Professional Documents
Culture Documents
Ipratropium (mechanism,
use, toxicity)use,
Beclomethasone,
fluticasone (mechanism,
toxicity)(mechanism, use,
Montelukast, zafirlukast
toxicity)
Zileuton (mechanism, use, toxicity)
Omalizumab (mechanism, use, toxicity)
Guaifenesin (mechanism, use, toxicity)
N-acetylcysteine (mechanism, use, toxicity)
Bosentan (mechanism, use, toxicity)
Dextromethorphanphenylephrine
(mechanism, use,
toxicity)
Pseudoephedrine,
(mechanism,
use, toxicity)
Difference in competitive
vs noncompetitve
inhibitors?
What is Km?
What is Vmax?
What is bioavailability?
Time
to steady
state depends
What
is rate
of elimination
in zeroon?
order
kinetics?
Give
three
drugs
are zero order
eliminated.
What
is the
ratethat
of elimination
for first
order
kinetics?
doestreat
ionization
relate
to urine
pH?
HowHow
do you
overdose
of weak
acid?
Give
drug
examples.
How do you treat overdose of weak base? Give
examples.
What is phasedrug
I drug
metabolism? What pt.
population
loses this?
What is phase II metaboloism?
What population
depend on this?
What is efficacy?
What
potency?
What happends
toisefficacy
when a partial
agonist and full agonist are mixed?
What is therapetuic index?
What
is a types
therapeutic
window?
What are the two
of Nicotonic
receptors?
What
kind
of
messenger
do
they
use?
Alpha-1 sympathetic receptor (G-protein
class,
major
function)
Alpha-2 sympathetic receptor(G-protein class,
majorreceptor(G-protein
function)
Beta-1 sympathetic
class,
major
function)
Beta-2 sympathetic receptor(G-protein class,
major function)
M-1 Parasymp receptor(G-protein
class, major
function)
M-2 Parasymp(G-protein class, major function)
M-3
parasymp(G-protein
class, for
major
function)
What
receptor is responsible
miosis
and
accomadation?
What receptor
is responsbile for mydriasis?
Dopamine
D-1 receptor(G-protein
class, major
function)
Dopamine D-2 receptor(G-protein
class, major
function)
Histamine H-1 receptor(G-protein
class, major
function)
Eculizumab(mechanism, use)
Cladribine(mechanism, use)
Trans-retinoic
Is an increase acid(use)
in serum creatinine normal after
starting ACE inhibitors?
Daptomycin(mechanism,
toxicity)
Ondansetron acts on 5HT3use,
receptors
in what
location,
in
order
to
decrease
nausea?
Why must mu agonists be avoided in suspected
pancreatic or biliary pain?
What drugs inhibit dihydrofolate reductase?
Varenicline(mechanism,
use)
What
class of drug can precipitate
mania in
those with bipolar disorder?
What
is thewhat
treatment
sleep
In
general,
is the for
best
drugenuresis?
to use for
edemadrug
of any
kind?
Which
used
for hyperthyroidism decreases
peripheral
T3->T3
conversion?
Can atropine be used
to block gastric
secretions? why or why not?
Fomepizole(mechanism, use)
Disulfiram(mechanism,
use)
hyperammonia caused by
a metabolic
derangement?
What is first dose effect, typically seen in A1
blockers?
Which
nitrate
bespecific
given PO?
Colchine
stopscan
what
cell to decrease
gout
symptoms?
What is the first line drug used to treat
hypertension
in pregnancy?
Why is MRSA resistant
to Naficillin but normal S.
Aureus is not?
Palizumab(mechanism, use)
Rhogam(mechanism, use)
Entacapone,
Tolcapone
(mechanism,
What
opioid effect
is most
resistant touse, tox)
tolerance?
Aldesleukin (mechanism, use)
Epoetin Alfa(mechanism, use)
Filgrastim, Sargramostim (mechanism, use)
alpha-inerferon(use)
B-Interferon(use)
gamma-interferon(use)
Oprelvekin(mechanism, use)
thromopoietin(use)
Muromonab-CD3 (mechanism, use)
Digoxin Immune Fab(mechanism, use)
Rasburicase (mechanism, use)
denosumab(mechanism,
What
keeps heparin fromuse)
crossing the placental
barrier?
cyclosporine(mechanism,
use, toxicity)
Isotretinoin,
tretinoin,
Acitretin(mechanism,use,toxicity
Calcipotrol(mechanism, use)
Orlistat(mechanism,
use)
giving what drug 30 minutes
before Niacin can
help
reduce
flushing?
