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394 Cards in this Set

  • Front
  • Back
28-year-old chemist presents
with MPTP exposure. What neurotransmitter is depleted?
Dopamine.
Woman taking tetracycline
exhibits photosensitivity.
Rash on sun-exposed regions of
the body.
African-American man who
goes to Africa develops a
hemolytic anemia after taking
malarial prophylaxis.
Glucose-6-phosphate
dehydrogenase deficiency
Farmer presents with dyspnea,
salivation, miosis, diarrhea,
cramping, and blurry vision.
Insecticide poisoning; inhibition of acetylcholinesterase.
27-year-old female with a history of psychiatric illness now has urinary retention due to a neuroleptic. What do you treat it with?
Bethanechol.
Patient with recent kidney
transplant is on cyclosporine for
immunosuppression. Requires
antifungal agent for candidiasis. What antifungal drug would result in cyclosporine toxicity?
Ketoconazole.
Patient is on carbamazepine. What routine workup should always be done?
LFTs.
23-year-old female who is on
rifampin for TB prophylaxis and
on birth control (estrogen) gets
pregnant. Why?
Rifampin augments estrogen
metabolism in the liver, rendering it less effective.
Km reflects
the affinity of the
enzyme for its substrate.
Vmax is directly proportional
to
the enzyme concentration.
The lower the Km, the
The lower the Km, the higher
the affinity.
The ???? the Km, the higher
the affinity.
lower
Competitive inhibitors
vs
Noncompetitive inhibitors

WRT Resemble substrate
Competitive-- Yes

Noncompetitive-- NO
Competitive inhibitors
vs
Noncompetitive inhibitors

WRT Overcome by ↑ [S]
Competitive-- Yes

Noncompetitive-- NO
Competitive inhibitors
vs
Noncompetitive inhibitors

WRT Bind active site
Competitive-- Yes

Noncompetitive-- NO
Competitive inhibitors
vs
Noncompetitive inhibitors

WRT Effect on Vmax
Competitive-- no change

Noncompetitive-- decrease
Competitive inhibitors
vs
Noncompetitive inhibitors

WRT Effect on Km
Competitive-- increase

Noncompetitive-- no change
Volume of
distribution (Vd)

describe and altered by
Relates the amount of drug in the body to the plasma concentration.

Vd of plasma
protein–bound drugs can be altered by liver and kidney disease.
Vd equation
amount of drug in the body /
plasma drug concentration
Vd ranges and what the mean for where the drug is
low Vd distribute in plasma

medium Vd distribute in extracellular space

high Vd distribute in tissues
t1/2 =
0.7 × Vd/CL
0.7 × Vd/CL =
half life
concentration after # of half-lives
1 - 50%
2 - 75%
3 - 87.5
3.3 - 90%
4 - 94%
Loading dose =
Cp × Vd/F.
28 year old chemist presents with MPTP exposure What NT is depleted?
Dopamine
Woman taking tetracycline exhibits photosensitivity What are the clinical manifestations?
Rash on sun-exposed regions of body
Nondiabetic patient presents with hypoglycemia but low levels of C peptide What is the diagnosis
Surreptitious insulin injection
African American male who goes to Africa develops hemolytic anemia after taking malaria prophylaxis What is the enzyme defficiency
Glucose 6 phosphate dehydrogenase
27 year old female with history of psychiatric illness now has urinary retention due to neuroleptic What do you treat it with?
Bethanechol
Farmer presents with dyspnea, salivation, miosis, diarrhea, cramping and blurry vision What caused this and what is the mechanism
Insecticide poisoning, inhibition of acetylcholinesterase
Patient with recent kidney transplant is on cyclosporine for immunosuppresion, he requires antifungal agent for candidiasis What antifungal drug would result in cyclosporine toxicity?
Ketoconazole
Man on several medications including antidepressants and antihypertensives, has mydriasis and becomes constipated What is the cause of symptoms?
TCA
55 year old postmenopausal woman on tamoxifen therapy What is she at increased risk of acquiring?
Endometrial carcinoma
Woman on MAO inhibitor has hypertensive crisis after meal What did she ingest?
Tyramine (wine or cheese)
After taking clindamycin, patient develops toxic megacolon and diarrhea What is the mechanism of diarrhea?
Clostridium difficile overgrowth
Man starts a medication for hyperlipidemia. He then develops rash, pruritus and GI upset What drug was it?
Niacin
Patient is on carbamazepine What routine workup should be done?
LFT's
23 year old female who is on rifampin for TB prophylaxis and on birth control (estrogen) gets pregnant Why?
Rifampin augments estrogen metabolism in liver rendering it less effective
Patient develops cough and must discontinue captopril WHat is a good replacement drug and why doesnt it have the same side effects?
Losartan - an angiotensin II receptor antagonist, does not increase bradykinin as captopril does
Relates the amount of drug in the body to plasma concentration
Vd - volume of distribution
Formule for volume of distribution
Vd = amount of drug in the body/plasma drug concentration
Vd of plasma protein-bound drugs can be altered by what disease?
Liver and kidney
Relates the rate of elimination to plasma concentration
CLEARANCE
Formula for clearance
Cl = rate of elimination of drug/plasma drug concentration
The time required to change the amount of drug in the body by 1/2 during elimination (or during constant infusion) is called _
Half life T1/2
After 1 half life concentration of drug equals _ %
50%
After 2 half lifes concentration of drug equals_
75%
A drug infused at constant rate reaches about _ % of steady state after 4 T1/2
94
Formula for T1/2
T1/2 = 0.7 * Vd/CL
Loading dose formula
Loading dose = Cp * Vd/F

