Flashcards for USMLE Step 1 Pharmacology

Michaelis-Menten Kinetics
Michaelis-Menten Kinetics
[S] = Concentration of substrate
V = Velocity
Km is inversely related to the affinity of the enzyme for its substrate
Vmax = Directly proportion to the enzyme concentrationMost enzymatic reactions follow of hyperbolic curve [Michaelis-Menten] kinetics
Enzymatic reactions that exhibit a sigmoid curve [Hemoglobin] exhibit positive cooperativity

Lineweaver-Burk
Lineweaver-Burk
↑ y-intercept, ↓ Vmax
The further to the right, the x-intercept [Closer to zero], the greater the Km, and the lower the affinity
Enzyme Inhibition
Enzyme Inhibition
Reversible competitive inhibitors cross each other competitively, whereas nonreversible inhibitors do not [parallel]
Reversible Competitive Inhibitiors
Resemble Substrate: Yes
Overcomed by ↑ [S]: Yes
Binds Active Site: Yes
Effect on Vmax: Unchanged
Effect on Km: ↑
Pharmacodynamics: ↓ Potency
Irreversible Competitive Inhibitors
Resemble Substrate: Yes
Overcomed by ↑ [S]: No
Binds Active Site: Yes
Effect on Vmax: ↓
Effect on Km: Unchanged
Pharmacodynamics: ↓ Efficacy
Noncompetitive Inhibitors
Resemble Substrate: No
Overcomed by ↑ [S]: No
Binds Active Site: No
Effect on Vmax: ↓
Effect on Km: Unchanged
Pharmacodynamics: ↓ Efficacy
Bioavailability [F]
Fraction of administered drug reaching systemic circulation unchanged
For an IV dose, F = 100%
Oral, F < 100%, due to incomplete absorption and first pass metabolism
Volume of distribution [Vd]

Theoretical volume occupied by total amount of drug in the body relative to the plasma concentration

Apparent Vd of plasma protein-bound drugs can be altered by LIVER and KIDNEY DISEASE [↓ protein binding, ↑ Vd]

Vd = [Amount of drug in body]/[Plasma drug concentration]

Low Vd
Compartment: Blood
Drug/Types: Large/charged molecules, plasma protein bound
Medium Vd
Compartment: ECF
Drugs/Types: Small hydrophilic molecules
High Vd
Compartment: All tissues including FAT
Drugs: Small, lipophilic molecules, especially if bound to tissue protein
Clearance [CL]
The volume of plasma cleared of drug per unit time
CLEARANCE MAY BE IMPAIRED w/ DEFECTS IN CARDIAC, HEPATIC, or RENAL FUNCTIONCL = [Rate of elimination of drug]/[Plasma concentration of drug] = Vd x Kc [Elimination constant]
Half-life [T1/2]

The time required to change the amount of drug in the body by 1/2 during elimination [or constant infusion]

PROPERTY OF FIRST ORDER ELIMINATION

A drug infused at a constant rate takes 4-5 half lives to reach steady state.
It takes 3.3 half lives to reach 90% of the steady-state level

T1/2 = [0.693 x Vd]/CL

# of Half-lives/Percent Remaining
1. 1 [50%] 2. 2 [25%] 3. 3 [12.5%] 4. 4 [6.25%]

Dosage Calculations

Loading Dose = [Cp x Vd]/F

Maintenance Dose = [Cp x CL x T]/F
Cp = Target plasma concentration at steady state
T = Dosage interval [Time between doses], if not administered continuously

IN RENAL AND LIVER FAILURE, MAINTENANCE DOSE ↓ and LOADING DOSE IS UNCHANGED

Time to steady state depends primarily on T 1/2 and is independent of dose and dosing frequency

Zero-order elimination
Zero-order elimination
The rate of elimination is CONSTANT regardless of Cp [Constant amount of drug is eliminated per unit time] Cp ↓ linearly w/ time
Example:
1. Phenytoin
2. Ethanol
3. Aspirin [At high or toxic concentrations]CAPACITY LIMITED ELIMINATION
PEA = A pea is round, shaped like a zero

First order elimination
First order elimination

Rate of elimination is DIRECTLY PROPORTIONAL to the drug concentration [Constant fraction of drug eliminated per unit time]

