- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
75 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
How does ionization affect resorption/excretion?
How do you increase excretion for an acid? |
only ionized molecules are excreted. Non ionized molecules will diffuse.
|
You make the urine more basic (basic environment with ionize the molecule and prevent diffusion/resorption) |
|
What is the bioavailability of a drug administered IV?
If a drugs has 25% oral bioavailability, how much of it needs to be taken in order to reach 100mg IV equivalence? |
100%
|
400mg x = 100/.25 |
|
what is Vd?
How is it calculated? |
Volume of distribution. Tells you how much space the drug is occupying (and by extension, where the drug is located).
|
Vd = drug amount/[drug] mg/1 * volume/mg = volume |
|
What organ determines clearance?
How is it calculated? |
how quickly the kidney can get rid of the drug
|
CL = rate of drug elimination/[plasma drug] |
|
What is a loading dose?
How is it calculated? |
a large dose given at the beginning of a treatment in order to increase plasma drug concentrations to a therapeutic level quickly
|
LD = Cp * Vd target concentration times the amount of space it's going to occupy |
|
what are standard fluid compartment levels?
|
plasma = 3L
Extracellular = 12L (includes plasma) Total = 41L |
|
|
What is steady state concentration?
How does it relate to dose and clearance? |
the concentration the drug remains at after a few days of taking it
|
it is proportional to dose and inversely proportional to clearance (the higher the clearance, the lower the Css will be, the higher the dose, the higher the Css will be) |
|
What is phase I metabolism? What is phase II metabolism?
How is this different than first pass metabolism? |
Phase 1 = first modification, drug becomes more water soluble. Prodrugs require this step to become active (eg - codein).
Phase 2 = second and final modification. Drug becomes polar and inactivated in preparation for excretion. |
First pass metabolism refers to the amount of drug lost in the initial metabolism of the drug (usually in the liver via P450) even before reaching the general circulation. This is Phase 1 metabolism. |
|
Major metabolism inducers (many enzymes)
What are the effects of inducers? |
rifampin, rifabutin
barbiturates phenytoin carbamazepine glucocorticoids St. John's worth |
the enzyme's activity increases (can be good or bad, lead to more prodrug being converted quicker leading to an increase in bioavailability or lead to more drug being inactivated quicker leading to a decrease in bioavailability) |
|
CYP1A2 inducers
|
smoking (benz(a)pyrene)
charcoal broiled foods cruciferous vegetables dioxine |
|
|
Major enzyme inhibitors
What are the effects of inhibitors? |
cimetidine
amiodarone paroxetine fluoxetine |
enzyme activity is inhibited. Drugs like codein become ineffective because of this. |
|
CYP3A4 inhibitors
|
ketoconazole
itraconazole HIV protease inhibitors (ritonavir) erythromycin clarithromycin diltiazem nicardipine verapamil grapefruit juice |
|
|
CYP2D6 inhibitors
What important drug is converted into its active form via this enzyme? |
quinidine
SSRIs |
codein |
|
What is efficacy?
What is potency? |
refers to the maximal effect a drug can have (related to Tmax)
|
relates a drugs concentration level to its effect. A lower concentration for an equal effect makes it more potent (related to Km. |
|
What does a competitive antagonist do to a drug's effect?
What does it look like on a graph? |
affects Km (potentcy) but has no affect on the Tmax (efficacy).
It's basically like you're diluting the drug so you just need more of it. |
the line gets shifted over to the right |
|
What does a non-competitive antagonist do to a drug's effect?
What does it look like on a graph? |
affects the Tmax but not the Km.
it's like you're taking away enzymes. Potency of the drug stays the same but the drug can't exhibit as strong of a reaction because the enzymes become saturated sooner (less efficacy). |
the line gets shorter |
|
What is the effect of a partial agonist?
|
it is not as effective as the full agonists so the Vmax is decreased. Km can be either more or less.
|
|
|
Physiologic antagonism
|
a different mechanism causes a counter effect (eg - stimulation of the SNS system in the lungs to dilate counteract the constrictive effects of the PNS)
|
|
|
Therapeutic index
|
the bigger the value the safer it is
|
|
|
What are the phases of drug development?
|
Phase 1 = small test size, is it safe?
Phase 2 = larger, is it effective? Phase 3 = very large, is it effective even in a double blind study |
|
|
Where is the PNS located?
What length are its pre/postsynaptic fibers? What receptor/neurotransmitter is located at the ganglia and at the target organ? How is the innervation compared from presynaptic to post synaptic? Are there any exceptions? |
Cranial/Sacral
Pre=long; Post=short Ganglia= Nicotinic/Ach; Target organ=Muscarinic/Ach pointed, 1:1 ratio of innnervation no |
|
|
Where is the SNS located?
What length are its pre/postsynaptic fibers? What receptor/neurotransmitter is located at the ganglia and at the target organ? How is the innervation compared from presynaptic to post synaptic? Are there any exceptions? |
Thoraco/lumbar
Pre=short; Post=long Ganglia=Nicotinic/Ach; Organ=alpha/beta/NE/Epi diffuse, 1 nerve pre, many nerves post yes - Sweat glan=Muscarinic/Ach at organ - adrenal=no synapse, direct Ach/nicotinic innervation |
|
|
What are the actions of alpha-1?
Alpha-2? |
constrict blood vessels, dilate pupils
|
inhibit insulin release, general inhibition |
|
How are the beta receptor actions the same?
