Pharmacology Flashcards
Pramlintide
Amylin analog. MOA = decrease gastric emptying and decrease glucagon. Used for type 1 + type 2 DM.
Dopamine MOA
At low doses stimulates D1 receptors in the renal vasculature and tubules, thereby increasing GFR, RBF, and sodium excretion. Big heart in middle of room + normal sized christian is squeezing it/at high doses stimulates beta-1 adrenergic receptors in the heart, thereby increasing cardiac contractility + pulse pressure + systolic BP. Huge air force one plane by the left that monster Christian is driving/at highest doses stimulates alpha-1 receptors in the systemic vasculature.
Why do you give dopamine for shock?
To stimulate a1 receptors in the systemic vasculature, causing vasoconstriction.
Amiloride vs. amiodarone vs.
Amiloride –> K+ sparing diuretic.
amiodarone –> K channel blocker
amlodipine –> Ca channel blocker
Ergotamine
o Code: Elisabeth with Erik backpack/ergotamine. Smoking a huge blunt + walking out of air force one/MOA = partial agonist/antagonist activity at tryptaminergic + dopaminergic + alpha-adrenergic receptors. Feet and arms are gangrenous/SE’s = peripheral vascular ischemia + potentially gangrene.
o Location: /usually used for migraines.
How can morphine therapy lead to toxicity?
Morphine is metabolized to active metabolites that accumulate and can cause CNS depression.
Drugs contraindicated in CHF
Diltiazem and verapamil.
Hydralazine MOA
Smooth muscle relaxant and vasodilator in arteries and arterioles. Exact mechanism unclear.
Phenoxybenzamine MOA
Non-selective irreversible alpha blocker
labetalol MOA
Mixed alpha/beta adrenergic antagonist
What is Vmax proportional to?
Enzyme concentration
Relationship of Km to Vmax
Km is enzyme saturation at 1/2Vmax
competitive inhibitor vs. noncompetitive inhibitor
FA 236
What does a change in y-intercept on Lineweaver-Burk plot indicate?
Increased y-intercept = decreased Vmax since y-axis is the reciprocal of Vmax
What does x-intercept represent on lineweaver-Burk plot?
The further to the right (i.e. the closer to zero), the greater the Km and the lower the affinity since x-axis is reciprocal of negative Km.
What is slope on Lineweaver-Burk plot?
Km/Vmax
How do you differentiate competitive inhibitors from noncompetitive on Lineweaver-Burk plot?
Reversible competitive inhibitors cross each other competitively, whereas noncompetitive inhibitors do not.
Competitive inhibitors, reversible
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?
1) Yes
2) Yes
3) Yes
4) Unchanged
5) Increased
6) Decreased potency
Competitive inhibitors, IRREVERSIBLE
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?
1) Yes
2) No
3) Yes
4) Decreased
5) Unchanged
6) Decreased efficacy
NONcompetitive inhibitors
1) resemble substrate?
2) overcome by increased saturation?
3) bind active site?
4) effect on Vmax?
5) effect on Km?
6) potency? efficacy?
1) No
2) No
3) No
4) Decreased
5) Unchanged
6) Decreased efficacy
What is bioavailability?
Fraction of administered drug reaching systemic circulation unchanged
bioavailability of IV dose of drug
100%
Why is bioavailability usually less than 100%
Incomplete absorption + first pass metabolism
How do liver and kidney disease affect Vd?
Decreased protein binding leads to increased volume of distribution.
Drugs that stick to blood compartment characteristics…
Large/charged molecules; plasma protein bound
Relative Vd of ECF, tissue, Blood compartments
Blood = low
ECF = medium
All tissues including fat = high
Characteristics of drugs that stay in ECF compartment?
Small hydrophilic molecules
Characteristics of drugs that stay in fat/tissue compartment?
Small lipophilic molecules, especially if bound to tissue protein.
Steady state in a drug with first-order kinetics?
Takes 4-5 lives to reach steady state and 3.3 half lives to reach 90% of steady-state.
What happens to maintenance and loading dose with renal or liver disease?
You need need to decrease maintenance dose. Loading dose is usually unchanged.
What does time to steady state depend on?
Primarily half life. Independent of dose and dosing frequency.
Additive drug interaction?
Effect of substance A and B together is equal to the sum of their individual effects.