Cp= target plasma concentration F = bioavailibility
Formula for maintenance dose
Cp * CL / F

Cp = target plasma concentration F = bioavailibility
In patients with impaired renal or hepatic function, the loading dose decreases, increases or remains unchanged? Maintenance dose?
Loading dose remains unchanged Maintenance dose decreases
Rate of elimination is constant (constant amount of drug is eliminated per unit time) - what order elimination? What happens to target plasma concentration?
Zero order elimination Target plasma concentration decreases linearly with time
Rate of elimination is proportional to drug concentration (constant fraction of drug eliminated per unit time) - what order elimination? What happens to target plasma concentration?
First order elimination Cp decreases exponentially with time
Give examples of drugs with zero order elimination
Ethanol Phenytoin Aspirin (at high or toxic concentration)
Phase I metabolism
products, what happens and how eliminated
(reduction, oxidation, hydrolysis) yields _ slightly polar, water-soluble metabolites (often still active) not yet eliminated
What phase of metabolism associated with cytochrome P450
Phase I
What phase of metabolism associated with conjugation
Phase II
Phase II metabolism
products, what happens and how eliminated
acetylation, glucoronidation, sulfation) yields Very polar, inactive metanolites (renally excreted)
Geriatric patients lose which phase of metabolism first?
Phase I
Is it safe? Pharmacokinetics? - which phase of clinical testing of the drug
Phase I
Does it work in patients?- which phase of clinical testing of the drug
Phase II
Does it work? Double blind - which phase of clinical testing of the drug
Phase III
What happens in phase IV of clinical testing of the drug
Postmarketing surveillance
A competitive antagonist shifts agonist curve where?
To the right
A noncompetitive antagonist (irreversible) shifts agonist curve where?
Downward
Urine pH and drug elimination

what is trapped
Ionized species get trapped.
Urine pH and drug elimination

Ionized species
Ionized species get trapped.
Urine pH and drug elimination

Weak acids what and Tx
Trapped in basic environments. Treat overdose with bicarbonate.
Urine pH and drug elimination

Weak bases what and Tx
Trapped in acidic environments. Treat overdose with
ammonium chloride.
Urine pH and drug elimination

Trapped in basic environments.
Weak acids
Urine pH and drug elimination

Trapped in acidic environments.
Weak bases
dose response curves and

different antagonists
A. A competitive antagonist shifts curve to the right, decreasing potency and ↑ EC50.

B. A noncompetitive antago-
nist shifts the agonist curve downward, decreasing efficacy.
dose response curves and

shifts curve to the right, decreasing potency and ↑ EC50.
competitive antagonist
dose response curves and

shifts the curve downward, decreasing efficacy.
noncompetitive antago-
nist
dose response curves and

in a system with spare receptors
the EC50 is lower than the Kd, indicating that to achieve 50% of maximum effect, < 50% of the receptors must be activated. EC50: dose causing 50% of maximal effect. Kd: concentration ofdrug required to bind 50% of receptor sites.
dose response curves and

different agonists
1. The partial agonist acts on the same receptor system as the full agonist but has a lower maximal efficacy no matter the dose.

A partial agonist
may be more potent (as in the figure), less potent, or equally potent; potency is an independent factor.
dose response curves and

may be more potent (as in the figure), less potent, or equally potent; potency is an independent factor.
A partial agonist
Efficacy
= maximal effect
Potency
= amount needed for a given effect
= amount needed for a given effect
Potency
= maximal effect
Efficacy
Therapeutic index
TILE

LD50/ED50
pre and postsynaptic nervous system neurotransmitters

Parasymp
ACh
(nicotinic)

ACh
(muscarinic)
pre and postsynaptic nervous system neurotransmitters

Somatic
only one
ACh (nicotinic)
pre and postsynaptic nervous system neurotransmitters

Sympathetic
pre = ACh (nicotinic)

Ach (muscarinic)- sweat glands

NEα,β - Cardiac and smooth
muscle, gland cells,
nerve terminals

D1 - Renal vascular smooth muscle
nicotinic receptor mech
ACh ligand gated Na+/K+ channels
muscarinic receptor mech
ACh G- protein coupled receptors that act through 2nd messengers
ACh ligand gated Na+/K+ channels
nicotinic receptor
ACh G- protein coupled receptors that act through 2nd messengers
muscarinic receptor
G-protein-linked 2nd messengers
give G protein and major function

