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224 Cards in this Set
- Front
- Back
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28 y/o chemist presents w/ MPTP exposuree. what NT is depleted
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dopamine
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woman taking tetracycline exhibits photosensitivity. What are the clinical manifestations?
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rash on sun exposed retions of body
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African American man who goes to Africa develops a hemolytic anemia after taking malarial prophylaxis. what is the enzyme deficiency
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glucose 6 phosphate dehydrogenase
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farmer presents w/ dyspnea, salivation, miosis, diarrhea, cramping, and blurry vision. What caused this, and what is the MOA
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insecticide poisoning; inhibition of acetylcholinesterase
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27 y/o female w/ hx of psych illness now has urinary retention due to a neuroleptic. What do you tx it with?
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bethancechol
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pt w/ recent kidney transplant is on cyclosporine for immunosuppression. Requires antifungal agent for candidiasis. What antifungal drug would result in cyclosporine toxicity
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ketoconazole
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pt is on carbamazepine. What routine workup should always be done?
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LFTs
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23 y/o female who is on rifampin for TB prophylaxis and on birth control (estrogen) gets pregnant. why
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rifampin augments estrogen metabolism in the liver, rendering it less effective
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what is the volume of distribution
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relates the amount of drug in the body to the plasma concentration
=amount of drug in body/plasma drug concentration |
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Vd of plasma protein bound drugs can be altered by dzs in these 2 organ systems
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liver and kidney
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what is clearance (CL)
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relates the rate of elimination to the plasma concentration
Cl=rate of elimination of drug/plasma drug concentration |
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what is the half life (t1/2)
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the time required to change the amount of drug in the body by 1/2 during elimination (or constant infusion). A drug infused at a constant rate reaches about 94% of steady state after 4 t(1/2_
t(1/2)=0.7xVd/Cl |
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what is concentration of drug in the body after 1 half life
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50%
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what is concentration of drug in the body after 2 half lives
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75%
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what is concentration of drug in the body after 3 half lives
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87.5%
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what is concentration of drug in the body after 4 half lives
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~94%
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Cp =
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target plasma concentration
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F=
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bioavalability
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Loading dose=
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Cp x Vd/F
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maintenance dose=
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CpxCL/F
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what happens to the loading dose and maitenance dose in pts will impared renal or hepatic fxn
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loading dose remains the same
maitenence dose is decreased |
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this order elimination describes a constant rate of elimination regardless of C (i.e. constant AMOUNT of drug eliminated per unit time). Cp decreases linearly with time. E.g., etoh, phenytoin, and asprin (at high or toxic concentrations)
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zero order elimination
image. p. 195 |
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this order elimination describes a rate of elimination proportional to the drug concentration (i.e., constant FRACTION of drug eliminated per unit time). Cp decreases exponentially with time.
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first order elimination
image. p. 195 |
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In drugs with 1st order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195 |
proportional to
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In drugs with 0 order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195 |
independant of
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give some examples of phase I metabolism
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reduction, oxidation, hydrolysis.
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describe the metabolites of phase I metabolism(aka are they active)
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slightly polar, water soluble, often still active
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give some examples of phase II metabolism
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acetylation, glucuronidation, sulfation
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describe the metabolites of phase II metabolism(aka are they active)
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yields very polar, inactive metabolites (renally excreted
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what pump is key in phase I metabolism
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cytocrome P-450
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by what method are drugs metabolized in phase II metabolism
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conjugation
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what phase of metabolism do geriatric pts lose first
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phase I
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image p. 196-agonist dose response curves in the presence of competitive and irreversable antagonists
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--
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competitive antagonist shifts the curve _______
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to the right
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noncompetitive antagonist shifts the curve ______
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downward
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EC50:
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dose causing 50% of maximal effect.
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Kd:
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concentration of drug required to bind 50% of receptor sites
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image p. 196-percent of maximum efect as a fx of dose
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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.