Example of additive drug interaction
Aspirin + acetaminophen
Permissive drug interaction?
Presence of substance A is required for the full effects of substance B.
Example of permissive drug interaction?
Cortisol on catecholamine responsiveness
synergistic drug interaction?
Effect of substance A and B together is greater than the sum of their individual effects.
Classic example of synergistic drug interaction?
Clopidogrel with aspirin
tachyphylactic drug interaction?
Acute decrease in response to a drug after initial/repeated administration.
classic examples of tachyphylactic drug interactioN?
MDMA and LSD
Graph of plasma concentration of drug vs. time with zero-order elimination?
linear
Drugs with zero-order elimination?
1) phenytoin
2) ethanol
3) aspirin (at high or toxic concentrations)
term for elimination in zero-order elimination?
“Capacity-limited elimination”
What is rate of elimination proportional to in first-order clearance?
Directly proportional to drug concentration (constant fraction eliminated per unit time)
term for elimination in first-order elimination?
“flow-dependent elimination”
Graph of plasma concentration of drug vs. time with first-order elimination?
exponential
Difference between ionized drugs and non-ionized in terms of renal clearance?
Ionized species are trapped in urine and cleared quickly. Neutral forms can be reabsorbed.
Examples of drugs that are weak acids…
1) phenobarbital
2) methotrexate
3) aspirin
Treating overdose for weak acid drugs…
Trapped in basic environments so treat overdose with bicarbonate.
Examples of drugs that are weak bases…
1) amphetamines
2) TCAs
Treating overdose for weak base drugs…
Trapped in acidic environments so treat with ammonium chloride.
Drug metabolism changes with age.
1) Geriatric patients lose phase I metabolism first.
2) More Phase II
What is Phase I metabolism?
Reduction, oxidation, hydrolysis with CYP-450 usually yielding slightly polar, water-soluble metabolites.
Caveat about drugs after Phase 1 metabolism…
Often still active.
What is Phase II metabolism?
Conjugation (MGAS - Methylation, glucuronidation, acetylation, sulfating), usually yields very polar, inactive metabolites (really excreted).
Problem with people who are slow acetylators?
They have increased side effects from certain drugs because of decreased rate of Phase II metabolism.
What is efficacy proportional to?
Vmax
How is potency represented on maximal effect vs. dose graph?
X-axis (EC50), left shift = decreased EC50 = increased potency = decreased drug needed.
partial agonist vs. agonist
partial agonists have lower efficacy.
effect of competitive antagonist
Shifts curve right (decreased potency, no change in efficacy.
effect of NONcompetitive antagonist
Shifts curve down (decreasing efficacy).
phenoxybenzamine MOA
noncompetitive antagonist on alpha receptors
Therapeutic index?
Difference between TD50 and ED50
TD50?
median toxic dose
ED50?
median effective dose
therapeutic window
Dosage range that can safely and effectively treat disease.
How to calculate therapeutic index?
TD50/ED50
Drugs with lower therapeutic indexes?
1) Digoxin
2) Lithium
3) theophylline
4) warfarin
Implication of drugs with low therapeutic indices?
Frequently require monitoring
LD50?
Basically TD50 in animal studies.
Caveat about adrenal medulla and sweat glands
Part of sympathetic nervous system but innervated by cholinergic fibers
Somatic nervous system structure + neurotransmitter
Voluntary motor nerves synapsing on skeletal muscle and release ACh.
Parasympathetic nervous system structure + neurotransmitter
1) Long preganglionics releasing ACh and synapsing on nicotinic receptors
2) short postganglionics releasing ACh and synapsing on muscarinic receptors at target organ
What receives sympathetic innervation?
1) sweat glands
2) cardiac and smooth muscle (both PS and S)
3) gland cells (both PS and S)
4) renal vasculature
5) vessels
Sympathetic vs. parasympathetic nerve structure
1) In parasympathetic, you have long preganglionics and short postganglionics.
2)
Sympathetic pregalgnionics
All release ACh onto Nicotinic receptors.
Sweat gland innervation
Sympathetic. ACh on muscarinic receptors.
Cardiac and smooth muscle, gland cells, nerve terminals innveration in sympathetic
NE synapsing on adrenergic receDptors
Dopamine 1 receptors expressed in…
1) renal vasculature
2) smooth muscle
Adrenal meddle neuromuscular transmission
preganglionics release ACh onto nicotinic receptors in the adrenal medulla. Catecholamines are released into blood. NE acts on A1,A2,B1, Epi on A1,A2, B1,B2
Structure of nicotinic ACh receptors?
