Term
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Definition
Induce emesis
Ipecac should not be used if toxin is- corrosive, a petroleum distillate, a rapid-acting convulsant |
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Term
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Definition
Chemical adsorption
Given 10:1, charcoal:toxin
Does not bind iron, lithium, potassium; poorly binds alcohol and cyanide |
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Term
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Definition
Prostaglandin- PGE1
Smooth muscle relaxant-> maintain patent ductus arteriosus in newborns awaiting surgery and treatment of impotence |
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Term
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Definition
Prostaglandin- PGE1 derivative
MOA: acid inhibitory and mucosal protective-> stimulates mucus and bicarbonate secretion; binds to PG receptors on parietal cells, reducing cAMP productions-> decreased acid
Cytoprotective-> prevention of NSAID induced peptic ulcer disease
Can be used in combo w/ mifepristone for terminating pregnancy
Half-life 30mins-> must be given 3-4times daily
SE: abdominal discomfort, diarrhea, bone pain, hyperostosis
C/I: pregnancy-> stimulates uterine contraction |
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Term
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Definition
Prostaglandin- PGF2 derivative
Treatment of open angle glaucoma |
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Term
| Prostacyclin (PGI2/Epoprostenol) |
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Definition
Prostaglandin
Synthesized by vascular endothelium-> vasodilator/inhibitor of platelet aggregation
Used to treat pulmonary and portopulmonary HTN |
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Term
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Definition
NSAID- salicylic acid derivative
MOA: irreversibly acetylates and inactives COX-1 and COX-2 (creating inactivated COX and salicylic acid), reducing TXA2 synthesis-> prevent clotting b/c platelets cannot make new COX
At low concentrations, preferential inhibition of COX-1
Use: anti-inflammatory, anti-pyretic, analgesic; prevention of cardiovascular disease; benefit in colon cancer
Toxicity: tinnitus; uncouples oxidative phosphorylation (overdose); gastric upset and ulcers; exacerbates gout
Contraindications: hemophilia |
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Term
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Definition
Selective COX-2 Inhibitor-> high anti-inflammatory w/ low GI side effects
Problems: very expensive; constitutive expression of COX-2 in kidneys-> decreased synthesis of renal PGs (toxicity); increased risk/worsening HTN; lack of anti-platelet effects-> inhibition of COX-2 in vascular endothelial cells results in unfavorable TxA2 (pro-clot) vs. PGI2 (cardio protective) ratio-> increased risk of atherosclerotic/cardiovascular disease
Only used in patients w/o CV disease, renal disease, and atherosclerosis who are experiencing high GI symptoms w/ other drugs |
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Term
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Definition
NSAID- enolic acid
Somewhat selective for COX-2
Treatment of osteoarthritis |
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Term
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Definition
NSAID- heteroaryl acetic acid Very potent COX inhibitor
MOA: non-selective COX inhibitor
GI toxicity caused by PGE2 release, but lessened when given w/ misoprostol
Tox: GI ulcers, impaired renal blood flow and glomerular filtration; elevation of serum aminotransferases |
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Term
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Definition
NSAID- salicylic acid derivative
MOA: non-selective COX inhibitor
Potent anti-inflammatory
Poor CNS penetration so poor anti-pyretic
Clearance depends on hepatic and renal function
Treatment: rheumatoid arthritis; cancer w/ bone metastasis and dental surgery |
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Term
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Definition
NSAID- indole and indene acetic acid
MOA: non-selective COX inhibitor
Fewer GI side effects b/c large difference b/w dosing amount that is anti-inflammatory and that which causes decreased GI PG synthesis |
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Term
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Definition
NSAID- arylpropionic acid
Similar to ibuprofen-> low incidence of GI side effects
MOA: non-selective COX inhibitor and affects TNF-alpha and NO synthesis
Hepatic metabolism |
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Term
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Definition
NSAID- arylpropionic acid
MOA: non-selective COX inhibitor
Low incidence of GI side effects
Effective in closing ductus arteriosus
Concomitant use w/ Aspirin antagonizes Aspirin's irreversible platelet inhibition
Tox: agranulocytosis/aplastic anemia
Contraindications: nasal polyps, angioedema, bronchospasmic reactivity to Aspirin |
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Term
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Definition
NSAID- indole and indene acetic acid
Very potent COX inhibitor; non-selective
Use: acute treatment of gout; suppress uterine contractions; induce closure of ductus arteriosus
High degree of side effects w/ chronic use-> headache, pancreatitis, psychosis w/ hallucinations, thrombocytopenia/aplastic anemia |
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Term
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Definition
NSAID- arylpropionic acid
MOA: non-selective COX inhibitor, lipoxygenase inhibitor, and also stabilizes lysosome membranes, thereby antagonizing bradykinin actions (i.e. decreased BP)
SE: GI and CNS |
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Term
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Definition
NSAID- heteroaryl acetic acid
MOA: non-selective COX inhibitor
Potent analgesic but poor anti-inflammatory
Use: post-op pain
Can be given IM or IV for systemic use
Tox: renal |
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Term
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Definition
NSAID- alkanone=> only nonacid NSAID
MOA: nonselective COX inhibitor-> prodrug
Half-life > 24 hrs
Tox: pseudoporphyria, photosensitivity |
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Term
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Definition
NSAID- arylpropionic acid=> only single enantiomer NSAID
MOA: nonselective COX inhibitor
20X more potent than Aspirin but w/out an increase in GI side effects
