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224 Cards in this Set

  • Front
  • Back
28 y/o chemist presents w/ MPTP exposuree. what NT is depleted
dopamine
woman taking tetracycline exhibits photosensitivity. What are the clinical manifestations?
rash on sun exposed retions of body
African American man who goes to Africa develops a hemolytic anemia after taking malarial prophylaxis. what is the enzyme deficiency
glucose 6 phosphate dehydrogenase
farmer presents w/ dyspnea, salivation, miosis, diarrhea, cramping, and blurry vision. What caused this, and what is the MOA
insecticide poisoning; inhibition of acetylcholinesterase
27 y/o female w/ hx of psych illness now has urinary retention due to a neuroleptic. What do you tx it with?
bethancechol
pt w/ recent kidney transplant is on cyclosporine for immunosuppression. Requires antifungal agent for candidiasis. What antifungal drug would result in cyclosporine toxicity
ketoconazole
pt is on carbamazepine. What routine workup should always be done?
LFTs
23 y/o 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
what is the volume of distribution
relates the amount of drug in the body to the plasma concentration

=amount of drug in body/plasma drug concentration
Vd of plasma protein bound drugs can be altered by dzs in these 2 organ systems
liver and kidney
what is clearance (CL)
relates the rate of elimination to the plasma concentration

Cl=rate of elimination of drug/plasma drug concentration
what is the half life (t1/2)
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
what is concentration of drug in the body after 1 half life
50%
what is concentration of drug in the body after 2 half lives
75%
what is concentration of drug in the body after 3 half lives
87.5%
what is concentration of drug in the body after 4 half lives
~94%
Cp =
target plasma concentration
F=
bioavalability
Loading dose=
Cp x Vd/F
maintenance dose=
CpxCL/F
what happens to the loading dose and maitenance dose in pts will impared renal or hepatic fxn
loading dose remains the same
maitenence dose is decreased
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)
zero order elimination
image. p. 195
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.
first order elimination
image. p. 195
In drugs with 1st order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
proportional to
In drugs with 0 order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
independant of
give some examples of phase I metabolism
reduction, oxidation, hydrolysis.
describe the metabolites of phase I metabolism(aka are they active)
slightly polar, water soluble, often still active
give some examples of phase II metabolism
acetylation, glucuronidation, sulfation
describe the metabolites of phase II metabolism(aka are they active)
yields very polar, inactive metabolites (renally excreted
what pump is key in phase I metabolism
cytocrome P-450
by what method are drugs metabolized in phase II metabolism
conjugation
what phase of metabolism do geriatric pts lose first
phase I
image p. 196-agonist dose response curves in the presence of competitive and irreversable antagonists
--
competitive antagonist shifts the curve _______
to the right
noncompetitive antagonist shifts the curve ______
downward
EC50:
dose causing 50% of maximal effect.
Kd:
concentration of drug required to bind 50% of receptor sites
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.
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
what is the therapeutic index
mean toxic dose/mean effective dose

TD50/ED50

high TI is good
image p. 197- drug development
--
on average how long does it take for a drug to be in In-vitro stidues
2 yts
on average how long does it take for a drug to be in animal stidues
2 years
this phase of clinical testing for a drugs looks at if it is safe, and the pharmakinetics
phase 1
this phase of clinical testing for a drugs looks at if it works in pts
phase 2
this phase of clinical testing for a drugs looks at does it work, in a double blind study
phase 3
this phase drug development involves postmarketing surveillance
phase 4
On average how many years of drug development does it take to file a NDA (new drug application)
9
how long after filing of application does patent expire on a drug and generics become available
20 years
image p. 198-central and peripheral nervous system
--
given the receptor, give the G-protein class and the major fx: α1
increases vascular smooth mm contraction

G protien class: q
given the receptor, give the G-protein class and the major fx: α2
Decrease sympathetic outflow, decrease insulin release

G protien class: i
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
given the receptor, give the G-protein class and the major fx: ϐ2
vasodilation, bronchodilation, increase glucagon release