Ligand-gated Na+/K+ channels.
Subdivisions of nicotinic receptors and expression
1) Nn (autonomic ganglia + adrenal medulla)
2) Nm (found in NMJ of skeletal muscle)
Muscarinic ACh receptor structure
G-protein-coupled receptors that usually act through 2nd messengers.
A1 functions
1) vascular smooth muscle contraction
2) Increase pupillary dilator muscle contraction (Mydriasis)
3) increase intestinal and bladder sphincter muscle contraction
A2 receptor functions
1) decrease sympathetic (adrenergic) outflow
2) decrease insulin release
3) lipolysis
4) decrease platelet aggregation
5) decrease aqueous humor production
B1 receptor functions
1) increase HR
2) increase contractility
3) increase renin release
4) increase lipolysis
B2 receptor functions
1) vasodilation
2) bronchodilation
3) increased lipolysis
4) increase insulin release
5) decrease uterine tone (tocolysis)
6) ciliary muscle relaxation
7) increase aqueous humor production
beta 3 class
Gs
Beta 3 functions
1) increased lipolysis
2) thermogenesis in skeletal muscle
M1 functions
1) CNS
2) enteric nervous system
M2 class
Gi
M2 functions
1) decrease heart rate
2) decrease contractility of atria
M3 functions
1) exocrine gland secretions (lacrimal, sweat, salivary, gastric acid)
2) increase gut peristalsis
3) increase bladder contraction
4) bronchoconstriction
5) Increase pupillary sphincter muscle contraction (mitosis)
6) ciliary muscle contraction (accommodation)
D1 receptors
Gs
D1 functions
1) relax renal vascular smooth muscle
D2 receptor
Gi
D2 receptor functions
1) modulates transmitter release, especially in brain
H1 receptor g protein class
Gq
H1 receptor function
1) Increase nasal and bronchial mucus production
2) increase vascular permeability
3) contraction of bronchioles
4) pruritus
5) pain
H2 receptor class
Gs
H2 receptor function
1) increase gastric acid secretion
V1 receptor class
Gq
V1 receptor function
Increase vascular smooth muscle contraction
V2 receptor class
Gs
V2 receptor function
1) ADH
Gq pathway
PIP2 (phospholipase C) –> DAG –> PKC
OR
PIP2 (phospholipase C) –> IP3 –> increased calcium concentration –> smooth muscle contraction
Gs/Gi pathway
adenylyl cyclase –> ATP to cAMP –> PKA –> increased calcium in heart OR myosin light-chain kinase (smooth muscle)
Hemicholinium
enzyme that inhibits choline uptake into neurons
vesamicol
enzyme that inhibits ACh uptake into vesicles
Metyrosin MOA
inhibits conversion of tyrosine to DOPA
Reserpine MOA
inhibits dopamine uptake into vesicles
ephedrine cell bio MOA
stimulates release of NE from vesicles
Bretylium MOA
Inhibit NE release from vesicles.
Guanethidine MOA
Inhibit NE release from vesicles. indirect general agonist + releases stored catecholamines, thus activating alpha and beta receptors
How is NE release from sympathetic nerves modulated?
NE regulates itself, by feeding back and acting on presynaptic alpha2 receptors.
How do amphetamines get into presynaptic terminal?
NET transporter (NE transporter) (NET)
How do amphetamines get into vesicles? What happens after?
VMAT, vesicular monoamine transporter. This displace NE from the vesicles. Once NE reaches a concentration threshold within the presynaptic terminal, the action of NET is reversed, and NE is expelled into the synaptic cleft, contributing to the characteristics and effects of increased NE observed in patients taking amphetamines.
Excess tyramine mechanism
It enters presynaptic vesicles and displaces other neurotransmitters (eg, NE) –> increasing amount of active presynaptic neurotransmitters, which diffuse into the synaptic cleft, leading to increased sympathetic simulation and hypertensive crisis.