α1 Receptor
q

↑ vascular smooth muscle contraction
G-protein-linked 2nd messengers
give G protein and major function

α2 Receptor
i

↓ sympathetic outflow, ↓ insulin release
G-protein-linked 2nd messengers
give G protein and major function

β1 Receptor
s

↑ heart rate, ↑ contractility, ↑ renin release, ↑ lipolysis, ↑ aqueous
humor formation
G-protein-linked 2nd messengers
give G protein and major function

β2 Receptor
s

Vasodilation, bronchodilation, ↑ glucagon release
G-protein-linked 2nd messengers
give G protein and major function

M1 Receptor
q

CNS
G-protein-linked 2nd messengers
give G protein and major function

M2 Receptor
i

↓ heart rate
G-protein-linked 2nd messengers
give G protein and major function

M3 Receptor
q

↑ exocrine gland secretions
G-protein-linked 2nd messengers
give G protein and major function

D2 Receptor
i

Modulates transmitter release, especially in brain
G-protein-linked 2nd messengers
give G protein and major function

D1 Receptor
s

Relaxes renal vascular smooth muscle
G-protein-linked 2nd messengers
give G protein and major function

H1 Receptor
q

↑ nasal and bronchial mucus production, contraction of bronchioles,pruritus, and pain
G-protein-linked 2nd messengers
give G protein and major function

H2 Receptor
s

↑ gastric acid secretion
G-protein-linked 2nd messengers
give G protein and major function

V1 Receptor
q

↑ vascular smooth muscle contraction
G-protein-linked 2nd messengers
give G protein and major function

V2 Receptor
s

↑ H2O permeability and reabsorption in the collecting tubules of
the kidney
Given the major function and G-protein class name the receptor

q
↑ vascular smooth muscle contraction
α1
Given the major function and G-protein class name the receptor

i
↓ sympathetic outflow, ↓ insulin release
α2
Given the major function and G-protein class name the receptor

s
↑ heart rate, ↑ contractility, ↑ renin release, ↑ lipolysis, ↑ aqueous
humor formation
β1
Given the major function and G-protein class name the receptor

s
Vasodilation, bronchodilation, ↑ glucagon release
β2
Given the major function and G-protein class name the receptor

q
CNS
M1
Given the major function and G-protein class name the receptor

i
↓ heart rate
M2
Given the major function and G-protein class name the receptor

q
↑ exocrine gland secretions
M3
Given the major function and G-protein class name the receptor

s
Relaxes renal vascular smooth muscle
D1
Given the major function and G-protein class name the receptor

i
Modulates transmitter release, especially in brain
D2
Given the major function and G-protein class name the receptor

q
↑ nasal and bronchial mucus production, contraction of bronchioles,
H1
Given the major function and G-protein class name the receptor

s
↑ gastric acid secretion
H2
Given the major function and G-protein class name the receptor

q
↑ vascular smooth muscle contraction
V1
Given the major function and G-protein class name the receptor

s
↑ H2O permeability and reabsorption in the collecting tubules of the kidney
V2
G-protein-linked 2nd messengers
Receptor G-protein class

how to remember which goes with which
α1, α2, β1, β2, M1, M2, M3, D1, D2, H1, H2, V1, V2

"QISS (kiss) and QIQ (kick) till you're SIQ (sick) of SQS (sex)."
G-protein-linked 2nd messengers
Receptor G-protein class

3rd messengers... for Gq
HAVe 1 M&M (H1, α1, V1, M1, M3)

↑ Phospholipase C to IP3 (↑Ca2+) and DAG (Protein Kinase C)
G-protein-linked 2nd messengers
Receptor G-protein class

3rd messengers... for Gs
β1, β2, D1 H2, V2

↑ Adenylcyclase (↑ATP to cAMP [ ↑ Protein kinase A])
G-protein-linked 2nd messengers
Receptor G-protein class

3rd messengers for... Gi
MAD 2's (M2, α2, D2)

↓Adenylcyclase (↓ATP to cAMP [ ↑ Protein kinase A])
Release of NE from a sympathetic nerve ending is modulated by

with mech
by NE itself, acting on presynaptic α2 autoreceptors, and by ACh,

angiotensin II, and other substances.
Cholinomimetics
direct
names
Bethanechol
Carbachol
Pilocarpine
Methacholine
Cholinomimetics
indirect
names
Neostigmine
Pyridostigmine
Edrophonium
Physostigmine
Echothiophate
Bethanechol

Mech
Cholinomimetics: Direct agonist
Carbachol

Mech
Cholinomimetics: Direct agonist
Pilocarpine

Mech
Cholinomimetics: Direct agonist
Methacholine

Mech
Cholinomimetics: Direct agonist
Neostigmine

Mech
Cholinomimetics: inirect agonist (anticholinesterase)

↑ endogenous ACh
Pyridostigmine

Mech
Cholinomimetics: inirect agonist (anticholinesterase)