Cp ↓ exponentially w/ time

FLOW-DEPENDENT ELIMINATION

Urine pH and drug elimination
Ionized species are trapped in urine and cleared quickly
NEUTRAL FORMS CAN BE REABSORBED
Urine pH and Drug Elimination: Weak Acids
Examples: Phenobarbital, methotrexate, aspirin, TCAs
TRAPPED IN BASIC ENVIRONMENT
Treat OVERDOSE w/ BicarbonateRCOOH [Lipid Soluble] → RCOO- + H+ [Trapped]
Urine pH and Drug Elimination: Weak Bases
Example: Amphetamine
TRAPPED IN ACIDIC ENVIRONMENTRNH3 [Trapped] → RNH2 + H+ [Lipid Soluble]
Drug Metabolism: Phase I
Reduction, oxidation, hydrolysis w/ Cytochrome P450
Usually yields, slightly polar, water soluble molecules [Often still active]GERIATRIC PATIENTS LOSE PHASE I FIRST

Drug Metabolism: Phase II
Conjugation [Glucuronidation], Acetylation, Sulfation
Usually yields VERY POLAR, inactive metabolites [Renally excretedGERIATRIC PATIENTS HAVE GAS [Phase II] Patients who are slow acetylators have ↑ side effects from certain drugs due to ↓ rate of metabolism

Efficacy
Efficacy
Maximal effect a drug can produce
Represented by y-value [Vmax] ↑ y-value = ↑ Vmax
PARTIAL AGONISTS HAVE LESS EFFICACY THAN FULL AGONISTS
Potency
Potency
Amount of drug needed for a given effect
↑ Potency [EC50] = ↓ Amount of drug needed
Represented by x-value
Left-shifting = ↓ EC50 = ↓ Potency
UNRELATED TO EFFICACY [Potent drugs can have high or low efficacy
Competitive Antagonist
Competitive Antagonist
Shifts curve RIGHT [↓ Potency], no change in efficacy
Can be overcome by the ↑ the concentration of agonist substrateExample: Diazepam [Agonist] + Flumazenil [Competitive antagonist] on GABA receptor

Noncompetitive Antagonist
Noncompetitive Antagonist
Shifts curve DOWN [↓ Efficacy] Cannot be overcome by ↑ the concentration of agonist substrateExample: Norepinephrine [agonist] + Phenoxybenzamine [Noncompetitive antagonist] on a-receptors

Partial Agonist [Alone]
Acts at the same site as a full agonist, but w/ lower maximal effect [↓ Efficacy] POTENCY IS AN INDEPENDENT VARIABLEMorphine [Full agonist] vs. Buprenorphine [Partial agonist] at opioid u-receptors

Therapeutic Index
Therapeutic Index
Measurement of drug safety
TD50/ED50 = Median Toxic Dose/ Median Effective DoseTherapeutic Window = Measure of Clinical Drug Effectiveness for a patient

TITE = Therapeutic Index = TD50/ED50
Safer drugs have higher TI values
Drugs w/ lower TI values include:
1. Digoxin
2. Lithium
3. Theophylline
4. Warfarin

LD50 [Lethal median dose] often replaces TD50 in animal studies

Parasympathetic Innervation [ACh, M]
1. Cardiac
2. Smooth muscle
3. Gland cells
4. Nerve terminalsFROM MEDULLA
ACh Nicotinic = Neuromuscular junction
ACh Muscarinic = End organ

Sympathetic Innervation [ACh, M]

1. Sweat glands

FROM SPINAL CORD
ACh , N = Ganglion
ACh, M = End organ [Sweat glands]

Sympathetic Innervation [NE, aB]
1. Cardiac
2. SMooth muscles
3. Gland cells
4. Nerve terminalFROM SPINAL CORD
ACh, N = Ganglion
NE, aB = End organ

Sympathetic [D, D1]
1. Renal vasculature
2. Smooth muscleFROM SPINAL CORD
ACh, N = Ganglion
D, D1 = Target organ

Adrenal Medulla
FROM SPINAL CORD
Ach, N = Adrenal Medulla → Norepi, EpiADRENAL MEDULLA AND SWEAT GLANDS ARE PART OF SNS BUT ARE INNERVATED BY CHOLINERGIC FIBERS

Somatic [ACh, N]

