Pharm 1 USMLE Flashcards
1
Q
28 y/o chemist presents w/ MPTP exposuree. what NT is depleted
A
dopamine
2
Q
woman taking tetracycline exhibits photosensitivity. What are the clinical manifestations?
A
rash on sun exposed retions of body
3
Q
African American man who goes to Africa develops a hemolytic anemia after taking malarial prophylaxis. what is the enzyme deficiency
A
glucose 6 phosphate dehydrogenase
4
Q
farmer presents w/ dyspnea, salivation, miosis, diarrhea, cramping, and blurry vision. What caused this, and what is the MOA
A
insecticide poisoning; inhibition of acetylcholinesterase
5
Q
27 y/o female w/ hx of psych illness now has urinary retention due to a neuroleptic. What do you tx it with?
A
bethancechol
6
Q
pt w/ recent kidney transplant is on cyclosporine for immunosuppression. Requires antifungal agent for candidiasis. What antifungal drug would result in cyclosporine toxicity
A
ketoconazole
7
Q
pt is on carbamazepine. What routine workup should always be done?
A
LFTs
8
Q
23 y/o female who is on rifampin for TB prophylaxis and on birth control (estrogen) gets pregnant. why
A
rifampin augments estrogen metabolism in the liver, rendering it less effective
9
Q
what is the volume of distribution
A
relates the amount of drug in the body to the plasma concentration
=amount of drug in body/plasma drug concentration
10
Q
Vd of plasma protein bound drugs can be altered by dzs in these 2 organ systems
A
liver and kidney
11
Q
what is clearance (CL)
A
relates the rate of elimination to the plasma concentration
Cl=rate of elimination of drug/plasma drug concentration
12
Q
what is the half life (t1/2)
A
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
13
Q
what is concentration of drug in the body after 1 half life
A
50%
14
Q
what is concentration of drug in the body after 2 half lives
A
75%
15
Q
what is concentration of drug in the body after 3 half lives
A
87.5%
16
Q
what is concentration of drug in the body after 4 half lives
A
~94%
17
Q
Cp =
A
target plasma concentration
18
Q
F=
A
bioavalability
19
Q
Loading dose=
A
Cp x Vd/F
20
Q
maintenance dose=
A
CpxCL/F
21
Q
what happens to the loading dose and maitenance dose in pts will impared renal or hepatic fxn
A
loading dose remains the same
maitenence dose is decreased
22
Q
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)
A
zero order elimination
image. p. 195
23
Q
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.
A
first order elimination
image. p. 195
24
Q
In drugs with 1st order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
A
proportional to
25
In drugs with 0 order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
independant of
26
give some examples of phase I metabolism
reduction, oxidation, hydrolysis.
27
describe the metabolites of phase I metabolism(aka are they active)
slightly polar, water soluble, often still active
28
give some examples of phase II metabolism
acetylation, glucuronidation, sulfation
29
describe the metabolites of phase II metabolism(aka are they active)
yields very polar, inactive metabolites (renally excreted
30
what pump is key in phase I metabolism
cytocrome P-450
31
by what method are drugs metabolized in phase II metabolism
conjugation
32
what phase of metabolism do geriatric pts lose first
phase I
33
competitive antagonist shifts the curve _______
to the right
34
noncompetitive antagonist shifts the curve ______
downward
35
EC50:
dose causing 50% of maximal effect.
36
Kd:
concentration of drug required to bind 50% of receptor sites
37
image p. 196-percent of maximum efect as a fx of dose
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.