↑ endogenous ACh
Edrophonium

Mech
Cholinomimetics: inirect agonist (anticholinesterase)

↑ endogenous ACh
Physostigmine

Mech
Cholinomimetics: inirect agonist (anticholinesterase)

↑ endogenous ACh
Echothiophate

Mech
Cholinomimetics: inirect agonist (anticholinesterase)

↑ endogenous ACh
Which Cholinergic Activates Bowel and Bladder smooth muscle;
Bethanechol
Which Cholinergic Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle)
Carbachol
Which Cholinergic Stimulates muscarinic receptors in airway when inhaled.
Methacholine
Which Cholinergic

Potent stimulator of sweat, tears, saliva
Pilocarpine
Which Cholinergic resistant to AChE
Bethanechol and Pilocarpine
Which Cholinergic ↑ endogenous ACh No CNS penetration
Neostigmine
Which Cholinergic ↑ endogenous ACh; ↑ strength
Pyridostigmine
Which Cholinergic is used for Postoperative and neurogenic ileus and urinary
retention
Bethanechol
and
Neostigmine
Which Cholinergic is used for Glaucoma, pupillary contraction, and release of intraocular pressure
Carbachol, Echothiophate and Physostigmine
Which Cholinergic is used for Potent stimulator of sweat, tears, saliva
Pilocarpine
Which Cholinergic is used for Challenge test for diagnosis of asthma
Methacholine
Which Cholinergic is used for reversal of
neuromuscular junction blockade (postoperative)
Neostigmine
Which Cholinergic is used for Myasthenia gravis
Neostigmine

Pyridostigmine does penetrate CNS
Which Cholinergic is used for Diagnosis of myasthenia gravis
Edrophonium
Which Cholinergic is used for atropine overdose
Physostigmine
Clinical applications of

Bethanechol
Postoperative and neurogenic ileus and urinary
retention
Clinical applications of

Carbachol
Glaucoma, pupillary contraction, and release of
intraocular pressure
Clinical applications of

Pilocarpine
Potent stimulator of sweat, tears, saliva
Clinical applications of

Methacholine
Challenge test for diagnosis of asthma
Clinical applications of

Neostigmine
Postoperative and neurogenic ileus and urinary
retention, myasthenia gravis, reversal of
neuromuscular junction blockade (postoperative)
Clinical applications of

Pyridostigmine
Myasthenia gravis; does penetrate CNS
Clinical applications of

Edrophonium
Diagnosis of myasthenia gravis (extremely short
acting)
Clinical applications of

Physostigmine
Glaucoma (crosses blood-brain barrier → CNS)
and atropine overdose
Clinical applications of

Echothiophate
Glaucoma
which anticholinesterase is extremely short acting
Edrophonium
Cholinesterase inhibitor poisoning

symps
DUMBBEL ASS.

Diarrhea, Urination, Miosis,
Bronchospasm, Bradycardia, Excitation of skeletal
muscle and CNS, Lacrimation, Abdominal cramping, Sweating, and Salivation
Cholinesterase inhibitor poisoning

Tx
Atropine (muscarinic antagonist) plus pralidoxime
chemical antagonist used to regenerate active cholinesterase
pralidoxime
pralidoxime

uses and mech
Cholinesterase inhibitor poisoning

chemical antagonist used to regenerate active cholinesterase
Parathion
organophosphate
organophosphate toxicity mech
Irreversible Cholinesterase inhibitor poisoning
Atropine,

mech
Muscarinic antagonist
Benztropine

mech
Muscarinic antagonist
Scopolamine

mech
Muscarinic antagonist
Ipratropium

mech
Muscarinic antagonist
Methscopolamine,
oxybutin,
glycopyrrolate

mech
Muscarinic antagonist
Atropine

clinical use
Produce mydriasis and cycloplegia
Benztropine

clinical use
Parkinson’s disease
Scopolamine

clinical use
Motion sickness
Ipratropium

clinical use
Asthma, COPD
Methscopolamine,
oxybutin,
glycopyrrolate

clinical use
Reduce urgency in mild cystitis and reduce bladder spasms
Glaucoma drugs mech and side effects

Epinephrine
↑ outflow of aqueous humor

Mydriasis, stinging; do not use
in closed-angle glaucoma
Glaucoma drugs mech and side effects

Brimonidine
↓ aqueous humor synthesis

No pupillary or vision changes
Glaucoma drugs mech and side effects

β-blockers
↓ aqueous humor secretion

No pupillary or vision changes
Glaucoma drugs mech and side effects

Acetazolamide
↓ aqueous humor secretion due to
↓ HCO3− (via inhibition of carbonic anhydrase)

No pupillary or vision changes
Glaucoma drugs mech and side effects

Cholinomimetics
↑ outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork;

Miosis, cyclospasm
Glaucoma drugs mech and side effects

Latanoprost (PGF2α)
↑ outflow of aqueous humor

Darkens color of iris (browning)
which glaucoma drug ↑ outflow of aqueous humor
Epinephrine