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image p. 197-percent of maximum efect as a fx of dose
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comparison of dose-response curves for a full agonist and a partial agonist. The partial agonist acts on the same receptor system as the full agonist but cannot produce an equivalently large effect (it has lower maximal efficacy) no matter how much the dose is increased. A partial agonist may be more potent (as in the figure), less potent, or equally potent; potency is an indipendant factor
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what is the therapeutic index
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mean toxic dose/mean effective dose
TD50/ED50 high TI is good |
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image p. 197- drug development
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--
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on average how long does it take for a drug to be in In-vitro stidues
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2 yts
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on average how long does it take for a drug to be in animal stidues
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2 years
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this phase of clinical testing for a drugs looks at if it is safe, and the pharmakinetics
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phase 1
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this phase of clinical testing for a drugs looks at if it works in pts
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phase 2
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this phase of clinical testing for a drugs looks at does it work, in a double blind study
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phase 3
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this phase drug development involves postmarketing surveillance
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phase 4
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On average how many years of drug development does it take to file a NDA (new drug application)
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9
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how long after filing of application does patent expire on a drug and generics become available
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20 years
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image p. 198-central and peripheral nervous system
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--
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given the receptor, give the G-protein class and the major fx: α1
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increases vascular smooth mm contraction
G protien class: q |
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given the receptor, give the G-protein class and the major fx: α2
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Decrease sympathetic outflow, decrease insulin release
G protien class: i |
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given the receptor, give the G-protein class and the major fx: ϐ1
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increase heart rate, increase contractility, increase renin release, increase lipolysis, incease aqueous humor formation
G protien class: s |
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given the receptor, give the G-protein class and the major fx: ϐ2
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vasodilation, bronchodilation, increase glucagon release
G protien class: s |
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given the receptor, give the G-protein class and the major fx: M1
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CNS
G protien class: q |
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given the receptor, give the G-protein class and the major fx: M2
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decrease heart rate
G protein class: i |
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given the receptor, give the G-protein class and the major fx: M3
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increase exocrine gland secretions
G protein class: q |
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given the receptor, give the G-protein class and the major fx: D1
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relaxes renal vascular sm mm
G protein class: s |
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given the receptor, give the G-protein class and the major fx: D2
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modulates NT release, esp in the brain
G protein class:i |
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given the receptor, give the G-protein class and the major fx: H1
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increase nasal and bronchial mucus production, contraction of bronchioles, pruritis, and pain
G protein class:q |
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given the receptor, give the G-protein class and the major fx: H2
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increase gastric acid secretion
G-protein class:s |
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given the receptor, give the G-protein class and the major fx: V1
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increase vascular sm mm contraction
G-protein class:q |
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given the receptor, give the G-protein class and the major fx: V2
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increase H2O permeability and reabsorption in the collecting tubules of the kidney
G-protein class:s |
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flowchart p. 199-receptors: α1,M1,M3,H1,V1
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--
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flowchart p. 199-receptors: ϐ1,ϐ2,D1,H2,V2
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--
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flowchart p. 199-receptors: α2,M2,D2
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--
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image p.200-Autonomic drugs
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--
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image p.200-noradrenergic nerve terminal
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--
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release of NE from a sympathetic nn ending is modulated by ______, acting on these receptors.
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NE, ACH, ATN II, othr substances
presynaptic α2 autoreceptors |
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Bethanechol is a cholinomimetic with direct agonist actions. Give its clinical applications
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postop and neurogenic ileus and urinary retention
it acts by activating Bowel & Bladder smooth mm. It is resistant to AChE |
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Carbachol, pilocarpine is a cholinomimetic with direct agonist actions. Give its clinical applications
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Used for glaucoma
it activates ciliary mm of eye (open angle), pupillary sphicter (narrow angle); It is resistant to AChe |
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Neostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
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postop & neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular jxn blockade (postop)
It acts by inceasing endogenous ACh |
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Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
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used to tx myasthenia gravis
It acts by inceasing endogenous ACh, thereby increasing strength |
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Edrophonium is a Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
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myasthenia gravis (short acting)
It acts by inceasing endogenous ACh |
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physostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
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glaucoma (crosses blood brain barrier) and atropine OD
works by increasing endogenous ACh |
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Echothiophateis a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
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Glaucoma
works by increasing endogenous ACh |
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give some signs of cholinesterase inhibitor poisoning
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Diarrhea (abd cramping), Urination, Miosis, Bronchospasm, Bradycardia, Exitation of skeletal mm and CNS, Lacrimation, Sweating, and Salivation,
mneu: DUMBBELSS or SLUD effects |
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what can cause cholinesterase inhibitor poisoning
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Parathion and other organophosphates
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how do you tx cholinesterase inhibitor poisoning
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Antidote--atropine (muscarinic antagonist) plus pralidoxime (chemical antagonist used to regenerate active cholinesterase)
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Atropine, homotropine, and tropicamide are cholinoreceptor blockers taht act on they eye to do what?
