]
  4. Peptic Ulcer Exacerbation
  5. Hyperglycemia Risk
  6. Hepatitis
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12
Q

Fibrates

  • A: Adverse Effects*
  • B: Contraindications (3)*
  • C: What are the Drugs in this class (2)*
A

A:

  1. INC gallstones
  2. Rhabdomyolysis (common with Gemfibrozil)
  3. Hepatitis
  4. Myopathy

B: Contraindicated in [Severe Liver OR Renal Dz Pts] / [Gallbladder Dz Pts]

C:

  • Gemfibrozil
  • Fenofibrate
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13
Q

A: Which [Bile Acid Binding Resins] have Drug Interaction problems?

B: What are the drug interactions (4)

A

“BABRs, Tyra and Pol didn’t get along with Dudes Who Play Tennis”

A:

  • Cholestyramine
  • Colestipol

B: DEC Absorption of

Digoxin / Warfarin / Phenobarbital / Tetracycline

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14
Q

Fibrates

  • A: Drug Interactions (2)*
  • B: Indications (2)*
A
  1. Fibrates are Strong Protein Binders—> [INC Warfarin and Sulfonylurea] –> bleeding and hypOglycemia
  2. Fibrates Inhibit [OATP2/glucoronidation] —> INC ALL STATINS —> Rhabdomyolysis

B: Fibrates are used for:

  • HIGH VLDL
  • Low HDL
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15
Q

Ezetimibe

  • A: Indication (2)*
  • B: Mechanism of Action*
A

A:

  • [High LDL in pt with Primary Hypercholesterolemia] since it doesn’t fully rely on [Hepatic LDL Receptor INC]
  • Adjunct with Statin

B: Prevents [Cholesterol Intestinal absorption] by inhibiting NPCL1. —> DEC Hepatic Cholesterol —> [INC LDL Receptors] —> [DEC Serum LDL by 18%]

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16
Q
  • niACin*
  • A: Indications (3)*
  • B: Mechanism of Action (7)*
A

A: [Low HDL] OR [HIGH VLDL OR HIGH LDL] in pt with Familial Combined Hyperlipidemias and [Familial Dysbetalipoproteinemia]

B: “ niACin Dec MALT”

  1. [INC ApoA-1 half life]—> NIACIN IS MOST EFFECTIVE HDL INCREASER (by [10-30%] )
  2. [ApoC-3] hepatic expression blocker –> [INC LPL] –> [INC VLDL CLEARANCE!]
  3. Inhibits DGAT2 –> [DEC VLDL hepatic synthesis]
  4. DEC Macrophage recruitment to atherosclerosis
  5. DEC Adipocyte Lipolysis as an agonist for [Gi-GPR109A] –> [DEC VLDL from FFA]
  6. DEC LPA —> DEC Thrombosis–> DEC Atherosclerosis
  7. DEC TAG by 30-80% —> DEC VLDL
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17
Q

Fibrates

A: Mechanism of Action (4)

B: Effect On Serum Lipids (4)

A

A: Ligands for [PPARalpha TF]:

  • DEC Apo-C3
  • INC LPL Expression
  • INC Fatty Acid Oxidation
  • INC [Apo-A1 Expression]

**** and this all

(x) [DEC VLDL synthesis]
(x) [DEC TriAcylGlycerides]
(x) [INC VLDL Clearance]
(x) [INC HDL production]

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18
Q

PCSK9 Inhibitors

A: What are the 2 Drugs

B: Effect On Serum Lipids

A

A:

  • Alirocumab
  • Evolocumab

B: DEC LDL by more than 50%

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19
Q

PCSK9 Inhibitors

Indications (2)

A
  1. HETEROzygous Familial Hypercholesteremia
  2. [HIGH LDL that is STATIN RESISTANT]
20
Q

PCSK9 Inhibitors

Mechanism of Action

A

Inhibits PCSK9 –> prevents [LDL Receptor] from being sent to lysosome –> INC LDL clearance

21
Q

loMiTaPide

  • A: Indications*
  • B: Adverse Effects*
  • C: Contraindications*
  • D: Drug Interactions*
A

A: Homozygous Familial Hypercholesteremia

B:

(x) Hepatotoxic
(x) CONTRAINDICATED IN PREGNANCY

D: loMiTaPide inhibits [CYP3A4 and P-gp]

22
Q

loMiTaPide

Mechanism of Action

A

Inhibits MTP in [Enterocytes AND Liver] —> DEC production of

  • Chylomicrons
  • VLDL
  • LDL
23
Q

Mipomersen

  • A: Indications*
  • B: Adverse Effects*
  • C: Contraindications*
A

A: homozygous Familial Hypercholesteremia

B: Hepatotoxic

C: CONTRAINDICATED IN MILD/MODERATE HEPATIC IMPAIRMENT

24
Q

Mipomersen

  • A: Mechanism of Action*
  • A: Effect On Serum Lipids (2)*
A

A: [Antisense Oligonucleotide] that’s specific for DECREASING ApoB100 Expression —>

B: DEC VLDL and LDL

25
Q

A: List the 5 Steps of how [Endothelial Injury] + LDL cause Atherosclerotic Plaques

B: ____ Cells contribute to this in what 3 ways?