How are they different? |
both increase HR, contractility
|
B2 also dilates cardiac vessels, releases glucagon and increases lipolysis (counteracts insulin) |
|
what are the actions of M1? M2? M3?
|
M1=activates enteric NS, inc peristalsis
M2=decrease HR M3=GI/GU activated (increase peristalsis etc), bronchoconstriction, pupil constriction |
|
|
What are the actions of D1?
D2? |
relaxes renal smooth muscle
|
CNS receptors, inhibitors will cause parkinson-like symptoms |
|
What are the actions of V1? V2?
|
smooth muscle contraction
|
increases aquaporins -> increase water absorption |
|
Inhibition at the ganglia will do what to the target organ?
|
shut it down. Will prevent autonomic reflexes (eg-bradycardia)
|
|
|
Direct Muscarinic Agonists
click for hint |
Beth and Nic are on Var(sity), they have sex in the C(h)evi and then have some Pilo talk.
|
Bethanecol Pilocarpine Cevimiline Nicotine Varenecline |
|
Indirect Muscarinic Agonists
(Cholinsesterase inhibitors) click for hint |
Don and Ed are Neo-Phys(iologist) who are on the Pral(prowl) for Organ(s) to Echo(cardiogram)
|
Donepezil Edrophonium Neostigmate Physostigmine Pralidoxime Organophosphate Echothiophate |
|
What cholinesterase inhibitor results in poisoning?
|
Organophosphates. Usually in farmers due to their use in insecticides.
What are the symptoms? |
DUMBBELSS Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation, Lacrimation, Sweating, Salivation |
|
Muscarinic/Cholinergic Antagonists
click for hint |
Iprah(oprah) is a Dic and has no Sol, she caused a Tropic Oxy(gen) supply to become depleted by a printer business called Glycopy, on a Diph(erent) note, the guy who At(e) the Tol booth was high on Scopolamine.
|
Atropine Scopolamine Tolterodine Oxybutynin Glycopyrrolate Dicyclomine Solifenacin Ipratropium Tropicamide Diphenoxylate-atropine |
|
Varenecline
|
stop smoking
|
|
|
Cevimiline
|
increase salivation
|
|
|
Pilocarpine
|
tx glaucoma, contracts ciliary muscles, makes a lot of seat sweating and saliva
|
|
|
Neostigmine
|
prototype,
|
|
|
Physostigmine
|
into CNS
|
|
|
Edrophonium
|
dx of myasthenia gravis
ds pathology? |
ds blocks Ach receptors at post synaptic -> muscle weakness |
|
Echothiophate
|
tx eye (glaucoma)
|
|
|
Organophosphates
|
irreversible bind
tx? |
atropine |
|
Atropine
|
prototype, tx Av block
|
|
|
Scopolamine
|
motion sickness
(fyi - called the zombie drug in a recent episode of Castle) |
|
|
Glycopyrrolate
|
slows heart, used in surgery
|
|
|
Ipratropium
|
tx asthma/COPD
|
|
|
Diphenoxylate
|
tx diarrhea, slows peristalsis
|
|
|
what drugs are absolutely contraindicated in narrow angle glaucoma?
|
cholinergic antagonists
|
|
|
d-tubocurare
|
prototype, surgery paralysis
|
|
|
Succinylcholine
|
binds Ach receptors, depolarizes muscle, SE - malignant hyperthermia
tx for MH? |
dantrolene |
|
what are ganglion blockers used for?
|
prevents reflex responses
|
|
|
Isoproterenol
|
B1 and B2, dec BP by musclar BV dilation
|
|
|
Epinephrine
|
DOC anaphylaxis
(fyi - why?) |
anaphylactic shock causes profound vasodilation, need to vasoconstrict, also no SE |
|
Pseudophedrine
|
nasal decongestant
|
|
|
Ephedrine
|
like Epi
|
|
|
Clonidine
|
tx HTN
|
|
|
Acroclonidine
|
tx glaucoma, put into eye
|
|
|
DA
|
lower BP
|
|
|
Amphetamine
|
increase catecholamine release
|
|
|
Cocaine
|
decrease catecholamine uptake
|
|
|
Phentolamine
|
tx HTN crisis
|
|
|
Phenoxybenzamine
|
tx pheochromocytoma (adrenal gland tumor)
|
|
|
what would happen to BP if you were to block alpha receptors and administer epinephrine?
|
drop
|
|
|
what would happen to BP if you were to block beta receptors and administer epinephrine?
|
rise
|
|
|
Prazosin
|
SE - postural hypotension
|
|
|
Propranolol
|
Chronic Tx results in decrease BP
|
|
|
Timolol
|
tx glaucoma
|
|
|
Betaxalol
|
tx glaucoma
|
|
|
what is the benefit of mixed beta/alpha antagonists?
|
no reflexive tachycardia
|
|
|
Acetazolamide
|
SE: metabolic acidosis
|
|
|
Loop Diuretics
|
most effective
SE: alkalosis |
|
|
Thiazides
|
open K channels causes...
relaxation of arteries decreased insulin release compensatory ↑ lipid release |
|
|
Indapamide
|
best vasodilator, least effect on lipids
|
|
|
K sparing should not be combined with?
|
ACEI and ARBs
|
|
|
Eplerenone
|
reduces MI mortality after attack
|
|
|
Inamrinone
|
acute CHF tx
|
|
|
DA
|
acute CHF tx
|