Paclitaxil or sirolimus are commonly used in
cardiac
why?
What is stents.
the drug
used for Pre-eclampsi and
ecplamsia?
Bortezomib(mechanism,use,
toxicity)
What causes nitroprusside toxicity?
What is the
antidote?
Memantine(mechanism, use, toxicity)
What
is used
in alzheimer's
In
gasvitamin
anesthesias,
what
is the lipid treatment?
solubility
and the blood
solubility?tacalcitol (mechanism,
Calcitrol,
calcipotriene,
use)
Usetekinumab(mechanism,
Why
is it required to wait 14use)
days after stoping
a MAO-i before starting an SSRI?
Lepirudin, Bivalirudin (mechanism, use)
Ropinirole, Pramipexole (mechanism, use)
what
the usescan
of amantidine
for of
parkinsons?
What are
compound
cause sickling
sickle cell
trait
RBC's?
How do atypical antipsychotics avoid causing
parkinson's
symptoms and will
tardive
dyskinesia?
Which anti-inflammatories
not impair
platlet
aggregation? why?
Natalizumab(mechanism,
use,
toxicity) induced
What drugs are preferred in
medication
parkinson's
treatment?
What defines
induction why?
and potency in gas
anesthetics?
Cause NO release -> vasodilation (veins >>> arteries); used in angina; fast
tolerance, hypotension, flushing, headache
and
muscle breakdown
Inhibits lipolysis andHepatoxicity
reduces VLDL
secretion,
lowering LDL and raising HDL;
hyperlipidemia;
flushing
and
hyperuricemia
Inhibits reabsorption of bile acids -> lower LDL with slight increase in HDL;
unpigmented gallbladder stones and malabsorption
reabsorption
->HDL
lower
LDL
Upregulates LPLPrevents
-> lowercholesterol
triglycerides,
slightly inc.
and
slightly dec. LDL;
myositis
and
hepatoxicity
inc. contractility; stimulates the vagus; causes cholinergic symptoms and
hyperkalemia
cause torsades de pointes, cinchonism
(qunidine), procainamide (drug-induced
lupus) dec. AP duration especially in
Lidocaine, mexiletine, and tocainide;
depolarized/ischemia
tissue;
following tachycardias;
MI
Flecainide, propafenone;
no effect on AP,
used best
in ventricular
do not
use
post-MI due
risk for
arrhythmias
Blocks Na channels,
decreasing
theto
slope
of phase
0 depolarization; toxicity
bySA
hyperkalemia
Beta-blockers; reduces exacerbated
cAMP, slowing
and AV node activity, increases PR
interval; adverse
effects
include
impotence,
asthma
exacerbation,
sedationand
Amiodarone,
ibutilide,
dofetilide,
sotalol;
K channel
blockers;
inc. AP duration
QT interval
Pulmonary
fibrosis,
hepatotoxicity,
thyroid
dysfunction
Ca channel blockers;
verapamil
and
diltiazem; dec.
conduction
velocity and inc. PR
interval;
cause
constipation,
flushing,
and
edema
Inc. K efflux, hyperpolarizing the cell; used in supraventricular tachycardias; can
cause flushing, hypotension, and chest pain
Used in torsades de pointes and digoxin toxicity
Bromocriptine or cabergoline (dopamine agonists)
Spironolactone (or other AT2 antagonist)
Octreotide (somatostatin analogues)
Lispro, aspart, and glulisine
Regular
NPH
Glargine
detemir
decreases gluconeogenesis; can
causeand
lactic
acidosis (don't use in renal failure
First-generation sulfonylureas; closepatients)
beta-cell K channels, causing depolarization
and increased
insulin release;
causesKdisulfuram-like
effects
Second-generation
sulfonylureas;
close beta-cell
channels, causing
depolarization
and increased
insulin
release; causes
hypoglycemia
Thiazolidinediones;
activates
PPAR-gamma,
increasing
insulin sensitivity and
adiponectin
levels;
causes
weight
gain,
hepatotoxicity,
and heart failure
Alpha-glucosidase inhibitors; prevent sugar hydrolysis and absorption,
reducing
blood sugar levels
Amylin analog; reduces glucagon secretion; causes hypoglycemia
GLP-1
analogues;
increase
insulin,
decrease
glucagon
secretion;
causes
pancreatitis
DPP-4
inhibitors;
increase
insulin,
decrease
glucagon
secretion;
causes
mild
urinary/respiratory
infections
Blocks thyroid peroxidase and 5'-deiodinase; used to treat hyperthyroidism; causes
agranulocytosis, aplastic anemia, hepatotoxicity
Blocks thyroid peroxidase; used to treat hyperthyrodism; teratogenic
Thyroid hormone analogs; causes thyrotoxicosis
Used
to SIADH;
control can
uterine
hemhorrage
ADH antagonist used to
treat
cause
photosensitivty and bone/teeth
abnormalities
suppression; can cause Cushing's syndrome, adrenal insufficiency (if withdrawn
quickly)cimeditine is a P-450 inhibitor and has
H2 antagonists; used to treat hyperchloridia;
antiandrogenic
effects,
both
creatinine secretion
Irreversibly inhibit
the H/K pump;
used
to reduce
treat hyperchloridia;
increased risk of C.