A
  1. Endothelial Injury allows LDL Entry
  2. LDL is oxidized and [OxLDL] activates endothelium to express [Monocyte adhesion]
  3. Monocytes adhese to damaged endothelium and extravasate into [Tunica Intima]–> macrophages
  4. Macrophages uptake [OxLDL] and become FOAM CELLS
  5. FOAM CELLS secrete [proteases and growth factors] that
  • INC smooth muscle migration and proliferation
  • promote Extracell matrix synthesis
  • Foam cells eventually become necrotic–>release cholesterol —> Contributes to Fatty Streak production
26
Q

Composition of Lipoprotein particles (3)

A
  • Lipid Membrane - Phospholipids/Cholesterol
  • Hydrophobic core - Triglycerides and Cholesterol Esters
  • Apolipoproteins - structural proteins & ligands for particle uptake
27
Q

LDL Lipid Composition (2)

A

60% of serum Cholesterol

25% of serum Triglyceride

28
Q

iDL Lipid Composition (2)

A

35% of serum Cholesterol

25% of serum Triglyceride

29
Q

VLDL Lipid Composition (2)

A

20% of serum Cholesterol

55% of serum Triglyceride

30
Q

Chylomicron Composition (2)

A

85% of serum Triglyceride
~3% Dietary Cholesterol

31
Q

HDL Lipid Composition (3)

A

20% Cholesterol

5% Triglyceride

35% Phospholipid

32
Q

A: Which vasculature do Chylomicrons utilize to travel to Peripheral tissues?

B: 4 Uses for Cholesterol

A

A: Lymphatics / [Thoracic Duct]

B: [Steroid Hormones] / lipoproteins / Membranes / [bile acids]

33
Q

A: Which Receptor does HDL use to enter the Liver (transporting Cholesterol Esters) ?

B: Which Transporter does HDL use to uptake cholesterol from Foam Cells?

A

A: [SR-B1 scavenger receptor] to enter Liver

B: [ABCA1 Transporter] to take up Cholesterol from Foam Cells

34
Q

Protective roles of HDL from atherosclerosis (4)

A

1) inhibit oxidation of LDLs via paraoxonase enzyme (PON1) present on HDL surface (also has anti-oxidant activity)
2) Inhibits expresion of endothelial adhesion molecules—>prevents recruitment of monocytes to atherosclerotic plaque
3) inhibit the formation of FOAM cells
4) Transports Cholesterol from periphery to the Liver where it’s excreted as Bile

35
Q

3 Main Causes of HyperLipidemia / Hyperlipoprotienemia

B: Also list examples of each

C: When is Drug therapy indicated in Hypercholesterolemia specifically? (2)

A
  • Genetics ([Monogenic LDL Receptor disorder] vs. [Polygenic Familial combined Hyperlipoproteinemia] )
  • [Lifestyle(smoking and EtOH) / Diseases(DM and Anorexia) / Drugs(BCP and Corticosteroids)]
  • Combination of Genetics and Lifestyle (mutant ApoE2 allele–> Type 3 Dysbetlipoprotinemia)

C: [Severe Hypercholesterolemia] and/or [High Cardiovascular Risk]

36
Q

7 Risk Factors for Developing [Coronary Artery Disease]

A

CHD Risk Factors: “ CHAD has Family Medical Hx of CAD “

  1. DM - Type2
  2. Hypertension (Greater than 140/90)
  3. HDL lower than 40
  4. [Metabolic Syndrome X]
  5. Family history of CAD (<55yrs M; <65 yrs W),
  6. Cigarettes
  7. Age: M > 45yrs; W > 55yrs
37
Q

A: Tx Criteria for [Primary Prevention with STATINS] (3)

B: Tx Criteria for [Secondary HIGH RISK] prevention with STATINS]

C: What is the difference between these two Preventions?

A

A: Stain Primary Prevention Criteria

  1. LDL Greater than 190
  2. [LDL Greater 70 + DM]
  3. 10 Year [Cardiovascular Disease Risk] > 7.5%

B: Stain Secondary Prevention Criteria:

-Current clinical evidence of CVD

C:

Primary = LDL is within normal range

Secondary= HIGH RISK or hx of CAD + LDL elevation

38
Q

Why does Doubling a STATIN Dose not necessarily better for therapy?