38
image p. 197-percent of maximum efect as a fx of dose
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
39
what is the therapeutic index
mean toxic dose/mean effective dose
TD50/ED50
high TI is good
40
on average how long does it take for a drug to be in In-vitro stidues
2 yts
41
on average how long does it take for a drug to be in animal stidues
2 years
42
this phase of clinical testing for a drugs looks at if it is safe, and the pharmakinetics
phase 1
43
this phase of clinical testing for a drugs looks at if it works in pts
phase 2
44
this phase of clinical testing for a drugs looks at does it work, in a double blind study
phase 3
45
this phase drug development involves postmarketing surveillance
phase 4
46
On average how many years of drug development does it take to file a NDA (new drug application)
9
47
how long after filing of application does patent expire on a drug and generics become available
20 years
48
given the receptor, give the G-protein class and the major fx: α1
increases vascular smooth mm contraction
G protien class: q
49
given the receptor, give the G-protein class and the major fx: α2
Decrease sympathetic outflow, decrease insulin release
G protien class: i
50
given the receptor, give the G-protein class and the major fx: ϐ1
increase heart rate, increase contractility, increase renin release, increase lipolysis, incease aqueous humor formation
G protien class: s
51
given the receptor, give the G-protein class and the major fx: ϐ2
vasodilation, bronchodilation, increase glucagon release
G protien class: s
52
given the receptor, give the G-protein class and the major fx: M1
CNS
| G protien class: q
53
given the receptor, give the G-protein class and the major fx: M2
decrease heart rate
G protein class: i
54
given the receptor, give the G-protein class and the major fx: M3
increase exocrine gland secretions
G protein class: q
55
given the receptor, give the G-protein class and the major fx: D1
relaxes renal vascular sm mm
G protein class: s
56
given the receptor, give the G-protein class and the major fx: D2
modulates NT release, esp in the brain
G protein class:i
57
given the receptor, give the G-protein class and the major fx: H1
increase nasal and bronchial mucus production, contraction of bronchioles, pruritis, and pain
G protein class:q
58
given the receptor, give the G-protein class and the major fx: H2
increase gastric acid secretion
G-protein class:s
59
given the receptor, give the G-protein class and the major fx: V1
increase vascular sm mm contraction
G-protein class:q
60
given the receptor, give the G-protein class and the major fx: V2
increase H2O permeability and reabsorption in the collecting tubules of the kidney
G-protein class:s
61
release of NE from a sympathetic nn ending is modulated by ______, acting on these receptors.
NE, ACH, ATN II, othr substances
presynaptic α2 autoreceptors
62
Bethanechol is a cholinomimetic with direct agonist actions. Give its clinical applications
postop and neurogenic ileus and urinary retention
it acts by activating Bowel & Bladder smooth mm. It is resistant to AChE
63
Carbachol, pilocarpine is a cholinomimetic with direct agonist actions. Give its clinical applications
Used for glaucoma
it activates ciliary mm of eye (open angle), pupillary sphicter (narrow angle); It is resistant to AChe
64
Neostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
postop & neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular jxn blockade (postop)
It acts by inceasing endogenous ACh
65
Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
used to tx myasthenia gravis
It acts by inceasing endogenous ACh, thereby increasing strength
66
Edrophonium is a Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
myasthenia gravis (short acting)
It acts by inceasing endogenous ACh
67
physostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
glaucoma (crosses blood brain barrier) and atropine OD
works by increasing endogenous ACh
68
Echothiophateis a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
Glaucoma
works by increasing endogenous ACh
69
give some signs of cholinesterase inhibitor poisoning
Diarrhea (abd cramping), Urination, Miosis, Bronchospasm, Bradycardia, Exitation of skeletal mm and CNS, Lacrimation, Sweating, and Salivation,
mneu: DUMBBELSS
or SLUD effects
70
what can cause cholinesterase inhibitor poisoning
Parathion and other organophosphates
71
how do you tx cholinesterase inhibitor poisoning
Antidote--atropine (muscarinic antagonist) plus pralidoxime (chemical antagonist used to regenerate active cholinesterase)
72
Atropine, homotropine, and tropicamide are cholinoreceptor blockers taht act on they eye to do what?
produce mydriasis and cycloplegia
73
Benzotropine is a cholinoreceptor blocker that acts on the CNS to tx?
Parkinson's dz
74
Scopolamine is a cholinoreceptor blocker that acts on the CNS to tx?
Motion skickness
75
Ipratropium is a cholinoreceptor blocker that acts on the Respiratory system to tx?
Asthma, COPD
76
Methscopolamine, oxybutin, glycopyrrolateis a cholinoreceptor blocker that acts on the GU system to tx?
urgency in mild cystitis and reduce bladder spasms
77
atropine is a muscarinic _______
antagoinist
mneu: blocks SLUD:
salivation, Lacrimation, Urination, Defication
78
give the effect atropine would have on the eye
pupil dilation, cycloplegia
79
give the effect atropine would have on the airway
decrease secretions
80
give the effect atropine would have on the stomach
decrease acid secretion
81
give the effect atropine would have on the gut
decrease motility
82
give the effect atropine would have on the bladder
decrease urgency in cystitis
83
what would an atropine toxicity look like
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
```
84
watch out cuz atropine can cause this in the elderly
acute angle-closure glaucoma
85
watch out cuz atropine can cause this in men with BPH
urinary retention
86
watch out cuz atropine can cause this in infants
hyperthermia
87
mechanism of hexamethonium
nicotinic ACh receptor antagoinist
88
hexamethonium clinical use
ganglionic blocker. Used in experimental models to prevent vagal reflex responses to changes in blood pressue -- e.g., prevents reflex bradycardia caused by NE
89
this catecholamine sympathomimetic is a derect general agonist (α1α2β1β2). It is used for open angle glaucoma, asthma, and hypotension
epinephrine
90
this catecholamine sympathomimetic acts on α1α2β1. It is used for hypotension (but decreases renal perfusion)
NE
91
this catecholamine sympathomimetic acts on β1=β2. It is used for AV block (rarely)
Isoproterenol
92
this catecholamine sympathomimetic acts on D1=D2>β>α. It is used for shock(increases renal perfusion), heart failure
Dopamine
93
this catecholamine sympathomimetic acts on β1>B2. It is used for shock and heart failure
dobutamine
94
this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for narcolepsy, obesity, ADD.