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produce mydriasis and cycloplegia
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Benzotropine is a cholinoreceptor blocker that acts on the CNS to tx?
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Parkinson's dz
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Scopolamine is a cholinoreceptor blocker that acts on the CNS to tx?
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Motion skickness
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Ipratropium is a cholinoreceptor blocker that acts on the Respiratory system to tx?
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Asthma, COPD
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Methscopolamine, oxybutin, glycopyrrolateis a cholinoreceptor blocker that acts on the GU system to tx?
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urgency in mild cystitis and reduce bladder spasms
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atropine is a muscarinic _______
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antagoinist
mneu: blocks SLUD: salivation, Lacrimation, Urination, Defication |
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give the effect atropine would have on the eye
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pupil dilation, cycloplegia
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give the effect atropine would have on the airway
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decrease secretions
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give the effect atropine would have on the stomach
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decrease acid secretion
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give the effect atropine would have on the gut
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decrease motility
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give the effect atropine would have on the bladder
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decrease urgency in cystitis
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what would an atropine toxicity look like
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increase body temp; rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation
SE: Hot as a hare Dry as a bone Red as a beet Blind as a bat Mad as a hatter |
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watch out cuz atropine can cause this in the elderly
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acute angle-closure glaucoma
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watch out cuz atropine can cause this in men with BPH
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urinary retention
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watch out cuz atropine can cause this in infants
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hyperthermia
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mechanism of hexamethonium
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nicotinic ACh receptor antagoinist
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hexamethonium clinical use
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ganglionic blocker. Used in experimental models to prevent vagal reflex responses to changes in blood pressue -- e.g., prevents reflex bradycardia caused by NE
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this catecholamine sympathomimetic is a derect general agonist (α1α2β1β2). It is used for open angle glaucoma, asthma, and hypotension
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epinephrine
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this catecholamine sympathomimetic acts on α1α2β1. It is used for hypotension (but decreases renal perfusion)
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NE
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this catecholamine sympathomimetic acts on β1=β2. It is used for AV block (rarely)
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Isoproterenol
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this catecholamine sympathomimetic acts on D1=D2>β>α. It is used for shock(increases renal perfusion), heart failure
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Dopamine
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this catecholamine sympathomimetic acts on β1>B2. It is used for shock and heart failure
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dobutamine
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this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for narcolepsy, obesity, ADD.
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amphetamine
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this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for nasal decongestion, urinary incontinance, hypotension
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ephedrine
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this sympathomimetic acts on α1>α2. It is used as a pupil dilator, vasoconstrictor, and nasal decongestor.
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phenylephrine
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this sympathomimetic acts on β2>β1. It is used for asthma
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albuterol, terbutaline
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this sympathomimetic is an indirect general agonist which releases stored and uptake inhibitor . It causes vasoconstriction and local anesthesia
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cocaine
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this sympathomimetic is a centrally acting α-agonist which decreases central adrenergic outflow. It is used for hypertension, especially with no renal dz (no decrease in blood flow to the kidney)
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clonadine
α-methyldopa |
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image [sympathomimetics p. 203]
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--
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this nonselective α-blocker is used for pheochromocytoma. Toxicity can cause orthostatic hypotension and reflex tachycardia.
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Phenoxybenzamine (irreversible) and pentolamine (reversable)
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This α1 selective blocker is used for hypertension, urinary retension in BPH. Toxicities include 1st dose orthostatic hypotension, idzziness, headache.
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prazosin, terazosin, doxazosin
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this α2 selective blocker is used for depression. Toxicity includes sedation, increased serum cholesterol and increased appetite
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mirtazapine
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image. p. 204- effects of α-blockers on blood pressure responses to epi and phenylephrine.
