DPT 5010 Pharmacology- Drugs

Question 1

Signs & Symptoms of Inflammation

Answer 1

Rubor
Calor
Tumor
Dolor

Question 2

NSAIDs: Non Steroidal anti-inflammatory drugs

Answer 2

(Aspirin)

a. Antithrombotic: inhibits platelets, clotting
b. Antipyretic: inhibits fever
c. Analgesic: inhibits pain
d. Anti-inflammatory: inhibits inflammation @ injury site

Question 3

Side Effects of NSAIDs (Aspirin)

Answer 3

a. GI: inhibition of protective prostaglandins in stomach
gastritis –> bleeding –> pain –> ulcers –> perforation

b. Liver: Reyes syndrome in KIDS w/ viral infections
virus + aspirin –> hepatotoxicity –> liver failure

c. Hearing
high dose –> ringing in ears –> “hair cell” damage –> deafness

d. Respiration/acid base balance
high dose –> stimulate respiration from acid
super high dose –> inhibits respiration

Question 4

NSAIDs apart from Aspirin

Answer 4

a. All still inhibit cycle-oxygenase pathway
b. Therapeutic effects are similar
c. Potency and therapeutic range differ
d. Side effects- esp. GI- are reduced
e. Examples: ibuprofen, naproxen, advil,
f. Cox-2 inhibitors: celecoxib
major increases in risk of MI & stroke

Question 5

Non-narcotic analgesic/antipyretic: Acetominophen

Answer 5

a. Effects: inhibits pain & fever, decreases GI side effects, NOT anti-inflame. @ inj. site.
b. Mechanism of action: inhibits cox enzyme –> in blood to CNS
c. Major side effect: Hepatotoxicity

Question 6

Drug Implications on Rehab:

Answer 6

Decrease Pain + Decrease Inflammation
=
Increased mobility & effort

Question 7

Glucocorticoids

Answer 7

Glucose/ Adrenal Cortex/ Steroids

Question 8

Normal physiology of Cortisol:

Answer 8

Glucose metabolism & stress response of adrenal cortex:

a. Cyclic (higher in am)
b. Stress (higher during stress)
c. Mechanism (fat soluble–> intra-cellular receptor, change protein synthesis)
d. Effects and Control: (@ Ant. pituitary, which affects cortisol in adrenal cortex to help adjust glucose levels)

Question 9

Anabolic Steroids

Answer 9

ALL related to testosterone
take to increase muscle
DIFFERENT from glucocorticoids

Question 10

Pharmacological use of glucocorticoids:

Answer 10

Anti-inflammatory effects through the inhibition of the phospholipase pathway.

Question 11

Reasons to prescribe glucocorticoids:

Answer 11

a. Adrenal insufficiency (Addison’s disease)
b. Immune system suppresion
c. Decrease inflammation
(allergies, dermatologic disorders, GI disorders, blood disorders, cancer, neurotrauma-decrease brain swelling, respiratory disorders, rheumatologic disorders

Question 12

Methods of Administering glucocorticoids

Answer 12

Topical
Oral
Injection
Use of mist/drops
-lungs
-nasal
-otic and ophthalmic

Question 13

General Side effects of glucocorticoids

2° to overloaded normal metabolic effects

Answer 13

i. General catabolic effects
(breakdown skeletal muscle, bone, CTs)
inhibit growth and healing

ii. Adrenocortical suppression
(block normal cortisol production)

iii. Immunosuppression

iv. Drug-induced Cushing’s syndrome
(extremity wasting, osteoporis, trunk obesity, “moon face, buffalo hump”)

Question 14

Examples of glucocorticoids used pharmacologically

Answer 14

Short 1/2 life (cortisone)
Intermediate 1/2 life (prednisone)
Long 1/2 life (dexamethasone)

Question 15

Pharmacodynamics

Answer 15

How drugs exert their effects

Question 16

Pharmacodynamics: Receptors

Answer 16

ALWAYS proteins (drug is ligand --> binds to protein)
Intracellular Receptors (fat soluble)
Membrane Receptors (water soluble)

Question 17

Intracellular Receptors

Answer 17

Fat Soluble
Drug-receptor-binding will affect cell nucleus
Changes cell’s protein synthesis

Question 18

Membrane Receptors

Answer 18

Water Soluble (can’t easily pass phospholipid bilayer)

i. ion channels (ionotropic receptors)
opens or closes ion channels

ii. second messenger mechanism (metabotropic receptors)
Receptor –> G protein (GTP) -like ATP but w/ Guanine
usu. enzyme adenylate cylcase
*cAMP in cell
Act inside cell

Question 19

Drug-receptor interactions : Affinity

Answer 19

drug binds to receptor- how tightly does it bind?

non-competitive: irreversible binds, no let go, nothing competes with it.

competitive: reversible: binds or does not bind, concentration dependent
Law of Mass action:
Lots of drug= lots of binding
Less drug = less binding

Question 20

Drug-receptor interactions: Efficacy

Answer 20

drug produces an effect

i. agonist: drug binds – has normal effect
ii. antagonist: drug binds – block normal effect

Question 21

Drug-receptor interactions: Selectivity

Answer 21

how selective drug is

i. Primary effect (beneficial or desired)– drug binds to specific desired receptors

ii. Side effect (usu, but not always undesired effect)
drug binds to other undesired receptors

Question 22

Drug-receptor interactions: Receptor Regulation

Answer 22

Cells often adjust #s of receptors

Reason for addictions

Question 23

Dose-Response Terminology

Answer 23

ED-50: effective dose in lrg population for 50% of population

TD- 50: toxic dose for 50% population

LD- 50: lethal dose for 50% of population

Question 24

What is TI?

Answer 24

Therapeutic index: measure of safety
TD- 50
TI = ——————–
ED- 50

i.e. Aspirin’s TI > 30
Tylenol = 27
Demerol = 8
Some Chemo treatments ~ 1

Factors:
age
weight
gender
liver/kidney health -alcohol

Question 25

Drug potency graph

Answer 25

More potent if lower dose gets you the same effect

A: most potent
D: lease potent

Question 26

Efficacy Drug Graph

Answer 26

How big of an effect

Tallest= most effect
Shortest: least effect