amphetamine
95
this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for nasal decongestion, urinary incontinance, hypotension
ephedrine
96
this sympathomimetic acts on α1>α2. It is used as a pupil dilator, vasoconstrictor, and nasal decongestor.
phenylephrine
97
this sympathomimetic acts on β2>β1. It is used for asthma
albuterol, terbutaline
98
this sympathomimetic is an indirect general agonist which releases stored and uptake inhibitor . It causes vasoconstriction and local anesthesia
cocaine
99
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)
clonadine
| α-methyldopa
100
this nonselective α-blocker is used for pheochromocytoma. Toxicity can cause orthostatic hypotension and reflex tachycardia.
Phenoxybenzamine (irreversible) and pentolamine (reversable)
101
This α1 selective blocker is used for hypertension, urinary retension in BPH. Toxicities include 1st dose orthostatic hypotension, idzziness, headache.
prazosin, terazosin, doxazosin
102
this α2 selective blocker is used for depression. Toxicity includes sedation, increased serum cholesterol and increased appetite
mirtazapine
103
image. p. 204- effects of α-blockers on blood pressure responses to epi and phenylephrine.
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
104
name some beta blockers
propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
105
how do the β blockers effect hypertension
decrease cardiac output, decrease renin secretion
106
how do the β blockers effect angina pectoris
decreasee HR & contractility, resulting in less O2 consumption
107
how do the β blockers effect MI
decrease mortality
108
how do the β blockers effect SVT (propranolol, esmolol only)
decrease AV conduction velocity
109
how do the β blockers effect CHF
slows progression of chronic failure
110
how do the β blockers effect glaucoma(timolol only)
decreases secretion of aqueous humor
111
give some toxicities of β blockers
impotensce, exacerbation of asthma, bradycardia, AV block, CHF, sedation, sleep alteration; use w/ caution in dbts
112
give the nonselective (B1=B2) B blockers
propranolol, timolol, nadolol, pindolol (partial agonist), and labetalol (partial agonist)
113
give the B1 selective (B1>B2) B blockers
Acebutolol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol
mneu: A BEAM of B1 blockers
114
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
epinephrine
115
this Rx for glaucoma is an α agonist. It acts by decreasing aqueous humor synthesis. It does not cause and pupillary or vision changes.
Brimonidine
116
this Rx for glaucoma is a β blocker. It acts by decreasing aqueous humor secretion. It does not cause and pupillary or vision changes.
timolol, betaxolol, carteolol
117
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.
