Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
77 Cards in this Set
- Front
- Back
|
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 |