Free fraction is greater in women than men, but equal half-lives
Tox: upper GI bleeding, allergic pneumonitis, leukocytoclastic vasculitis, pseudoporphyria |
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Term
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Definition
NSAID- arylpropionic acid
MOA: nonselective COX inhibitor
Long half-life: 50-60 hrs
Uricosuric- increases secretion of uric acid in the urine-> treatment of gout |
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Term
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Definition
NSAID- enolic acid
MOA: nonselective COX inhibition and also inhibits neutrophil activation in the presences of PGs; may also inhibit collagenase and proteoglycanase
Long half-life: 50hrs
Tox: increased risk of peptic ulcer bleeding |
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Term
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Definition
NSAID- indole and indene acetic acid
MOA: nonselective COX inhibitor
Pro-drug that is activated in the liver
Suppresses familial intestinal polypsosis, may inhibit some cancers
Tox: fewer GI side effects; elevation of amino transferases; Stevens-Johnson syndrome, thrombocytopenia, agranulocytosis, nephrotic syndrome |
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Term
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Definition
NSAID- heteroaryl acetic acid
MOA: nonselective COX inhibitor
Well tolerated; often used for children
Short half-life
Tox: thrombocytopenic purpura |
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Term
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Definition
NSAID- aka Tylenol
Poor inhibitor of COX outside of CNS and in presence of radical oxygen species (inflammation)
Use: analgesic, anti-pyretic, but NOT anti-inflammatory
Conjugated for excretion; unconjugated drug is deactivated by GSH in liver, but children lack GSH-> reacts w/ protein sulfhydryl groups in liver = toxicity
Toxicity: therapeutic index = 4 (i.e. 4X the normal limit induces toxicity); hepatic toxicity (fatal if untreated)
Treat toxicity w/ N-acetylcysteine |
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Term
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Definition
NSAID- salicylic acid derivative Azo link of mesalamine (5-ASA) with sulfapyridine-> allows it to not be broken down until it reaches intestinal flora, and can exert effects in large intestine
MOA: COX inhibitor; DHFR inhibitor; scavenging free radicals
Use: IBD (mainly UC); rheumatoid arthritis
SE: nausea/vomiting; headaches, arthralgias; myalgias; bone marrow suppression; malaise; hypersensitivity; oligospermia |
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Term
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Definition
NSAID- salicylic acid derivative Azo link of mesalamine (5-ASA) with 4-aminobenzoyl-beta-alanine-> allows it to not be broken down until it reaches intestinal flora, and can exert effects in large intestine
Use: IBD (mainly UC); rheumatoid arthritis |
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Term
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Definition
NSAID- salicylic acid derivative Azo link of two mesalamine (5-ASA) molecules-> allows it to not be broken down until it reaches intestinal flora, and can exert effects in large intestine
Use: IBD (mainly UC); rheumatoid arthritis
SE: secretory diarrhea |
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Term
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Definition
NSAID- salicylic acid derivative
Pentasa- timed release mesalamine
Asacol/Lialda- mesalamine that dissolves at pH 7
Rowasa- enema formulation
Canasa- suppository
Use: IBD (mainly UC); rheumatoid arthritis |
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Term
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Definition
Adrenocorticosteroid
Anti-inflammatory and immunosuppressive
MOA: ↓ arachidonic acid metabolism (both PGs and LTs)-> ↓ COX-2 mRNA and protein and ↓ PLA2 activity; ↓ cytokine expression (esp ILs); ↓ cell-adhesion molecule expression (traps neutrophils in vascular compartment); ↓ fibroblast DNA synthesis/proliferation
Adverse effects: adrenal suppression, fluid and electrolyte abnormalities, metabolic changes, edema, hypertension, osteoporosis, growth suppression in children, cataracts, behavioral changes
Must taper off; do not abruptly stop-> adrenal glands begin to shut down so you have to allow them to start back up |
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Term
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Definition
Cortisol- naturally occurring; hydrocortisone- synthetic
Short to medium acting glucocorticoid; half life 60-90mins
Oral, injectable, topical; production governed by ACTH
Increased w/ stress, hypothyroidism, and liver disease
Greatest metabolism in liver; 20% by 11-hydroxysteroid dehydrogenase in kidney
Given as enemas, foams, or suppositories for IBD |
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Term
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Definition
Glucocorticoid
Rapid 1st pass effect-> low oral bioavailability
Controlled released oral version available
Treatment of IBD |
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Term
AZATHIOPRINE
6-Mercaptopurine |
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Definition
Purine Analogs
MOA: azathioprine converted to 6-mercaptopurine; 6-MP activated by HGPRT-> inhibits purine synthesis, esp in B/T cells
Oral bioavailability: azathioprine > 6-MP
Induction and maintenance of remission of IBD-> delay of 17 wks for therapeutic benefit
Toxicity: inhibits proliferation of any rapidly dividing cell populations (i.e. epithelial)-> nausea/vomiting, bone marrow depressions, hepatic toxicity
Should not be given to pts w/ no TPMT activity
Can cross placenta-> low risk of teratogenicity |
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Term
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Definition
Antimetabolite
MOA: inhibition of DHFR
Used in treatment of Crohn's disease
SE: bone marrow depression, magaloblstic anemia, alopecia, mucositis; in pts w/ psoriasis-> hepatic damage
Recommended folate supplementation |
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Term
INFLIXIMAB
Adalimumab
Certolizumab |
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Definition
MOA: anti-TNF alpha
Infliximab/Certolizumab- chimeric monoclonal Abs
Adalimumab- fully humainzed monoclonal Ab
Neutralizes soluble TNF and membrane bound TNF
Only Infliximab/Adalimumab-> induce apoptosis and complement mediated cyotoxicity of cells expressing membrane bound TNF
Infliximab- IV; Adalimumab/Certolizumab- subcutaneous
