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201 Cards in this Set

  • Front
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positive agonist opiods
most mu- produce analgesia
act at specific opiod receptor sites
antagonist
block opiod receptors
agonist PK
well absorbed via SC, IM, PO routes
1st pass effect
variable protein binding
metabolized by the liver, renally excreted
phenylpiperidines
opiod agonist- cyp450 metabolism
agonist CI/caution
allergies, diarrhea caused by toxic poisons/ respiratory depression, recent GI/GU surgery, ulcerative colitis, head injury, alcoholism, liver/renal dysfunction, pregnancy or lactation
opiod agonist adverse effects
sedation, respiratory depression, n/v, postural hypotension, constipation, urinary retention, pruritis, allergic reactions
Opiod tolerance
Chronic toxicity: neuroadaptation by the body during chronic use
opiod physical dependence
Chronic toxicity: seen only when opiates are stopped suddenly or dose is markedly decreased
opiod addiction
chronic toxicity: dysfunctional pattern of use for purposes other than the alleviation of pain
hydromorphone
opiod agonist, more potent, better oral absorption
oxymorephone
opiod agonist, active metabolite of oxycodone, no pharmacological advantages
codeine
opiod agonist, prodrug of morphine, often combined with other compounds
hydrocodone
opiod agonist, used in combination products, pharmacological properties similar to morphine
oxycodone
opiod agonist, good analgesia when combined with peripherally acting nonopiod agent
morphine
opiod agonist, prototype
PK: 1/2 life 2 hrs, converted to active metabolite that's 2x more potent, excreted by kidneys
meperidine
opiod agonist, pharmacological profile similar to morphine
-not as potent, shorter duration
- metabolite accumulates with high doses and in renal failure
-causes CNS excitability --> seizures
fentanyl
opiod agonist, high potency and high lipid solubilty
-transdermal patch, oral transmucosal, parenteral and lozenge
-metabolized by CYP3A4
methadone
opiod agonist, synthetic, similar to morphine
- longer 1/2 life= more sedation
-extended duration of action
- DOA prolonged with repeated doeses
Mixed agonist/ antagonist opiods
stimulate one receptor, block another
- produce analgesia and respiratory depression but has ceiling effect= plateau
-lower abuse potential
-effect dependent on previous opiate exposure- dependent= withdrawal symptoms
mixed agonist/antagonist pharmicokinetics
readily absorbed, metabolized by the liver, excreted in urine or feces
mixed agonist/ antagonist opiods adverse effects
respiratory depression, n/v, constipation, dizziness, anxiety, hallucinations
pentazocine
mixed agonist/ antagonist opiod
-significant CV effects: high doses increase BP, HR
-can cause dizziness. hallucinations, nightmares
-mostly used in anesthesia
buprenorphine
mixed agonist/antagonist opiod
-used in detox
-less sedation, respiratory depression and hypotension
-long DOA, respiratory depression CANNOT be reversed, nausea, dizziness
nalbuphine and butorphanol
mixed agonist/ antagonist opiods
- limited role in chronic pain
- no CV effects
opiod antagonists
-MOA: compete with endogenous and exogenous opiods @ mu receptor sites= prevent or reverse opiod induced side effects
opiod antagonist adverse effects
acute narcotic abstinence syndrome, CNS excitement, increased heart rate, BP changes, pulmonary edema
Naloxone
opiod antagonist
- binds competitively to opiod receptors but no analgesia
- used to reverse toxic effects of agonist/mixed narcotics
-repeated dosing req. to reverse coma and respiratory depression
naltrexone
opiod antagonist
-longer DOA
- hepatotoxic
tramadol
-MOA: weak opiod receptor binding (mu), inhibition of NA and serotonin reuptake
- less respiratory depression and constipation
- PO only
-can cause seizures
- used with chronic pain b/c less dependence and tolerance
acetominophen
non opiod agent
-alternative to aspirin
- minimal anti-inflammatory effects, -no effect on platelets
-MOA: weak prostaglandin inhibitor in CNS