Voluntary motor nerve → Skeletal Muscle

FROM SPINAL CORD
ACh, N = Skeletal Muscle

Botulinum toxin
Prevents release of Ach at cholinergic terminals
ACh receptors
Nicotinic ACh receptors are LIGAND GATED Na+/K+ channels
1. NN = Found on autonomic ganglia
2 NM = Found in neuromusclar junctionMuscarinic ACh receptors are G-protein-coupled receptor that usually act through 2nd messengers, 5 subtypes:
1. M1
2. M2
3. M3
4. M4
5. M5

Sympathetic a1 receptor
G-protein class: Q
Major functions:
1. ↑ Vascular smooth muscle contraction
2. ↑ Pupillary dilator muscle contraction [Mydriasis] 3. ↑ Intestinal and bladder sphincter muscle contraction
Sympathetic a2 receptor
G-protein class: I
Major Function
1. ↓ Sympathetic outflow
2. ↓ Insulin release
3. ↓ Lipolysis
4. ↓ Aqueous humor
5. ↑ Platelet aggregation
Sympathetic B1 receptor
G-protein class: S
Major Function:
1. ↑ HR
2. ↑ Contractility
3. ↑ Renin release
4. ↑ Lipolysis
Sympathetic B2 receptor
G-protein class: S
Major Function:
1. Vasodilation
2. Bronchodilation
3. ↑ Lipolysis
4. ↑ Insulin release
5. Aqueous humor production
6. ↓ Uterine tone [Tocolysis] 7. Ciliary muscle relaxation
Parasympathetic M1 receptor
G-protein class: Q
Major Function
1. CNS
2. Enteric nervous system
Parasympathetic M2 receptor
G protein class: I
Major Function:
1. ↓ Heart rate
2. ↓ Contractility of atria
Parasympathetic M3 receptor
G-protein class: Q
Major Function
1. ↑ Exocrine gland secretion [Lacrimal, salivary, gastric acid] 2. ↑ Gut peristalsis
3. ↑ Bladder contraction, bronchoconstriction
4. ↑ Pupillary sphincter muscle contraction [Miosis] 5. Ciliary muscle contraction [Miosis]
Dopamine D1 receptor
G-protein class: S
1. Relaxes vascular smooth muscle
Dopamine D2 receptor
G-protein class: I
1. Modulates transmitter release, especially in the brain
Histamine H1 receptor
G-protein class: Q
1. ↑ Nasal and bronchial mucus production
2. ↑ Vascular permeability
3. Contraction of bronchioles
4. Pruritis
5. Pain
Histamine H2 receptor
G-protein class: S
1. ↑ Gastric acid secretion
Vasopressin V1 receptor
G-protein class: Q
Major function:
1. ↑ Vascular smooth muscle contraction
Vasopressin V2 receptor
G-protein class: S
Major Function:
1. ↑ H2O permeability and reabsorption in collecting tubules of kidneys [Found in the 2 Kidneys]
Mnemonic for G-protein linked receptors
QISS [Kiss] and QIQ [Kick], till your SIQ [Sick] of SQS [Super Qinky Sex]
Gq receptors

A1,M1, M3, H1, V1 HAVe 1 M&M

Ligand binds receptor → Gq activation → Phospholipase C activation →
Causes PIP2 to split into:
1. DAG → Protein lipase C
2. PIP3 → ↑ Ca2+ → Smooth muscle contraction

Gs and Gi receptors

Ligands bind receptors → Activates Gs/Gi → Adenylyl cyclase → ↑ cAMP [From ATP]

↑ cAMP [From ATP] → Protein Kinase A →
1. ↑ Ca2+ [Heart] 2. Myosin light chain kinase [Smooth muscle] — MAD 2’s

Norepinephrine release
Release of Norepinephrine from a sympathetic nerve ending is modulated by norepinephrine itself acting on presynaptic a2-autoreceptors
Bethanechol

CHOLINOMIMETIC AGENTS: DIRECT AGONIST

Clinical Applications:
1. Postoperative ileus
2. Neurogenic ileus
3. Urinary retention

Action:
1. Activates Bowel and Bladder smooth muscle
2. Resistant to AChE

Carbachol

CHOLINOMIMETIC AGENT: DIRECT AGONIST

Clinical Applications:
1. Constricts pupil and relieves intraocular pressure in glaucoma