difficile infection and hypomagnesemia
Coats ulcer base and protects underlying tissue
PGE1 analog that decreases acid production and increases bicarb production; used
to prevent NSAID ulcers; abortifacient
Somatostatin analog; used to treat VIPoma and carcinoid syndrome
Hypokalemia
Anti-TNF; used
treat IBD and
RA; can cause
activation
of latentacid
microbes
Combination
of to
sulfapyridine
(antibacterial)
and
5-aminosalicylic
(antiinflammatory); used to treat IBD; causes oligospermia
antagonist;
used activity
as an antiemetic
D2 antagonist; used 5-HT3
to increase
gut muscle
and as an antiemetic; causes
parkinson signs
Cromolyn sodium
Dimercaprol
andsome
EDTA,patients
succimer
in kidsantibodies to platelet
coagulation and in pregnant
women;
develop
4 half-life,
(HIT)
Same actions as heparin, but has afactor
longer
does not have to be monitored
as closely, andofhas
a reduced
of C,
HIT
Inactivated gamma-carboxylation
factors
II, VII, risk
IX, X,
and S; used for longterm and non-immediate anticoagulation; can cause tissue necrosis, teratogenic
Converts
plasminogen
to plasmin;
usedand
as aanti-inflammatory;
thrombolytic
Irreversibly inhibits
COX-1
and COX-2;
anti-platelet
gastric
ulcers,
tinnitus,
Reye's
syndrome
in
childhood
viral
infections
Irreversibly blocks ADP receptors on platelets, preventing degranulation; used for
acure coronary
syndrome;
ticlodipine
causes
neutropenia
Phosphodiesterase
inhibitor,
increases
cAMP and
decreases
ADP, preventing
platelet degranulation; nausea, headache, facial flushing, hypotension
GPIIb/IIIa
preventing
platelet
aggregation;
bleeding,
thrombocytopenia
Inhibits inhibitors,
dihydrofolate
reductase,
inhibiting
DNA synthesis;
myelosuppression,
fatty
change
in liver synthase, inhibiting
Pyrimidine analog thatmacrovesicular
is activated and
inhibits
thymidylate
DNAthat
synthesis;
photosensitivity
Pyrimidine analog
inhibitsmyelosuppression,
DNA polymerase; leukopenia,
thrombocytopenia,
megaloblastic
anemia
Purine analogs that are activated by HGPRT and inhibit purine synthesis; toxicity is
increased with allopurinol, causes bone marrow, GI, and liver toxicity
DNA intercalator; usedan
for
childhood
tumors;
myelosuppression
cardiomyopathy(Dexrazoxone,
iron
chelator,
prevents
this), myelosuppression,
alopecia
Generates free radicals that cause DNA
strand breaks; pulmonary fibrosis with
Crosslinks DNA (must be minimal
activatedmyelosuppression
by liver); myelosuppression, hemhorragic
cystitis (can be minimized with mesna)
Used to treat CNS tumors
Alkylates
DNA; pulmonary
fibrosis,causes
hyperpigmentation
Block microtubule
polymerization;
vincristine
neurotoxicity, vinblastine
causes bone marro suppression
Blocks
microtubule(minimize
breakdown;
Crosslinks DNA;
nephrotoxicity
withmyelosuppression
chloride diuresis, amifostine),
acoustic n. damage
Inhibits topoisomerase
II; and
myelosuppression,
GI upset,
alopecia
Inhibits ribonucleotide
reductase
increases HbF; used
in cancers
and HbSS
disease; bone marrow suppression
Unknown but
may trigger
apoptosis
in dividing
cells; Cushingoid
symptoms
osteoporosis;
tamoxifen
increases
the risk
of endometrial
cancer due
to agonist
effects. Raloxifene = no increase in endometrial cancer.
