Pharmacology Final Content Flashcards
Tetracyclines
Vacuum Her Bedroom
Doxycycline, Minocycline, Demclocycline
Tularemia,
Vibrio cholerae, acne, chlamydiae, ureaplasma, urealyticum, Mycoplasma Pneumoniae, H. Pylori, Borrellia Burgdorferi, Brucella, Rickettsiae
also malaria, gonococcals, prophylaxis of chronic bronchitis
Doxycycline
Fat soluble, used in infectious prostatitis in the young, fat soluble so broken down in the liver
Minocycline
water soluble used by dentists
Demeclocycline
not really used as an antibiotic, Blocks the ADH receptors and is therefore used as a treatment for SIADH
Chelation and Tetracylcines
tetracyclines chelate divalent cations, go after calcium in teeth, brown teeth, Contraindicated CI in Preggers, children —> due to calcium disruption in bones and teeth
Chloramphenicol
50S inhibitor RNA inhibitor, PHEN= lipid soluble, used in sepsis and meningitis b/c it penetrates CSF.
- Dose dependent Bone marrow Supression
- inhibitor of CYP450
- “gray baby syndrome” bilirubin kernicterus and lack of UDPglucouronyl transferase so it remains un-metabolized in the body
AmiNOglycosides
GNATS: Gentamycin, Neomycin, Amikacin, Tobramycin, Streptomycin
- used for gram(-) rods
- used P.aeruginosa
- O2 dependent uptake,
- nephrotoxicity, ototoxicity, NMJ blockade
- -Bacteriocidal due to misfolded protein and kinking, remember —–Raymond’s drawing
Streptomycin
for TB, DOC for bubonic plague and tularemia
Neomycin
- -Only aminoglycoside used topically,
- -can cause contact dermatitis
Resistance to Aminoglycosides
Production of conjugating enzymes: acetylases, adenylases
Macrolides
Wide Spectrum Bacteriostatic
- Erythromycin, Azithromycin, clarithromycin
- -“thromycin” = macrolide
- -Gram+ cooci (not MRSA)
- -good for atypicals: chalmydia, mycoplasma, ureaplasma, LEGIONELLA, c.jejuni, Mycobaterium Avium Cellulare (MAC), H.pylori
Toxicity:
- QT prolongation –> predisposes to Torsades de Pointes
- CYP3A4 inhibition (can cause increase coumadin, theophylline)
- hepatotoxicity and upset GI
Azithromycin doesn’t inhibit CYP3A4
Macrolides
-pharmacokinetics
inhibit CYP450
-EXCEPT Azithromycin (slightly water soluble no crossing of placenta preggers)
side effects: GI distress, stimulates MOTILIN RECEPTORS–> more peristalsis. (looks like just erythromycin)
–reversible ototoxicity
Telithromycin
ketolide, used in macrolide resistant strept. Pneumoniae
Macrolide mode of resistance
Methylation of the 50S RNA, methylation of bacteria by methyltransferases hence no inhibition of translocation
Clindamycin
- -not a macrolide, but same MOA and Resistance
- -Gram + great for S. Aureus therefore great for osteomyelitis
- -good in mixed pneumonias
Linezolid
- -MOA inhibits the formation of initiation complexes in 50S subunits
- treats VRSA, VRE, drug resistant pneumoccociae
- Side effects: bone marrow supression
Quinupristin-Dalfopristin
AKA Streptogramins MOA: like A site but on 50S site spectrum: VRSA and VRE ---resistance to enterococci MO resistance for Vancomycin? --replace D-ALA to D-Lactate
Lincosamides
Clindamycin and Lincomycin
- -> lincomycin rarely used
- -like macrolides they bind the 23S rRNA of the 50S subunit, block translocation from the A site to the P site
- -inhibits formation of initiation complex
- -Supresses peptidyltransferase activity
- -Useful against anaerobes B. Fragillis, C. Perfringens
- -malaria, Gram+ in PCN allergic pt.’s
- ***Goldstein)) blocks transpeptidation by Reversible binding of the 50 S subunit at site near macrolides
Clindamycin
- -Can cause a C DiFF overgrowth
- -Wide distribution! but can’t go into CSF even when meninges are inflamed
- t.5= 2-3 hours but can vary based on the route
Clindamycin Activity
Gram + cocci
- -pneumococci, S. Pyogenes, viridians streptococci, MSSA, some MRSA and Nocardia
- -MRSA D TEST for Clindamycin!!