Cholinomimetics

Prostaglandin (Latanoprost
(PGF2α))
which glaucoma drug ↓ aqueous humor synthesis
Brimonidine
which glaucoma drug ↓ aqueous humor secretion
β-blockers: Timolol, betaxolol,
carteolol

Diuretics: Acetazolamide
which glaucoma drug causes Mydriasis, stinging; do not use
in closed-angle glaucoma
Epinephrine
which glaucoma drug causes Miosis, cyclospasm
Cholinomimetics
which glaucoma drug causes Darkens color of iris (browning)
Prostaglandin: Latanoprost
(PGF2α)
Atropine effects
dilates pupils and Blocks SLUD:
↓Salivation
↓Lacrimation
↓Urination
↓Defecation
Atropine Toxicity
Hot as a hare
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter
Can cause acute angle-closure glaucoma in elderly, urinary retention in men with prostatic hypertrophy, and hyperthermia
in infants.
Atropine
Hexamethonium

Mechanism
Nicotinic ACh receptor antagonist. Ganglionic blocker.
Hexamethonium

Clinical use
Ganglionic blocker. Used in experimental models to prevent vagal reflex responses to
changes in blood pressure– –e.g., prevents reflex bradycardia caused by NE.
prevents reflex bradycardia caused by NE
Hexamethonium
Used in experimental models to prevent vagal reflex responses to
changes in blood pressure
Hexamethonium
selectivity for Sympathomimetics

Epinephrine
α1, α2, β1, β2, low doses selective for β1
selectivity for Sympathomimetics

NE
α1, α2 >β1
selectivity for Sympathomimetics


Isoproterenol
β1 =β2
selectivity for
Sympathomimetics

Dopamine
D1 = D2 >β >α
selectivity for Sympathomimetics

Dobutamine
β1 >β2
Mechanism for Sympathomimetics

Amphetamine
Indirect general agonist, releases stored
catecholamines
Mechanism for Sympathomimetics

Ephedrine
Indirect general agonist, releases stored
catecholamines
Mechanism forSympathomimetics

Cocaine
Indirect general agonist, uptake inhibitor
Mechanism for Sympathomimetics

Clonidine, α-methyldopa
Centrally acting α-agonist, ↓ central
adrenergic outflow
selectivity for Sympathomimetics

Phenylephrine
α1 >α2
selectivity for Sympathomimetics


Albuterol
β2 >β1
Mechanism/selectivity for Sympathomimetics

terbutaline
β2 >β1
name the Sympathomimetic

α1, α2, β1, β2, low doses selective for β1
Epinephrine
name the Sympathomimetic

α1, α2 >β1
NE
name the Sympathomimetic

β1 =β2
Isoproterenol
name the Sympathomimetic

β1 >β2
Dobutamine
name the Sympathomimetic

D1 = D2 >β >α
Dopamine
name the Sympathomimetic

Indirect general agonist, releases stored catecholamines
Amphetamine

and

Ephedrine
name the Sympathomimetic

α1 >α2
Phenylephrine
name the Sympathomimetic

β2 >β1
Albuterol,

terbutaline
name the Sympathomimetic

Indirect general agonist, uptake inhibitor
Cocaine
name the Sympathomimetic

Centrally acting α-agonist, ↓ central adrenergic outflow
Clonidine,
α-methyldopa
effect on BP and HR of

Norepinephrine
(α > β)

↑ BP

↓ HR (reflex bradycardia)
effect on BP and HR of


Epinephrine
nonselective

NC BP( increases systolic, but decreases diastolic)
effect on BP and HR of

Isoproterenol
(β > α)

↓ BP

↑ HR
Applications of Sympathomimetics

Epinephrine
Anaphylaxis, glaucoma (open
angle), asthma, hypotension
Applications of Sympathomimetics

NE
Hypotension (but ↓ renal
perfusion)
Applications of Sympathomimetics

Isoproterenol
AV block (rare)
Applications of Sympathomimetics

Dopamine
Shock (↑ renal perfusion),
heart failure
Applications of Sympathomimetics

Dobutamine
Shock, heart failure cardiac
stress testing
Applications of Sympathomimetics

Amphetamine
Narcolepsy, obesity, ADHD
Applications of Sympathomimetics

Ephedrine
Nasal decongestion, urinary
incontinence, hypotension
Applications of Sympathomimetics

Phenylephrine
Pupil dilator, vasoconstriction,
nasal decongestion
Applications of Sympathomimetics

Albuterol,
terbutaline
Asthma
Applications of Sympathomimetics

Cocaine
Causes vasoconstriction and
local anesthesia
Applications of Sympathomimetics

Clonidine,
α-methyldopa
Hypertension, especially with
renal disease (no ↓ in blood
flow to kidney)
name the Nonselective α-blockers
Phenoxybenzamine

phentolamine
name the α1 selective α-blockers
Prazosin, terazosin,
doxazosin
name the α2 selective α-blockers
Mirtazapine
Nonselective α-blockers

