Pharmacology Flashcards
Drugs easily displaced from albumins –> ____ plasma drug level
INCREASE
- Sulfonamides
- Phenylbutazone
- Tolbutamide
- Coumarin
Drugs that induce P450 –> _____ plasma drug levels
DECREASE
- Alcohol
- Barbiturates
- Phenytoin
- Rifampicin
Drugs that inhibit P450 –> ______ plasma drug levels
INCREASE
- Chloramphenicol
- Sulfonamides
- Phenylbutazone
Drugs that compete for renal transporters –> ______ plasma drug levels
INCREASE
- Uric acid
- Probenecid
- Penicillins
- Sulfonamides
- Salicylates
- Thiazides
Risk of severe hemorrhage if coumarins are combined with
any other drug that competes for albumin
_______ displace sulfonureas from albumin leading –> hypoglycemia
Sulfonamides
What is the effect of Barbiturates on MAO-I?
induce P450 enzymes –> enhanced metabolism of MAO inhibitors –> ineffective tx of depression
What effect does P450 induction have on estrogen?
It enhances estrogen metabolism, which reduces oral contraceptive effects
What effect do steroids have on MAO-I?
they compete with MAO-I for P450 enzymes –> reduced metabolism of MAO-I –> risk of OD
NEVER combine aminoglycosides with:
- Neuromuscular blockers (enhanced block)
- Loop diuretics (compounds ototoxicity)
NEVER combine MAO-I with:
- Levadopa (HTN crisis)
- Amphetamine (HTN crisis)
- Tricyclic antidepressants
Famous SE of Penicillin
Anaphylactic shock
Famous SE of Isoniazid
Hepatotoxicity
Famous SE of Cyclosporin
Renal toxicity
Famous SE of Aminoglycosides (Neomycin)
Ototoxicity
Famous SE of Hydralazine
Drug-induced Lupus
Famous SE of Tetracyclines (Doxycycline, Minocycline)
Photosensitivity (skin)
Cutaneous flushing is a famous SE cz’d by
Niacin
Niacins is also HEPATOTOXIC
Famous SE of Zidovudine aka Azidothymidine (AZT)
Bone marrow suppression
Antidote to Acetominophen intoxication
NAC
Antidote to Opiate intoxication
Naloxone
Antidote to Benzo intoxication
Flumazenil
Antidote to Methanol or Ethylene Glycol intoxication
Ethanol
Antidote to CO intoxication
100% O2
Antidote to Cyanide intoxication
Amyl nitrate
Antidote to Organophosphate intoxication
- Atropine
- Pralidoxime
Antidote to iron intoxication
deferoxamine
Antidote to lead intoxication
EDTA
Antidote to coumarin intoxication
Vitamin K
Antidote to Heparin intoxication
Protamine
What does alpha-1 do?
- Tubules
- Tightening/contraction of b.v.
- Paralysis/relaxation of GI tube
What does alpha-2 do?
- Affects CNS
- Emergency break on SNS
What does Beta-1 do?
- Pro-sympathetic
- Affects heart
What does Beta-2 do?
- Pro-sympathetic
- Affects lungs
What ADR can B6 cause?
peripheral neuropathy
MOA of statins
HMG-CoA reductase inhibitors
Simvastatin and Atorvastatin
- Class: Statins (lipid-lowering agent)
- MOA: HMG-CoA reductase inhibitors
- give CoQ10!
- ADR: rhabdomyolysis
What labs should you check with statins rx?
Check AST and ALT prior to Rx and 6 weeks post-Rx
Common and serious ADR of statins
Rhabdomyolysis
*d/c statins if pt. has mm. pain, even if LFTs are normal
Colesevelam
- Class: Bile sequesterant (lipid-lowering agent)
- MOA: combines w/ bile to form insoluble compound that is then excreted
- ADR: constipation, fecal impaction, abdominal pain, nausea
Gemfibrozil
- Class: Fibrates (lipid-lowering agent)
- MOA: inhibits peripheral lypolysis, decr. hepatic FFA extraction, inhibits synthesis and incr. clearance of VLDL carrier Apo B
- ADR: often hepatotoxic (so falling out of favor)
When would you use carbonic anhydrase inhibitors?