G protien class: s
given the receptor, give the G-protein class and the major fx: M1
CNS
G protien class: q
given the receptor, give the G-protein class and the major fx: M2
decrease heart rate

G protein class: i
given the receptor, give the G-protein class and the major fx: M3
increase exocrine gland secretions

G protein class: q
given the receptor, give the G-protein class and the major fx: D1
relaxes renal vascular sm mm

G protein class: s
given the receptor, give the G-protein class and the major fx: D2
modulates NT release, esp in the brain

G protein class:i
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
given the receptor, give the G-protein class and the major fx: H2
increase gastric acid secretion

G-protein class:s
given the receptor, give the G-protein class and the major fx: V1
increase vascular sm mm contraction

G-protein class:q
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
flowchart p. 199-receptors: α1,M1,M3,H1,V1
--
flowchart p. 199-receptors: ϐ1,ϐ2,D1,H2,V2
--
flowchart p. 199-receptors: α2,M2,D2
--
image p.200-Autonomic drugs
--
image p.200-noradrenergic nerve terminal
--
release of NE from a sympathetic nn ending is modulated by ______, acting on these receptors.
NE, ACH, ATN II, othr substances

presynaptic α2 autoreceptors
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
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
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
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
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
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
Echothiophateis a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
Glaucoma

works by increasing endogenous ACh
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
what can cause cholinesterase inhibitor poisoning
Parathion and other organophosphates
how do you tx cholinesterase inhibitor poisoning
Antidote--atropine (muscarinic antagonist) plus pralidoxime (chemical antagonist used to regenerate active cholinesterase)
Atropine, homotropine, and tropicamide are cholinoreceptor blockers taht act on they eye to do what?
produce mydriasis and cycloplegia
Benzotropine is a cholinoreceptor blocker that acts on the CNS to tx?
Parkinson's dz
Scopolamine is a cholinoreceptor blocker that acts on the CNS to tx?
Motion skickness
Ipratropium is a cholinoreceptor blocker that acts on the Respiratory system to tx?
Asthma, COPD
Methscopolamine, oxybutin, glycopyrrolateis a cholinoreceptor blocker that acts on the GU system to tx?
urgency in mild cystitis and reduce bladder spasms
atropine is a muscarinic _______
antagoinist