Action: CARbon copy of acetylcholine

Methacholine
CHOLINOMIMETIC AGENT: DIRECT AGONIST
Clinical Application: Challenge test for diagnosis of asthma
Action: Stimulates muscarinic receptors in the airway when inhaled
Pilocarpine
CHOLINOMIMETIC AGENT: DIRECT AGONIST
Clinical Application:
1. Potent stimulator of sweat, tears, and saliva
2. Open angle and closed-angle glaucoma
Action:
1. Contracts ciliary muscle of eye [Open-angle glaucoma] 2. Pupillary sphincter [Closed-angle glaucoma] 3. Resistant to AChE”YOU CRY DROOL AND SWEAT ON YOUR PILlow’

Donepezil, Galantamine, Rivastigmine
INDIRECT AGONISTS [ANTICHOLINESTERASES] Clinical Application: Alzheimer’s Disease
Action: ↑ ACh
Edrophonium
INDIRECT AGONISTS [ANTICHOLINESTERASES] Clinical Application:
1. Historically diagnosis of myasthenia gravis [Short acting] *** Now diagnosed by anti-AChR Ab [Anti-acetylcholine receptor antibody test] Action: ↑ ACh
Neostigmine
INDIRECT AGONISTS [ANTICHOLINESTERASES] Clinical Application:
1. Post-operative and neurogenic ileus
2. Urinary retention
3. Myasthenia gravis
4. Reversal of neuromuscular junction blockade [Postoperative] Action: ↑ AChNeo CNS = No CNS penetrtion

Physostigmine
INDIRECT AGONISTS [ANTICHOLINESTERASES] Clinical Application:
1. Anticholinergic toxicity
2. Crosses BBB → CNS
Action: ↑ AChUSED FOR ATROPINE OVERDOSE

Pyridostigmine
INDIRECT AGONISTS [ANTICHOLINESTERASES] Clinical Applications:
1. Myasthenia gravis [Long-acting] 2. Does not penetrate CNSAction:
1. ↑ ACh
2. ↑ Muscle strength
3. GETS RID OF MYASTHENIA GRAVIS

With all cholinomimetic agents, what do you have to watch out for?
Exacerbation of:
1. COPD
2. Asthma
3. Peptic ulcers
Cholinesterase Inhibitor Poisoning
DUMBBELSS
Often due to organophosphates [PARATHION] = Irreversible inhibit AChE
*** Often components of insecticides
*** Poisoning usually seen in farmersClinical manifestation
1. Diarrhea
2. Urination
3. Misosi
4. Bronchospasm
5. Bradycardia
6. Excitation
7. Lacrimation
8. Sweating
9. Salivation

Antidote = Atropine [Competitive inhibitor] + Pralidoxime [Regenerates AChE if given early]

Atropine, Homatropine, Tropicamide
Muscarinic antagonists
Organ systems: Eye
Applications: Produce mydriasis and cycloplegia
Benzotropine
Muscarinic antagonist
Organ System: CNS
Applications:
1. PARKinson disease [PARK my BENZ] 2. Acute dystonia
Glycopyrrolate
Muscarinic antagonist
Organ System: GI, respiratory
Applications:
1. Parenteral = Postoperative use to reduce airway secretions
2. Oral: Drooling, peptic ulcer
Hyoscyamine, Dicyclomine
Muscarinic antagonist
Organ System: GI
Application: Antispasmodics for IBS
Ipratropium, Titropium
Muscarinic antagonist
Organ System: Respiratory
Applications:
1. COPD, asthma
Oxybutynin, Solifenacin, Tolterodine
Muscarinic antagonist
Organ System: Genitourinary
Applications:
1. Reduce bladder spasms and urge urinary incontinence [Overactive bladder]
Scopolamine
Muscarinic antagonist
Organ System: CNS
Applications:
1. Motion sickness
Atropine
Muscarinic antagonist
Used to treat BRADYCARDIA and OPHTHALMIC APPLICATIONS
Action:
1. ↑ Pupil dilation, cycloplegia [Eye] 2. ↓ Secretions [Airway] 3. ↓ Acid secretions [Stomach] 4. ↓ Motility [GI] 5. ↓ Urgency in cystitis [Bladder]Blocks skeletal muscle and CNS excitation by nicotinic receptors