MOA?
Emergency situations
This diuretic works by blocking HCO3 reabsorption in the proximal convoluted tubule –> resorbs 67% Na and H20 (A LOT!)
Furosemide
- Class: Loop Diuretic
- MOA: works at ascending loop of Henle and resorbs 25% Na
- ADR: hypokalemia (K+ wasting) and hyperglycemia
Hydrochlorothiazide
- Class: Thiazide diuretic
- MOA: works at the distal tubule/collecting duct via Na-Cl transporter and resorbs 8% Na
- ADR: hypokalemia (K+ wasting) and hyperglycemia
Hydrochlorothiazide is C/I in pt with a hypersensitivity to _____
sulfonamide drugs
1st line drugs for HTN
HCTZ (thiazide diuretics)
How to loop diuretics and thiazide diuretics affect blood sugar?
cause hyperglycemia
Triamterene
- Class: Potassium sparing diuretic
- MOA: acts on distal tubules
- ADR: HYPERkalemia
Why do you commonly use HCTZ and Triamterene together?
HCTZ is a potassium wasting diuretic and Triamterene is a potassium sparing diuretic so they can balance each other out
Spironolactone
- Class: Potassium sparing diuretic
- MOA: Acts on distal tubule; aldosterone receptor antagonist
- ADR: HYPERkalemia
Note: also used for PCOS
Atenolol
- Class: Beta blocker (selective)
- MOA: acts on B1 adrenergic receptor
- ADR: fatigue, bronchospasm, hypotension, bradycardia
**Abrupt discontinuation is dangerous
Carvedilol
- Class: Beta blocker (non-selective)
- MOA: acts on B1 and B2 adrenergic receptors
- ADR: fatigue, hypotension, bradycardia
**Abrupt discontinuation is dangerous
Propanolol
- Class: Beta blocker (non-selective)
- MOA: acts on B1 and B2 adrenergic receptors
- ADR: fatigue, hypotension, bradycardia
**Abrupt discontinuation is dangerous
Carvedilol
- Class: Beta blocker (non-selective)
- MOA: acts on B1 and B2 adrenergic receptors
- ADR: fatigue, hypotension, bradycardia
**Abrupt discontinuation is dangerous
Propanolol
- Class: Beta blocker (non-selective)
- MOA: acts on B1 and B2 adrenergic receptors
- ADR: fatigue, hypotension, bradycardia
**Abrupt discontinuation is dangerous
Timolol
- Class: Beta blocker (non-selective)
- MOA: acts on B1 and B2 adrenergic receptors
- ADR: fatigue, hypotension, bradycardia
**Abrupt discontinuation is dangerous
What is a common off-label use for B1 and B2 adrenergic receptor blockers?
migraines
Diltiazem
- Class: CCB
- MOA: makes Ca++ plateau shorter –> weakening the pump
- ADR: CHF
Verapamil
- Class: CCB
- MOA: makes Ca++ plateau shorter –> weakening the pump
- ADR: CHF
Amlodipine
- Class: CCB
- MOA: makes Ca++ plateau shorter –> weakening the pump
- ADR: CHF
If a pt with CHF needs to be put on an antihypertensive drug, which drug class should be avoided?
CCB
What drug interaction do the CCBs have?
increase levels of cimetidine (H2 receptor antagonist)
What affect to all of the angiotensin agents (ACE-I and ARBs) have on potassium?
the sequester potassium
K+ sparing
Lisinopril
- Class: ACE-I
- MOA: inhibit angiotensin converting enzyme in the lungs
- ADR: dry, persistent cough; hyperkalemia
What is a big C/I for ACE-I?