Acute and chronic treatment of Crohn's disease; Infliximab also used for acute and chronic ulcerative colitis
Time to therapeutic response = 2wks
SE: infection due to TH1 suppression (must give PPD before therapy); Ab production-> hypersensitivity; serum-sickness like reaction; acute hepatic failure; demyelinating disorders; hematologic reactions, CHF; lymphoma |
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Term
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Definition
Antacid- baking soda, Alka Seltzer
MOA: reacts w/ HCl -> CO2 + NaCl
CO2-> gas production = belching; NaCl may exacerbate fluid retention
Unreacted alkali is absorbed-> potential alkalosis
Excessive doses w/ milk products-> hypercalcemia, renal insufficiency, metabolic alkalosis = milk-alkali syndrome |
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Term
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Definition
Antacid- Tums, Os-Cal
MOA: reacts w/ HCl -> CO2 + CaCl2
CO2-> gas production = belching; CaCl2 may cause belching or metabolic alkalosis
Excessive doses w/ milk products-> hypercalcemia, renal insufficiency, metabolic alkalosis = milk-alkali syndrome |
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Term
| Aluminum and Magnesium Hydroxides |
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Definition
Antacid; Mg(OH)2 = Milk of Magnesia (osmotic laxative)
MOA: reacts w/ HCl -> MgCl2 or AlCl3 + H2O
No gas production = no belching
Mg salt may cause diarrhea (use as laxative); Al may cause constipation-> usu given together in formulations (Gelusil, Maalox, Mylanta)
C/I: pts w/ renal insufficiency should not take long term; not to be given w/in 2 hrs of tetracyclines, fluoroquinolones, itraconazole, iron-> decreased absorption |
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Term
Cimetidine
Ranitidine
Nizatidine
Famotidine |
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Definition
H2 receptor antagonists
MOA: block histamine binding and lessens acid secretion induced by ACh and gastrin
USE: GERD, peptic ulcer disease (not by H. pylori), nonulcer dyspepsia, stress-related gastritis
C, R, and F- 1st-pass metabolism (not N); all cleared by hepatic and renal mechanisms
Potency: C < R= N < F
Have a more marked effect on nocturnal over meal-induced acid secretion
SE: diarrhea, constipation, headaches, fatigue, myalgia; mental status change (when given IV); bradycardia, hypotension; crosses placenta/breast milk; Cimetidine-> inhibits estrogen metabolism=> gynecomastia/impotence in men and glactorrhea in women
D/I: C interferes w/ P450 drug metabolism pathways; all except F inhibit gastric metabolism of ethanol; all compete w/ creatine for renal secretion |
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Term
Omeprazole
Esomeprazole
Lansoprazole
Rabeprazole
Pantoprazole |
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Definition
Proton pump inhibitors
MOA: prodrug becomes protonated in parietal cell canaliculus, activated, and then forms bond w/ and irreversibly inhibits H+,K+ ATPase
USE: GERD, peptic ulcer disease (esp duodenal), nonulcer dyspepsia, prevention of stress related mucosal bleeding (omeprazole), gastrinoma
All- oral; Eso and Panto- also available IV
Oral form has acid-resistant coating-> not dissolved/absorbed until alkaline intestinal lumen
Bioavailability decreased 50% by food-> given on empty stomach 1 hr before eating
Serum half-life ~1.5hrs; acid inhibition lasts 24hrs
Rapid 1st pass metabolism; all hepatic metabolism
Inhibits both fasting/nocturnal and meal stimulated acid secretion (unlike H2 blockers)
SE: diarrhea, headache, abdominal pain; decreased B12/Ca absorption; increased gastric bacterial contents; increased serum gastrin
D/I: decreased absorption of drugs relying on acidity; consume P450s during metabolism; Omep- inhibits metabloism of warfarin, diazepam, phenytoin; Esomep- inhibits metabolism of diazepam; Lanso- inhibits metabolism of theophylline |
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Term
| H. pylori "Triple Therapy" |
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Definition
14 days
PPI 2X daily + Clarithromycin 2X daily + Amoxicillin or Metronidazole 2X daily
After 14 days, PPI continued 1X daily for 4-6wks |
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Term
| H. pylori "Sequential Treatment" |
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Definition
10 days
Days 1-5: PPI 2X daily + Amoxicillin 2X daily
Days 6-10: PPI 2X daily + Clarithromycin 2X daily + Tinidazole 2X daily |
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Term
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Definition
Mucosal Protective Agent
MOA: salt of sucrose + sulfted aluminum hydroxide-> forms a paste in stomach acid that binds ulcers or erosions for up to 6hrs
Prevents further caustic damage while stimulating mucosal prostaglandin and bicarbonate secretion
Given on empty stomach at least 1 hr before a meal
SE: constipation
D/I: may interfere w/ the absorption of some drugs |
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Term
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Definition
Mucosal protective agent and Antidiarrheal
Bismuth + salicylate
MOA: dissociates in the stomach allowing absorption of salicylate-> bismuth coats ulcers and erosions; stimulates prostaglandin, mucus and bicarbonate secretion; reduces stool freq and liquidity in acute infectious diarrhea due to salicylate inhibition of prostaglandin and Cl secretion; direct antimicrobial effects
Treatment of dyspepsia, acute diarrhea, prevention of traveler's diarrhea, eradication of H. pylori infection
SE: blackening of tongue and stools
CI: renal insufficiency |
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Term
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Definition
Antimuscarinic
MOA: selective blockade of excitatory M1 muscarinic receptors on vagal ganglion cells innervating the stomach-> reduce gastric acid secretion with fewer SE compared to atropine |
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Term
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Definition
Alcohol
Peak blood concentration in 30min-> food delays absorption; women have higher peak concentration
Majority oxidized in liver via zero-order kinetics @ 7-10g/hr; some excreted via lungs and urine
Metabolized by alcohol dehydrogenase (ADH) and microsomal ethanol oxidizing system (MEOS-> P450s) to acetaldehyde-> acetaldehyde metabolized by aldehyde dehydrogenase (ALDH) to acetate
Can be used in the treatment of methanol poisoning (higher affinity for ADH)
Chronic consumption: fatty liver=> hepatitis, cirrhosis, liver failure; chronic pancreatitis; gastritis; diarrhea, weight loss, vitamin deficiency (folate, B12, thiamine, etc.)