Atropine toxicity
Clinical manifestations:
1. ↑ Body temperature [Due to ↓ sweating] 2. Rapid pulse
3. Dry mouth
4. DRY, FLUSHED SKIN
5. CYTOPLEGIA
6. Constipation
7. DISORIENTATIONCan cause acute angle-closure glaucoma in elderly [due to mydriasis] Urinary retention in men w/ prostatic hyperplasia
Hyperthermia in infants

Side Effects:
1. Hot as a hare
2. Dry as a bone
3. Red as a beet
4. Blind as a bat
5. Mad as a hatter

Jimson Weed [Datura]
Gardener’s pupil [Mydriasis due to plant alkaloids]
Tetrodotoxin
Highly potent toxin that binds voltage-gated Na+ in cardiac and nerve tissue
PREVENTS DEPOLARIZATION [Blocks action potential w/out changing resting potential] Clinical Manifestations:
1. Nausea
2. Diarrhea
3. Paresthesia
4. Weakness
5. Dizziness
6. Loss of reflexes
Treatment: SupportiveCaused by ingestion of poorly prepared pufferfish [Fugu], a delicacy in Japan

Ciguatoxin
Causes ciguatera fish poisoning
Opens Na+ channels CAUSING DEPOLARIZATION
Symptoms can be easily confused w/ cholinergic poisoningTemperature-related dysesthesia = COLD FEELS HOT, HOT FEELS COLD = Specific finding
Treatment is Supportive

Consumption of reef fish [Barracuda, snapper, moray eel]

Scombroid Poisoning
Caused by consumption of DARK-MEAT FISH [Bonito, Mackrel, Mahi-Mahi, Tuna] improperly stored at warm temperature
Bacterial histidine decarboxylase converts histidine → histamine
*** Histamine is not degraded by cooking
*** Frequently misdiagnosed as allergy to fish
Clinical Manifestations:
1. Acute onset of BURNING SENSATION of the mouth
2. Flushing of the face
3. Erythema
4. Urticaria
5. Pruritis
6. Headache
7. May cause anaphylaxis-like presentation [Bronchospasm, Angioedema, Hypotension]Treat supportively w/ antihistamines [If needed, antianaphylactics = Bronchodilators, epinephrine]
Albuterol, Salmeterol
Direct Sympathomimetics
B2 > B1
Treatment:
1. Albuterol = Acute asthma
2. Salmeterol = Long-term asthma or COPD control
Dobutamine
Direct Sympathomimetics
B1 > B2 > a
Treatment:
1. Heart failure [HF] = Inotropic > Chronotropic
2. Cardiac stress testing
Dopamine
Direct Sympathomimetics
D1 = D2 > B > a
Treatment:
1. Unstable bradycardia
2. HF
3. Shock
4. INOTROPIC AND CHRONOTROPIC a EFFECTS PREDOMINATE AT HIGH LEVELS
Epinephrine
Direct Sympathomimetics
B > a
Treatment:
1. Anaphylaxis
2. Asthma
3. Open-angle glaucoma
4. a EFFECTS DOMINATE AT HIGH DOSES
SIGNIFICANTLY STRONGER AT B2 THAN NOREPINEPHRINE
Isoproterenol
Direct Sympathomimetics
B1 = B2
Treatment:
1. Electrophysiologic evaluation of tachyarrhythmias
2. Can worsen ischemia
Norepinephrine
Direct Sympathomimetics
a1 > a2 > B1
Treatment:
1. Hypotension [But ↓ renal perfusion] 2. Significantly weaker effect at B2 than epinephrine
Phenylephrine
a1 > a2
Treatment:
1. Hypotension [Vasoconstrictor] 2. Ocular procedures [Mydriatic] 3. Rhinitis [Decongestant
Amphetamine
Indirect sympathomimetics
Indirect general agonist
Reuptake inhibitor
Releases store catecholaminesApplications:
1. Narcolepsy
2. Obesity
3. ADHD

Cocaine
Indirect sympathomimetics
Indirect general agonist
Reuptake inhibitorApplications:
1. Vasoconstriction and local anesthesia
2. NEVER GIVE B-Blockers IF COCAINE INTOXICATION IS SUSPECTED – can lead to unopposed a1 activation and extreme HTN