Pregnancy (b/c it can affect fetal lung development)
Ramipril
- Class: ACE-I
- MOA: inhibit angiotensin converting enzyme in the lungs
- ADR: dry, persistent cough; hyperkalemia
Irbesartan
- Class: ARB
- MOA: inhibit ANG-2 receptors
- ADR: hyperkalemia
**exist to give to pt w/ dry cough that are otherwise responsive to ACE-I
Losartan
- Class: ARB
- MOA: inhibit ANG-2 receptors
- ADR: hyperkalemia
**exist to give to pt w/ dry cough that are otherwise responsive to ACE-I
Clonidine
- Class: Alpha-2 Agonist Anti-hypertensive
- MOA: alpha-2 is an emergency break SNS
**this drug is used in emergency HTN crisis situations!
What is the typical dose of Reserpine?
- 1 - 0.25 mg BID
* impt to know this because they may asl question about how to dose Rauwolfia serpentina tincture (the extract will be standardized to mg reserpine)
Famous SE of NSAIDs
*Renal toxicity
Hepatotoxicity
Famous SE of Sulfonamides (Sulfamethoxazole, Sulfacetamide)
Photosensitivity (skin)
Hemolysis in pt. with G6PD-deficiency
Famous SE of Sulfonylureas (Glyburide)
Photosensitivity (skin)
Valsartan
- Class: ARB
- MOA: inhibit ANG-2 receptors
- ADR: hyperkalemia
**exist to give to pt w/ dry cough that are otherwise responsive to ACE-I
Do not give ________ to pt with G6PD-deficiency because it may cause hemolysis
Sulfonamides (Sulfamethoxazole, Sulfacetamide)
Warfarin
- Class: Anti-thrombotic, Anti-coagulation
- MOA: Vit K antagonist; acts on EXTRINSIC factors 2, 7, 9, 10
- ADR: Prolonged bleeding, hemorrhage
What do you need to monitor when pt is on warfarin?
prothrombin time (PT)
*from PT you can derive prothrombin ratio (PR) and international normalized ratio (INR)
Heparin
- Class: Anti-thrombotic, Anti-coagulation
- MOA: inhibits clotting factors by binding to antithrombin III (AT3); affects thrombin and fibrin; works downstream and doesn’t affect Vit K
- ADR: Hemorrhage
- MC injection (SC)
- IV is given to tx thromboembolism
Clopidogrel
- Class: Anti-thrombotic, Anti-coagulation
- MOA: inhibit platelets sticking together by preventing formation of thromboxane A2 (TXA2)
- ADR: Bleeding, Neutropenia, TTP
Aspirin
- Class: Anti-thrombotic, Anti-coagulation, NSAID
- MOA: inhibit platelets sticking together by preventing formation of thromboxane A2 (TXA2)
- ADR: Bleeding and salicylism (OD)
What is salicylism and how does it present?
OD of aspirin
characterized by acid-base disturbances, electrolyte imbalance and CNS effects
s/sx: tinnitus, deafness, N/V; early CNS stimulation (hyperkinetic agitation, excitement, mania, delirium, convulsions); later CNS depression (stupor and coma)
Digoxin
- Class: Class I Antiarrhythmic
- MOA: cardiac glycoside that inhibits Na-K pump and increases intracellular Ca++ –> contraction is stronger; also increase PNS flow and SA and AV nodes –> decreased HR
- ADR: death (problem is digoxin works everywhere in body so if dose is too high or brain is affected it can result in death)
Sx of Digoxin toxicity
fatigue, mm. weakness, agitation, anorexia, nausea, *yellow halos around vision
If a pt presents on digitalis/digoxin what should you always choose as an answer if available?
monitor their blood levels of digitalis/digoxin
this should be done first!
Quinine/Quinidine toxicity
Cinchonism
S/Sx: tinnitus, hearing loss, HA, nausea, dizziness, vertigo, visual changes
What are the 3 primary indications for Beta blockers in cardiology?
Antihypertensive, Antiarrhythmic, Antianginal
What are the 3 primary indications for CCB in cardiology?
Antihypertensive, Antiarrhythmic, Antianginal
Class I antiarrhythmics
Digoxin
Class II antiarrhythmics
BB
Class III antiarrhythmics
Amiodarone
Class IV antiarrhythmics
CCB