D/I: induction of P450s; increased conversion of acetaminophen to toxic metabolites |
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Term
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Definition
Management of alcohol withdrawal syndrome; antiemetic
MOA: enhances Cl- inflow through GABA-A receptor channels in the presence of GABA by increasing frequency of inflow (not duration) on inhibitory interneurons-> disinhibition of DA neurons
Oral or IV administration
Replacing for alcohol then gradually reducing the dose |
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Term
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Definition
Alcohol withdrawal syndrome
MOA: enhance GABA-A mediated influx of Cl- to prevent depolarization |
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Term
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Definition
Use: treatment of alcoholism
MOA: competitive μ-opiate receptor antagonist-> blocks reinforcing properties by inhibiting drug stimulated dopaminergic pathways
Success is linked to a polymorphism of μ opioid receptor; long acting (1/2 life 10hrs); oral or IM
Reduces cravings and relapse rate
SE: hepatotoxicity
D/I: increased liver damage if given w/ disulfiram; blocks the therapeutic effects of opioids |
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Term
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Definition
Use: treatment of alcoholism
MOA: competitive inhibitor of NMDA glu receptor and GABA-A activator
Reduces relapse rates
Food reduces absorption
SE: arrhythmia, altered BP, headache, insomnia, impotence, hallucinations in elderly
CI: renal impairment |
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Term
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Definition
Use: treatment of alcoholism
MOA: blocks aldehyde dehydrogenase (ADH) metabolism of etoh-> accumulation of acetaldehyde = flushing, respiratory difficulties, vomiting, and BP drop upon alcohol ingestion
12hrs is required for its full action
D/I: inhibits metabolism of phenytoin, anticoagulants, isoniazid |
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Term
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Definition
Treatment of alcoholism
MOA: induces closure of the inactivation gate in activated Na+ channels in depolarizing neurons, preventing further depolarization; |
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Term
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Definition
Found in canned heat and windshield-washing products; absorbed through skin, lungs, and GI tract
Metabolized by alcohol dehydrogenase (ADH) to formaldehyde and then by aldehyde dehydrogenase (ALDH) to formate; formate metabolized by a folate-dep pathway to CO2+H2O
Tox: visual disturbances w/ clear sensorium, bradycardia, coma, seizures, acidosis, respiratory failure
Treatment of poisoning: resp support; hemodialysis; IV etoh (etoh has a higher affinity for ADH than methanol); fomepizole; bicarbonate; folate |
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Term
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Definition
Found in antifreeze
Metabolized to toxic aldehydes and oxalate by alcohol dehydrogenase (ADH)
Tox: excitation followed by CNS depression, metabolic acidosis, renal insufficiency
Treatment: fomepizole; IV etoh; hemodialysis |
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Term
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Definition
Treatment of methanol and ethylene glycol poisoning
MOA: alcohol dehydrogenase inhibitor
Prevents breakdown of alcohols into toxic metabolites
SE: headache, nausea, dizziness, minor allergic reactions |
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Term
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Definition
Only NT in parasympathetic, first NT in sympathetic
Muscarninc and nictonic receptors
acetyl CoA + choline via choline acetyltransferase -> acetylcholine
Hydrophilic-> poorly absorbed, poorly distributed to CNS; rapidly hydrolyzed
Effects: DUMBELSS *diarrhea and emesis* |
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Term
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Definition
Muscarinic cholinergic receptor agonist
More resistant to hydrolysis than acetylcholine |
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Term
|
Definition
Nonselective muscarinic and nicotinic agonist
High resistance to hydrolysis |
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Term
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Definition
| Muscarinic cholinergic receptor agonist (partial agonist) Effects: DUMBBELS |
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Term
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Definition
Muscarinic cholinergic receptor agonist
MOA: stimulates M3 receptors in GI system
USE: postoperative ileus, congenital megacolon |
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Term
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Definition
AchE inhibitor; carbamate ester
MOA: forms covalent bond w/ AchE that is resistant to hydrolysis; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate=> DUMBELSS
Hydrolysis can occur but at a slow rate (30min-6hr)
Does not enter CNS; poorly soluble
Use: postop paralytic ileus and urinary retention
Short acting requiring frequent dosing; oral or parenteral every 4 hours |
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Term
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Definition
Antimuscarinic- competitive antagonist
MOA: reversible blockade of Ach receptors; inverse agonist
Effects: eye dilation (mydriasis); cycloplegia (loss of accommodation); tachydcardia; bronchodilation; dry mouth; reduced GI motility; reduced urination; reduced sweating
Use: cholinergic poisoning; eye examination
Given IV, topically (drops)-> well absorbed from conjunctival and gut membranes
Toxicity: increased intraocular pressure in closed angle glaucoma; dry mouth, flushed skin; agitation; delirium; hyperthermia-> dry as a bone, blind as a bat, red as a beet, mad as a hatter |
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Term
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Definition
Antimuscarinic
MOA: inhibits M3 receptors in the enteric plexus and on smooth muscle
Works as an antispasmodic in treatment of IBS
SE: dry mouth, visual disturbances, urinary retention, constipation |
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Term
METOCLOPRAMIDE
Domperidone |
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Definition
Antiemetic; Prokinetic
MOA: dopamine D2 receptor antagonist-> D2 activation inhibits cholinergic smooth muscle stimulation=> these drugs allow sm musc activity
