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

pharm: 9-29 Hyperlipidemia drugs Flashcards

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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)

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

PCSK9 Inhibitors

Mechanism of Action

Study These Flashcards
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*
Study These Flashcards
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

Study These Flashcards
A

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

  • Chylomicrons
  • VLDL
  • LDL
23
Q

Mipomersen

  • A: Indications*
  • B: Adverse Effects*
  • C: Contraindications*
Study These Flashcards
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)*
Study These Flashcards
A

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

B: DEC VLDL and LDL

25
A: List the 5 Steps of how [Endothelial Injury] + LDL cause **Atherosclerotic Plaques** B: ____ Cells contribute to this in what 3 ways?
1. Endothelial Injury allows LDL Entry 2. LDL is oxidized and [**O**x**L**DL] activates endothelium to express [Monocyte adhesion] 3. Monocytes adhese to damaged endothelium and extravasate into [Tunica Intima]--\> macrophages 4. Macrophages uptake [**O**x**L**DL] 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
Composition of Lipoprotein particles (3)
* Lipid Membrane - Phospholipids/Cholesterol * Hydrophobic core - Triglycerides and Cholesterol Esters * Apolipoproteins - structural proteins & ligands for particle uptake
27
LDL Lipid Composition (2)
60% of serum Cholesterol 25% of serum Triglyceride
28
iDL Lipid Composition (2)
35% of serum Cholesterol 25% of serum Triglyceride
29
**V**LDL Lipid Composition (2)
20% of serum Cholesterol 55% of serum Triglyceride
30
Chylomicron Composition (2)
85% of serum Triglyceride ~3% Dietary Cholesterol
31
HDL Lipid Composition (3)
20% Cholesterol 5% Triglyceride 35% Phospholipid
32
A: Which vasculature do **Chylomicrons** utilize to travel to Peripheral tissues? B: 4 Uses for *Cholesterol*
A: Lymphatics / [Thoracic Duct] B: [Steroid Hormones] / lipoproteins / Membranes / [bile acids]
33
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: [SR-B1 scavenger receptor] to enter Liver B: [ABCA1 *Transporter*] to take up Cholesterol from Foam Cells
34
Protective roles of HDL from atherosclerosis (4)
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
3 Main Causes of HyperLipidemia / Hyperlipoprotienemia B: Also list examples of each C: When is **Drug** therapy indicated in _Hypercholesterolemia_ specifically? (2)
* 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
7 Risk Factors for Developing [Coronary Artery Disease]
CHD Risk Factors: " **CHAD** has **F**amily **M**edical **H**x 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
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: 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
Why does Doubling a STATIN Dose **not** necessarily better for therapy?
Doubling the STATIN dose usually results in only a 5-6% further decrease in LDL, while significantly increasing potential for ADVERSE EFFECTS!!!
39
6 **"OTHER"** anti-atherogenic Effects of STATINS
**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
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: -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
A: Relationship between Grapefruit Juice and Statins? B: How do Statins enter the Liver? C: How are Statins metabolized and excreted?
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
**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: 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
A: 3 Common Disorders associated with [Elevated **T**ri**A**cyl**G**lycerdies] B: [Elevated **T**ri**A**cyl**G**lycerdies] is usually associated with what condition? C: What 2 medications are tx for this
A: [**Pancreatitis** / Atherosclerosis / CV Dz] B: [HIGH TAG] usually comes from [low HDL] C: *Niacin* and *Fibrates* both DEC TAG and INC HDL
44
A: Therapy of Choice for *Familial Dysbetalipoproteinemia* (2) B: Long term Fibrates do what clinically?
Fibrates or niACin B: DEC Coronary Events / Stroke / TIA
45
**[Fish Oils: O3pUFA** *(Omega 3 Polyunsaturated Fatty Acids)***]** A: Clinical Effect (2) B: MOA (2) C: Clinical USES D: Drug Interactions
**[Fish Oils: O3pUFA** *(Omega 3 Polyunsaturated Fatty Acids***)** ## Footnote 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
A: 4 Circumstances in which **Combination Drug Therapy** is indicated B: Which tx do you use for each circumstances
1. LDL levels are not reduced in high-risk individuals even with HIGHEST STAIN DOSE--\> Use Vytorin 2. BOTH LDL and **V**LDL are HIGH such as in [combined hyperlipoproteinemia] --\> Use Fenofibrate 3. HDL deficiency co-exist with other hyperlipidemias --\> [Use Niacin OR Fibrate] 4. **V**LDL levels are INC during [Bile Acid Binding Resin] Tx ---\> Use Niacin
47
4 Steps to how Gut Microbiota can INC risk for Atherosclerosis
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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