Application and Toxicity
-Pheochromocytoma

-Orthostatic hypotension,
reflex tachycardia
α1 selective α-blockers

Application and Toxicity
-Hypertension, urinary retention in BPH

-1st-dose orthostatic hypotension, dizziness, headache
α2 selective α-blockers

Application and Toxicity
-Depression

-Sedation, ↑ serum cholesterol, ↑ appetite
Nonselective α-blockers

names and differences
Phenoxybenzamine (irreversible)


phentolamine (reversible)
effects of an α-blocker (e.g., phentolamine) on BP responses to epinephrine and phenylephrine.
The epinephrine response exhibits reversal of the mean blood pressure change, from a net increase (the α response) to a net decrease (the β2 response). The response to phenylephrine is suppressed but not reversed because phenylephrine is a “pure” α-agonist without β action.
β-blockers

non selective ones
Nonselective (N or later)(β1 = β2)––propranolol, timolol, nadolol, pindolol (partial agonist), and

labetalol (partial agonist, and exception to the after N rule and the olol rule)
β-blockers

selective ones
Before N

β1 selective (β1 > β2)–– Betaxolol, Esmolol (short acting), Atenolol,
Metoprolol

Acebutolol (partial agonist hes and Ass),
β-blocker effect WRT

Hypertension
↓ cardiac output, ↓ renin secretion
β-blocker effect WRT

Angina pectoris
↓ heart rate and contractility, resulting in ↓ O2 consumption
β-blocker effect WRT

MI
β-blockers ↓ mortality
β-blocker effect WRT

SVT
↓ AV conduction velocity
β-blocker effect WRT

CHF
Slows progression of chronic failure
β-blocker effect WRT Glaucoma
↓ secretion of aqueous humor
which β-blockers

Tx for Glaucoma
timolol
which β-blockers

Tx for SVT
propranolol, esmolol
β-blockers

Toxicity (non cardiac)
1. Impotence,
2. exacerbation of asthma,
3. CNS adverse effects (sedation, sleep alterations);
4. diabetics can't feel low sugar
β-blockers

Toxicity (cardiac)
-bradycardia,
-AV block,
-CHF
antidote for

Acetaminophen
1. N-acetylcysteine
antidote for

Salicylates
2. Alkalinize urine, dialysis
antidote for

Anticholinesterases, organophosphates
3. Atropine, pralidoxime
antidote for

Antimuscarinic, anticholinergic agents
4. Physostigmine salicylate
antidote for

β-blockers
5. Glucagon
antidote for

Digitalis
6. Stop dig, normalize K+,
lidocaine, anti-dig Fab
fragments, Mg2+
antidote for

Iron
7. Deferoxamine
antidote for

Lead
8. CaEDTA, dimercaprol,
succimer, penicillamine
antidote for

Arsenic, mercury, gold
9. Dimercaprol (BAL),
succimer
antidote for

Copper, arsenic, gold
10. Penicillamine
antidote for

Cyanide
11. Nitrite, hydroxocobalamin,
thiosulfate
antidote for

Methemoglobin
12. Methylene blue
antidote for

Carbon monoxide
13. 100% O , hyperbaric O
antidote for

Methanol, ethylene glycol (antifreeze)
14. Ethanol, dialysis, fomepizole
antidote for

Opioids
15. Naloxone/naltrexone
antidote for

Benzodiazepines
16. Flumazenil
antidote for


TCAs
17. NaHCO3 (nonspecific)
antidote for

Heparin
18. Protamine
antidote for

Warfarin
19. Vitamin K, fresh frozen
plasma
antidote for

tPA, streptokinase
20. Aminocaproic acid
antidote for

Basic amphetamines
NH4CL (acidify urine)
This antidote is used for

NH4CL (acidify urine)
Basic amphetamines
This antidote is used for

Aminocaproic acid
tPA, streptokinase
This antidote is used for

Vitamin K, fresh frozen
plasma
Warfarin
This antidote is used for

Protamine
Heparin
This antidote is used for

NaHCO3 (nonspecific)
TCAs
This antidote is used for

Flumazenil
Benzodiazepines
This antidote is used for

N-acetylcysteine
1. Acetaminophen
This antidote is used for

Alkalinize urine, dialysis
2. Salicylates
This antidote is used for

Atropine, pralidoxime
3. Anticholinesterases, organophosphates
This antidote is used for

Physostigmine salicylate
4. Antimuscarinic, anticholinergic agents
This antidote is used for

Glucagon
5. β-blockers
This antidote is used for

Stop dig, normalize K+,
lidocaine, anti-dig Fab
fragments, Mg2+
6. Digitalis
This antidote is used for

Deferoxamine
7. Iron
This antidote is used for

CaEDTA, dimercaprol,
uccimer, penicillamine
8. Lead
This antidote is used for

Dimercaprol (BAL),
succimer
9. Arsenic, mercury, gold
This antidote is used for

Penicillamine
10. Copper, arsenic, gold
This antidote is used for

Nitrite, hydroxocobalamin,
thiosulfate
11. Cyanide
This antidote is used for

Methylene blue
12. Methemoglobin
This antidote is used for

100% O2, hyperbaric O2
13. Carbon monoxide
This antidote is used for

Ethanol, dialysis, fomepizole
14. Methanol, ethylene glycol (antifreeze)
This antidote is used for

Naloxone/naltrexone
15. Opioids
signs of Lead poisoning
LEAD.