Ephedrine
Indirect sympathomimetics
Indirect general agonist
Releases stored catecholaminesApplications:
1. Nasal decongestion
2. Urinary incontinence
3. Hypotension

Norepinephrine vs. Isoproterenol
Norepinephrine vs. Isoproterenol

Norepinephrine ↑ systolic and diastolic pressures as a result of a1-mediated vasoconstriction → ↑ mean arterial pressure → Reflex bradycardia

Isoproterenol [No longer used] has little a effect but causes B2-mediated vasodilation → ↓ mean arterial pressure and ↑ HR through B1 and reflex activity

Clonidine
Sympatholytics [A2-agonists] Applications:
1. Antihypertensive urgency [Limited situations] 2. DOES NOT DECREASE RENAL BLOOD FLOW
3. ADHD, Tourette syndromeToxicity:
1. CNS depression
2. Bradycardia
3. Hypotension
4. Respiratory depression
5. Miosis

a-methyldopa
Sympatholytics [A2-agonists] Applications: HYPERTENSION IN PREGNANCYToxicity:
1. Direct Coombs + hemolysis
2. SLE-like syndrome

Phenoxybenzamine
a-blockers
Irreversible, Nonspecific
Applications:
1. Pheochromocytoma [Used preoperatively] to prevent catecholamine [hypertensive crisis]
Phentolamine
a-blockers
Reversible, Nonspecific
Applications:
1. Given to patients on MAO inhibitors who eat tyramine-containing foods
Side Effects:
1. Orthostatic Hypotension
2. Reflex tachycardia
Prazosin, Terazosin, Doxazosin, Tamsulosin [-osin]
a1 selective blockers
Applications:
1. Urinary symptoms of BPH
2. PTSD [Prazosin] 3. HTN [Except Tamsulosin] Side Effects:
1. First dose orthostatic hypertension
2. Dizziness
3. Headache
Mirtazapine
a2 selective blockers
Applications:
1. Depression
Side Effects:
1. Sedation
2. ↑ Serum cholesterol
3. ↑ Appetite
a-blockade of epinephrine vs. phenylephrine
a-blockade of epinephrine vs. phenylephrine

Shown are the effects of an a-blocker [Phentolamine] on blood pressure responses to epinephrine and phenylephrine

The epinephrine response exhibits reversal of mean blood pressure change, from a net increase [a response] to a net decrease [B response] The response to phenylephrine is suppressed by revered because phenylephrine is a pure a-agonist

B-blockers [-olol] Indications
Application/Effect
1. Angina pectoris = ↓ HR and contractility, ↓ O2 consumption
2. MI = ↓ Mortality [Metoprolol, Carvedilol, Bisoprolol] 3. SVT = ↓ AV conduction velocity [Class II antiarrhythmic] – Metoprolol, esmolol
4. HTN = ↓ CO, ↓ renin secretion [B1 blockade on JGA] 5. HF = ↓ Mortality
6. Glaucoma = ↓ Aqueous humor production
B-Blockers Toxicity
1. Impotence
2. Cardiovascular effects [Bradycardia, AV block, HF] 3. CNS effects [Seizures, sedation, sleep alterations] 4. Dyslipidemia [Metoprolol] 5. Asthma/COPD exacerbations*** Avoid in cocaine users due to risk of unopposed a-adrenergic receptor agonist activity