-PK: well absorbed, peak concentration 30-60 min
-AE: overdose assoc w/ fatal hepatic necrosis
NSAIDS method of action
MOA: inhibits COX-1- protective prostaglandins (kidney and GI function) and COX-2- inflammatory prostaglandins
- anti inflammatory, analgesic, antipyretic and anti-platelet effects
NSAIDs pharmacokinetics
different potency and 1/2 life- lower for milder pain, higher for more severe
-absorbed rapidly from GI, metabolized in liver, excreted in urine
NSAIDs cautions/contraindications
allergies, history of peptic ulcer, GI bleeding, bleeding, surgery associated blood loss, asthma, renal impairment, dehydration, hypersensitivity to aspirin, renal/hepatic dysfunction
NSAIDs adverse effects
dyspepsia, d/n/v, gastric bleeding, ulceration, acute renal insufficiency, rashes, bronchospasm, bleeding, fluid retention, peripheral edema
ibuprofen
NSAID
naproxen
NSAID
diclofenae
NSAID
indomethacin
NSAID
ketorolac
NSAID
-parenteral, short term management of moderate- severe pain
-associated with severe bleeding post op
-increases liver enzymes, limit therapy to maximum of 5 days
celecoxib
NSAID
-COX-2 inhibitor
- decreases GI toxicity, doesn't effect platelet aggregation
-CI in pts with sulfa allergy
- increase risk for CV event
aspirin
NSAID
- irreversible inhibition of COX enxyme
-AE: Gi, dizziness, deafness, tinnitus, Reyes Syndrom in kids w/ viral infections, increased risk of bleeding with warfarin
nonspecific analgesic
absorptive therapy for migraines
- not considered 1st line for migraines b/c of adverse effects
- ibuprofen, aspirin, opiods, other NSAIDs, acetominophen
ergot derivative
- used to treat migraines
- precise MOA unknown
ergot derivative adverse effects
hallucinations, alters prolactin release, vasoconstriction, uterine stimulation, n/v/d
ergot derivative pharmacokinetics
metabolized by liver and excreted by kidneys
ergot derivative contraindications
cardiac, peripheral and cerebral vascular disease, liver disease, pregnancy- category x b/c of uterine stimulation
-interaction w/ triptans
dihydroergotamine
ergot derivative
ergotamine
ergot derivative
triptans
1st line in migraine treatment
triptan MOA
selective stimulation of serotonin 1b and 1d receptors, relieve pain by constricting intracranial blood vessels and suppress release of inflammatory neuropeptides
triptan pharmacokinetics/ contraindications/ adverse effects
-metabolized by liver, excreted by urine, variable 1/2 life
- CI: hypertension, peripheral vascular disease, CAS, MI, angina
-AE: n/v, malaise, dizziness, injection site pain, chest pressure
beta lactams
antibacterial
Cell wall synthesis inhibitor
MOA: interfere with the last step og bacterial cell wall synthesis- prevent cross linkage
- time dependent killing
penicillins method of action
antibacterial
beta lactams
interfere with the ability of susceptible bacteria to build their walls when they're dividing (cross linkage)
penicillin PK
inhibit cell wall synthesis: beta lactam
- absorption variable, most incomplete
- distributed well into most body tissues, not well in eye, CSF or prostate
- mostly excreted by kidneys
- metabolism: only semisynthetic
hepatically metabolized and excreted in bile
penicillin adverse effects
inhibit cell wall synthesis: beta lactam
hypersensitivity, diarrhea, interstital nephritis, CNS effects, increased liver enzymes
natural penicilins
antibacterial
inhibit cell wall synthesis: beta lactam
penicillin G- IM/IV and penicillin V-PO
- narrow spectrum of activity: gram+/-, few anaerobes, few spirocettes
-DOC for syphillis
penicillin-resistant penicillins
antibacterial
inhibit cell wall synthesis:beta lactams
narrow spectrum- gram + only, use limited to MSSA
nafcillin
antibacterial
inhibit cell wall synthesis: beta lactam
parenteral penicillin
oxacillin
antibacterial
inhibit cell wall synthesis: beta lactam
parenteral penicillin
cloxacillin
antibacterial
inhibit cell wall synthesis: beta lactam
oral penicillin
dicloxacillin
antibacterial
inhibit cell wall synthesis: beta lactam
oral penicillin
aminopenicillins
beta lactam-penicillin
narrow spectrum: some gram+/-
