Pharm final Flashcards by Alex Lang

Stereoisomerism

Same chemical formula but different 3D structure and drug effects

How well did you know this?

Not at all

Perfectly

differ toxins and poisons

Toxins are biological (snake venom) while poisons are pharmaceutical (cyanide, arsenic, alcohol)

How well did you know this?

Not at all

Perfectly

Strongest combination of agonists, weakest?

Agonist + allosteric activator

Agonist + allosteric inhibitor

How well did you know this?

Not at all

Perfectly

Pharmacokinetics vs pharmacodynamics

What the body does to the drug (ADME) vs what the drug does to the body (effects, binding, etc.)

How well did you know this?

Not at all

Perfectly

If pH < pKa

favors protonated form (has Hydrogen attached)

How well did you know this?

Not at all

Perfectly

if pH > pKa

Favors unprotonated form (no Hydrogen ion attached)

How well did you know this?

Not at all

Perfectly

Weak Acid: pKa 3.5, pH 1.5

Protonated, non-charged

How well did you know this?

Not at all

Perfectly

Weak base: pKa 7.0, pH 4.5

Protonated, Charged

How well did you know this?

Not at all

Perfectly

Weak Acid: pKa 2.5, pH 5.0

Unprotonated, charged

How well did you know this?

Not at all

Perfectly

Weak base: pKa 4.0, pH 6.5

Unprotonated, non-charged

How well did you know this?

Not at all

Perfectly

What’s the therapeutic ratio?

TD50/ED50

How well did you know this?

Not at all

Perfectly

Most potent curve on graph is

the one that starts showing effect the earliest

How well did you know this?

Not at all

Perfectly

What’s the goal of rational dosing?

Achieve desired beneficial effect with minimal adverse effects

How well did you know this?

Not at all

Perfectly

the bond strength is indirectly proportional to

specificity

How well did you know this?

Not at all

Perfectly

Drug safety is directly proportional to

therapeutic index

How well did you know this?

Not at all

Perfectly

Volume of distribution is directly proportional to

concentration of drug outside systemic circulation

How well did you know this?

Not at all

Perfectly

First order elimination vs zero order elimination

first order elimination elimination rate changes with concentration, whereas zero-order has max and CONSTANT elimination rate until it reaches first order concentration levels.

In first order, the fraction elimination rate is constant. e.g. 10% of the drug is eliminated every hour, so the elimination rate changes but not the fractional change

How well did you know this?

Not at all

Perfectly

How long does it take a drug to reach full effectiveness if the half-life is 4 hours?

How long does it take to be removed from the body/no effectiveness?

16 hours (4 half-lives), then another 16 hours. Totals 32 hours.

How well did you know this?

Not at all

Perfectly

Parameters that affect passive diffusion

Weight of the drug, pKa, lipid solubility, and plasma protein binding

How well did you know this?

Not at all

Perfectly

Four basic mechanisms of transmembrane signaling

-Direct crossing to intracellular receptor due to having lipid solubility (think aldosterone)

Enzymatic action mediated by ligand binding (TKR)

-Ligand gated ion channel (ACH in skeletal muscle)

-GPCRs

How well did you know this?

Not at all

Perfectly

GPCR structure

7 trans-membrane alpha-helices

-Pleiotropy: several downstream effects possible

-G-proteins: trimeric
-alpha subunit dissociates when active (GDP -> GTP) and binds to effector protein to produce second messenger cells)

How well did you know this?

Not at all

Perfectly

Describe desensitization

The GPCR is phosphorylated by GRKs, enabling beta-arrestin to bind to the phosphorylated receptor, thereby inactivating it. The receptor-beta-arrestin complex is then internalized into a clathrin-coated pit, where the receptor can either be recycled to the membrane or degraded in lysosomes

How well did you know this?

Not at all

Perfectly

Drug efflux transporters

ATP-binding cassete (ABC) transporters
-major drug efflux transporters are B, C, G and found in

How well did you know this?