Antibody against HER-2 receptor; cardiotoxicity
Antibody
tyrosinelymphoma
kinase
Antibody against CD20;
used against
to treat bcr-abl
non-Hodgkin's
and rheumatoid
arthritis
B-raf kinase inhibitor (V600 mutation); used in metastatic melanoma
Antibody
against
Reversible COX inhibitor; gastric
ulcers,
renalVEGF
ischemia (due to constriction of
afferent arteriole)
Reversible COX-2 inhibitor; anti-inflammatory
without damage to gastric mucosa;
sulfa allergy, thrombosis
Muscarinic
antagonist,
and
Inhibit
cytokine
synthesis,prevents
reducingbronchoconstriction;
inflammation due toasthma
asthma;
1stCOPD
line for
chronic asthma
Leukotriene
receptor
antagonists; especially
in aspirin-induced
asthma
Inhibits activity
of 5-lipoxygenase,
inhibiting useful
leukotriene
production; reduces
inflammation
Anti-IgE antibody; used in refractory allergic asthma
Thins
secretions
Loosens mucus plugs; used
in CFrespiratory
patients and
as an antidote to acetominaphen
posioning
Antagonizes endothelin-1 receptors, reducing vascular resistance in the pulmonary
vessels; used
in pulmonary
hypertension
Antagonizes NMDA receptors,
inhibiting
coughing;
produces opioid effects in large
and
carries
mild
abuse
potentialrhinitis; hypertension,
Alpha-1 agonists thatdoses
reduce
edema
and
nasal
congestion;
quick tolerance (recurrence of symptoms despite continued treatment)
competitive = decrease potency, noncompetitive = decrease efficacy.
Inverse relation of affinity of enzyme for its substrate.
Direct proportion to enzyme concentration
Fraction of administered drug that reaches systemic circulation unchanged.
depends on half-life. Does not depend on frequency or size of dose.
constant amount eliminated per time.
PEA - phenytoin, Ethanol, Aspirin.
A constant FRACTION is eliminted, variable by concentration!
Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed.
Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin.
Treat with ammonium
chloride.
exp:Often
amphetamines.
Reduction, Oxidation,
hydrolysis with
CYP450.
gives neutral products.
Geriatrics
lose
this
phase.
Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products.
Geriatrics depend on this, old people have GAS.
maximal effect a drug can produce.
amount of drug needed for the same effect.
DECREASEDMedian
efficacy.
fightdose
for same
binding
site, full
agonistdose.
cantSafer
exert drugs
full effect.
LD50/ED50.
lethal
divded
by median
effective
have
a higher TI.
Minimum
effective
dose
to
minimum
toxic Two
dose.
Think oftypes:
it as range
of use.
1. Nicotinic - Ligang gated Na/K channels.
nicotinic
Nm(NMJ)
and
Nn(autonomic
ganglia.
2.
Muscarinic
G-proteins.
5
types,
M1-M5.
q, increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction,
intestinal outflow,
and bladder
sphincter
i, decrease: sympathetic
insulin
release,contaction.
lipolysis. increase: platlet
aggregation.
s, increase:
heart rate,
contractilty,
renincontractility,
release, lipolysis
s, vasodilation,
brochodilation,
increase:
heart rate,
lipolysis, insulin
release, aqueous humor production. decrease: uterine tone, ciliary muscle tone.
q, CNS, enteric nervouse system.
i, decease: heart
rate, contractility
of atria
contraction, bronchoconstriction,
pupillary
spinchter contraction,
cilliary muscle
contraction.
Parasympathetic M-3.
Sympathetic Alpha-1.
s, relaxes renal vascular smooth muscle
i, modulates transmitter release especially in brain.
q, increase: mucus production, contraction of bronchioles, pruritus, pain.
Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and
causes tachycardia.
release.Used in hypertension, especially
renal disease due to no increase in renal
blood
flow!
IRREVERSIBLE nonslective alpha blocker.
Used in pheochromosytoma BEFORE
surgery!
toxic:
orhtostatic
hypotension,
reflec tachycardia.
