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77 Cards in this Set

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penicillin and cephalosporins
antibiotic
beta lactam
1. inhibits transpeptidase (suicide substrate)
2. activates autolysins

resistance
1. beta lactamase
2. autolysin deficient
3. decrease permeability

penicillin is static but not cidal to autolysin deficient strains
aminoglycosides
70s ribosome inhibitor (30s)

resistance: decreased uptake of aminoglycosides
cycloserine
antibiotic
D alanine mimetic

reversibly inhibits transpeptidase and all nzs that interact with D-ala
clavulanate
beta lactamase inhibitor
(suicide substrate)

used with penicillin
sulbactam
beta lactamase inhibitor
(suicide substrate)

used with penicillin
prontosil
sulfonamide antibiotic (antimetabolite)

inhibits folate synthesis
(bact make folate, mamm cells dont)
sulfonamide alone is static
sulfonamide + trimethorprim = great combo -> prevents resistance
trimethorprim
antibiotic (antimetabolite)

inhibits DHF reductase, no THF regeneration, folate depletion
(antimetabolite)


sulfonamide + trimethorprim = great combo -> prevents resistance
tetracyclines
70s ribosome inhibitor (30s)

resistance: tetracyclines actively pumped out
pancreatic supplement (cotazym)
pancreatic enzymes (bovine)

use: pancreatic insufficiency, CF patient
dehydrocholate (dechoin)
bile acid
oxidized bile acid. forms small micelles and increases osmotic pressure of bile, increasing bile flow. isn't reabsorbed.

use: slow bile, biliary sludge, (liver transplant)
medium chain fatty acids
c8-c12 dont require bile acids to solubilize them

use: liver disease, CF, anyone with biliary insufficiency
chendeoxycholate
use: cholelithiasis

moa: inhibits HMG CoA reductase
less cholesterol, bile is not supersaturated with cholesterol and is more soluble
ursodeoxycholate

(URSODIOL)
URSODIOL
use: cholelithiasis

moa: hypdrophilic and shifts the bile acid:phospholipid:cholesterol phase diagram so that liquid crystals form rather than cholesterol stones
cholate, heparin, monooctanoin
treat bile stones stuck in common bile duct
NaHCO3
antacid.

sodium can be problem
CaCO3
antacid.

calcium can cause nocturnal acid secreation.
Al(OH)3
antacid.

slower acid neutralization.
constipation
Mg(OH)2
antacid
insoluble, must take in pill form
diarrhea
SULCRALFATE
mucosal protecting agent

binds to ulcer and acts like a shield

will not work without acid activation, so dont give with an H2 blocker or PPI
MISOPROSTOL
prostaglandin

1. increases mucus production
2. reduces cAMP and acid production in parietal cell
CIMETIDINE
H2 blocker

active agent. not a prodrug

decreases acid production by blocking histamine receptor on parietal cell

use:
1. gastric and duodenal ulcers
2. acid reflux
3. z-e syndrome (must give higher dose...)

* remember, no effect on gastric emptying, LES pressure, biliary and pancreatic secretions
s/e: gynecomastia and low sperm count. can change effects of other drugs
RANITIDINE
H2 blocker

8x more potent than cimetidine (qd instead of qid)
OMEPRAZOLE
PPI

moa: irreversible inactivation of H+/K+ ATPase

highly selective for parietal cell caniculi because it diffuses there, gets protonated and is trapped

uses:
gastric ulcer
z-e syndrome
do not give with cimetidine!
tetracycline/metranidazole/bismuth subsalicylate
treatment for h. pylori

not front line. only use in pts with major ulcer recurrence after treatment with H2 blockers or sucralfate
DIMENHYDRINATE
h1 antagonist

use: motion sickness (n/v)

s/e: drowsiness and dry mouth

= dramamine
DIPHENHYDRAMINE
h1 antagonist

use: motion sickness (n/v)

s/e: drowsiness and dry mouth

= benadryl
CISAPRIDE
dopamine agonist

antinausea (does NOT prevent motion sickness!)

use: GI endoscopy, migraine and chemotherapy associated nausea

moa: increases GE sphincter pressure, increases upper GI motility, relaxes pyloric sphincter (closes tap and opens spigot)

similar:
domperidone
CISAPRIDE
METOCLOPRAMIDE
dopamine agonist

antinausea (does NOT prevent motion sickness!)