Increase esophageal peristaltic amplitude, increase LES pressure, enhance gastric emptying but have no effect on the intestines; also block D2 receptors in area postrema-> anti-nausea
USE: GERD, impaired gastric emptying, nonulcers dypepsia, postop nausea/vomiting, pospartum lactation stimulation
SE: Metoclopramide-> restlessness, drowsiness, insomnia, anxiety, agitation, EPS, tardive dyskinesia, elevated prolactin levels (galactorrhea, gynecomastia, impotence); Domperidone-> doesn't cross BBB; well tolerated |
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Term
PSYLLIUM
Methylcellulose
POLYCARBOPHIL |
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Definition
Bulk-forming laxatives
MOA: indigestible, hydrophilic colloids that absorb water, forming a bulky gel that distends the colon and promotes peristalsis
SE: bloating, flatulence |
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Term
|
Definition
Stool softener
MOA: softens stool material, permitting water and lipid penetration
Oral or enema; prevents constipation and minimizes straining
SE: impaired fat soluble vitamin absorption |
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Term
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Definition
Stool softener
MOA: clear, viscous oil that lubricates fecal material, retarding water absorption from stool
Prevents and treats fecal impaction in young children and debilitated adults
SE: impaired fat soluble vitamin absorption |
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Term
|
Definition
Osmotic laxative
MOA: nonabsorbable sugar-> increased fluid in GI lumen to increase liquid stool volume and promote release
Prevent or treat chronic obstruction
SE: metabolized by bacteria-> severe flatus and cramps |
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Term
| Polyethylene Glycol (PEG) |
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Definition
Osmotic laxative
MOA: inert, nonabsorbable, osmotically active sugar given w/ salts-> increased fluid in stool to allow release
Given via lavage-> colonic cleansing before endoscopic procedures; orally-> chronic constipation
Can be used in decontamination after ingestion of iron tablets, enteric coated medicines, illicit drug filled packets, and foreign bodies |
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Term
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Definition
Stimulant laxatives (Cathartics)
MOA: direct stimulation of the ENS and colonic electrolyte and fluid secretion
BM w/in 6-12hrs taken orally, 2hrs rectally
Chronic use lease to melanosis coli-> brown pigmentation of the colon |
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Term
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Definition
Stimulant laxative (Cathartic)
MOA: direct stimulation of the ENS and colonic electrolyte and fluid secretion
Treatment of acute and chronic constipation; cleansing prior to colonoscopy
BM w/in 6-10hrs taken orally, 30-60mins rectally |
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Term
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Definition
Laxative
MOA: activation of type 2 Cl channel (ClC-2) in sm intestine-> increases Cl rich fluid secretion=> increased motility and decreased intestinal transit time
USE: chronic constipation, IBS w/ predominant constipation in women
BM w/in 24hrs
SE: teratogenic, nausea
C/I: not to be used in women of child bearing age |
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Term
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Definition
Laxative
MOA: μ-opioid receptor antagonist
Treatment of opioid induced constipation-> opioids may cause constipation by decreasing intestinal motility
Does not cross BBB
Given subcutaneously |
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Term
|
Definition
Laxative
MOA: μ-opioid receptor antagonist
Treatment of postop ileus after small or large bowel resection
Does not cross BBB
Given orally
SE: cardiovascular toxicity |
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Term
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Definition
Laxative; Prokinetic
MOA: partial 5-HT4 agonist-> enhances release of calcitonin gene related peptide which stimulates neurons to promote proximal bowel contraction and distal bowel relaxation
Treatment of chronic constipation due to IBS in women
SE: cardiovascular toxicity-> inhibition of 5-HT1A receptors |
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Term
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Definition
Laxative; Prokinetic
MOA: partial 5-HT4 agonist-> enhances release of calcitonin gene related peptide which stimulates neurons to promote proximal bowel contraction and distal bowel relaxation
SE: QT prolongation-> inhibition of cardiac K channels
D/I: Erythromycin |
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Term
|
Definition
Macrolide antibiotic; GI Motility Stimulant
MOA: directly stimulates motilin receptors on GI smooth muscle and promotes onset of a MMC
USE: treatment of gastroparesis; promote gastric emptying before endoscopy
Tolerance develops quickly
D/I: cisapride-> compound cardio toxicity |
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Term
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Definition
Antidiarrheal
MOA: μ-opioid receptor agonist-> inhibition of presynaptic cholinergic nerves-> increased colonic transit time w/ increased fluid absorption
Does not cross BBB-> no analgesia, no addiction
Nonperscription |
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Term
|
Definition
Antidiarrheal
MOA: μ-opioid receptor agonist-> inhibition of presynaptic cholinergic nerves-> increased colonic transit time w/ increased fluid absorption
No analgesia; does cross BBB-> potential for addiction
Prescription formulations made w/ atropine to discourage overdose
SE: high doses can cause opioid toxicity and effects |
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Term
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Definition
Antidiarrheal-> Kaopectate
MOA: absorbent of bacterial toxins and fluid-> decreasing stool liquidity and number
Kaolin- hydrated Mg/Al silicate
Pectin- indigestible carb derived from apples
Used for acute diarrhea
SE: constipation
D/I: should not be taken w/in 2 hrs of other medications |
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Term
CHOLESTYRAMINE
COLESTIPOL
Colesevelam |
|
Definition
Antidiarrheal
MOA: bile salt-binding resins-> terminal ileum dysfunction causes decreased bile acid resorption which can cause diarrhea
Taken before meals
SE: flatulence, bloating, constipation, fecal impaction; exacerbation of fat malabsorption
D/I: Cholestyramine and Colestipol should not be taken w/in 2 hrs of other drugs-> decreased absorption |
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Term
|
Definition