REVERSBILE nonselective alpha blocker. give to patients
on MAOI who each
tyramine
contraining
foods.
Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox:orthostatic
dizziness,
headache.
Alpha-2 blocker. Used in hypotension,
depression. tox:
sedation,
hypercholesterolemia, increased
apetite.
Before blockade: Both epi and phen RAISES BP. After alpha blockade: only epi
raises, CHF
no change
phenyl. Why:
Epi has B- decrease
binding, phenyl
does
secretion.
- slowsinprogression.
Glaucoma
secretion
of NOT.
aqueous
humor.
impotence, asthma exacerbation,
bradycardia, seizures, sedation, hides
hypoglycemia.
A BEAM. acebutolol, betaxolol, Esmolol,
Atenolol, Metoprolol. Useful in comorbid
pum. disease.
Please Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B = B-blocker.
Carvedilol, labetalol.
Pindolol, Acebutolol.
N-Acetylcysteine (replenishes glutathione).
NaHCO3 (alkalinize urine)
NH4Cl (acidify urine)
Phygostigmine and control the hyperhermia.
Glucagon
(KLAM) normalize K, Lidocaine, Anti-dig fab fragments, Mg2
deFEroxamine, deFErasirox.
CaEDTA, dimercaprol, succimer, penicillamine
Dimercaprol, succiner
penillamine
nitrite + thiosulfate, hydroxocobalamin
Methylene blue, vitamin c
100% oxygen or hyperbaric oxygen
Fomepizole>Ethanol, dialysis
naloxone/naltrexone
flumazenil
NaHCO3 (alkalinize plasma)
protamine
Vitamin K, fresh frozen plasma
aminocaproic acid
B-Blockers
atropine + pralidoxime
cocaine, sumatriptan, ergots
(VANC) Vancomycin, Adenosine, Niacin, Ca blocker
doxorubicin, daunorubicin
class III (sotalol) and class Ia (quinidine)
Clozapine, Carbamazepine, Colchine, Propylthiouracil, Methimazole, Dapsone
chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole
methyldopa, penicillin
(hemolysis IS PAIN)isoniazid, chloramphenicol
sulfonamides, primaquine, aspirin, ibuprofen,
nitrofurantoin
(females with PMS are on full BLAST mode) Phenytoin, Methotrexate, Sulfa drugs
OCPs like estrogen
ACE inhibitors
Bleomycin, amiodarone, Busulfan
erthryomycin
Halothane, Amanita Phalloides, Valrpoic acid, Acetaminophen
isoniazid
clindamycin, ampicillin
glucocorticoid
HPA suppression
`(Some drugs create
awkward withdrawl
knockers) via
spironolactone,
digitalis, cimetidine,
chronic alcohol use, ketoconazole
estrogen, clomophene
niacin, tacrolimus, protease inhibitor, HCTZ, corticosteriods
lithium, amiodarone, suldonamides
glucocoricoids, protease inhibitors
phenytoin, verpamil
furosemide,
thiazides, niacin,interferon-alpha,
cyclosporine
fibrates, niacin, colchine,
hydroxychloroquine,
penicillamine,
statins, glucocorticoids
corticosteroids, heparin
for a PHOTO)
Sulfonamides,
amiodarone,
tetracycline
penicillin, (SAT
ethosuximide,
carbamazepine,
sulfa
drugs, lamotrigine,
allopurinol,
phenytoin, phenobarbital
Hydralazine, isonizid, procainamine, phenytoin
tetracyclines
fluoroquinolones
lithium, demeclocycline
expired tetracycline
Cyclophosamide, ifosfamide
methicllin, NSAID, furosemide
carbamazepine, cyclophosamide
Quinidine, qunine
antipsychotics,
(with seizures, I BITE
My tongue)resperine,
isoniazid, metoclopramide
Buproprion, imipenem, Tramadol,
Enflurane, Metoclopramide
antipsychotics
Atropine, TCA, H1-blocker, neuoleptics
metronidazole, some cephalosporins, procarbazine, 1st gen sulphonoureas
aminoglycosides,
vancomycin,
loop dieuetics,
cisplatin
Barbiturates,
St. John wart, phenytoin,
rifampin,
griseofulvin,
carbamazepine,
chronic
use. ketoconazole, sulfonamides,
cimetidine, ritonavir actue alcohol
use,alcohol
ciprofloxacin,
gemfibrozil,
quinidine.