Bethanechol impt pharmacology point
resistant to AChE
Bethanechol
direct agonist at bowel and bladder smooth muscle
bethanechol uses
1) postoperative ileus
2) neurogenic ileus
3) urinary retention
carbachol MOA
direct cholinomimetic
carbachol applications
constricts pupil and relives intraocular pressure in open-angle glaucoma (increases aqueous humor outflow)
pilocarpine MOA
direct agonist – contracts ciliary muscle of eye (open-angle glaucoma) + pupillary sphincter (closed-angle glaucoma).
pilocarpine impt pharmacology ypoint
resistant to AChe
pilocarpine uses
1) potent stimulator of sweat, tears, and saliva.
2) open-angle and closed-angle glaucoma
3) xerostomia (Sjogren’s)
rivastigmine MOA
indirect, increases ACh
galantine MOA
indirect, increases ACh
options for AD
1) donepezil
2) galantine
3) rivastigmine
How is MG actually diagnosed now?
Anti-AChR Ab (anti-acetylcholine receptor antibody) test.
edrophonium MOA
indirect, increases ACh
All cholinomimetics can exacerbate…
1) COPD
2) asthma
3) peptic ulcers
neostigmine impt pharmacology poitn
Neo CNS = NO CNS penetration
neostigmine uses
1) postoperative and neurogenic ileus and urinary retention
2) MG
3) reversal of neuromuscular junction blockade (postop)
physostigmine is used for anticholinergic toxicity because…
it crosses BBB into CNS
pyridostigmine and CNS
Long acting but does NOT penetrate CNS.
organophosphate commonly causing cholinesterase inhibitor .
parathion
Why do organophosphates cause poisoning?
They irreversibly inhibit AChE
How is pralidoxime affective?
Regenerates AChE if given early.
Major concern with untreated cholinesterase inhibitor poisoning…
respiratory failure
DUMBBELSS
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, and Salivation.
What does muscarinic antagonism create in the eye?
1) mydriasis
2) cycloplegia
cycloplegia
paralysis of ciliary muscle
benztropine MOA
muscarinic antagonist in the CNS
benztropine uses
1) PD
2) Acute dystonia
glycopyrrolate MOA
Muscarinic antagonist targeting GI + respiratory
glycopyrrolate uses
1) parenteral: preoperative use to reduce airway secretions
2) oral: drooling + peptic ulcers
drug like hyoscyamine
dicyclomine
dicyclomine, hyoscyamine uses
Antispasmodics for IBS
Ipratropium, tiotropium uses
1) COPD
2) asthma
Ipratropium, tiotropium MOA
muscarinic antagonists targeting respiratory system
muscarinic antagonists targeting GU system
1) oxybutynin
2) solifenacin
3) tolterodine
Atropine affects
1) mydriasis, cycloplegia
2) decrease airway secretions
3) decrease acid secretion in stomach
4) decrease gut motility
5) decrease urgency in cystitis
AE’s of atropine
1) Hot as a hare
2) Dry as a bone (dry, flushed skin)
3) Red as a beet
4) Blind as a bat
5) Mad as a hatter (disorientation)
rapid pulse + dry mouth + constipation.
Atropine AE’s/contranidcations
1) urinary retention in men with BPH
2) hyperthermia in infants
3) acute angle-closure glaucoma
albuterol vs. salmeterol clinical applications
1) albuterol for acute asthma or COPD
2) salmeterol for long-term asthma or COPD control.
Dobutamine primarily targets…
B1 more so than B2, alpha
dobutamine uses
1) HF (inotropic more so than chronotropic)
2) cardiac stress testing
Dopamine targets…
D1 = D2, then B, then A
dopamine uses
1) unstable bradycardia
2) HF
3) shock
4) inotropic AND chronotropic effects at lower doses
5) vasoconstriction at high doses due to alpha effects
epinephrine targets primarily
beta more so than alpha
isoproterenol uses
1) electrophysiologic evaluation of tachyarrhythmias
isoproterenol contraindications
CAD (can worsen ischemia)
midodrine MOA
alpha1 agonist
norepinephrine uses
1) hypotension
2) septic shock
norepinephrine targets
alpha1, then alpha 2, then beta1
phenylephrine targets
alpha1 primarily, but also alpha 2
phenylephrine uses
1) hypotension (vasoconstrictor)
2) ocular procedures
3) rhinitis (decongestant)
what are the indirect sympathomimetics?