Antidiarrheal; Treatment of variceal hemorrhage; Prokinetic (in low doses)
MOA: similar effects as somatostatin-> decreased GI hormone secretion, decreased fluid and pancreatic/gallbladder secretion, slow GI motility, contraction of vascular smooth muscle; in low doses however it stimulates motility
IV half-life 1.5hr; longer in IM preps
Use: inhibition of endocrine tumor effects, diarrhea, inhibits pancreatic secretion in pancreatic fistula, GI bleeding
SE: steatorrhea/fat-soluble vitamin deficiency/cholecystitis (decreased pancreatic/GB secretion), nausea, vomiting, abdominal pain, flatulence, diarrhea, hyperglycemia, bradycardia, hypothyroidism |
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Term
ODANSETRON
Granisetron
Dolasteron
Palonosetron |
|
Definition
Antiemetic; Treatment of alcoholism
MOA: serotonin 5-HT3 receptor antagonists-> blockade of peripheral receptors on extrinsic vagal and spinal afferent nerves
Use in chemotherapy, postop, and postradiation nausea/vomiting
O, G, and D-> half life 4-9hrs; P-> half-life 40hrs
Hepatic metabolism
Most effective when given before chemo, esp in combo w/ a corticosteroid and NK1 receptor antagonist
SE: headache, dizziness, constipation, prolonged QT interval (esp dolasteron)
C/I: prolonged QT syndrome |
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Term
|
Definition
Antiemetic-> Corticosteroid
MOA: unknown
Enhances efficacy of 5-HT3 receptor antagonists for prevention of chemotherapy induced nausea/vomiting |
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Term
|
Definition
Antiemetic
MOA: neurkinin-NK1 receptor antagonist-> central blockade in area postrema (aka chemoreceptor trigger zone)
Aprepitant- oral; Fosaprepitant- IV, converted to aprepitant
Half-life 12hrs, hepatic metabolism
Used in combo w/ 5-HT3 receptor antagonists and corticosteroids for acute and delayed chemotherapy induced nausea/vomiting
SE: fatigue, dizziness, constipation
D/I: CYP3A4 metabolized drugs |
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Term
PROCHLORPERAZINE
Promethazine |
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Definition
Antiemetic-> phenothiazines (antipsychotics)
MOA: inhibition of DA-D2 and Muscarinic receptors (antiemetic) and antihistamine effects (sedative) |
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Term
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Definition
Antiemetic-> butyrophenones (antipsychotics)
MOA: central DA receptor blockade
Used for postop nausea/vomiting, also heavily sedating
Given IV or IM
SE: EPS, hypotension, QT prolongation |
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Term
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Definition
Antiemetic
MOA: muscarinic receptor antagonist
USE: prevention of motion sickness
SE: high anticholinergic effects (less when given as transdermal patch) |
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Term
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Definition
Antiemetic
MOA: 1st generation H1 antagonist w/ cholinergic activity
USE: chemo induced nausea/vomiting, sedation |
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Term
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Definition
Antiemetic
MOA: H1 antagonist w/ minimal anticholinergic activity
USE: motion sickness and vertigo |
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Term
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Definition
Antiemetic-> cannabinoids
Active ingredient-> delta9-tetrahydrocannabinol (THC)
Oral ingestion, high 1st pass metabolism
USE: appetite stimulant, antiemetic
SE: euphoria, dysphoria, sedation, hallucinations, dry mouth, increased appetite, tachycardia, orthostatic hypotension |
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Term
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Definition
Pancreatic enzyme replacement
Mixture of amylase, lipase, and protease
Pancrelipase enzmye concentration > pancreatin
USE: exocrine pancreatic deficiency in CF, pancreatitis, or pancreatic resection
Enzymes irreversibly inactivated by gastric acids-> given in enteric coated formulas or w/ acid inhibitor
Given w/ each meal and snack; swallowed and not chewed-> chewing may cause oropharyngeal mucositis
SE: diarrhea, abdominal pain, hyperuricosuria, renal stones, colonic strictures |
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Term
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Definition
Bile acid therapy for gallstones
MOA: bile acid that is absorbed, conjugated, and excreted in bile
Decreases cholesterol content of bile by reducing hepatic cholesterol secretion
USE: dissolution of small cholesterol gallstones and prevention of gallstones in obese pts undergoing rapid weight loss |
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Term
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Definition
Chemo- colon cancer
MOA: inhibits thymidylate synthase (TS)-> prevents conversion of dUMP to TMP for DNA synthesis; also inhibits RNA processing and incorporates itself into DNA
Activation to FdUMP req PRPP; MOA req cofactor N5-10methylene FH4Glu-n
MOR: increased TS
Combos: FOLFOX- leucovorin+5-FU+oxaliplatin; FOLFIRI- leucovorin+5-FU+irinotecan |
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Term
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Definition
Chemo- colon cancer
MOA: inhibits thymidylate synthase (TS)-> prevents conversion of dUMP to TMP for DNA synthesis
Oral version converted to 5-FU-> activated by carboxyesterase, cysteine deaminase, and sugar cleavage
SE: swelling, numbness of hands/feet, inflammation of mucus membranses |
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Term
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Definition
Used in combo w/ 5-FU
MOA: enhances thymidylate synthase inhibition by increasing required cofactor N5-10methyleneFH4 |
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Term
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Definition
Chemo- Used in combo w/ 5-FU
Given 24hrs before 5-FU
Synergism: blocks purine production which increases PRPP reserves for 5-FU activation |
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Term
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Definition
Chemo- advanced metastatic colon cancer
MOA: topoisomerase I inhibitor-> prevents breakage/resealing during DNA repair
Prodrug-> activated by carboxylesterase; low therapeutic index
Used in combo w/ 5-FU
Tox: severe diarrhea |
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Term
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Definition
Chemo- colon cancer
Used in combo w/ 5-FU and Irinotecan
MOA: prevents DNA synthesis via alkylation
Synergism: blocks feedback mechanisms that would increase levels of thymidylate synthase |