-Lead Lines on gingivae and on epiphyses on x-ray.
-Encephalopathy and RBC basophilic stippling.
-Abdominal colic and sideroblastic Anemia.
-Drops––wrist and foot drop.
Drug reaction by system

Cardiovascular Atropine-like side
effects
-Tricyclics
Drug reaction by system

Cardiac toxicity
-Doxorubicin (Adriamycin), -daunorubicin
Drug reaction by system

Coronary vasospasm
Cocaine
Drug reaction by system

Cutaneous flushing
-Niacin,
-Ca2+ channel blockers,
-adenosine,
-vancomycin
Drug reaction by system

Torsades des pointes
-Class III (sotalol),
-class IA (quinidine)
-cisapride
Drug reaction by system

Agranulocytosis
-Clozapine,
-carbamazepine,
-colchicine
Drug reaction by system

Aplastic anemi
-Chloramphenicol,
-benzene,
-NSAIDs
Drug reaction by system

Gray baby syndrome
Chloramphenicol
Drug reaction by system

Hemolysis in G6PD-
deficient patients
IS PAIN

isoniazid (INH),
Sulfonamides,

primaquine,
aspirin,
ibuprofen,
nitrofurantoin
Drug reaction by system

Thrombotic complications
OCPs (e.g., estrogens and progestins)
Drug reaction by system

Cough
ACE inhibitors
Drug reaction by system

Pulmonary fibrosis
Bleomycin,
amiodarone,
busulfan
Drug reaction by system

Acute cholestatic
hepatitis
Macrolides
Drug reaction by system

Focal to massive
hepatic necrosis
Halothane,
valproic acid,
acetaminophen,
Amanita phalloides
Drug reaction by system

Hepatitis
INH
Drug reaction by system

Pseudomembranous
colitis
Clindamycin, ampicillin
Drug reaction by system

Gynecomastia
(Some Drugs Create Awesome, Excellent Knockers)

Spironolactone,
Digitalis,
Cimetidine,
Alcohol chronicuse,
Estrogens,
Ketoconazole
Drug reaction by system

Hot flashes
Tamoxifen
Drug reaction by system

Gingival hyperplasia
Phenytoin
Drug reaction by system

Osteoporosis
Corticosteroids, heparin
Drug reaction by system

Photosensitivity
(SAT for a photo)

Sulfonamides,
Amiodarone,
Tetracycline
Drug reaction by system

SLE-like syndrome
(it’s not HIPP to have lupus)
Drug reaction by system

Tendonitis, tendon rupture, and cartilage damage (kids)
Fluoroquinolones
Drug reaction by system

Fanconi’s syndrome
Expired tetracycline
Drug reaction by system

Interstitial nephritis
Methicillin
Drug reaction by system

Hemorrhagic cystitis
Cyclophosphamide,
ifosfamide
Drug reaction by system

Cinchonism
Quinidine,
quinine
Drug reaction by system

Diabetes insipidus
Lithium,
demeclocycline
Drug reaction by system

Tardive dyskinesia
Antipsychotics
Drug reaction by system

Disulfiram-like
reaction
Metronidazole,
certain cephalosporins,
procarbazine,
sulfonylureas
Drug reaction by system

Nephrotoxicity/
neurotoxicity
Polymyxins
Drug reaction by system

Nephrotoxicity/
ototoxicity
Aminoglycosides,
loop diuretics,
cisplatin
P-450 Inducers
"Queen Barb takes Phen-phen
and Refuses Greasy Carved Steak"

Quinidine (can inhibit too), Barbiturates, Phenytoin, Rifampin, Griseofulvin, Carbamazepine,
St. John’s wort
P-450 Inhibitors
Inhibitors Stop Cyber-Kids
from Eating Grapefruit.

Isoniazid
Sulfonamides
Cimetidine
Ketoconazole
Erythromycin
Grapefruit juice
Iron Poisioning

Mech
Cell death due to peroxidation of membrane lipids
Iron Poisioning

Symps
acute - gastric bleeding

chronic - metabolic acidosis, scarring (leading to GI obstruction)
INHIBITED BY DISULFIRAM
Acetaldehyde dehydrogenase
COMPETITIVE SUBSTRATES
FOR Alcohol
dehydrogenase
-Ethylene glycol
-Methanol
-Ethanol
Alcohol toxicity