B1 selective antagonists (B1 > B2)
1. Acebutolol [Partial agonist] 2. Atenolol
3. Betaxolol
4. Esmolol
5. Metoprolol
[A to M, with first half of the alphabet]
Nonselective B antagonists [B1 = B2]
1. Nadolol
2. Pindolol [Partial agonist] 3. Propranolol
4. Timolol
[B2 M to T, second half of the alphabet]
Nonselective a- and b- antagonists
Carvedilol
Labetalol
[Modified suffixes, instead of -olol]
Nebivolol
Combines cardiac-selective B1-adrenergic blockade w/ stimulation of B3-receptors [Activate nitric oxide synthase in the vasculature]
Antidote for Acetaminophen
N-acetylcysteine [Replenishes glutathione]
Antidote for AChE inhibitors, organophosphates
Atropine > Pralidoxime
Antidote for Amphetamines [Basic]
NH4Cl [Acidifies urine and traps]
Antidote for Antimuscarinic, anticholinergic agents
Physostigmine salicylate, control hyperthermia
Antidote for Benzodiazapems
Flumazenil
Antidote for B-Blockers
Glucagon
Antidote for Carbon Monoxide
100% O2, hyperbaric O2
Antidote for Copper, arsenic, gold
Penicillamine
Antidote for cyanide
Nitrite + thiosulfate, hydroxycobalamin
Antidote for Digitalis [Digitoxin]
Anti-dig Fab fragments
Antidote for Heparin
Protamine sulfate
Antidote for Iron [Fe]
DeFERoxamine, DeFERasirox
Antidote for Lead
EDTA, dimercaprol, succimer, penicillamine
Antidote for Mercury, arsenic, gold
DiMERCaprol [BAL], succimer
Antidote for Methanol, ethylene glycol
Fomepizole > ethanol, dialysis
Antidote for Methemoglbolin
METHylene blue, vitamin C
Antidote for Opioids
Naloxone, nalrexone
Antidote for Salicylates
NaHCO3 [Alkalinize urine], dialysis
Antidote for TCA
NaHCO3 [Plasma alkalinization]
Antidote for tPA, streptokinase, urokinase
Aminocaproic acid
Warfarin
Vitamin K [Delayed effect], Fresh frozen plasma [Immediate
Which drugs cause coronary vasospasm?
1. Cocaine
2. Sumatriptan
3. Ergot alkaloids
Which drugs cause Cutaneous flushing?
“VANC”
1. Vancomycin
2. Adenosine
3. Niacin
4. Ca2+ channel blockers
Which drugs cause dilated myopathy?
1. Anthracyclines [Doxorubicin, Daunorubicin] PREVENT W/ DEXRAZOXANE
Which drugs cause Torsades de pointes?
1. Class III [Sotalol] and IV [Quinidine] antiarrhythmics
2. Macrolide antibiotics
3. Antipsychotics
4. TCA
Which drugs causes Adrenocortical Insufficiency?
HPA suppression secondary to glucocorticoid withdrawal
Which drugs cause Hot Flashes?
1. Tamoxifen
2. Clomiphene
Which drugs cause Hyperglycemia?
Taking Pills Necessitates Having blood Checked
1. Tacrolimus
2. Protease Inhibitors [Cushing Syndrome}
3. Niacin
4. HCTZ
5. Corticosteroids
Which drugs cause Hypothyroidism?
1. Lithium
2. Amiodarone
3. Sulfonamides
Acute cholestatic hepatitis, jaundice?
1. Erythromycin
Which drugs cause Diarrhea?
Might Excite Colon On Accident
1. Metformin
2. Erythromycin
3. Colchicine
4. Orlistat
5. Acarbose
Which drugs cause Focal to massive hepatic necrosis?
Liver HAVAc
1. Halothane
2. Amanita phalloides [Death cap mushroom] 3. Valproic acid
4. Acetaminophen
Which drugs cause Hepatitis?
1. Rifampin
2. Isoniazid
3. Pyrazinamide
4. Statins
5. Fibrate
Which drugs cause pancreatitis?
Drugs Causing A Violent Abdominal Distress
1. Didanosine
2. Corticosteroids
3. Alcohol
4. Valproic Acid
5. Azathioprine
6. Diuretics [Furosemide, HCTZ]
Which drugs cause Pseudomembranous colitis?
1. Clindamycin
2. Ampicillin
3. Cephalosporins
Antibiotics predispose to superinfection by resistant C. difficle
Which drugs cause Agranulocytosis
Gangs CCCrush Myeloblasts and Promyelocytes
1. Ganciclovir
2. Clozapine
3. Carbamazepine
4. Colchicine
5. Methimazole
6. Propylthiouracil