Acetazolamide
118
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
pilocarpine, carbachol, physostigmine, echothiophate
119
this Rx for glaucoma is a prostaglandin. It acts by increaseing outflow of aqueous humor. SE include darkening of the iris (browning)
lantanoprost (PGF2α0
120
what is the anitidote/tx for acetaminophen overdose
N-acetylcysteine
121
what is the anitidote/tx for salicylate overdose
alkanize urine, dialysis
122
what is the anitidote/tx for anticholinesterases, organophosphatesoverdose
atropine, pralidoxime
123
what is the anitidote/tx for antimuscarinic, anticholinergic agentsoverdose
physostigmine salicylate
124
what is the anitidote/tx for B-blocker overdose
glucagon
125
what is the anitidote/tx for digatis overdose
stop dig, normalize K+, lidocaine, anti-dig Fab fragments, Mg++
126
what is the anitidote/tx for iron overdose
deferoxamine
127
what is the anitidote/tx for lead overdose
CaEDTA, dimercaprol, succimer, penicillamine
128
what is the anitidote/tx for arsenic, mercury, gold overdose
Dimercaprol (BAL), succimer
129
what is the anitidote/tx for copper, arsenic, gold overdose
penicillamine
130
what is the anitidote/tx for cyanide overdose
nitrite, hydroxycobalamin, thiosulfate
131
what is the anitidote/tx for methemoglobin overdose
methylene blue
132
what is the anitidote/tx for CO overdose
100% O2, hyperbaric O2
133
what is the anitidote/tx for methanol, ethylene glycol (antifreeze) overdose
ethanol, dialysis, fomepizole
134
what is the anitidote/tx for opiods overdose
naloxone/naltrexone
135
what is the anitidote/tx for benzodiazepines overdose
flumazenil
136
what is the anitidote/tx for TCAs overdose
NaHCO3 (nonspecific
137
what is the anitidote/tx for heparin overdose
protamine
138
what is the anitidote/tx for warfarin overdose
vitamin K, fresh frozen plasma
139
what is the anitidote/tx for tPA, streptokinase overdose
aminocaproic acid
140
give some signs of lead poisioning
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
141
what is the tx for Lead poisoning in adults and kids
adults: Dimercarol and EDTA
kids: Succimer
mneu: It "sucks" to be a kid with lead poisoning
142
when someone ODs on a weak acid (phenobarbital, methotrexate, aspirine) what do you do
alkalinize urine with bicarb to increase clearance
143
when someone ODs on weak bases (e.g., amphetamines) what do you do
acidify urine to increase clearance (give NH4Cl)
144
someone comes in with atropine like side effects. What do you suspect
tricyclics
145
someone comes in with cardiac toxicity. what do you suspect?
doxorubicin (adriamycin), daunorubicin
146
someone comes in with coronary vasospasm. what do you suspect?
cocaine
147
someone comes in with cutaneous flushing. what do you suspect?
niacin, Ca++ channel blockers, adenosine, vancomycin
148
someone comes in with torsades de pointes. what do you suspect?
class III (sotalol, class IA (quinidine) antiarrhythmics, cisapride
149
someone comes in with agranulocytosis. what do you suspect?
clozapine, carbamazepine, colchicine
150
someone comes in with aplastic anemia . what do you suspect?
chloramphenicol, benzene, NSAIDS
151
someone comes in with grey baby syndrome. what do you suspect?
chloramphenicol
152
someone comes in with hemolysis in G6PD-deficient pts. what do you suspect?
sulfonamines, isoniazid (INH, aspirin, ibuprofen, primaquine, nitrofurantoine
153
someone comes in with thrombotic complications. what do you suspect?
OCPs (e.g., estrogens and progestins)
154
someone comes in with cough. what do you suspect?
ACE inhibitors (losartan-no cough)
155
someone comes in with pulmonary fibrosis. what do you suspect?
bleomycin, amiodarone, busulfan
156
someone comes in with acute cholestatic hepatitis. what do you suspect?
macrolides
157
someone comes in with focal to massive hepatic necrosis. what do you suspect?
halothane, valproic acid, acetaminophen, amanita phalloides
158
someone comes in with hepatitis. what do you suspect?
INH
159
someone comes in with pseudomembranous colitis. what do you suspect?
clindamycin, ampicillin
160
someone comes in with adrenocortical insufficency. what do you suspect?
glucocorticoid withdrawal (HPA supression
161
someone comes in with gynomastia. what do you suspect?
Spironolactone, Digitalis, Cimetidine, Alcoholism, estrogens, Ketoconazole
mneu: Some Drugs Create Awesom Knockers
162
someone comes in with hot flashes. what do you suspect?
tamoxifin
163
someone comes in with gingival hyperplasia. what do you suspect?
phenytoin
164
someone comes in with osteoporosis. what do you suspect?
corticosteroids, heparin
165
someone comes in with photosensitivity. what do you suspect?
Sulfonamindes, Amiodarone, Tetracycline
mneu: SAT for a photo
166
someone comes in with SLE like syndrome. what do you suspect?
Hydralazine, INH, Procainamide, Phenytoin
mneu: it's not HIPP to have lupus
167
someone comes in with tendonitis, tendon rupture, and cartilage damage (kids). what do you suspect?
fluoroquinolones
168
someone comes in with Fanconi's syndrome. what do you suspect?
expired tetracycline
169
someone comes in with interstitial nephritis. what do you suspect?
methacillin
170
someone comes in with hemorrhagic cystitis. what do you suspect?
cyclophosphamide, ifosfamide
171
someone comes in with cinchonism. what do you suspect?
quinidine, quinine
172
someone comes in with diabetes insipidus. what do you suspect?
lithium, demeclocycline
173
someone comes in with seizures. what do you suspect?