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the peinephrine response exhibits a reversal of the mean BP change, from a net increase (the α response) to a net decrease (the B2 response). The response to phenylephrine is supressed but not reversed because the phenylephrine is a "pure" α agonist w/out B action
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name some beta blockers
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propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
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how do the β blockers effect hypertension
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decrease cardiac output, decrease renin secretion
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how do the β blockers effect angina pectoris
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decreasee HR & contractility, resulting in less O2 consumption
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how do the β blockers effect MI
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decrease mortality
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how do the β blockers effect SVT (propranolol, esmolol only)
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decrease AV conduction velocity
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how do the β blockers effect CHF
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slows progression of chronic failure
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how do the β blockers effect glaucoma(timolol only)
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decreases secretion of aqueous humor
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give some toxicities of β blockers
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impotensce, exacerbation of asthma, bradycardia, AV block, CHF, sedation, sleep alteration; use w/ caution in dbts
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give the nonselective (B1=B2) B blockers
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propranolol, timolol, nadolol, pindolol (partial agonist), and labetalol (partial agonist)
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give the B1 selective (B1>B2) B blockers
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Acebutolol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol
mneu: A BEAM of B1 blockers |
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this Rx for glaucoma is an α agonist. It acts by increasing the outflow of aqueous humor. Its SE include mydriasis, stinging. This drug should not be used in closed- angle glaucoma
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epinephrine
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this Rx for glaucoma is an α agonist. It acts by decreasing aqueous humor synthesis. It does not cause and pupillary or vision changes.
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Brimonidine
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this Rx for glaucoma is a β blocker. It acts by decreasing aqueous humor secretion. It does not cause and pupillary or vision changes.
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timolol, betaxolol, carteolol
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this Rx for glaucoma is a diuretic. It acts by decreasing aqueous humor secretion due to decreased HCO3- via inhibition of carbonic anhydrase. It does not cause and pupillary or vision changes.
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Acetazolamide
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this Rx for glaucoma is a cholinomimetic. It acts by increaseing outflow of aqueous humor by contracting the ciliary mm and opening the trabecular meshwork. SE include miosis and cyclospasm
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pilocarpine, carbachol, physostigmine, echothiophate
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this Rx for glaucoma is a prostaglandin. It acts by increaseing outflow of aqueous humor. SE include darkening of the iris (browning)
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lantanoprost (PGF2α0
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what is the anitidote/tx for acetaminophen overdose
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N-acetylcysteine
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what is the anitidote/tx for salicylate overdose
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alkanize urine, dialysis
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what is the anitidote/tx for anticholinesterases, organophosphatesoverdose
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atropine, pralidoxime
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what is the anitidote/tx for antimuscarinic, anticholinergic agentsoverdose
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physostigmine salicylate
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what is the anitidote/tx for B-blocker overdose
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glucagon
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what is the anitidote/tx for digatis overdose
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stop dig, normalize K+, lidocaine, anti-dig Fab fragments, Mg++
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what is the anitidote/tx for iron overdose
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deferoxamine
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what is the anitidote/tx for lead overdose
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CaEDTA, dimercaprol, succimer, penicillamine
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what is the anitidote/tx for arsenic, mercury, gold overdose
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Dimercaprol (BAL), succimer
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what is the anitidote/tx for copper, arsenic, gold overdose
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penicillamine
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what is the anitidote/tx for cyanide overdose
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nitrite, hydroxycobalamin, thiosulfate
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what is the anitidote/tx for methemoglobin overdose
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methylene blue
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what is the anitidote/tx for CO overdose
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100% O2, hyperbaric O2
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what is the anitidote/tx for methanol, ethylene glycol (antifreeze) overdose
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ethanol, dialysis, fomepizole
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what is the anitidote/tx for opiods overdose
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naloxone/naltrexone
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what is the anitidote/tx for benzodiazepines overdose
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flumazenil
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what is the anitidote/tx for TCAs overdose
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NaHCO3 (nonspecific
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what is the anitidote/tx for heparin overdose
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protamine
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what is the anitidote/tx for warfarin overdose
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vitamin K, fresh frozen plasma
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what is the anitidote/tx for tPA, streptokinase overdose
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aminocaproic acid
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give some signs of lead poisioning
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Lead Lines on gingivae and on epiphyses of long bones on x-ray
Encephalopathy and Erythrocyte basophilic stippling Abdominal colic and sideroblastic Anemia Drops--wrist and foot drop mneu: LEAD |
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what is the tx for Lead poisoning in adults and kids
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adults: Dimercarol and EDTA
kids: Succimer mneu: It "sucks" to be a kid with lead poisoning |
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when someone ODs on a weak acid (phenobarbital, methotrexate, aspirine) what do you do
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alkalinize urine with bicarb to increase clearance
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when someone ODs on weak bases (e.g., amphetamines) what do you do
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acidify urine to increase clearance (give NH4Cl)
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someone comes in with atropine like side effects. What do you suspect
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tricyclics
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someone comes in with cardiac toxicity. what do you suspect?