amoxicillin
antibacterial
inhibit cell wall synthesis: beta lactam
aminopenicillin
ampicillin
antibacterial
inhibit cell wall synthesis: beta lactam
aminopenicillin
antipseudomonal penicillins
antibacterial
inhibit cell wall synthesis: beta lactam
penicillin
broad spectrum- increased activity against gram -
- used to treat pseudomonas infections
ticarcillin
antibacterial
inhibit cell wall synthesis: beta lactam
antipseudomonal penicillin
pipercillin
antibacterial
inhibit cell wall synthesis: beta lactam
antipseudomonal penicillin
beta lactamase inhibitors
antibacterial
inhibit cell wall synthesis: beta lactam
-used with penicillin to expand spectrum of action
-mimic beta lactam, bind to enzymes and inhibit their activity
-broad spectrum: dependent on parent beta lactam- gram +/-, anaerobes
clavulonic acid
antibacterial
inhibit cell wall synthesis: beta lactam
beta lactamase inhibitor
sulbactam
antibacterial
inhibit cell wall synthesis: beta lactam
beta lactamase inhibitor
tazobactam
antibacterial
inhibit cell wall synthesis: beta lactam
beta lactamase inhibitor
cephalosporin
antibacterial
inhibit cell wall synthesis: beta lactam
- all end in cef
-1st generation treats gram + w/ narrow spectrum ---> 4th gen treats gram - with broad spectrum
- well absorbed, widely distributed, some into CSF, metabolized in liver, renal excretion
cephalosporin adverse effects
antibacterial
inhibit cell wall synthesis: beta lactam
hypersensitivity, IM admin painful, diarrhea, interstitial nephritis, CNS effects, billiary sludge
monobactam
antibacterial
inhibit cell wall synthesis
monocyclic beta lactam
-narrow spectrum: gram --, pseudomonas
-used in pts with PCN allergy
-PK: IM/IV only, not absorbed in GI, wide distribution, renal excretion, 1/2 life 2 hrs
-AE: rash
carbapenems
antibacterial
inhibit cell wall synthesis: beta lactam
- differ in 5 member ring structure
-used in serious and life threatening infections and polymicrobial infections
-broad spectrum: gram +/--, anaerobes
-broadest of all beta lactams
-PK: well distributed, renal excretion
-AE: hypersensitivity, diarrhea, seizures
doripenem
antibacterial
inhibit cell wall synthesis: beta lactam
carbapenem
ertapenem
antibacterial
inhibit cell wall synthesis: beta lactam
carbapenem
imipenem-cilastin
antibacterial
inhibit cell wall synthesis: beta lactam
carbapenem
meropenem
antibacterial
inhibit cell wall synthesis: beta lactam
carbapenem
glycopeptides
antibacterial
cell wall synthesis inhibitor
vancomycin
antibacterial
inhibit cell wall synthesis: glycopeptide
-MOA:inhibits 2nd stage of peptidoglycan- cell wall
-broad spectrum: gram + only, incl. MRSA
-poorly absorbed in gut, IV systemic distribution, excreted by kidney
- measure trough levels for therapeutic levels
-AE: red man syndrome: infusion related, red rash of head, face, neck and upper trunk, hypotension, nephrotoxicity, ototoxicity
- time dependent killin
inhibit protein synthesis
antibacterial
inhibit the binding of 50s and 30s (combine to form 70s) ribosome to mRNA
chloraphenicol
antibacterial
protein synthesis inhibitor
-spectrum: gram +/-, anaerobic
-MOA: bind to 50s ribosomal subunit
-PK: well absorbed, widely distributed incl CSF, hepatically metabolized, metabolite excretion in urine
- bacteriostatic
-AE: hypersensitivity, reversible bone marrow supression, fatal anemia, gray baby syndrome
tetracyclines
antibacterial
protein synthesis inhibitor
-MOA: bind to 30s subunit, block incoming tRNA
-narrow spectrum: some gram +/-
- PK: widely distributed incl CSF, excreted in bile and urine
-bacteriostatic
-AE: GI irritation, diarrhea, photosensitivity, kidney and liver toxicity, permanent brown discoloration of teeth
demeclicycline
antibacterial
inhibit cell wall synthesis: tetracycline
doxycycline
antibacterial
inhibit cell wall synthesis: tetracycline
-complete oral absorption
-excreted in feces
minocycline
antibacterial
inhibit cell wall synthesis: tetracycline
-complete oral absorption
-metabolized by the liver
glycylcycline
antibacterial
protein synthesis inhibitor