(Popular FACTSSS) probenacid,
furosemide,
acetazolamide, celecoxib, thiazide,
sulfonamide antibiotics, sulfaasalazine, sulfonylureas
G = effective
IV and IM.on
V G+,
= oral.
peptidoglycans;most
also N. Meningitidis,
Treponema;hypersensitivy
reaction,
anema.blocking Bbind transpeptidases, penicillanse resistant duehemolytic
to bukly r-group
Lactamse;
S. Aureus, except MRSA; hypersensitivity and interstitial nephritis.
E.coli,Listera,Proteus,Salmonella,Shigella,enterococci;hypersensitivity
reaction,rash,pseudomemrane colitis.
amOxicllin has better Oral bioavilability.
B-lactamse
inhibitor
transpeptidase inhibitor but extended
spectrum;pseduomonas
and g- rods, use with
claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction.
(CAST) Clavulanic
Acid, Sulbactam,Tazobactem.
bactericidal;use depends
on generation,
there are four;hypersensitivty reactions,
vitamin
K defiency, increased
nephrotoxicity
of aminoglycosides.
1st generation
cephalosporins.
PEcK. Proteus,
E.coli,Klebsiella.
Cefazolin used preop
to prevent
infections.
2nd generation cephalosporins.
HENA.aureus
PEcKs. H.ib,
Enterbacter, Neisseria, Proteus,
E.coli,Klebsiella,
Serratia.
3rd gen. cephalosporins. Serious
gram - infections.
Ceftriaxone = meningitis and
gonorrhea. Ceftazidime = pseudomonas.
increased
activity
against pseudomonas
G+ bugs.
a monobactem resistant
to B-lactamases,
preventsand
binding
to PBP3 and is
synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset.
aztreonam.do not;G+ cocci,G- rods, anerobes.
renal dehydropeptidase. later carbepenems
used only in life
events;skin
rash, CNS
toxicity,onces;NOT
seizures. bacterialcidal;
G+ threating
only, especially
for multidrug
resistant
nephrotoxicity, ototoxicity, thrombophlebitis, red man syndrome.
slow infusion and rate and antihistamines.
amino
acid
change of D-alaTetracyclines.
D-ala to D-ala50S
D-lac.
AT 30, CCEL at 50.
30S =
Aminoglycosides,
= Chloramphenicol,
Clindamycin,
Erythromycin,
Linezolid.
uptake;ineffective in anaerobes,use in gram - rod infections and before bowel
ototoxicity,
teratogen.
transferase surgery;
enzymesnephrotoxicty,
that inactivateNMJ
theblock,
drug by
acetylation,
phosphorylation, or
adenylation.
Chlamysia; can't take with milk, antacids, iron because ions bind it, GI distress,
discoloration of teeth, inhibition of bone growth, contraindication in pregnancy.
uptake into cells
or increased
effluxchlamydia,
by pumps.gram + cocci;
bacteriostatic,decrease
blocks translocation;
atypical
pneumonias,
MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia.
23s rRNAanemia,
binding site.
countries due to being methylation
cheap; dose of
dependent
dose independent aplastic
anemia, gray baby syndrome.
use of chloramphenicol in premature infants, they lack UDO-glucuronyl-transferase.
plasmid-encoded
acetyltransferase.
Bacteriostatic. Blocks peptide
transfer; anaerobic
infections in lung infections and
oral
anerobes;
C.
Diff
infection,
fever,
Nocardia, Chlamydia, UTI; hypersensitivty, hemolysisdiarrhea.
in G6PD, nephrotoxic,
kernicterus, displaces other drugs from albumin.
altered
bacterial dihydropteroate
or increased
PABA synthesis.
used in UTI,
PCP (prophylacis
and treatment),
shigella, salmonella;
megaloblastic
anemia,
leukopenia,
granulocytopenia.
Neisseria, some G+;( lones hurt the bones) tenonitis and tendon rupture,
superinfections, don't give to kids or pregnant women due to cartilage damage.
mutation in DNA gyrase or efflux pumps.
older than
60 or taking
prednisone
damage; (GET GAP) Giardia,
Entamoeba,
trichomonas,
Gardnerella, Anaerobes,
Pylori;
causes
disulfiram
like
reaction,
headache,
metallic
taste.
activate INH; TB drug, only one used as prophylaxis and in
latent TB;
peripheral
neuropathy,
hepatoxic, lupis
like
drug interaction,
pyridoxine
antagonist.
inhibits DNA-dependent
RNA
polymerase;
TB, Leprosy,
prophylaxis
in
meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids.