Which drugs cause Aplastic Anemia
Can’t Make New Blood Cells Properly
1. Carbamazepine
2. Methimazole
3. NSAIDs
4. Benzene
5. Chloramphenicol
6. Propylthiouracil
Which drugs cause Direct Coombs Positive Hemolytic Anemia
1. Methyldopa
2. Penicillin
Which drugs cause Hemolysis in G6PD Deficiency?
Hemolysis IS D PAIN
1. Isoniazid
2. Sulfonamides
3. Dapsone
4. Primaquine
5. Aspirin
6. Ibuprofen
7. Nitrofurantoin
Which drugs cause MegaloBLASTic anemia?
Having a blast w/ PMS
1. Phenytoin
2. Methotrexate
3. Sulfa drugs
Which drugs cause thrombocytopenia?
Heparin
Which drugs cause thrombotic complications?
1. OCPs
2. Hormone Replacement Therapy
Which drugs cause Fat Redistribution [Cushing Syndrome]
FAT PIG
1. Protease Inhibitors [HAART] 2. Glucocorticoids
Which drugs cause gingival hyperplasia?
1. Phenytoin
2. Ca2+ Channel blockers
3. Cyclosporine
Which drugs cause hyperuricemia [Gout]?
Painful Tophi and Feet Need Care
1. Pyrazinamide
2. Thiazides
3. Furosemide
4. Niacin
5. Cyclosporine
Which drugs cause myopathy?
1. Fibrates
2. Niacin
3. Colchicine
4. Hydroxychloroquine
5. IFN-a
6. Penicillamine
7. Statins
8. Glucocorticoids
Which drugs cause osteoporosis?
1. Corticosteroids
2. Heparin
Which drugs cause photosensitivity?
SAT For Photo
1. Sulfonamides
2. Amiodarone
3. Tetracyclines
4. 5-FU
Which drugs cause rash [SJS]?
1. Antiepileptic drugs [Lamotrigine] 2. Allopurinol
3. Sulfa drugs
4. Penicillin
Which drugs cause SLE-like syndrome?
Having lupus is SHIPP-E
1. Sulfa drugs
2. Hydralazine
3. Isoniazid
4. Procainamide
5. Phenytoin
6. Etanercept
Which drugs cause teeth discoloration?
Tetracyclines
Which drugs cause tendonitis, tendon rupture, and cartilage damage?
Fluoroquinolones
Which drugs cause Cinchonism?
Flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity),[1] vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea.
Quinidine, quinine
Which drugs cause Parkinson-like syndrome?
Cogwheel rigidity of the ARM
1. Antipsychotics
2. Reserpine
3. Metoclopramide
Which drugs cause seizures?
With seizures, I BItE my tongue
1. Isoniazid [Vitamin B6 deficiency] 2. Bupropion
3. Imipenem/Cilastatin
4. Enflurane
Which drugs cause tardative dyskinesias?
1. Antipsychotics
2. Metoclopramide
Which drugs cause diabetes insipidus?
1. Lithium
2. Demeclocycline
Which drugs cause Fanconi syndrome?
Expired tetracycline
Which drugs cause hemorrhagic cystitis?
1. Cyclophosphamide
2. Ifosfamide
*** Prevent by coadministering w/ mesna
Which drugs cause interstitial nephritis?
1. Methicillin
2. NSAIDs
3. Furosemide
Which drugs cause SIAD
Can’t Concentrate Serum Sodium
1. Carbamazepine
2. Cyclophosphamide
3. SSRIs
Which drugs cause dry cough?
ACE inhibitors
Which drugs cause pulmonary fibrosis?
Breathing Air Badly from Medications
1. Bleomycin
2. Amiodarone
3. Busulfan
4. Methotrexate
Which drugs cause antimuscarinic effects?
1. Atropine
2. TCAs
3. H1-blockers
4. Antipsychotics
Which drugs cause disulfiram-like reactions?
1. Metronidazole
2. Certain cephalosporins
3. Griseofulvin
4. Procarbazine
5. 1st generation sulfonyureas
Which drugs cause nephrotoxicity/ototoxicity?
1. Aminoglycosides
2. Vanc
3. Loop diuretics
4. Cisplatin [Respond to w/ amifostine]
Sulfa drugs
Popular FACTSSS
1. Probenecid
2. Furosemide
3. Acetazolamide
4. Celecoxib
5. Thiazides
6. Sulfonamide antibiotics
7. Sulfasalazine
8. SulfonylureasPatient’s w/ sulfa allergies may develop:
1. Fever
2. UTIs
3. SJS
4. Hemolytic anemia
5. Urticaria
6. Thrombocytopenia
7. Agranulocytosis

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