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Term
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Definition
Chemo- colon cancer
MOA: EGFR-tyrosine kinase reversible inhibitor-> blocks EGFR autophosphorylation and signal transduction=> decreased proliferation/angiogenesis/metastasis and increased apoptosis
Orally active
Used in combo w/ FOLFOX
Tox: diarrhea, rash |
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Term
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Definition
Chemo- EGFR(+) metastatic colon cancer in pts unable to tolerate Irinotecan
MOA: chimeric monoclonal Ab that blocks binding of ligand (EGF, TGFalpha) to EGFR=> decreased proliferation/angiogenesis/metastasis and increased apoptosis
SE: infusion reaction (mild to severe hypotension)-> limit w/ anti-inflammatory (i.e. dexamethasone) |
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Term
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Definition
Chemo- colon cancer
MOA: humanized monoclonal Ab against VEGF-> inhibits interaction with VEGF receptors (VEGF-Trap)=> inhibits angiogenesis in tumors
Tox: severe HTN, proteinurea, congestive HF, hemorrhage, stroke, MI, gastric perforation |
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Term
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Definition
Chemo- colon cancer
MOA: displacement of Cl in cisplatin by water activates-> crosslinks DNA by binding guanines to prevent replication; cisplatin-DNA complex attracts HMG-1 (high mobility group-1) repair proteins which become irreversibly bound-> prevents effective repair and leads to apoptosis
MOR: increased nucleotide excision repair protein; loss of function of mismatch repair (HMG-1)
Tox: nephrotoxicity, ototoxicity, marked nausea/vomiting (given w/ anti-emetic) |
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Term
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Definition
Chemo- carcinoma of pancreas, stomach, and small intestine
MOA: nitrosourea-> alkylation of DNA=> inhibits synthesis
Sugar group attached directs it to beta-cells of pancreas-> decreases toxicity
Does not produce a carbamoylated protein like most nitrosoureas-> lacks severe myelosuppression
SE: nausea, mild renal/hepatotoxicity |
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Term
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Definition
Chemo- mainly pancreatic cancer; also stomach and colon
MOA: dual alkylator-> crosslinks DNA @ G and A
Req activation for alkylation and chromosome breaks
MOR: decreased activation, efflux pump
SE: myelosuppression, nephrotoxicity |
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Term
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Definition
Chemo- pancreatic, esophageal, and NSC lung cancer
MOA: enters cell via nucleotide transporter; binds DNA as a nucleoside analog-> chain termination and apoptosis
Effective for both rapidly dividing and solid tumor cells
Synergistic w/ platinum based drugs
Inactivated by deoxycytidine deaminase
MOR: increased deoxycytidine deaminase
Tox: myelosuppression
Contraindications: radiation use |
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Term
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Definition
Chemo- esophagus, ovary, breast, cervix, lung, bladder
MOA: inhibit mitosis by binding to beta-tubulin-> blocks disassembly of microtubule strands
MOR: multidrug resistance pumps, beta-tubulin mutations
Tox: neutropenia, peripheral neuropathy, hypersensitivity (can prevent w/ dexamethasone) |
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Term
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Definition
Chemo
MOA: intercalates, inhibits topoisomerase II, ROS
Given IV
SE: cardiotoxicity, bone marrow suppression, alopecia, GI, red urine |
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Term
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Definition
Chemo
MOA: binds beta-tubulin to prevent cell division
Given IV
MOR: efflux pump
Tox: neurological (peripheral neuropathy), limited myelosuppresion, alopecia |
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Term
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Definition
Antimicrobial
Treatment of: severe colitis caused by C. difficle
MOA: binds D-Ala-D-Ala to prevent transglycosylation and inhibiting cell wall synthesis
Vancomycin- IV only
Teicoplanin- IV and IM
MOR: alteration of D-Ala-D-Ala to D-Ala-D-Lactate or D-Ala-D-Serine |
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Term
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Definition
Antimicrobial
MOA: prevents dephosphorylation (activation) of lipid transport molecule which carries peptidoglycan building blocks for cell wall synthesis
Given topical (dermatologic and opthalmic)
Can be given oral for C. difficile b/c not readily absorbed-> what is absorbed causes nephrotoxicity |
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Term
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Definition
Antimicrobial
MOA: inhibits transpeptidase-> blocks cell wall synthesis
Oral agents: Penicillin V, Oxacillin, Cloxacillin, Dicloxacillin, Ampicillin, Carbenicillin indanyl (R group) |
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Definition
Antimicrobial
MOA: inhibits transpeptidase-> blocks cell wall synthesis
Oral agents:
1st Gen: Cefalexin, Cefadroxil
2nd Gen: Cefaclor, Loracarbef (Cefzil)
3rd Gen: Cefpodoxime proxetil |
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Term
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Definition
Antimicrobial
Treatment of: Yersinia enterocolitica
MOA: prevent tRNA binding to 30S
MOR: influx/efflux, binding site mutation, inactivation
SE: GI, photosenitivity, brown teeth for fetus/young children, nephrotoxicity (not in doxycycline b/c not secreted by kidney-> excreted in feces)
Oral agents: doxcycycline, minocycline |
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Term
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Definition
Antimicrobial
Can be used in pregnant women in place of tetracyclines
MOA: binds 50S peptidyltransferase
MOR: plasmid encoded acetyltransferase, decreased permeability, binding site mutation
SE: inhibits synthesis of IMM proteins, anemia/leukopenia/thrombocytopenia, aplastic anemia/fatal pancytopenia (<1%); gray baby syndrome (cyanosis, HTN)-> due to failure to glucuronidate
Given orally |
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Term
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Definition
Antimicrobial- Sulfamethoxazole
MOA: competitive inhibitor of dihydropteroate synthase-> prevents incorporation of PABA into folic acid
MOR: mutation of DHOS, efflux, decreased PABA production
SE: crystaluria, THF deficiency, agranulocytosis, hemolytic anemia, anorexia, nausea/vomiting |