bupropion, imipenem/cilastin
174
someone comes in with tarditive dyskinesia. what do you suspect?
antipsychotics
175
someone comes in with disulfram-like reaction. what do you suspect?
metronidazole, certain cephalosporins, procarbazine, sulfonyurease
176
someone comes in with nephrotoxicity/neurotoxicity. what do you suspect?
polymyxins
177
someone comes in with nephrotoxicity/ototoxicity. what do you suspect?
aminoglycosides, loop diuretics, cysplatin
178
P-450 inducers
```
Quinidine
Barbituates
Phenytoin
Rifampin
Griseofulvin
Carbamazapine
```
mneu: Queen Barb takes Phen-Phen and Refuses Greasy Carbs
179
P-450 inhibitors
```
Isoniazid
Sulfonamides
Cimetidine
Ketoconazole
Erythromycin
Grapefruit juice
St. John's wort
```
mneu: Inhibitors Stop Cyber Kids from Eating GrapefruitS
180
ethylene glycol is transformed into oxalic acid by alcohol dehydrogenase which can have this result
acidosis, nephrotoxicity
181
methanol is transformed into formaldehyde and formic acid by alcohol dehydrogenase which can have this result
severe acidosis, retinal damage
182
ethanol is transformed into acetic acid and acetaldehyde by alcohol dehydrogenase. Acetaldehyde can have this result
nausea, vomiting, headache, hypotension
183
ethanol is a competitive substrate for this hormone
ADH
184
this herbal agent is sometimes used for the common cold. Toxicities can be GI distress, dizziness, and headache
echinacea
185
this herbal agent is sometimes used as a stimulent. Toxicities can be CNS and CV stimulation, arrhythmias, stroke, and seizures at high doses
ephedra
186
this herbal agent is sometimes used for migranes. Toxicities can be GI distress, ulcers, antiplatelet actions
feverfew
187
this herbal agent is sometimes used for the intermittent claudication. Toxicities can be GI distress, anxiety, insomnia, headache, and antiplatelet action
ginkgo
188
this herbal agent is sometimes used for anxiety. Toxicities can be GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity
Kava
189
this herbal agent is sometimes used for viral hepatitis. Toxicities can be loose stools
milk thistle
190
this herbal agent is sometimes used for BPH. Toxicities can be GI distress, decreased libido, hypertension
Saw palmetto
191
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
192
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
193
this herbal agent is sometimes used for jet lag and sinsomnia. Toxicities can be sedation, suppresses midcycle LH, hypoprolactemia
melatonin
194
drugs ending in -afil, are usually for . . .
erectile dysfunction
e.g., Sildenafil
195
drugs ending in -ane, are usually for . . .
inhalational general anesthetic
e.g., halothane
196
drugs ending in -azepam, are usually . . .
benzodiazepines
e.g. diazepam
197
drugs ending in -azine, are usually . . .
phenothiazines (neuroleptics, antiemetics)
e.g., chlorpromazine
198
drugs ending in -azole, are usually . . .
antifungals
e.g., ketoconazole
199
drugs ending in -barbital, are usually . . .
barbiturates
e.g., phenobarbital
200
drugs ending in -caine, are usually . . .
local anesthetics
e.g., lidocaine
201
drugs ending in -cillin, are usually . . .
penicillins
e.g., methicillin
202
drugs ending in -cycline, are usually . . .
antibiotic, protein synthesis inhibitors
e.g., tetracycline
203
drugs ending in -ipramine, are usually . . .
TCA
e.g., imipramine
204
drugs ending in -navir, are usually . . .
protease inhibitors
e.g., saquinavir
205
drugs ending in -olol, are usually . . .
Beta agonist
e.g., propranolol
206
drugs ending in -operidol, are usually . . .
Butyrophenones (neuroleptics)
e.g., haloperidol
207
drugs ending in -oxins, are usually . . .
cardiac glycosides (inotropic agents)
e.g., digoxin
208
drugs ending in -phylline, are usually . . .
methylxanthine
e.g., theophylline
209
drugs ending in -pril, are usually . . .
ACE inhibitors
e.g., Captopril
210
drugs ending in -terol, are usually . . .
beta2 agonist
e.g., albuterol
211
drugs ending in -tidine, are usually . . .
H2 antagonist
e.g., cemetidine
212
drugs ending in -triptyline, are usually . . .
TCA
e.g., amitriptyline
213
drugs ending in -tropin, are usually . . .
pituitary hormone
e.g., somatotropin
214
drugs ending in -zosin, are usually . . .
alpha1 antagonist
e.g., prazosin
