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Cardio/Renal 2 Midterm > Midterm > Flashcards

Midterm Flashcards

Pharmacology

1
Q

Kinectics of Statins

A

Extensive first-pass hepatic uptake (OATPIBI)-> (organic anion transporter protein 1B1)

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2
Q

Lovastatin

A

First statin
Metabolized by CYP3A4
DDI- CYP3A4 inhibitors increase risk of myopathy

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3
Q

Reductace inhibitors MOA

A

Competitive/reversible inhibitors
Increase in high-affinity LDL receptors (liver)-> decrease blood LDL levels
Mechanism is transcription
Reduces Rho and Rab proteins (leads to blood vessel relaxation)

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4
Q

Atorvastatin

A

Lipitor
With food AM or PM (better in evening)
Metabolism- CYP3A4
Half life 14 hrs
Monitor- Liver Function test (LFT) and Creatine Kinase (SCR)

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5
Q

AE and DDI of lipitor

A

AE- Myalgia
Discontinue if symptoms of renal failure or myopathy due to rhabdomyolysis develop
DDI- Gemfibrozil, Niacin-> myopathy

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6
Q

Simvastatin

A

Zocor
Very potent 5mg-40mg daily
Monitor- Liver function test (LFT) and signs of myopathy

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7
Q

Pravastatin

A

Pravachol
Should be given either 1 hr or more before or at least 4 hrs following resin
Not a prodrug

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8
Q

Rosuvastatin

A

Crestor
Use low doses with gemfibrozil and cyclosporine

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9
Q

AE and caution of crestor

A

AE - Myalgia
Caution- Renal failure may predispose to rhabdomyolysis, increase INR with concurrent warfarin (due to CYP2C9), heavy alcohol drinkers, Liver disease, proteinuria, Japanese/Chinese- predisposition to myopathy

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10
Q

Pitavastatin

A

Livalo
CI drugs- fibrates, cyclosporine
Does not affect warfarin’s effect (no increase in bleeding risk)

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11
Q

MOA of Bile acid binding resins

A

MoA
Oldest/safest because it does not get absorbed into blood
The bile acid sequestrants are highly positively charged and bind negatively charged bile acids Increases hepatic bile acid synthesis and hepatic triglyceride synthesis
Decreases LDL by stimulating the production of LDL receptors, similar to statins

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12
Q

AE of Bile acid binding resins

A

Chloride salts-> hyperchloremic acidosis, Severe hypertriglyceridemia is a CI (because they increase triglyceride levels), CI in diverticulitis, Malabsorption of vitamin K (clotting issues)
DDI with all anionic drugs

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13
Q

MOA of fibrates

A

PPAR- Alpha (agonist) activation induces fatty acid oxidation/ lipoprotein lipase
Have antithrombotic effects

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14
Q

PK of gemfribozil and fenofibrate

A

Gemfibrozil (does not undergo change), Fenofibrate (undergoes hydrolyzation-> has ester) Gemfibrozil- undergoes enterohepatic circulation, and eliminated through kidneys mostly unmodified
Fenofibrate- isopropyl ester prodrug that is hydrolyzed completely in the intestine

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15
Q

Thera of Fibrates

A

Useful for hypertriglyceridemia
Feno is more effective than gem at increasing HDL
Not much effect on LDL-C
Feno is the fibrate of choice for combo with a statin

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16
Q

AE of fibrates

A

Rashes, Myopathy (gem more than feno), Liver toxicity
Risk of Myopathy increases when given with statins
Avoid fibrates if pts have hepatic or renal dysfunction
Increase risk of cholithiasis (gallstones) when administered with ezetimibe Caution- coumarin anticoagulant

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17
Q

MOA of Ezetimibe

A

Allosteric Non-competitive inhibitor of NPC1L1
Inhibits intestinal absorption of phytosterols and cholesterol
Inhibits cholesterol uptake by inhibiting the transport protein NPC1L1

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18
Q

PK of Ezetimibe

A

Highly water insoluble
Glucuronidated in the intestinal epithelium
Excreted in the feces

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19
Q

Thera of Ezetimibe

A

Monotherapy- used in statin intolerant pts
Synergistic with statin for dyslipidemia
Useful for phytosterolemia

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20
Q

AE of Ezetimibe

A

Low chance for causing myopathy
Bile acid sequestrants inhibit absorption of ezetimibe and should not be administered together

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21
Q

What are the PCSK9 antibodies and their MOA

A

Proprotein convertase subtilisin/ kexin type 9 is a protease that binds to the LDL receptor on the surface of hepatocytes and enhances lysosomal degradation of the LDL receptor, resulting in higher plasma LDL concentrations which decreases LDL levels

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22
Q

Niacins 2 places of action and their MOA

A

Adipose tissue- inhibits the lipolysis of triglycerides by lipase and decreases hepatic triglyceride synthesis
Liver- reduces triglyceride synthesis by inhibiting synthesis and esterification of fatty acids This reduces hepatic VLDL production and LDL levels

23
Q

Omega 3 Fatty Acid / Fish Oil

A

Available OTC up to 1g daily, capsules
Acts on PPAR-alpha (same as fibrates)
Reduces VLDL, triglycerides
Prescription- if triglycerides higher than 1000, pancreatitis

24
Q

Agents decreasing O2 demand

A

(HR, Contractility, Preload, Afterload)- Beta blockers, Some CCB, Organic nitrates,