Not at all

Perfectly

Where are B C and G ABC drug efflux transporters found?

Intestines, liver, kidneys, BBB, placenta

How well did you know this?

Not at all

Perfectly

What's the research target of the blood brain barrier?

Block efflux transporters, increase delivery to brain tight junction!!

Biotransformation

Some drugs become active AFTER going through liver, but it could also be inactivation of metabolite

Examples of second messengers in a GPCR activation cascade

DAG cAMP IP3 cGMP *adenylyl cyclase is NOT a second messenger!!!*

Neurotransmitter class: Esters

ACh - Cholinergic

Neurotransmitter class: Monoamines

Norepi, serotonin, dopamine - ADRENERGIC

Neurotransmitter class: Amino acids

Glutamate, GABA

Neurotransmitter class: Purines

Adenosine, ATP

Neurotransmitter class: Peptides

Substance P, endorphins

Neurotransmitter class: Inorganic gases

Nitric oxide

Sympathetic vs parasympathetic fibers

Symp: thoracolumbar region of spinal cord, consists of short pre and long post Para: brain and sacral region, long pre and short post

a1 and a2 activates what?

Phospholipase C

b1 2 and 3 stimulates what?

Adenylate cyclase

M1 3 and 5 activate what?

Phospholipase

M2 and 4 inhibit what?

andeylate cyclase

MOA of phospholipase C activation (whole pathway)

Agonist binds to a1 receptor, GDP -> GTP, alpha subunit binds to effector protein phospholipase C, secrets DAG and IP3, releases stored calcium

MOA of adenylyl cyclase activation (whole pathway)

Agonist binds to beta receptor or a2 receptor, alpha subunit turns to GTP, stimulates effector protein adenylyl cyclase, ATP -> cAMP, activates protein kinase -> downstream effects

Receptors in heart for sympathetic activity are

B1 and B2

Receptors on skeletal muscle blood vessels

Receptors on smooth vessels for sympathetic activity are

alpha

Bronchiolar smooth muscle receptors for sympathetic activity are

Receptors in heart for parasympathetic activity are

Receptors in bronchioles smooth muscle for parasympathetic activity are

Receptors on smooth vessels for parasympathetic activity are

What are the second messengers for alpha 1 receptor binding?

DAG and IP3

direct acting Adrenergic agonist

Albuterol, clonidine, dobutamine, dopamine, epi, norepi, isoproterenol

Cardiac output equation

SV x HR (70 x 75) = 5250ml/min

Isoproterenol receptors

B1/B2

dopamine receptors

D1-5, higher doses are A1/B1

dobutamine receptors

Adrenoreceptor agonist drugs are used for

pheochromocytoma ex: phentolamine, tolazoline, prazosin, labetalol

Whats an irreversible adrenoceptor antagonist?

Phenoxybenzamine

Non-specific beta blockers

propranolol

B1 specific beta blockers

metoprolol and atenolol

Ultra short acting beta blockers

Esmolol

Muscarinic agonists cause what in the eyes?

Miosis and increase intraocular drainage

Major uses of cholinomimetics

eye disease, GI/urinary tracts, NMJ issues (MG), atropine overdose

Symptoms of organophosphate exposure

SLUDGE-M tx with atropine and pralidoxime (ONLY for this exposure)

Poisonous mushrooms are a what overdose and how to treat? S/S?

Cholinomimetic, atropine, SLUDE-M

How to treat atropine overdose?

Physostigmine (belladona is a thing to OD on, symptoms are BRAND)

What kind of receptors are adrenergic receptors?

GPCRs

AHA angina classifications of stable, unstable, and variant

Stable: angina with effort Unstable: angina with rest, emergency. Variant: vasospasms, rare

Good and bad of nitrates/nitrites

Good: increased venous capacity, decreased ventricular preload, decrease heart size and CO Bad: orthostatic hypotension, syncope, reflex tachycardia.

Dihydropyridines CCB are specific to what?

