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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
|