mneu: blocks SLUD:
salivation, Lacrimation, Urination, Defication
give the effect atropine would have on the eye
pupil dilation, cycloplegia
give the effect atropine would have on the airway
decrease secretions
give the effect atropine would have on the stomach
decrease acid secretion
give the effect atropine would have on the gut
decrease motility
give the effect atropine would have on the bladder
decrease urgency in cystitis
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
watch out cuz atropine can cause this in the elderly
acute angle-closure glaucoma
watch out cuz atropine can cause this in men with BPH
urinary retention
watch out cuz atropine can cause this in infants
hyperthermia
mechanism of hexamethonium
nicotinic ACh receptor antagoinist
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
this catecholamine sympathomimetic is a derect general agonist (α1α2β1β2). It is used for open angle glaucoma, asthma, and hypotension
epinephrine
this catecholamine sympathomimetic acts on α1α2β1. It is used for hypotension (but decreases renal perfusion)
NE
this catecholamine sympathomimetic acts on β1=β2. It is used for AV block (rarely)
Isoproterenol
this catecholamine sympathomimetic acts on D1=D2>β>α. It is used for shock(increases renal perfusion), heart failure
Dopamine
this catecholamine sympathomimetic acts on β1>B2. It is used for shock and heart failure
dobutamine
this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for narcolepsy, obesity, ADD.
amphetamine
this sympathomimetic is an indirect general agonist which releases stored catecholamines. It is used for nasal decongestion, urinary incontinance, hypotension
ephedrine
this sympathomimetic acts on α1>α2. It is used as a pupil dilator, vasoconstrictor, and nasal decongestor.
phenylephrine
this sympathomimetic acts on β2>β1. It is used for asthma
albuterol, terbutaline
this sympathomimetic is an indirect general agonist which releases stored and uptake inhibitor . It causes vasoconstriction and local anesthesia
cocaine
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
image [sympathomimetics p. 203]
--
this nonselective α-blocker is used for pheochromocytoma. Toxicity can cause orthostatic hypotension and reflex tachycardia.
Phenoxybenzamine (irreversible) and pentolamine (reversable)
This α1 selective blocker is used for hypertension, urinary retension in BPH. Toxicities include 1st dose orthostatic hypotension, idzziness, headache.
prazosin, terazosin, doxazosin
this α2 selective blocker is used for depression. Toxicity includes sedation, increased serum cholesterol and increased appetite
mirtazapine
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
name some beta blockers
propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
how do the β blockers effect hypertension
decrease cardiac output, decrease renin secretion
how do the β blockers effect angina pectoris
decreasee HR & contractility, resulting in less O2 consumption
how do the β blockers effect MI
decrease mortality
how do the β blockers effect SVT (propranolol, esmolol only)
decrease AV conduction velocity
how do the β blockers effect CHF
slows progression of chronic failure
how do the β blockers effect glaucoma(timolol only)
decreases secretion of aqueous humor
give some toxicities of β blockers
impotensce, exacerbation of asthma, bradycardia, AV block, CHF, sedation, sleep alteration; use w/ caution in dbts
give the nonselective (B1=B2) B blockers
propranolol, timolol, nadolol, pindolol (partial agonist), and labetalol (partial agonist)
give the B1 selective (B1>B2) B blockers
Acebutolol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol

mneu: A BEAM of B1 blockers
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
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
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
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
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
this Rx for glaucoma is a prostaglandin. It acts by increaseing outflow of aqueous humor. SE include darkening of the iris (browning)
lantanoprost (PGF2α0
what is the anitidote/tx for acetaminophen overdose
N-acetylcysteine
what is the anitidote/tx for salicylate overdose
alkanize urine, dialysis
what is the anitidote/tx for anticholinesterases, organophosphatesoverdose
atropine, pralidoxime
what is the anitidote/tx for antimuscarinic, anticholinergic agentsoverdose
physostigmine salicylate
what is the anitidote/tx for B-blocker overdose
glucagon
what is the anitidote/tx for digatis overdose
stop dig, normalize K+, lidocaine, anti-dig Fab fragments, Mg++
what is the anitidote/tx for iron overdose
deferoxamine
what is the anitidote/tx for lead overdose
CaEDTA, dimercaprol, succimer, penicillamine
what is the anitidote/tx for arsenic, mercury, gold overdose
Dimercaprol (BAL), succimer
what is the anitidote/tx for copper, arsenic, gold overdose
penicillamine
what is the anitidote/tx for cyanide overdose
nitrite, hydroxycobalamin, thiosulfate
what is the anitidote/tx for methemoglobin overdose
methylene blue
what is the anitidote/tx for CO overdose
100% O2, hyperbaric O2
what is the anitidote/tx for methanol, ethylene glycol (antifreeze) overdose
ethanol, dialysis, fomepizole
what is the anitidote/tx for opiods overdose
naloxone/naltrexone
what is the anitidote/tx for benzodiazepines overdose
flumazenil
what is the anitidote/tx for TCAs overdose
NaHCO3 (nonspecific
what is the anitidote/tx for heparin overdose
protamine
what is the anitidote/tx for warfarin overdose
vitamin K, fresh frozen plasma
what is the anitidote/tx for tPA, streptokinase overdose
aminocaproic acid
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
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
when someone ODs on a weak acid (phenobarbital, methotrexate, aspirine) what do you do
alkalinize urine with bicarb to increase clearance
when someone ODs on weak bases (e.g., amphetamines) what do you do
acidify urine to increase clearance (give NH4Cl)
someone comes in with atropine like side effects. What do you suspect
tricyclics
someone comes in with cardiac toxicity. what do you suspect?
doxorubicin (adriamycin), daunorubicin
someone comes in with coronary vasospasm. what do you suspect?
cocaine
someone comes in with cutaneous flushing. what do you suspect?
niacin, Ca++ channel blockers, adenosine, vancomycin
someone comes in with torsades de pointes. what do you suspect?
class III (sotalol, class IA (quinidine) antiarrhythmics, cisapride
someone comes in with agranulocytosis. what do you suspect?
clozapine, carbamazepine, colchicine
someone comes in with aplastic anemia . what do you suspect?
chloramphenicol, benzene, NSAIDS
someone comes in with grey baby syndrome. what do you suspect?
chloramphenicol
someone comes in with hemolysis in G6PD-deficient pts. what do you suspect?
sulfonamines, isoniazid (INH, aspirin, ibuprofen, primaquine, nitrofurantoine
someone comes in with thrombotic complications. what do you suspect?
OCPs (e.g., estrogens and progestins)
someone comes in with cough. what do you suspect?
ACE inhibitors (losartan-no cough)
someone comes in with pulmonary fibrosis. what do you suspect?
bleomycin, amiodarone, busulfan
someone comes in with acute cholestatic hepatitis. what do you suspect?
macrolides
someone comes in with focal to massive hepatic necrosis. what do you suspect?
halothane, valproic acid, acetaminophen, amanita phalloides
someone comes in with hepatitis. what do you suspect?
INH
someone comes in with pseudomembranous colitis. what do you suspect?
clindamycin, ampicillin
someone comes in with adrenocortical insufficency. what do you suspect?
glucocorticoid withdrawal (HPA supression
someone comes in with gynomastia. what do you suspect?
Spironolactone, Digitalis, Cimetidine, Alcoholism, estrogens, Ketoconazole