use: GI endoscopy, migraine and chemotherapy associated nausea

moa: increases GE sphincter pressure, increases upper GI motility, relaxes pyloric sphincter (closes tap and opens spigot)

similar:
domperidone
METOCLOPRAMIDE
ipecac syrup
induction of vomitting

moa: irritant to chemoreceptor trigger zone in medulla

contraind: corrosive substance, cardiotoxic, coma, convulsions
apomorphine
induction of vomitting

moa: opiate which is irritant to chemoreceptor trigger zone in medulla

s/e: resp depression. have naloxone available
loperamide
opiate antidiarrheal

loperamide = immodium

use: diarrhea

moa: increase muscle tone(spasm) in GI, but reduce peristalsis

nonaddictive opiate b/c cant cross BBB
lomotil
opiate antidiarrheal

use: diarrhea

moa: increase muscle tone(spasm) in GI, but reduce peristalsis
kaopectate
antidiarrheal
kaolin + pectin - absorbs water
charcoal
lots of surface area
binds organic substances (and others) but not water?

use for diarrhea? and overdoses
cholestyramine
moa: binds and sequesters bile salts

use: bile salt malabsorption
(such as radiation ileitis and ileal resection). bile salts are cathartics and cause colonic mucosal secretion (blockable with propanolol)
epsom salts
cathartic

similar: go lyte ly

moa: osmotic diarrhea. Mg also activates water secretion in colon (think antacid s/e)
docusate
stool softener

lubrication and softening

s/e: may enhance absorption of some drugs
castor oil
cathartic

moa: mucosal irritation
methyl cellulose / bran
increases bulk
sulfasalazine
use: inflammatory bowel disease

antinflammatory

moa: inhibits cyclooxygenase, lipoxygenase, and thromboxane synthase

split in colon to form 5ASA and sulfapyridine

sulfapyridine s/e: fever rash aplastic anemia, AI hemolysis
olsalazine
use: inflammatory bowel disease

two 5ASA joined together
no sulfapyridine s/e

moa: inhibits c-o, l-o, and thromboxane synthase
phenolphthalen
cathartic
senna
cathartic
bismuth subsalicylate
promotes ulcer healing

moa is unclear

in peptobismol
bismuth subsalicylate
promotes ulcer healing

moa is unclear

in peptobismol
carbon monoxide
toxin

moa: binds to hemoglobin with much higher affinity than oxygen

effects: mental confusion, muscle weakness, hypoxia, cardiovascular toxicity
treatment:
1. remove person from CO
2. hyperbaric oxygen
methanol
toxin

moa: metabolized by alcohol DH to formaldehyde, which is toxic

effects: kills retinal ganglion cells

treatment:
1. ethanol - competes for alcohol DH
2. 4-methylpyrazole - inhibts alcohol DH
3. hemodialysis to remove methanol from blood before it's converted to formaldehyde
acetominophen
overdose

moa: normally metabolized by reduction by glutathione. when glutathione is used up (massive dose), a toxic intermediate, NAPQI accumulates.

NAPQI is hepatotoxic and causes LIVER FAILURE

treatment:
1. n-acetylcysteine - increases glutathione
cyanide
toxin

sign: bright red blood

moa: binds to cytochrome oxidase and inhibits electron transport chain and oxphos

treatment
1. sodium nitrite - oxidizes Fe in Hb to Fe3+, which will pull the cyanide off of cytochrome oxidase
2. sodium thiosulfate - reacts with cyanide to form thiocyanide, which is excreted by kidneys
benzene
toxin

effects:
1. leukemia
2. aplastic anemia
arsenic
toxin

moa: arsenate, arsenite
1. arsenate: phosphate analog which prevents ATP synthesis
2. arsenite: reacts with lipoic acid (pyruvate DH - no acetylcoa can enter tca cycle)

GI irritation: n/v/d/pain
muscle weakness and aching, paresthesia in stocking glove distrib
skin problems

carcinogenic in skin, bladder, lung, and liver

treatment: chelation therapy
lead
toxin

moa: inhibits heme synthesis

effects:
1. CNS manifestations - deterioration in mental function, problems in school. reversable.
2. hypochromic microcytic anemia
mercury
toxin

methyl mercury bioaccumulates
also inorganic mercury?