-broad spectrum: gram +/--, anaerobes, NO pseudomonas
- PK: IV only, large distribution, elimated through feces
-AE: n/v, hepatic toxicity
tigecycline
antibacterial
protein synthesis inhibitor- glycylcycline
macrolides
antibacterial
protein synthesis inhibitor
-MOA: binds to 23s subunit- component 50s
-narrow spectrum: gram+/-
-widely distributed except CSF
-AE: GI intolerance, cholestatic hepatitis, ototoxicity, cardiac arrythmias
azythromycin
antibacterial
protein synthesis inhibitor:macrolide
clarithromycin
antibacterial
protein synthesis inhibitor: macrolide
dirithromycin
antibacterial
protein synthesis inhibitor: macrolide
erythromycin
antibacterial
protein synthesis inhibitor: macrolide
clindamycin
antibacterial
protein synthesis inhibitor
-MOA: binds to 50s
- narrow spectrum: gram+, anaerobes
-PK: almost completely absorbed, distribute everwhere excp CSF
-bacteriostatic
-AE: diarrhea, rash
licosamide
antibacterial
protein synthesis inhibitor- clindamycin
streptogramins
antibacterial
protein synthesis inhibitor
-quinupristin/dalofopristin- combo, ehance activity of each other
-MOA: binds to 50s in 2 places
-narrow spectrum: gram +- used in serious infections (MRSA,VRE)
-PK: IV only, incompatible w/ saline, no CSF, hepatic metabolism, biliary excretion
-bacteriostatic, together may be bacteriocidal
-AE: thrombophlebitis, muscle and joint pain, increased liver enzymes and hyperbilirubinemia
oxazolidinones
antibacterial
protein synthesis inhibitor
-synthetic
-MOA: binds to 50s- inhibits formation of initiation complex
-broad spectrum: gram +only
-PK: complete absorption PO, widely distributed incl CSF, metabolized in liver
-bacteriostatic
- AE: n/v/d, bone marrow suppression
linezolid
antibacterial
protein synthesis inhibitor: oxazolidinones
aminoglycosides
antibacterial
protein synthesis inhibitor
MOA: interfere w/ initiation @ 30s
-broad spectrum: gram-- only, in combo for gram+
- distributed only in lean body mass
-rapidly bacteriocidal, concentration dependent
-post antibiotic effect:bacteria fail to grow despite concentration falling below MIC
-AE: nephrotoxicity (reversible), ototoxicity (irreversible), neuromuscular blockade
-extended interval dosing
amikcan
antibacterial
protein synthesis inhibitor: aminoglycosides
gentamicin
antibacterial
protein synthesis inhibitor: aminoglycosides
kanamycin
antibacterial
protein synthesis inhibitor: aminoglycosides
momycin
antibacterial
protein synthesis inhibitor: aminoglycosides
streptomycin
antibacterial
protein synthesis inhibitor: aminoglycosides
tobramycin
antibacterial
protein synthesis inhibitor: aminoglycosides
fluorquinolones
antibacterial
alter nucleic metabolism
-MOA: inhibits activity of topoisomerase- interferes with replication
- spectrum: gram --, some pseudomonas
-concentration dependent, bactericidal
-PK: well absorbed except w/ multivalent cations, wide distribution, metabolized by liver, excreted by kidneys
- AE: n/v, rashes, photosensitivity, atropathy, tendonitis, increased liver enzymes, cardiac arrhythmias, dizziness, seizures, hallucination
ciprofloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
gemifloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
levofloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
lomefloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
moxifloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
norfloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
ofloxacin
antibacterial
alter nucleic acid metabolism: fluorquinolones
trimethoprim/sulfamethoxazole
antibacterial
inhibit folate metabolism
-MOA: inhibits synthesis of tetrahydrofolic acid= unable to synthesize DNA,RNA and proteins
-spectrum: limited gram +/-
-DOC for immunosuppressed
-PK: analogs of PABA, well absorbed, widely distributed, excreted via kidneys
-AE: hypersensitivity, rashes, stevens johnson syndrome (sloughing of skin), hematologic abnormalities, kidney inflammation, hepatitis, pancreatitis, encephalopathy in infants
metronidazole
antibacterial
-MOA: binds to and breaks DNA- inhibits synthesis
-anaerobic bacteria only- treats C.Diff