25
Agents increasing O2 supply
(coronary blood flow, Regional myocardial blood flow)- Statins, vasodilators (esp. CCB), antithrombotics
26
MOA of antianginals and its molecular mechanism
Decrease myocardial oxygen requirement. In some pts, the nitrates and CCB cause a redistribution of coronary flow which relieve spasm and increase oxygen delivery. Increase cGMP, Decrease intracellular Ca++, and stabilizes vascular smooth muscle cell membrane
27
What muscles do nitrates work on and do not work on
Effect mostly smooth muscles but not cardiac and skeletal muscles
28
What are the effects of nitrates on smooth muscle
relaxation of veins with increased venous capacitance and decreased ventricular preload, heart size and output decreases, reflex responses: tachycardia and increased cardiac contractility. Redistribution of coronary flow from normal to ischemic regions
29
MOA of nitrates
Release nitric oxide which activates soluble guanylate cyclase (sGC) causing an increase in cGMP activating PKG, which activates myosin phosphate resulting in blood vessel relaxation
30
PK of nitrates
High first pass metabolism (oral bioavailability is low) Excretion- glucuronide derivatives of the denitrated metabolites by the kidney CAUTION (all nitrates)- don't use with sildenafil
31
AE of NTG
Throbbing headache, Hypotension, Tachycardia (reflex), Sublingual bruning, Contact dermatitis (patch-> that's why you change patch location every time), Tolerance buildup
32
Isosorbide Dinitrate
Longer SL coverage than NTG Metabolized to active metabolites including the mononitrate (longer action) Sublingual dose rarely used because of high tolerance
33
Isosorbide mononitrate
Bypasses first pass metabolism (low tolerance liability) Metabolite of the dinitrate Prophylactic: not used during periods of angina
34
Extra info of NTG
Use Viagra before nitrates SL NTG is used for acute attack and prevention only because time of action is low
35
MOA of CCB
DHP- Bind alpha 1 and block from inside: open channels and inactivated channels Organ system effects- CCB have more effect on arteries, DHP have greater vascular effect than cardiac, Verapamil and diltiazem (they have major effect on heart) are both similar so use one.
36
Altepase (t-PA)
Low affinity for free plasminogen but a very high affinity for plasminogen bound to fibrin in a thrombus (fibrin-specific agent) Half life- 5 mins (continuous IV) Give within 3 hours of Acute ischemic stroke (acute MI or heart attack) Reteplase and Tenecteplase- slightly modified proteins that have longer half lives
37
AE and CI of Altepase
Hemorrhage (increased bleeding risk) CI- Heparin, pregnancy, bleeding liability, metastatic cancer Alternatives to Alteplase- mechanical reperfusion, mechanical thrombus extraction
38
Aspirin MOA
Causes platelet aggregation and is a potent vasodilator Irreversible Inhibition of COX-1 Action lasts for lifetime of the platelet (7 to 10 days)
39
AE of Aspirin
GI bleeding, Occult bleeding (bleeding without cause), prolongation of bleeding time, iron deficiency anemia, thrombocytopenia, leukopenia, hemolytic anemia CI- infants and small children (Reye’s syndrome), avoid in pregnancy Decreased effect- NSAIDs, Antagonize probenecid Increased effect- Methotrexate, Valproic acid, NSAI (GI bleed), Anticoagulants, Sulfonylurea hypoglycemics, Digoxin
40
Which of the P2Y12 ADP receptor agonists are reversible and which are irreversible
Irreversible - Ticlopidine, Clodpiogrel, Prasgurel Reversible - Ticagrelor and Cangrelor
41
Clopidogrel MOA, thera, and AE
MoA: P2Y12 receptor couples to Gi and is activated by ADP which inhibits adenylyl cyclase resulting in lower levels of intracellular cyclic AMP and platelet activation in lower levels of intracellular cyclic AMP and platelet activation Thera: Commonly used with baby aspirin AE: Bleeding (risk is higher with aspirin and anticoagulant) DDI- Inhibits CYP2C19
42
Prasugrel
MoA same as clopidogrel Efficacy is higher but toxicities (bleeding) also higher than Clopidogrel Faster onset of action- 30 mins Prodrug AE- Bleeding DDI- CYP3A4 inhibitors (protease inhibitors, statins, grapefruit)
43
Ticlopidine
Same MOA as Clopidogrek DDI - CYP3A4 inhibitors (PI, Statins, Grapefruit)
44
Ticlopidine
Same MOA as clopidogrel AE - 1% chance of Leukopenia
45
Ticagrelor MOA, Thera, AE, DDI
Non-competitive allosteric inhibitor Faster onset + offset of action than Clopidogrel Thera- Coronary stent thrombosis AE- Dyspnea (difficulty breathing~ 14%), bleeding DDI- CYP3A inhibitor, increases statin conc.
46
Cangrelor and AE
Used for precutaneous coronary intervention (PCI) AE - bleeding (more than clopidogrel)
47
What are the glycoprotein IIb/IIIa receptor blockers and their MOA
Abciximab, Eptifibatide, Tirofiban MOA - Platelet activation and aggregation
48
Info about Abciximab and its AE and CI
Fab fragment Platelet-bound:18-24 hrs AE- bleeding CI- Bleeding, cranial hemorrhage, thrombocytopenia
49
Eptifibatide
Ligand containing Arg-Gly-Asp (RGD) sequence Cyclic peptide derived from rattlesnake venom containing a variation of RGD motif (KGD) Renal elimination Similar CI and AE to abciximab
50
Tirofiban
RGD mimetic can bind to bile sequestering agent via anion exchange mechanism
51
Dipyridamole MOA
directly inhibits PDE5 which converts cyclic AMP to 3-5 AMP resulting in an increase in cAMP cascade platelets
52
Extra info about Dipyridamole
Vasodilator and antithrombotic (prevents platelet aggregation) Approved for secondary prevention of stroke when combined with aspirin Its metabolite has no impact on bleeding time or platelet aggregation
53
Cilostazol
Vasodilator Inhibits phosphodiesterase Treats intermittent claudication

Cardio/Renal 2 Midterm (1 decks)

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