effects:
CNS (mad hatter)
kidney failure
lots of stuff

treatment:
1. chelation for nonorganic mercurials.
a. SUCCIMER - oral
b. EDTA - IV, lots of S/E
2. hemodialysis
TXA2
1. vasoconstriction
2. platelet activation
PGI2
prostacyclin

counteracts TXA2

1.vasodilation
2. inhibits platelet activation
3. gastric cyto-protection
PGE2
1. vasodilation
2. bone resorption (at sites of inflamm)
3. pain sensitization (this is how NSAIDs are analgesic)
4. gastric cyto-protection
a. enhances mucosal blood flow
b. increases mucus secretion
c. enhances bicarbonate secretion
d. enhances epithelial growth
**** NSAID induced gastropathy
PGF2
F
1. uterine contraction - labor and menses
2. bronchoconstriction (impt in pathogenesis of asthma)
COX2 inhibitor
selectively inhibits COX2
this mostly targets pain, fever, manifestations of inflammation

in addition to being induced during inflammation, COX2 is constituitively expressed in kidney and CNS. in kidney, PG cause vasodilation and maintain renal blood flow and renal function. COX2 inhibitors decrease renal blood flow!

all NSAIDs probably increase thromboembolic events

COX2 may be the predominant form of COX in atheromatous lesions (inflammatory - induced). PGI2 produced in the vessel wall here is keeping the vessel vasodilated and compensating. COX2 inhibitor tips the balance b/t the PGI2 (inflamed endothelium - COX2 and TXA2 (platelets - COX1)
giving nonselective NSAIDs is better here b/c it keeps the balanse
NSAID
COX inhibitor

COX1- all over body, many functions, including gastric mucus
COX2- mostly induced during inflammation except for constitutive expression in kidney and CNS

s/e:
1. GI ulcers (PGE2, PGI2)
2. reduce renal blood flow (PGI2?)
a. sodium retention
b. enhanced renin release (kidney is too smart)
3. hypertension secondary to renal problems
4. hyperkalemia
5. azotemia
6. allergic interstitial nephritis, esp. with fenoprofen and flurbiprofen

*give PPI (omeprazole) with NSAID or COX2I to counter the gastropathy

drug interactions:
1. protein binding -> displacement
WARFARIN
2. p450
BETA BLOCKERS, SSRI
3. inhibition of renal clearance
METHOTREXATE, LITHIUM, AMINOGLYCOSIDES

CNS effects:
1. headache
2. confusion, lethargy (elderly)
3. salicylates -> tinitis
4. aseptic meningitis (SLE + ibuprofen)
aspirin
NSAID
ZILEUTIN
5-lipoxygenase inhibitor

use: severe asthma, severe allergic rhinitis
ZAFIRLUKAST
LT receptor antagonist (LTD4 and LTE4)


use: severe asthma, severe allergic rhinitis
MONTELUKAST
LT receptor antagonist (LTD4 and LTE4)


use: severe asthma, severe allergic rhinitis
piroxicam
long acting (qd) NSAID

more likely to be associated with ulcers
naproxen
intermediate acting (bid) NSAID
ibuprofen
short acting (tid) NSAID
CELECOXIB
COX2 inhibitor (celebrex)
MELOXICAM
COX2 inhibitor - less selective
aspirin
NSAID
ibuprofen
NSAID
indomethacin
NSAID

dont get excited, it's a regular old NSAID
methotrexate
inhibits dihydrofolate reducatase

halts the folate cycle
febuxostat
inhibitor of xanthine oxidase (like allopurinol), give to people allergic to allopurinol
allopurinol
use: gout

moa: competitively (noncomp at hi dose) inhibits xanthine oxidase, stopping formation urate crystals

drug interactions:
azathioprine, 6mercaptopurine - severe bone marrow suppression
warfarin
dont give with methotrexate
colchicine
antiinflammatory - not nsaid

moa: inhibits microtubule formation and neutrophil chemotaxis, neutrophil degranulation

use: acute gout - neutrophils

s/e: bone marrow suppression
GI toxicity
myopathy (monitor CK)
probenecid
use: gout
moa: uricosuric. decreases reabsorption of urate in kidney

must have good renal function for this to work.
salsalate
non acetylated salicylate
doesn't affect COX, works by other moa

analgesic, good for osteoarthritis pain in people with kidney problems, htn, etc