A

Doubling the STATIN dose usually results in only a 5-6% further decrease in LDL, while significantly

increasing potential for ADVERSE EFFECTS!!!

39
Q

6 “OTHER” anti-atherogenic Effects of STATINS

A

Inhibits…

  1. Endothelial Adhesion molecule–> Inhibits Monocyte adhesion
  2. Monocyte Proliferation / Migration
  3. Oxidation process of LDL
  4. Smooth Muscle Cell proliferation
  5. Inflammatory Responses
  6. Stimulates Endothelial Stabilization –> DEC Plaque Rupture Risk
40
Q

A: Symptoms of Rhabdomyolysis (5)

B: Which STATIN has less likely chance of developing these sx

C: Which 3 Demographics are at INC risk

A

A:

A:

-fever / malaise / [diffuse myalgia and/or tenderness] /
[marked elevation of serum (CK)], [myoglobin present in the urine-dark]

B: Pravastatin

C: Incidence INC in pt with [Renal and Liver Failure] or [STAIN Hepatic Anion Transporter- HAT polymorphism]

41
Q

A: Relationship between Grapefruit Juice and Statins?

B: How do Statins enter the Liver?

C: How are Statins metabolized and excreted?

A

A: Grapefruit Juice INC bioavailability of [SAL - Simvastatin / Atorvastatin / Lovastatin] (most STATINS are absorbed in intestine. Normal bioavailability is 5-30% )

B: STATINS are directly taken into Liver by OATP2 = STATINS have strong effect in the liver

C: Once in liver, STATINS are [CYP450 metabolized] and glucoronidated by [UGATA1 and 1A3] –> Excreted

42
Q

Which Statins are metabolized by these CYP450 enzymes?

A: CYP3A4 (3)

B: CYP2C9

C: CYP2C19

D: Which Statin is NOT metabolized by CYP450 system? How is this statin different in excretion?

A

A: CYP3A4 = SAL = Simvastatin/Atorvastatin/Lovastatin

B: CYP2C9 = Fluvastatin

C: CYP2C19 = Rosuvastatin

D: Pravastatin is NOT metabolized by CYP450 and is partially renal excreted (vs. all others are strictly hepatic):-)

43
Q

A: 3 Common Disorders associated with [Elevated TriAcylGlycerdies]

B: [Elevated TriAcylGlycerdies] is usually associated with what condition?

C: What 2 medications are tx for this

A

A: [Pancreatitis / Atherosclerosis / CV Dz]

B: [HIGH TAG] usually comes from [low HDL]

C: Niacin and Fibrates both DEC TAG and INC HDL

44
Q

A: Therapy of Choice for Familial Dysbetalipoproteinemia (2)

B: Long term Fibrates do what clinically?

A

Fibrates or niACin

B: DEC Coronary Events / Stroke / TIA

45
Q

[Fish Oils: O3pUFA (Omega 3 Polyunsaturated Fatty Acids)]

A: Clinical Effect (2)

B: MOA (2)

C: Clinical USES

D: Drug Interactions

A

[Fish Oils: O3pUFA (Omega 3 Polyunsaturated Fatty Acids)

A: [DEC TAG by 30-50%] / [INC HDL]

B: Inhibits [Hepatic TAG synthesis] Gene Expression and uses [Macrophage GPCR] to carry out antiinflammation

C:

1) Adjunct to Diet in Tx of Hypertriglyceridema in pt with TAG >500

D: ARE SAFE AND DO NOT INC RHABDOMYOLYSIS RISK WITH STATINS

46
Q

A: 4 Circumstances in which Combination Drug Therapy is indicated

B: Which tx do you use for each circumstances

A
  1. LDL levels are not reduced in high-risk individuals even with HIGHEST STAIN DOSE–> Use Vytorin
  2. BOTH LDL and VLDL are HIGH such as in [combined hyperlipoproteinemia] –> Use Fenofibrate
  3. HDL deficiency co-exist with other hyperlipidemias –> [Use Niacin OR Fibrate]
  4. VLDL levels are INC during [Bile Acid Binding Resin] Tx —> Use Niacin
47
Q

4 Steps to how Gut Microbiota can INC risk for Atherosclerosis

A

1st: Pt eats [L-Carnitine from Red Meat]
2nd: [Gut flora-Peptostrep Clostridiaceae] metabolizes [L-Carnitine from Red Meat] —> TMA
3rd: TMA is processed in Liver —> [Active TMAO]
4th: [Active TMAO] INC risk for Atherosclerosis development

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