-PK: high bioavailability PO and distribution incl CSF, liver metabolism, metabolites excreted by kidneys
-AE: ataxia, dysarthia, dizziness, confusion, excitation, depression, seizures, peripheral neuropathy, metallic taste, alcohol=vomiting
daptomycin
antibacterial
-MOA: Ca dependent binding and insertion of the lipophilic tail into gram + membrane--> ion leakage and collapse--> cell death
-PK: IV only, small distribution, , renal elimination
-concentration dependent bactericidal
-AE: reverse myositis
polymyxins
antibacterial
B and E
-MOA: cause permability changes in gram -
- used in ear/eye, multi resistant gram-
-PK: concentration dependent killing, tightly bound to tissues, poorly distribution into lung, CSF, bone
-AE: renal toxicity, neurotoxicity
amphotericin B
antifungal
-MOA: binds to ergosterol in fungal cell membrane
-PK: poor oral absorption, IV over 2-4 hrs, wide distribution, slow excretion via kidneys
-AE: infusion rlated rxns- fever, chills, vomitting; nephrotoxicity, electrolyte imbalance
flucytosine
antifungal
-MOA: inhibits thymidylate--> inhibits DNA synthesis
-combo
-PK: PO only, excreted by kidneys
-AE: bone marrow suppression, hepatoxicity
echinocandins
antifungals
-MOA: inhibits cell wall synthesis
-PK: IV only, liver metabolism
-AE: thrombophlebitis, abnormal liver enzymes
anidulafungin
antifungal
echinocandin
caspofungin
antifungal
echinocandin
micafungin
antifungal
echinocandin
azoles
antifungal
-MOA:inhibit synthesis of ergosterol- cell membrane component
-PK: variable absorption PO, hepatic metabolism CYP 450 3A4
-AE: local irritation, hepatotoxicity, visual disturbances
-inhibitor of CYP 450
fluconazole
antifungal
azole
itraconazole
antifungal
azole
ketoconazole
antifungal
azole
posaconazole
antifungal
azole
voriconazole
antifungal
azole
griseofluvin
antifungal
-active against dermatophytes
-MOA: disrupts microtubule function and inhibits mitosis
-PK: PO only, increase absorption with high fat meal, metabolized by liver
-AE: GI, hepatitis, phototoxicity, possibly carcinogenic
terbinafine
antifungal
-treats superficial dermatophyte infections
-MOA: inhibits ergosterol synthesis
-PK: 40% bioavailability, due to 1st pass effect, highly protein bound, extensive liver metabolism, long 1/2 life
-AE: GI disturbances, rash, dizziness, joint and muscle pains, hepatotoxicity
nystatin
antifungal
-polyene
-limited to direct contact surfaces- topical and PO swish
nucleoside analogs
antiviral-herpes
-MOA:prodrug, prevents synthesis of viral DNA
-PO, topical, IV
-PK: eliminated in kidneys
-AE: GI, headache, rash, neutropenia, thrombocytopenia,
acyclovir
antiviral-herpes
nucleoside analogue
-poor bioavailability
cidofovir
antiviral-herpes
nucleside analogue
-IV only
-long 1/2 life, dose 1-2 weeks
- AE: bone marrow suppression, very toxic
famiciclovir
antiviral-herpes
nucleside analogue
-best bioavailability
ganciclovir
antiviral-herpes
nucleside analogue
-IV, PO, poor bioavailability
-AE: bone marrow suppression- very toxic
valcyclovir
antiviral-herpes
nucleside analogue
-prodrug, metabolized to be acyclovir
valganciclovir
antiviral- herpes
nucleside analogue
-PO
-AE: bone marrow suppression- very toxic
foscarnet
antiviral-herpes
-pyrophosphate derivative
-MOA: prevents attachment of nucleotide precursors to DNA
-Main use CMV, IV only, renal excretion
-AE: toxic- nephrotoxicity, anemia, seizures, arrythmias, electrolyte imbalances
neuraminidase inhibitors
antiviral-influenza
-MOA: prevents release of new virons
-decreases symptoms and vaccine
-AE: GI discomfort, nausea, respiratory tract irritation
oseltamivir
antiviral-influenza
neuraminidase inhibitor
- PO active prodrug, rapidly hydrolyzed in liver, eliminated unchanged in urine
zanamivir
antiviral-influenza
neuraminidase inhibitor
-eliminated unchanged in urine, absorbed through respiratory tract
carbonic anhydrase inhibitors
diuretic
-MOA: inhibits carbonic anhydrase- req for Na resorption in PT- increases excretion of Na, H2O, HCO3
-used more for glaucoma and altitude sickness
-AE: metabolic acidosis, hypokalemia