mneu: Some Drugs Create Awesom Knockers
someone comes in with hot flashes. what do you suspect?
tamoxifin
someone comes in with gingival hyperplasia. what do you suspect?
phenytoin
someone comes in with osteoporosis. what do you suspect?
corticosteroids, heparin
someone comes in with photosensitivity. what do you suspect?
Sulfonamindes, Amiodarone, Tetracycline

mneu: SAT for a photo
someone comes in with SLE like syndrome. what do you suspect?
Hydralazine, INH, Procainamide, Phenytoin

mneu: it's not HIPP to have lupus
someone comes in with tendonitis, tendon rupture, and cartilage damage (kids). what do you suspect?
fluoroquinolones
someone comes in with Fanconi's syndrome. what do you suspect?
expired tetracycline
someone comes in with interstitial nephritis. what do you suspect?
methacillin
someone comes in with hemorrhagic cystitis. what do you suspect?
cyclophosphamide, ifosfamide
someone comes in with cinchonism. what do you suspect?
quinidine, quinine
someone comes in with diabetes insipidus. what do you suspect?
lithium, demeclocycline
someone comes in with seizures. what do you suspect?
bupropion, imipenem/cilastin
someone comes in with tarditive dyskinesia. what do you suspect?
antipsychotics
someone comes in with disulfram-like reaction. what do you suspect?
metronidazole, certain cephalosporins, procarbazine, sulfonyurease
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
alcohol toxicity p. 208
--
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
this herbal agent is sometimes used for the intermittent claudication. Toxicities can be GI distress, anxiety, insomnia, headache, and antiplatelet action
ginkgo
this herbal agent is sometimes used for anxiety. Toxicities can be GI distress, sedation, ataxia, hepatotoxicity, phototoxicity, dermatotoxicity
Kava
this herbal agent is sometimes used for viral hepatitis. Toxicities can be loose stools
milk thistle
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
this herbal agent is sometimes used for jet lag and sinsomnia. Toxicities can be sedation, suppresses midcycle LH, hypoprolactemia
melatonin
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