Ethylene glycol
Acidosis,
nephrotoxicity
Alcohol toxicity

Methanol
Severe acidosis,
retinal damage
Alcohol toxicity

Ethanol
Nausea, vomiting,
headache,
hypotension
which Alcohol toxicity

Acidosis, nephrotoxicity
Ethylene glycol
which Alcohol toxicity

Severe acidosis, retinal damage
Methanol
which Alcohol toxicity

Nausea, vomiting, headache,
hypotension
Ethanol
Alcohol toxicity

what causes the problem in Ethylene glycol
Build up of Oxalic acid
Alcohol toxicity

what causes the problem in Methanol
Build up of Formaldehyde
and formic acid
Alcohol toxicity

what causes the problem in Ethanol
Build up of Acetaldehyde
which Alcohol toxicity

Oxalic acid is the problem
Ethylene glycol
which Alcohol toxicity

Formaldehyde and formic acid is the problem
Methanol
which Alcohol toxicity

Acetaldehyde is the problem
Ethanol
Drugs that cause problems in patients with sulfa allergies
Celecoxib, furosemide, thiazides, TMP-SMX, sulfonyureas,
sufasalazine
Herbal agents Clinical uses and Toxicities

Echinacea
Common cold

no major
Herbal agents Clinical uses and Toxicities

Ephedra
As for ephedrine

CNS and cardiovascular stimulation; arrhythmias,
stroke, and seizures at high doses
Herbal agents Clinical uses and Toxicities

Feverfew
Migraine

mouth ulcers, antiplatelet actions
Herbal agents Clinical uses and Toxicities

Ginkgo
Intermittent claudication

anxiety, insomnia, antiplatelet actions
Herbal agents Clinical uses and Toxicities

Kava
Chronic anxiety

sedation, ataxia, hepatotoxicity,
phototoxicity, dermatotoxicity
Herbal agents Clinical uses and Toxicities

Milk thistle
Viral hepatitis

Loose stools
Herbal agents Clinical uses and Toxicities

Saw palmetto
Benign prostatic hyperplasia

↓ libido, hypertension
Herbal agents Clinical uses and Toxicities

St. John’s wort
Mild to moderate depression

phototoxicity; serotonin syndrome
with SSRIs; induces P-450 system
Herbal agents Clinical uses and Toxicities

Dehydroepiandrosterone
Symptomatic improvement in females with SLE or AIDS

Androgenization (premenopausal women), estrogenic effects (postmenopausal), feminization (young men)
Herbal agents Clinical uses and Toxicities

Melatonin
Jet lag,

Sedation, suppresses midcycle LH,
hypoprolactinemia
Drug name Ending / Category

-afil
Erectile dysfunction
Drug name Ending / Category

Erectile dysfunction
-afil
Drug name Ending / Category

-ane
Inhalational general anesthetic
Drug name Ending / Category

Inhalational general anesthetic
-ane
Drug name Ending / Category

-azepam
Benzodiazepine
Drug name Ending / Category

Benzodiazepine
-azepam
Drug name Ending / Category

-azine
Phenothiazine (neuroleptic, antiemetic)
Drug name Ending / Category

Phenothiazine (neuroleptic, antiemetic)
-azine
Drug name Ending / Category

-azole
Antifungal
Drug name Ending / Category

Antifungal
-azole
Drug name Ending / Category

-barbital
Barbiturate
Drug name Ending / Category

Barbiturate
-barbital
Drug name Ending / Category

-caine
Local anesthetic
Drug name Ending / Category

Local anesthetic
-caine
Drug name Ending / Category

-cillin
Penicillin
Drug name Ending / Category

Penicillin
-cillin
Drug name Ending / Category

-cycline
Antibiotic, protein synthesis inhibitor
Drug name Ending / Category

Antibiotic, protein synthesis inhibitor
-cycline
Drug name Ending / Category

-ipramine
TCA
gjkgjh
ghjkghjkgh
Drug name Ending / Category

Protease inhibitor
-navir
Drug name Ending / Category

-navir
Protease inhibitor
Drug name Ending / Category

-olol
β-antagonist
Drug name Ending / Category

β-antagonist
-olol
Drug name Ending / Category

-operidol
Butyrophenone (neuroleptic)
Drug name Ending / Category

Butyrophenone (neuroleptic)
-operidol
Drug name Ending / Category

-oxin
Cardiac glycoside (inotropic agent)
Drug name Ending / Category

Cardiac glycoside (inotropic agent)
-oxin
Drug name Ending / Category

-phylline
Methylxanthine
Drug name Ending / Category

Methylxanthine
-phylline
Drug name Ending / Category

-pril
ACE inhibitor
Drug name Ending / Category

ACE inhibitor
-pril
Drug name Ending / Category

-terol
β2 agonist
Drug name Ending / Category

β2 agonist
-terol
Drug name Ending / Category

-tidine
H2 antagonist
Drug name Ending / Category

H2 antagonist
-tidine
Drug name Ending / Category

TCA
-triptyline

or

-ipramine
Drug name Ending / Category

-ipramine
TCA
Drug name Ending / Category

-tropin
Pituitary hormone
Drug name Ending / Category

Pituitary hormone
-tropin
Drug name Ending / Category

-zosin
α1 antagonist
Drug name Ending / Category

α1 antagonist
-zosin