acetzolamide
diuretic
carbonic anhydrase inhibitor
methazolamide
diuretic
carbonic anhydrase inhibitor
loop diuretics
-most potent
-PO, IV
-MOA: inhibits Na/K symporter in ascending LOH
-increases excretion of Na and H2O by 25% and other electrolytes
-high bioavailibilty, short 1/2 life
-CI: allergy, electrolyte depletion, renal failure
-AE: hypotension, hyponatremia, hypochloremia, hypokalemia, hypomagnesia, hypocalcemia, ototoxicity
furosemide
loop diuretic
burnetamide
loop diuretic
torsemide
loop diuretic
ethacrynic acid
loop diuretic
thiazide diuretics
-MOA: inhibits Na/Cl symporter in the distal tubule, up to 10% Na, H2O and other electrolyte excretion
-PK: absorbed in GI, metabolized in liver, excreted in urine
-CI: sulfa allergy, fluid and electrolyte imbalances, severe renal disease
-effectiveness decreases when creatinine clearance falls below 30ml/min
-AE: low BP, hyponatremia, hypokalemia, hypomagnesia, hypocalemia, increased uric acid and plasma levels
hydrochlorothiazide,
thiazide diuretic
chlorothiazide
thiazide diuretic
metolazone
thiazide diuretic
chlorothalidone
thiazide diuretic
indapamide
thiazide diuretic
potassium sparing diuretics
-limited usefulness as a diuretic
-MOA: at collecting duct, up to 2% Na and H2O excretion
-PK: well absorbed, metabolized in liver, excreted in urine
-AE: lethargy, confusion, hypotension, hyperkalemia
amiloride
potassium sparing diuretic
spironolatone
potassium sparing diuretic
triamterene
potassium sparing diuretic
histamine (H2) receptor antagonists
treat GERD and ulcers
-available as OTC- moderate effectiveness
-MOA: reversibly inhibit gastric acid secretion by competitively antagonizing H2 receptors on parietal cells- only blocks one receptor out of 3
-PK: well/rapidly absorbed from GI, 1/2 life 1-4 hrs, DOA 12 hrs,
-AE: GI discomfort, diarrhea, constipation, sedation and delirium in elderly, gynecomastia and impotence in men
-intrxns: drugs requiring gastric acid for absorption
cimetidine
treat GERD and ulcers
histamine (H2) receptor antagonists
-hepatically metabolized
-CYP 450 inhibitor
famotidine
treat GERD and ulcers
histamine (H2) receptor antagonists
-hepatically metabolized
nizatidine
treat GERD and ulcers
histamine (H2) receptor antagonists
-eliminated renally, good for ppl with liver disease
ranitidine
treat GERD and ulcers
histamine (H2) receptor antagonists
-hepatically metabolized
proton pump inhibitors (PPI)
treat GERD and ulcers
-MOA:admin as inactive prodrug, activated by acid-inhibits active proton pump by irreversibly binding to H/K ATPase enzyme across the parietal cell
-PK: take w/food- oral bioavailibility decreases w/food, DOA 24 hrs, CYP 2C19 metabolism
-AE: diarrhea, headache, abdominal pain, dizziness
-intrxns: drugs via CYP 450 and requiring gastric acid for absorption
dexiansoprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
esomeprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
lansoprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
-approved to treat under 18
omeprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
-available OTC
pantoprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
raberprazole
treat GERD and ulcers
proton pump inhibitor (PPI)
antacids
treat GERD and ulcers
-least effective- only treat symptoms
-MOA: weak bases that react with acid to neutralize pH
-PK: multiple doses daily- short DOA
-intrxns: affect absorption of other drugs by binding to the drug b/c multivalent cation or by increasing pH-may cause enteric-coated to release early
aluminum salts
treat GERD and ulcers
antacid
-AE: constipation
-used in combo products w/ magnesium
calcium salts
treat GERD and ulcers
antacid
-AE:diarrhea, if absorbed: n/v, sedation
- used in combo products w/ aluminum
sodium bicarbonate
treat GERD and ulcers
antacid
-AE: bloating, belching, exacerbates: fluid retention, hypertension, kidney disease, heart failure
calcium salts
treat GERD and ulcers
antacid
-AE: bloating, belching, hypercalcemia, constipation, rebound acid secretion
sucralfate
treat GERD and ulcers
GI protectant