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doxorubicin (adriamycin), daunorubicin
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someone comes in with coronary vasospasm. what do you suspect?
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cocaine
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someone comes in with cutaneous flushing. what do you suspect?
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niacin, Ca++ channel blockers, adenosine, vancomycin
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someone comes in with torsades de pointes. what do you suspect?
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class III (sotalol, class IA (quinidine) antiarrhythmics, cisapride
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someone comes in with agranulocytosis. what do you suspect?
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clozapine, carbamazepine, colchicine
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someone comes in with aplastic anemia . what do you suspect?
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chloramphenicol, benzene, NSAIDS
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someone comes in with grey baby syndrome. what do you suspect?
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chloramphenicol
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someone comes in with hemolysis in G6PD-deficient pts. what do you suspect?
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sulfonamines, isoniazid (INH, aspirin, ibuprofen, primaquine, nitrofurantoine
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someone comes in with thrombotic complications. what do you suspect?
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OCPs (e.g., estrogens and progestins)
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someone comes in with cough. what do you suspect?
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ACE inhibitors (losartan-no cough)
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someone comes in with pulmonary fibrosis. what do you suspect?
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bleomycin, amiodarone, busulfan
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someone comes in with acute cholestatic hepatitis. what do you suspect?
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macrolides
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someone comes in with focal to massive hepatic necrosis. what do you suspect?
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halothane, valproic acid, acetaminophen, amanita phalloides
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someone comes in with hepatitis. what do you suspect?
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INH
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someone comes in with pseudomembranous colitis. what do you suspect?
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clindamycin, ampicillin
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someone comes in with adrenocortical insufficency. what do you suspect?
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glucocorticoid withdrawal (HPA supression
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someone comes in with gynomastia. what do you suspect?
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Spironolactone, Digitalis, Cimetidine, Alcoholism, estrogens, Ketoconazole
mneu: Some Drugs Create Awesom Knockers |
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someone comes in with hot flashes. what do you suspect?
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tamoxifin
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someone comes in with gingival hyperplasia. what do you suspect?
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phenytoin
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someone comes in with osteoporosis. what do you suspect?
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corticosteroids, heparin
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someone comes in with photosensitivity. what do you suspect?
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Sulfonamindes, Amiodarone, Tetracycline
mneu: SAT for a photo |
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someone comes in with SLE like syndrome. what do you suspect?
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Hydralazine, INH, Procainamide, Phenytoin
mneu: it's not HIPP to have lupus |
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someone comes in with tendonitis, tendon rupture, and cartilage damage (kids). what do you suspect?
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fluoroquinolones
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someone comes in with Fanconi's syndrome. what do you suspect?
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expired tetracycline
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someone comes in with interstitial nephritis. what do you suspect?
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methacillin
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someone comes in with hemorrhagic cystitis. what do you suspect?
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cyclophosphamide, ifosfamide
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someone comes in with cinchonism. what do you suspect?
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quinidine, quinine
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someone comes in with diabetes insipidus. what do you suspect?
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lithium, demeclocycline
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someone comes in with seizures. what do you suspect?
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bupropion, imipenem/cilastin
|
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someone comes in with tarditive dyskinesia. what do you suspect?
|
antipsychotics
|
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someone comes in with disulfram-like reaction. what do you suspect?
|
metronidazole, certain cephalosporins, procarbazine, sulfonyurease
|
|
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someone comes in with nephrotoxicity/neurotoxicity. what do you suspect?
|
polymyxins
|
|
|
someone comes in with nephrotoxicity/ototoxicity. what do you suspect?