1) amphetamine
2) cocaine
3) ephedrine
amphetamine MOA
1) Indirect general agonist
2) reuptake inhibitor
3) releases stored catecholamines
cocaine MOA
1) indirect general agonist
2) reuptake inhibitor
ephedrine MOA
1) indirect general agonist, releases stored catecholamines
ephedrine uses
1) nasal decongestion
2) urinary incontinence
3) hypotension
isoproterenol affects on BP, HR
vasodilation (via B2) + increased HR through both B1 + reflex activity
guanfacine MOA
A2 agonists
clonidine, guanfacine uses
1) hypertensive urgency in limited situations
2) ADHD
3) Tourettes
Clonidine, guanfacine AE’s
1) CNS depression
2) bradycardia
3) hypotension
4) respiratory depression
5) miosis
alpha-methyldopa AE’s
1) direct coombs positive hemolysis
2) SLE-like syndrome
beta blockers used for SVTs?
metoprolol + esmolol
beta blocker MOA for use in SVTs?
Decrease AV conduction velocity.
beta blocker MOA for use in HTN?
1) decrease cardiac output
2) *decrease renin secretion (beta1 blockade on JGA cells)
beta blockers used to decrease mortality in HF?
1) bisoprolol
2) carvedilol
3) metoprolol
timolol mechanism in glaucoma?
Decreases secretion of aqueous humor
Other BB usage?
Decrease variceal bleeding
BB’s to use to decrease variceal bleeding?
1) nadolol
2) propranolol
beta blocker MOA for use in variceal bleeding?
Decrease hepatic venous pressure gradient and portal HTN.
beta blocker AE’s
1) erectile dysfunction
2) cardiovascular AE’s (bradycardia, AV block, HF)
3) CNS (seizures, sedation, sleep alterations)
4) asthma/COPD exacerbations
metoprolol other AE
dyslipidemia
What’s the deal with using beta blockers in diabetics?
despite concern with masking hypoglycemia, benefits likely outweigh risk so they are indicated.
nonselective betablockers
1) nadolol
2) pindolol
3) propranolol
4) timolol
nonselective antagonism means what?
B1 = b2 (unlike selective, which primarily target B1) N
Nebivolol MOA
Blocks beta1 but stimulates B3, thus activating NO synthase in vasculature
tetrodotoxin source
pufferfish
tetrodotoxin MOA
Highly potent; binds fast voltage-gated Na+ channels in cardiac/nerve tissue, preventing depolarization.
tetrodotoxin symptoms
nausea + diarrhea + paresthesias + weakness + dizziness + loss of reflexes
tetrodotoxin treatment
primarily supportive
ciguatoxin sources
Reef fish…
1) barracuda
2) snapper
3) moray eel
ciguatoxin mechanism
1) OPENs Na+ channels, causing depolarization
ciguatoxin presentation
symptoms mimic cholinergic poisoning
ciguatoxin poisoning treatment
primarily supportive
scombroid poisoning is basically…
histamine poisoning
scombroid sources
spoiled dark-meat fish..
1) tuna
2) mahi-mahi
3) mackerel
4) bonito
scombroid mechanism
Bacterial histidine decarboxylase converts histidine to histamine
What is scombroid poisoning frequently misdiagnosed as?
Fish allergy
scombroid poisoning presentation…
anaphylaxis picture…
1) acute burning sensation of mouth
2) flushing of face
3) erythema
4) urticaria
5) itching
6) bronchospasm
7) angioedema
8) hypotension
scombroid treatment
Antihistamines. Albuterol + epinephrine if needed.
Treatment for amphetamine overdose…
ammonium chloride (amphetamines are basic so you want to acidify the urine)
Treatment for antimuscarinic/anticholinergic overdose…
physostigmine + *control hyperthermia
Treatment for arsenic overdose…
dimercaprol + succimer
Treatment for beta-blocker overdose…
saline + atropine + glucagon
Treatment for copper overdose…
penicillamine + trientine
Treatment for cyanide overdose…
Nitrite + thiosulfate + hydroxocobalamin
Treatment for digitalis overdose…
anti-dig Fab fragments
Treatment for gold overdose…
penicillamine + dimercaprol (BAL) + succimer
Treatment for heparin overdose…
protamine sulfate
Treatment for iron overdose…
deFERoxamine, deFERasirox, deFERipone
Treatment for lead overdose…
1) EDTA
2) dimercaprol
3) succimer
4) penicillamine
Treatment for amphetamine overdose…
diMERCaprol + succimer
Treatment for methanol, ethylene glycol (antifreeze) overdose…
Fomepizole. Also, ethanol or dialysis if fomepizole isn’t available.
