Pharmacology Final Content

Question 1

Tetracyclines

Vacuum Her Bedroom

Answer 1

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

Question 2

Doxycycline

Answer 2

Fat soluble, used in infectious prostatitis in the young, fat soluble so broken down in the liver

Question 3

Minocycline

Answer 3

water soluble used by dentists

Question 4

Demeclocycline

Answer 4

not really used as an antibiotic, Blocks the ADH receptors and is therefore used as a treatment for SIADH

Question 5

Chelation and Tetracylcines

Answer 5

tetracyclines chelate divalent cations, go after calcium in teeth, brown teeth, Contraindicated CI in Preggers, children —> due to calcium disruption in bones and teeth

Question 6

Chloramphenicol

Answer 6

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

Question 7

AmiNOglycosides

Answer 7

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

Question 8

Streptomycin

Answer 8

for TB, DOC for bubonic plague and tularemia

Question 9

Neomycin

Answer 9

• -Only aminoglycoside used topically,

- -can cause contact dermatitis

Question 10

Resistance to Aminoglycosides

Answer 10

Production of conjugating enzymes: acetylases, adenylases

Question 11

Macrolides

Answer 11

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:

1. QT prolongation –> predisposes to Torsades de Pointes
2. CYP3A4 inhibition (can cause increase coumadin, theophylline)
3. hepatotoxicity and upset GI

Azithromycin doesn’t inhibit CYP3A4

Question 12

Macrolides

-pharmacokinetics

Answer 12

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

Question 13

Telithromycin

Answer 13

ketolide, used in macrolide resistant strept. Pneumoniae

Question 14

Macrolide mode of resistance

Answer 14

Methylation of the 50S RNA, methylation of bacteria by methyltransferases hence no inhibition of translocation

Question 15

Clindamycin

Answer 15

• -not a macrolide, but same MOA and Resistance
• -Gram + great for S. Aureus therefore great for osteomyelitis
• -good in mixed pneumonias

Question 16

Linezolid

Answer 16

• -MOA inhibits the formation of initiation complexes in 50S subunits
• treats VRSA, VRE, drug resistant pneumoccociae
• Side effects: bone marrow supression

Question 17

Quinupristin-Dalfopristin

Answer 17

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

Question 18

Lincosamides

Answer 18

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

Question 19

Clindamycin

Answer 19

• -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

Question 20

Clindamycin Activity

Answer 20

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

Question 21

Clindamycin Resistance

Answer 21

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

Question 22

Clindamycin drug interactions

Answer 22

• –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

Question 23

Pharm HTN emergencies

Answer 23

• -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

Question 24

Sulfonylureas

Answer 24

Glyburide, Glipizide,
Tolbutamide

-reduce dose in Renal failure also reduce some in hepatic

Question 25

Alpha Glucosidase Inhibitors

Answer 25

- -Acarbose and Miglitol - -Disaccharidases prevent conversion to monosaccharides by brush border enzymes - -osmotic diarrhea presents more sugars to flora causing flatulence

Question 26

Biguanides

Answer 26

- --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

Question 27

Insulins Rapid Acting

Answer 27

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

Question 28

Short Acting Insulins

Answer 28

----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

Question 29

Intermediate Acting Insulin

Answer 29

--NPH (isophane) O) 1-2 hours P) 4-12 hours D) 18-24 hours

Question 30

Long Acting Insulin

Answer 30

--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

Question 31

Statins

Answer 31

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 )

Question 32

Fibrates

Answer 32

Gemfibrozil, Fenofibrate ---activation of nuclear transcription factor PPAR alpha --> upregulation of LPL --> increased clearance of TG rich lipoproteins ---Fibrates + statins ---> ATN, acute tubular necrosis

Question 33

Resins

Answer 33

(Bile Acid Sequestrants): Cholestyramine, colestipol, colsevelam --upregulation of hepatic LDL receptors

Question 34

Cardiac Glycosides

Answer 34

oral avail, .5 life, elim. Digoxin 75% 40 kidneys Digitoxin >90% 160 liver Ouabain 0% 20 kidneys