TB; hyperuricemia,
decreasedunknown;
carbohydrate
polymerizationhepatotoxic.
of TB cell wall, blocks
arabinosyltransferase; TB; optic neuropathy(red-green color blindness_
Themyoglobinuria,
naloxone is only
active if inected,
making
it hard
to abuse theoverdose.
combo.
rigidity,
autonomic
instability.
seen with
antipsychotics
treatment:
bromocriptine
(d2 agonist)
sterotypicaldantrolene
oral-facial and
movements,
from long
term antipsychotic use. often NOT
reversible.
hyperthermia, confusion, myoclonus, cardio collapse, flushing. tx: cyproheptadine
(5ht antagonist)
Translitional cell carcinoma of the bladder
renal damage
absence of digits, toes
CV VIII toxicity
neural tube defects, craniofacial defects
vaginal clear cell adenocarcinoma, congenital mullerian anomalies
neural tube defects
ebstein's anomaly -> atrialized right ventricle
fetal hydantoin syndrome->microcephaly,dysmorphic face
discolored teeth
limb defects like flipper arms
inhibitor of maternal folate absorption ->neural tube defects
bone deformities, fetal hemorrhage, abortion
3rd -8th week.
extremely high risk for spontaneous abortion
placental abruption, developmental abnormalities
preterm labor, placental problems, ADHD
alcohol
(OH DANG) Ototox, hypokalemia, dehydration, allergy(sulfa), Nephritis, Gout
(hyperGLUC)
hyperglycemia,
leads
to K leaving
all cells andhyperlipidemia,
thus H enteringhyperuricemia,
all cells. 3. in ahypercalcemia.
low K state, H is
exchanged instead of K for Na in the CCT leading to paradoxical aciduria.
OCP and dopemaine antagonists (antipsychotics)
PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase.
NO, they require some islet function to release insulin. type 1 - those cells are dead.
Insulins, amylin analongs(pramlintide).
allopurinol stops urate crystal collection -> no gout.
acute:
allopurinol,
probenacid,
colchicine
used inNSAID,
chronicindomethicin.
gout; inhibitsChronic:
reabsorption
of uric febuxostat,
acid in the proximal
tubule;
inhibits secretion of penicillin; do NOT use in renal dysfunction.
used
gout, inhibits
xanthine oxidase.
bindsin
tochronic
G- cell membrane
phospoholipids,
disrupting them; only works in g-;
peripheral
neuropathy,
dizziness,
nsytagmus,
nephrotoxicity.
increase catecholamines at synaptic cleft, especially
NE + dopamine; ADHD,
nacrolepsy, appetite control
this
is vitamin
in warfarin
overdose
folinic
acid, it isK,aused
metabolite
of folic
acid; given with methotrexate to replish the
body's
folate
stores.
antidote to heparin overdose. Protamine is a postive ion that binds to negative
heparin,
inactivating
it.MAO inhibitors eats hard cheeses and drinks wine, causing a
When
someone
taking
crisis.
it has
a MUCH
longer
plusrid
it is
while phentolamine
is reversible
out
some
ascites)
andhalf
alsolife,
it gets
ofirrversible
excess ammonia,
which is causing
the
encephalopathy.
Pharmacology
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pharmacology
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pharmacology
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
micro
reactions
micro
micro
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overdose
reactions
renal
psych
psych
pharmacology
pharmacology
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pharmacology
pharmacology
pharmacology
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pharmacology
psych
psych
psych
psych
renal
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reactions
reactions
reactions
reactions
reactions
reactions
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reactions
reactions
reactions
reactions
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pharmacology
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heme/onc
heme/onc
renal
micro
GI
neuro
general
neuro
psych
renal
renal
endocrine
GI
neuro
neuro
general
cardio
cardio
GI
repro
micro
micro
repro
neuro
Neuro
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
heme/onc
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heme/onc
general
heme/onc
heme/onc
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pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
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pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
pharmacology
heme/onc
GI
GI
cardio
repro
heme/onc
reactions
neuro
neuro
neuro
msK
msK
neuro
heme/onc
neuro
neuro
reactions
neuro
heme/onc
msk
psych
neuro