Treatment for opioid overdose…
naloxone
Treatment for salicylate overdose…
sodium bicarb (alkalinize urine) + dialysis
Drugs associated with coronary vasospasm…
1) cocaine
2) sumatriptan
3) ergot alkaloids
Drugs associated with cutaneous flushing…
VANCE Vancomycin Adenosine Niacin Ca2+ channel blockers Echinocandins
What do you give to prevent dilated cardiomyopathy with anthracyclines (doxorubicin, daunorubicin)?
Dexrazoxane
Drugs associated with torsades de pointes
1) 1A + III antiarrhythmics
2) macrolides
3) haloperidol
4) TCA’s
5) ondansetron
Drugs associated with hot flashes
1) tamoxifen
2) clomiphene
Drugs associated with hyperglycemia
1) tacrolimus
2) protease inhibitors
3) niacin
4) HCTZ
5) corticosteroids
Drugs associated with hypothyroidism
1) lithium
2) amiodarone
3) sulfonamides
Erythromycin AE’s
acute cholestatic hepatitis + jaundice
Drugs causing diarrhea
1) acamprosate
2) acarbose
3) cholinesterase inhibitors
4) colchicine
5) erythromycin
6) ezetimibe
7) metformin
8) misoprostol
9) Orlistate
10) pramlintide
11) quinidine
12) SSRIs
Drugs associated with focal to massive hepatic necrosis…
HAVAc Halothane Amanita phalloides Valproic acid Acetaminophen
drugs associated with hepatitis
Rifampin Isoniazid Pyrazinamide Statins Fibrates
Drugs associated with pancreatitis
Didanosine Corticosteroids Alcohol Valproic acid Azathioprine Diuretics (furosemide, HCTZ)
Drugs associated with pill-induced esophagitis
1) tetracyclines
2) bisphosphonates
3) potassium chloride
How do you minimize pill-induced esophagitis?
good posture + adequate water ingestion
Drugs associated with pseudomembranous colitis
Clindamycin
Ampicillin
Cephalosporins
Drugs associated with
agranulocytosis
Clozapine Carbamazepine propylthiouracil Methimazole Colchicine Ganciclovir
Drugs associated with aplastic anemia
Carbamazepine Methimazole NSAIDs Benzene Chloramphenicol PTU
Drugs associated with direct Coombs-positive hemolytic anemia
1) methyldopa
2) penicillin
Drugs associated with hemolysis in G6PD deficiency
Isoniazid Sulfonamides Dapsone Primaquine Aspirin Ibuprofen Nitrofurantoin
Drugs associated with megaloblastic anemia
Phenytoin
Methotrexate
Sulfa drugs
Drugs associated with thrombosis
1) OCPs
2) hormone replacement therapy
Drugs causing gingival hyperplasia
1) phenytoin
2) calcium channel blockers
3) cyclosporine
Drugs associated with hyperuricemia
1) pyrazinamide
2) thiazides
3) furosemide
4) niacin
5) cyclosporine
Drugs associated with myopathy
Vibrates Niacin colchicine hydroxycloroquine INF-alpha penicillamine statins GCs
Drugs associated with osteoporosis
corticosteroids, heparin
Drugs associated with photosensitivity
Sulfonamides
Amiodarone
Tetracyclines
5-FU
Drugs associated with Stevens-Johnson syndrome
1) lamotrigine
2) allopurinol
3) sulfa drugs
4) etanercept
drugs causing cinchonism
quinidine + quinine
Drugs associated with Parkinson-like syndrome
Cogwheel rigidity of ARM
1) antipsychotics
2) reserpine
3) metoclopromide
Drugs associated with seizures
1) isoniazid
2) bupropion
3) Imipenem/cilastatin
4) tramadol
5) enflurane
Drugs associated with tardive dyskinesia
1) antipsychotics
2) metoclopramide
Drugs associated with fanconi syndrome
1) tenofovir
2) ifosfamide
Drugs associated with hemorrhagic cystitis?
1) cyclophosphamide
2) ifosfamide
Drugs associated with interstitial nephritis?
1) methicillin
2) NSAIDs
3) furosemide
Drugs associated with SIADH?
