Pharmacology

Question 1

Pharmacokinetics

Answer 1

study of absorption, distribution, metabolism, and excretion/elimination from the body
(What the body does to the drug)

Question 2

Pharmacodynamics

Answer 2

study of responsiveness, of receptors to a drug and mechanisms by which these effects occur and impact the body
(What the drug does to the body)

Question 3

ADME

Answer 3

Absorption - drug movement from site of administration to circulatory system
Distribution - reaching the site of action at a high enough concentration for a sufficent period of time for a response to be produced
Metabolism - reached site of action and produced clinical effect (liver most often) (Oxidation, reduction, hydrolysis, hydration, conjunction)
Elimination - removal of drug from body (most often urine), liver, bile, sweat, lungs, milk, tears, saliva

Question 4

What can affect distribution?

Answer 4

Hypoalbuminemia
Acidemia
MDR 1

Question 5

Cellular Signaling

Answer 5

G-protein coupled receptors
cAMP, IP3, DAG
Adrenergic, opioids, vasopressors and insulin
Inotropic receptors - NMDA, GABA A receptors

Question 6

Chelation

Answer 6

Bind directly to metals in the body and promote elimination
EDTA - binds with calcium in blood to prevent clotting

Question 7

Receptor Interactions

Answer 7

Agonists - mimic affect of receptor
Antagonists - binds to receptor and blocks the response
Partial agonists - bind to receptor but have partial or incomplete efficacy

Question 8

Pediatric patients

Answer 8

Distribution may be altered due to increased total body water, decreased fat stores, hypoproteinemia
renal system not fully developed - drug clearance

Question 9

Geriatric patients

Answer 9

CKD - reduce GFR - decrease drug clearance

Question 10

Emetics

Answer 10

Apomorphine
Alpha 2 Agonists
Peripheral acting emetics - H2O2

Question 11

Antiemetics

Answer 11

Phenothiazine Derivatives
Metoclopramide
Serotonin (5HT3) Antagonists
Maropitant - NK1 antagonist

Question 12

Apomorphine

Answer 12

stimulates dopamine, serotonin, alpha adrenergic, opioid receptors, stimulates CRTZ
Reversed with metoclopramide or naloxone

Question 13

Alpha 2 Agonists

Answer 13

Xylazine, stimulation of CRTZ
Reversed with atipamazole

Question 14

Phenothiazine Derivatives

Answer 14

acepromazine, chlorpromazine, prochlorperazine
Block dopamine receptors in CRTZ
Alpha 1 antagonist effect = reduced SVR and vasodilation

Question 15

Metoclopramide

Answer 15

Prokinetic
dopamine and serotonin antagonist, cholinergic agonist
Gastric emptying, increases lower esophageal sphincter tone
Can interfere with other drugs that work on similar receptors
(DO NOT USE IN INTUSSUSCEPTIONS OR OBSTRUCTIONS)

Question 16

Serotonin (5HT3) Antagonists

Answer 16

ondansetron and dolasetron
block serotonin receptors in CRTZ

Question 17

Maropitant

Answer 17

NK 1 antagonist - blocks substance P at vomiting center (bone marrow suppression under 8 weeks old)
Confirmed no obstruction prior to use –> mask decline
Antitussive effect

Question 18

Gastroprotectant Drugs

Answer 18

Proton Pump Inhibitors
H2 histageneric Antagonists
Sucralfate
Misoprostol

Question 19

Proton Pump Inhibitors

Answer 19

Omeprazole, pantoprazole, esomeprazole
Inhibits Na/K ATPase pump activity –> controls proton deposition into gastric lumen and HCL secretion

Question 20

H2 Histageneric Antagonists

Answer 20

“H2 blockers”
Famotidine, ranitidine, cimetidine
Reduce histamine at receptors on gastric parietal cells and reduce stomach acid production

Question 21

Sucralfate

Answer 21

Sucrose sulfate aluminum complex drug - bind to locally injured GI lining and create a barrier
Separate by 2 hours from food or meds

Question 22

Misoprostol

Answer 22

Synthetic prostaglandin E1 analogue –> improve gastric blood flow, decrease gastric acid production, increase mucous production and bicarb secretion and promote cell turnover
Used to help prevent NSAID-induced GI injury and ulceration

Question 23

Antiarrhythmic Drugs

Answer 23

Class 1 - sodium channel blockers
Class 2 - beta blockers
Class 3 - potassium channel blockers
Class 4 - calcium channel blockers
Class 5 - Misc

Question 24

Class 1 antiarrythmics

Answer 24

Sodium Channel blockers
1A - quinidine, procainamide (ventricular and supraventricular arrythmias)
1B - lidocaine, mexiletine - ventricular arrythmias
1C - flecainide

Question 25

Class 2 antiarrhythmics

Answer 25

Beta blockers Reduce HR and myocardial oxygen demand, increase atrioventricular conduction time HCM, supraventricular and ventricular arrythmias Propanolol, esmolol, atenolol, metoprolol

Question 26

Class 3 antiarrythmics

Answer 26

Potassium Channel Blockers Amiodarone, sotolol Blocks, Na, K, Ca channels

Question 27

Class 4 antiarrythmics

Answer 27

Calcium channel blockers Diltiazem blocks Ca channels, lower SA/AV nodes, vasodiltion

Question 28

Anticholinergics

Answer 28

Atropine, Glycopyrrolate Inhibit acetycholine at muscarinic receptors Increases HR, resolving vagally mediated pupillary dilation, bronchodilations, urinary retention, drying secretions

Question 29

Loop diuretcs

Answer 29

Furosemide Bind to and inhibit the Na-K-2Cl symporter on apical membrane of ascending loop of Henle Blocks reabsorption of Na and Cl - H20 follows Hypercalcemia

Question 30

Osmotic Diuretics

Answer 30

Mannitol Filtered by kidney Improve brain oxygenation

Question 31

Potassium Sparing Diuretcs

Answer 31

Spironolactone Antagonizes aldosterone - binds to receptor sites in distal tubule and collecting duct Limits K loss Hyperaldosteronism Hyperkalemia - side effect

Question 32

Thiazide Diuretics

Answer 32

Hydrochlorothiazide Inhibits Na/Cl co transporter within distal tubule