-MOA: in H2o or acid, forms viscous paste- binds to damaged, ulcerated tissue forming a protective barrier
-PK: tablet or oral suspension, not absorbed, excreted in feces
-AE: constipation, dry mouth, nausea, rash, renal dysfunction= CNS effects, diarrhea
-intrxns: alter absorption of other PO drugs
misoprostol
treat GERD and ulcers
prostaglandin
-semi-synthetic- used only in prevention of gastric ulcer in pts w/ long term NSAID use
-MOA: inhibits gastric acid secretion and promotes the scretion of mucus and bicarbonate
-PK: rapid absorption, metabolized in liver, excreted in urine, 1/2 life-30 min
-CI: pregnancy- stimulates uterine contractions- category X
-AE: diarrhea, abdominal pain
phenothiazine
treats nausea and vomitting
-antipsychotic drugs that are can be used for antiemetic and sedative properties
-MOA: inhibits muscarinic and dopamine receptors (CTZ)- cause sedation by blocking histamine
-PK: IV/PO- onset 30 min, PR-60 min
-AE: sedation, hypotension, tardive dyskinesia, restlessness, muscular spasms, dryness, urinary retenion, constipation, pupil dilation, double vision, agitaion, tachycardia
promethazine
treats nausea vomiting
phenothiazine
prochiorperazine
treats nausea vomiting
phenothiazine
metoclopramide
treats nausea vomiting
nonphenothiazine
-MOA: inhibits dopamine and serotonin receptors in CTZ
-PK: PO/IV, rapidly absorbed, metabolized in liver, excreted in urine
-CI: GI tract obstruction
-AE: sedation, confusion, seizures, diarrhea
serotonin (5HT3) antagonists
treats nausea vomiting
-used for chemo induced and postoperative n/v
-MOA: competitively blocks 5-HT3 receptors in the CTZ and GI tract
-PK: 1/2 life of 4-9 hrs
-AE: infrequent- headache, sedation, dizziness, constipation
doiasetron
treats nausea vomiting
serotonin (5HT3) antagonist
granisetron
treats nausea vomiting
serotonin (5HT3) antagonist
ordansetron
treats nausea vomiting
serotonin (5HT3) antagonist
palonosetron
treats nausea vomiting
serotonin (5HT3) antagonist
-1/2 life of 40hrs- weekly dose
chemical stimulants
laxatives
-MOA: directly act on intestinal mucosa to alter fluid secretion--> stimulate perstalsis- increases amt of fluid in stool
-PK: 6-10 hr onset PO, PR 15min-2hr
-CI: appendicitis, fecal impaction, intestinal obstruction
-AE: n/v, cramping, flatulence, urine discoloration, dependence
bisacodyl
laxative
chemical stimulant
senna
laxative
chemical stimulant
bulk stimulants
laxative
-used to prevent constipation-safe for daily use
-MOA: absorbs liquid in GI tract--> causes stool to swell --> facilitates peristalsis and motility
-PK: begins in 12-24 hrs, full effect at 3 days
-CI: intestinal perforation/obstruction, inability to drink adequate amt of fluid
-AE: flatulence, bloating, cramps, n/v
psyllium
laxative
bulk stimulant
methylcellulose
laxative
bulk stimulant
polycarpophil
laxative
bulk stimulant
docusate
laxative-lubricant
-MOA: decreased surface tension of liquid in stool, causes additional liquid to be incorporated into feces
-prevents constipation in cardiac pts and opiod users
-1-3 day onset
-AE: stomach upset, diarrhea
loperamide
antidiarrheal
-MOA: direct action on muscle of GI to slow activity
-PK: PO only- poorly absorbed
-AE: constipation, abdominal discomfort, n/v, dry mouth
diphenoxylate/atropine
antidiarrheal
-MOA: activates opiod receptors in the GI tract- decreases intestinal motility- more time for fluid and electrolytes to be reabsorbed
-chem related to opioids, but doesn't exhibit analgesic except at high doses- mixed w/ atropine to discourage abuse
-PK: PO only
-AE: at high doses CNS effects- light headedness, hallucinations
bismuth subsalicylate
antidiarrheal
-MOA: decreased motility of GI tract through direct action on the lining to inhibit local reflexes
-coats ulcers and erosions- protective layer
-PK: subsalicyclate >90% absorbed, bismuth < 1%- converted to salicyclic acid and bismuth salts in GI, bismuth excreted in feces, subsalicylate in urine
-caution/CI: aspirin, warfarin, allergy
-AE: constipation, blackening of stool, darkening of tongue, toxicity in high doses