1) carbamazepine
2) cyclophosphamide
3) SSRIs
Drugs associated with pulmonary fibrosis?
1) methotrexate
2) nitrofurantoin
3) carmustine
4) bleomycin
5) busulifan
6) amiodarone
Drugs with antimuscarinic side effects?
1) TCA’s
2) H1-blockers
3) antipsychotics
Drugs associated with disulfiram-like reaction?
1) metronidazole
2) certain cephalosporins
3) griseofulvin
4) procarbazine
5) 1st generation sulfonylureas
Drugs associated with nephrotoxicity/ototoxicity?
1) aminoglycosides
2) vancomycin
3) loop diuretics
4) cisplatin
What can you treat cisplatin toxicity with?
Amifostine
CYP 450 inducers
1) Chronic alcohol
2) *St. John’s wort
3) phenytoin
4) phenobarbital
5) nevi rapine
6) rifampin
7) griseofulvin
8) carbamazepine
CYP-450 substrates
1) Anti-epileptics
2) theophylline
3) warfarin
4) OCPs
CYP-450 inhibitors
1) acute alcohol abuse
2) ritonavir
3) amiodarone
4) cimetidine/ciprofloxacin
5) ketoconazole
6) sulfonamides
7) isoniazid
8) grapefruit juice
9) quinidine
19) macrolides (*except azithromycin)
sulfa allergic reaction presentation…
fever + UTI + SJS + hemolytic anemia + thrombocytopenia + agranulocytosis + urticaria
Sulfa drugs
1) sulfonamide antibiotics
2) sulfasalazine
3) probenecid
4) furosemide
5) acetazolamide
6) celecoxib
7) thiazides
8) sulfonylureas
-azole suffix means…
ergosterol synthesis inhibitor
-cillin means…
peptidoglycan synthesis inhibitor
-ivir suffix means…
neuraminidase inhibitor (oseltamivir)
-ovir suffix means..
DNA polymerase inhibitor (acyclovir)
-ane suffix means
inhalation general anesthetic
thioridazine
typical antipsychotic (ends in -azine)
-caine means…
local anesthetic
-etine means…
SSRI
-curium, -curonium
*nondepolarizing paralytic
atracurium, vecuronium
non depolarizing paralytics
-terol means…
Beta2 agonist
prazosin
alpha *1 antagonist
-afil means…
PDE-5 inhibitor
-dipine means..
dihydropyridine Ca2+ channel blocker
-xaban means…
direct factor Xa inhibitors
examples of factor Xa inhibitors
1) apixaban
2) edoxaban
3) rivaroxaban
-glitazone means…
PPAR-gamma activator
Example of PPAR-gamma activator
Rosiglitazone
-prost means…
prostaglandin analog
-tidine means
H*2 antagonist
-tropin means
pituitary hormone
-ximab means…
Chimeric monoclonal Ab (eg basiliximab)
-zumab means
Humanized monoclonal Ab (daclizumab)
daclizumab vs. basiliximab
Basiliximab is a chimeric monoclonal Ab, daclizumab is a monoclonal Ab.
ergot alkaloids
bromocriptine + cabergoline
nitrosoureas
Carmustine
Lomustine
Semustine
Streptozocin
NNRTIs
Delaviridine
Efavirenz
Nevirapine
Cholinergic effects
o Code: Coleen: Huge red inflatable car man to left + she’s in a gocart with nitrous boosters (nitric oxide code)/receptors present on endothelial surface of peripheral blood vessels. Binding promotes release of NO, thus producing vasodilation. NO activates guanylate cyclase and increases intracellular cGMP. She’s shitting on a towel + drenched in sweet + crying + salivating saliva everywhere + brady in passenger seat + neon eyes/effects = increase tone of smooth muscle of visceral walls + increase motility and secretion in GI tract, manifesting as nausea + vomiting + abdominal cramps + diarrhea + sweating + lacrimation + decreased contractility of heart + decreased conduction velocity + pupillary constriction (via M3 agonism). /decreased conduction velocity may result in heart block. Fizz cartoon and sally cooper resuscitating colleen + waving fan over her on the left/antidote = physostigmine salicylate + control hyperthermia. Erin in car next to brady/NOTE vasodilation can result in baroreceptor-mediated tachycardia.
o Location: Entryway
