Drugs Week 2 Flashcards
Amoxicillin
Resistance is around 1%, possibly increasing.
More than twice as acid stabile as ampicillin, thus twice the blood levels are achieved w/ the same oral dose –> never substitute.
MOA: Cell wall inhibitor –> binds to PBP –> inhibits transpeptidases
A.E. = Hypersensitivity reactions
Bismuth Subsalicylate
AKA petpo bismol
MOA:
- ) Antimicrobial: disrupt cell wall, prevents adhesion, inhbits urease
- ) Protects surface –> coat, increase secretion of mucus and increase HCO3-
Bismuth is active ingredient in stomach
Drug dissociates in stomach into Bismuth and Salicylate
A.E. Black tongue and stool (benign), salicylate toxicity (vomting, tinnitus, confusion, hypothermia, resp. alkalosis –> metabolic acidosis)
Clarithromycin
Resistance is 10-15%
Has the lowest MIC50 of the macrolides and is the most acid stabile.
MOA: It binds to 23S rRNA, a component of the 50S subunit of the bacterial ribosome, thus inhibiting the translation of peptides.
A.E. - GI effects (stimulates MMC). Drug interactions (CYP 3A4). Increased risk of miscarriage in 1st trimester.
Bacteriostatic
Rifabutin
MOA: Inhibits DNA dependent RNA polymerase blocking transcription.
Bacteriocidal
A.E. HS rxn, hepatotoxicity, inhbitis CYP450, Orange/Red fluids
Tetracycline
Antacids will chelate tetracyclines and render them less efficacious.
Incomplete absorbtion –> give w/ food.
MOA: Binds 30s subunit inhibiting protein synthesis.
A.E. - GI Irritation, Photosensitivity, Discoloration of growing teeth, Don’t give to pregnant women or kids.
Bacteriostatic
Metronidozole
Resistance is 25-35%
MOA: Electron sink
A.E. GI/CNS toxicity, disulfiram reaction, teratogenic
Inhibits CYP2C9 ( increase Warfarin and affects H2 blocker)
Tinidazole has decreased A.E. and dosing
Triple Therapy
Regimens to treat H. pylori ulcers always have 3 key components:
- ) Multiple ABs for eradication of the bacteria
- ) A mechanism for treating pain (usually a PPI) and facilitating healing
- ) Long duration (10-14 days), which can cause problems w/ compliance
Current standard = PPI + Clarithro + Amox or Tinidazole)
Alternatives if resistance = Quadruple therapy:
PPI + Bismuth + Tetracycline + Metronidazole
Or
PPI + Amox + Rifabutin + Cipro
Sucralfate
Requires an acid environment to be activated, thus can’t be given w/ PPIs, H2 blockers or antacids
MOA: H+ converts to paste –> sticks to ulcer.
Use: Stress induced ulcers in ICU “band-aid”
A.E. Constipation, binds drug
Aluminum Hydroxide
MOA: Weak base used to buffer stomach acid.
Rapid onset, but short duration of action, no prevention of ulcer recurrence –> useful for intermittent dyspepsia.
Not systemically absorbed (good)
Significant for constipation (often given w/ Mg(OH)2)
Drug interactions:
- Increase gastric PH
- Bind drugs (tetracycline)
- Increase gastric emptying
- ) Alkalinize urine (changes drug elimination)
Calcium Carbonate
MOA: Weak base used to buffer stomach acid.
Rapid onset, but short duration of action, no prevention of ulcer recurrence –> useful for intermittent dyspepsia.
Rapid onset, long duration.
A.E. Mild systemic alkalosis, hypercalcemia (milk-alkali syndrome)
Drug interactions:
- Increase gastric PH
- Bind drugs (tetracycline)
- Increase gastric emptying
- ) Alkalinize urine (changes drug elimination)
Magnesium Hyroxide
MOA: Weak base used to buffer stomach acid.
Rapid onset, but short duration of action, no prevention of ulcer recurrence –> useful for intermittent dyspepsia.
Not systemically absorbed (good)
Significant for diarrhea (often given w/ Al(OH)3.
Drug interactions:
- Increase gastric PH
- Bind drugs (tetracycline)
- Increase gastric emptying
- ) Alkalinize urine (changes drug elimination)
Sodium Bicarbonate
MOA: Weak base used to buffer stomach acid.
Rapid onset, but short duration of action, no prevention of ulcer recurrence –> useful for intermittent dyspepsia.
Extremely rapid onset.
A.E’s severe metabolic alkalosis, alkalinizes urine.
Drug interactions:
- Increase gastric PH
- Bind drugs (tetracycline)
- Increase gastric emptying
- ) Alkalinize urine (changes drug elimination)
Misoprostol
MOA: PGE1 is the drug of choice for treatment of ulcers induced by NSAIDs.
Adverse effects and frequent dosing lead to limited use.
A.E.’s: Abortifacient, Uterine contractions, diarrhea, severe nausea, cramping, abdominal pain in 25%.
PK: Rapid absorbtion and metabolism. Excreted in urine.
Simethicone
MOA: Antifoaming agent –> decreases gas pain.
-prazoles
MOA: Irreversibly block the final common pathway in acid secretion, the H/K ATPase. AKA PPI.
OTC
Slow onset of action, very long duration of action, excellent prevention. Drugs of choice for ZE syndrome, GERD, and ulcer treatment
PK: Prodrugs (acid labile) –> pass through stomach and absorbed in small intestine before being distributed to the entire body. Then selective for acidic compartments.
Timing is critical –> give in fasting state (don’t want to crush drug) approximately 1/2 hr. before meal –> concentration of drug is highest when pumps turn on.
Short half life, but are irreversibly –> once a day dosing. Full inhibition in 3-4 days; recovery in 3-4 days. High initial dose –> taper off.
A.E.’s - no significant in healthy people. 1-5%: HA, diarrhea, nausea, rash.
Rebound acid secretion when stopped
Concerns:
- Decreased B12, iron, Ca, and Zn –> increase incidence of hip fracture.
- Increased respiratory and enteric infections (from increased pH)
- ECL hyperplasia –> increase carcinoid tumors (only in animals so far).