Peripheral vasculature

Verapamil and diltiazem are more specific to what?

heart

Toxicity of CCBs

AV block, CHF, bradycardia, cardiac arrest

Beta blockers, are they vasodilators?

Beneficial effects of beta blockers

decreased HR, BP, contractility

Hydraulic equation

BP = CO x PVR

Adrenoceptor antagonist are what?

beta blockers

2 examples of CNS sympathoplegics

Methyldopa, clonidine

how do CNS sympathoplegics help blood pressure?

Decrease it by decreasing sympathetic stimulation in brainstem, bind more tightly to A2

Examples of a1 blockers

Prazosin, terazosin, doxazosin. Block in the periphery.

How does minoxidil vasodilate?

Opens K channels in smooth muscle, decreasing excitability.

How does hydralazine work?

Increases NO production, dilating arterioles.

How does sodium nitroprusside work?

Dilates arterial and venous vessels, used for HTN emergency, releases NO

How does fenoldopam work?

Rapid peripheral arteriolar dilator, HTN emergencies and post-op HTN. Agonist of D1 receptors and increases flow to kidneys.

ACE-I and ARB examples

ACE: captopril ARB: losartan, valsartan.

Where does digoxin work on the cell?

inhibits Na/K pumps, positive inotrope

Compare systolic and diastolic failure in regards to cardiac output and ejection fraction

Systolic: decreased CO and ejection fraction, typical for acute HF Diastolic: decreased CO but normal ejecetion fraction, wont respond to positive inotropic drugs, typical for hypertrophy

4 factors of cardiac performance

preload, afterload, contractility, heart rate

Toxicity of digoxin levels

EC50 1ng/mL, TC50 only 2ng/mL

How do PDE inhibitors work?

inactivate cAMP and cGMP, causing vasodilation and positive inotropy. milrinone

order of nodal tissue

SA, AV, Bundle, purkinjie

Cardiac action potential ion channels need to know

Phase 0: Na+ in Phase 1: K, Cl out Phase 2: Ca in, K out Phase 3: K+ out phase 4: K+ inward rectifier 200ms

Causes of impulse conduction re-entry?

Scar tissue, unidirectional block, long conduction time

Class II antiarrhythmics

Sympatholytic

Class III antiarrhythmics

Prolong action potential duration (K channel blockers)

Class IV antiarrhythmics

Block cardiac calcium channels

Examples of sodium channel blockers

Quinidine, lidocaine, flecainide

Drug of choice for VTach and why?

Amiodarone - has effects as all 4 classes by blocking sodium channels, inhibits receptors, increases action potential, and blocks calcium channels

Treatment for bradycardia

Assess underlying cause, D/C drugs If symptomatic, atropine and api/dopamine If chronic: pacemaker

Treatment for heart block

not usually treated for 1st degree. If symptomatic, atropine and transcutaneous pacing Chronic: pacemaker

Treatment for SVT

assess cause, rule out atrial flutter Adenosine If chronic, CCBs, beta blockers

Treatment for sinus tach

rule out wide complex Adenosine, CCBs, cardioversion If chronic, catheter ablation, ICD

Treatment for Vtach

amiodarone, lidocaine, magnesium (torsades) Chronic: amiodarone, satolol

Treatment for Afib

diltiazem, verapamil Chronic: Beta-blockers, amiodarone

Treatment for Vfib

CPR, defibrillation, epi, vasopressin Chronic: amiodarone, lidocaine, magnesium

H1 receptors are stimulated and cause

Bronchoconstriction and vasodilation

What receptors do antihistamines act on?

Selective H1 inverse agonists such as Benadryl which is most useful for type I hypersensitivity

Histamine effects

Nervous system: stimulates pain and itching Cardiac: Decreased BP, Increased HR

1st gen H1 receptor antagonist

For sedation (children make have reverse effects), anti nausea, and antiparkinsonism e.g. Benadryl

Pharm final Flashcards

(106 cards)