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Term
| Trimethoprim-Sulfamethoxazole |
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Definition
Antimicrobial (Bactrim)
Treatment of: Shigella diarrhea
MOA: inhibits 2 steps of the THF synthesis pathway; sulfamethoxazole inhibits incorporation of PABA into folic acid; trimethoprim inhibits DHFR
20:1 sulfamethoxazole:trimethoprim concentration
MOR: altered DHFR
Tox: myelosuppression, Stevens-Johnson syndrome, nausea/vomiting |
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Term
Ciprofloxacin
Levofloxacin |
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Definition
Antimicrobial- Fluoroquinolones
Treatment of: Salmonella, Shigella, Campylobacter, E. coli diarrhea; main diarrheal treatment
MOA: inhibits DNA gyrase and topoisomerase IV
Given orally
MOR: DNA gyrase mutation
SE: GI distress, arthritis in children
C/I: children |
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Term
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Definition
Antimicrobial- macrolide
Treatment of: Salmonella (Typhoid fever in children), Campylobacter diarrhea
MOA: binds 50S subunit of bacterial ribosome
MOR: methylation of 50S subunit
Given as enteric coated tablet for oral use
SE: diarrhea, cholestatic hepatitis |
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Term
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Definition
Antimicrobial- ketolide
MOA: binds to 50S subunit of ribosome
MOR: less susceptible to methylase and efflux mediated resistance than macrolides
SE: pseudomembranous colitis |
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Term
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Definition
Antimicrobial
MOA: binds 50S peptidyltransferase to block translocation
SE: diarrhea, pseudomembranous colitis |
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Term
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Definition
Antimicrobial/Antiprotozoal
Treatment of: C. difficile diarrhea; Giardia; Entamoeba
MOA: activated reactive hydroxylamine which degrades DNA in anaerobic organisms
MOR: decreased oxygen scavenging
SE: interferes w/ ethanol metabolism (inhibits aldehyde dehydrogenase), headache, nausea/vomiting, dry mouth-> fewer GI SE w/ tinidazole |
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Term
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Definition
Antiprotozoal
Treatment of: Giardia; Entamoeba
MOA: luminal aminoglycoside-> binds 30S ribosomal subunit and interferes with protein synthesis
Not absorbed
Used in combo w/ Metronidazole |
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Term
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Definition
Antiprotozoal
Treatment of: Cryptosporidium
MOA: interferes w/ ferredoxin oxidoreductase (PFOR)
No MOR, Little SE |
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Term
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Definition
Antiprotozoal
Treatment of: Entamoeba
MOA: chelating ferrous ions essential for metabolism
Luminal-> not absorbed; little SE |
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Term
| Pyrimethamine-Sulfadiazine |
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Definition
Antiprotozoal
MOA: inhibits 2 steps of the THF synthesis pathway; sulfadiazine inhibits incorporation of PABA into folic acid; pyrimethamine inhibits DHFR |
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Term
Mebendazole
Albendazole
Thiabendazole |
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Definition
Antihelminthic- roundworms, hookworms (nematodes)
MOA: inhibit microtubule polymerization by binding to beta-tubulin
Not toxic |
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Term
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Definition
Antihelminthic- flukes (trematodes), tapeworms (cestodes)
MOA: causes influx of Ca to produce paralysis of worm musculature
SE: dose related transient abdominal distress |
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Term
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Definition
Antihelminthic- roundworms, hookworms (nematodes)
MOA: activates glutamate gated Cl- channels-> causes tonic paralysis of the worm musculature
Well tolerated |
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Term
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Definition
Antihelminthic- flukes (trematodes)
MOA: organophosphate converted to dichlorvos-> AChE inhibitor |
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Definition
Antihelminthic- tapeworms (cestodes)
MOA: uncouples oxidative phosphorylation
No longer used in US |
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Term
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Definition
Antihelminthic
MOA: DNA binding, resulting in contraction and paralysis of the worms
Acts mainly on male worms
No longer used in US |
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Term
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Definition
Antihelminthic- nematodes
MOA: GABA-receptor agonist-> increasing Cl- conductance => muscle relaxation and flaccid paralysis |
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Term
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Definition
Antihelminthic- pinworm, roundworm, and hookworm (nematodes)
MOA: open nonselective cation channels and induce persistent activation of nicotinic acetylcholine receptors and spastic paralysis of the worm
SE: neuromuscular blockade |
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Term
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Definition
Antihelminthic
MOA: unknown
Not used in US unless supplied by CDC |
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Definition
Antiviral- HBV
MOA: inhibits viral polymerase/reverse transcriptase and causes chain termination
SE: nephrotoxicity, hepatotoxicity, lymph toxicity |
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Definition
Antiviral- HBV and HIV
MOA: inhibits viral polymerase/reverse transcriptase and causes chain termination
High resistance rates; well tolerated |
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Term
| Pegylatged interferon-alpha |
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Definition
Antiviral- HCV
MOA: inhibits viral replication and the translation of viral protein synthesis at multiple sites
Pegylation prevents renal elimination
SE: influenza like syndrome, reversible anemia
Used in combo w/ Ribavirin |
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Term
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Definition
Antiviral- HCV
MOA: inhibits viral mRNA synthesis
SE: cough, fatigue, rash, anemia
Used in combo w/ IFNalpha |
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