- –>disc approximation test
- -Gram + and Gram - bacteria, C. Prefringens (not C.DIFF)
- actinomyces, Bacteroides fragillis
- -Pneumocystits Jiroveci is second line: clindamycin +primarquine (anti-malarial)
- -toxoplasma gondii encephalitis clindamycin + pyramethamine (antimalarial, toxoplasma is a protozoa)
- -clindamycin is no good against UTI but is used in Pelvic inflammatory disease
Clindamycin Resistance
Gram (-), aerobic bacteria and enterobacteriaceae poorly penetrate the outer membranes
- -enterococci and C DIFF
- -MRSA and coagulase staph
- -RIBOSOMAL METHYLATION, erm encoding, D test , iMSLB inducible resistance that can occur during therapy
Clindamycin drug interactions
- –macrolides, chloramphenicol and clindamycin all attack the same site on the 50S. don’t use together
- –NMJ blockers and clind. lincoasamides inhibit release of Ach and enhance effects of NMJ for anesthesia
- –Device Interaction: oleaginous base in clindamycin vaginal cream may weaken condoms and diaphragms
Pharm HTN emergencies
- -get a vasodilator on board, IV
- -Sodium Nitroprusside, Fenaldopam, Diazoxide
- -Sodium Nitroprusside= MONITOR Thiocyanate levels!
- -Fenaldopam is only selective D1 dopamine receptor agonist for IV emergencies
Sulfonylureas
Glyburide, Glipizide,
Tolbutamide
-reduce dose in Renal failure also reduce some in hepatic
Alpha Glucosidase Inhibitors
- -Acarbose and Miglitol
- -Disaccharidases prevent conversion to monosaccharides by brush border enzymes
- -osmotic diarrhea presents more sugars to flora causing flatulence
Biguanides
- –Metformin
- -activates AMPCK –> increase expression of orphan nuclear receptor (Small Heterodimer Partner) inhibits expression of liver PEPCK and glucose 6 phosphate thus repressing hepatic gluconeogenesis
Insulins Rapid Acting
Rapid-Acting)
-Humalog or LISPRO
O) 15-30 min P) 30-90 min D) 3-5 hours
-Novolog or ASPART
O) 10-20 min. P) 40-50 min. D) 3-5 hours
-Apidra or GLULISINE
O)20-30 min. P) 30-90 min.
D) 1-2½ hours
Short Acting Insulins
—-Regular (R) humulin or novolin O) 30 min.-1 hour P) 2-5 hours D) 5-8 hours
–Velosulin (for use in the insulin pump)
O) 30 min.-1 hour P)2-3 hours D)2-3 hours
Intermediate Acting Insulin
–NPH (isophane)
O) 1-2 hours
P) 4-12 hours
D) 18-24 hours
Long Acting Insulin
–Lantus (GLARGINE)
O) 1-1.5 hours P) none, steady D) 20-24 hours
–Levemir (DETEMIR)
O) 1-2 hours P) 6-8 D) up to 24 hours
Statins
Rosuvastatin >Atorvastatin> Simvastatin> Lovastatin ~~ pravastatin > Fluvastatin
MOA) inhibition HMG-COA reductase
Cholesterol Synthesis))) Acetyl COA –> HMG-COA –> Mevalonate –> Farnesyl Pyrophosphate
–HMG COA –> mevalonate = 2NADPH –> NADP+ + HSCOA
HMG COA reductase
- -> insulin (increases action)
- -> Glucagon, phosphorylation (decreases action )
Fibrates
Gemfibrozil, Fenofibrate
—activation of nuclear transcription factor PPAR alpha –> upregulation of LPL –> increased clearance of TG rich lipoproteins
—Fibrates + statins —> ATN, acute tubular necrosis
Resins
(Bile Acid Sequestrants): Cholestyramine, colestipol, colsevelam
–upregulation of hepatic LDL receptors
Cardiac Glycosides
oral avail, .5 life, elim.
Digoxin 75% 40 kidneys
Digitoxin >90% 160 liver
Ouabain 0% 20 kidneys