|
aminoglycosides, loop diuretics, cysplatin
|
|
|
P-450 inducers
|
Quinidine
Barbituates Phenytoin Rifampin Griseofulvin Carbamazapine mneu: Queen Barb takes Phen-Phen and Refuses Greasy Carbs |
|
|
P-450 inhibitors
|
Isoniazid
Sulfonamides Cimetidine Ketoconazole Erythromycin Grapefruit juice St. John's wort mneu: Inhibitors Stop Cyber Kids from Eating GrapefruitS |
|
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alcohol toxicity p. 208
|
--
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ethylene glycol is transformed into oxalic acid by alcohol dehydrogenase which can have this result
|
acidosis, nephrotoxicity
|
|
|
methanol is transformed into formaldehyde and formic acid by alcohol dehydrogenase which can have this result
|
severe acidosis, retinal damage
|
|
|
ethanol is transformed into acetic acid and acetaldehyde by alcohol dehydrogenase. Acetaldehyde can have this result
|
nausea, vomiting, headache, hypotension
|
|
|
ethanol is a competitive substrate for this hormone
|
ADH
|
|
|
this herbal agent is sometimes used for the common cold. Toxicities can be GI distress, dizziness, and headache
|
echinacea
|
|
|
this herbal agent is sometimes used as a stimulent. Toxicities can be CNS and CV stimulation, arrhythmias, stroke, and seizures at high doses
|
ephedra
|
|
|
this herbal agent is sometimes used for migranes. Toxicities can be GI distress, ulcers, antiplatelet actions
|
feverfew
|
|
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this herbal agent is sometimes used for the intermittent claudication. Toxicities can be GI distress, anxiety, insomnia, headache, and antiplatelet action
|
ginkgo
|
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this herbal agent is sometimes used for anxiety. Toxicities can be GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity
|
Kava
|
|
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this herbal agent is sometimes used for viral hepatitis. Toxicities can be loose stools
|
milk thistle
|
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this herbal agent is sometimes used for BPH. Toxicities can be GI distress, decreased libido, hypertension
|
Saw palmetto
|
|
|
this herbal agent is sometimes used for mild to moderate depression. Toxicities can be GI distress, phototoxicity, serotonin syndrome with SSRI, inhibits P-450 system
|
St. Johns wart
|
|
|
this herbal agent is sometimes used for symptomatic improvement in females with SLE or AIDS. Toxicities can include androgenization (premenopausal women), estrogenic effects (postmenopausal), feminization (young men)
|
Dehydroepiandrosterone
|
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|
this herbal agent is sometimes used for jet lag and sinsomnia. Toxicities can be sedation, suppresses midcycle LH, hypoprolactemia
|
melatonin
|
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|
drugs ending in -afil, are usually for . . .
|
erectile dysfunction
e.g., Sildenafil |
|
|
drugs ending in -ane, are usually for . . .
|
inhalational general anesthetic
e.g., halothane |
|
|
drugs ending in -azepam, are usually . . .
|
benzodiazepines
e.g. diazepam |
|
|
drugs ending in -azine, are usually . . .
|
phenothiazines (neuroleptics, antiemetics)
e.g., chlorpromazine |
|
|
drugs ending in -azole, are usually . . .
|
antifungals
e.g., ketoconazole |
|
|
drugs ending in -barbital, are usually . . .
|
barbiturates
e.g., phenobarbital |
|
|
drugs ending in -caine, are usually . . .
|
local anesthetics
e.g., lidocaine |
|
|
drugs ending in -cillin, are usually . . .
|
penicillins
e.g., methicillin |
|
|
drugs ending in -cycline, are usually . . .
|
antibiotic, protein synthesis inhibitors
e.g., tetracycline |
|
|
drugs ending in -ipramine, are usually . . .
|
TCA
e.g., imipramine |
|
|
drugs ending in -navir, are usually . . .
|
protease inhibitors
e.g., saquinavir |
|
|
drugs ending in -olol, are usually . . .
|
Beta agonist
e.g., propranolol |
|
|
drugs ending in -operidol, are usually . . .
|
Butyrophenones (neuroleptics)
e.g., haloperidol |
|
|
drugs ending in -oxins, are usually . . .
|
cardiac glycosides (inotropic agents)
e.g., digoxin |
|
|
drugs ending in -phylline, are usually . . .
|
methylxanthine
e.g., theophylline |
|
|
drugs ending in -pril, are usually . . .
|
ACE inhibitors
e.g., Captopril |
|
|
drugs ending in -terol, are usually . . .
|
beta2 agonist
e.g., albuterol |
|
|
drugs ending in -tidine, are usually . . .
|
H2 antagonist
e.g., cemetidine |
|
|
drugs ending in -triptyline, are usually . . .
|
TCA
e.g., amitriptyline |
|
|
drugs ending in -tropin, are usually . . .
|
pituitary hormone
e.g., somatotropin |
|
|
drugs ending in -zosin, are usually . . .
|
alpha1 antagonist
e.g., prazosin |
