DPT 5010 Pharmacology- Drugs Flashcards
Signs & Symptoms of Inflammation
Rubor
Calor
Tumor
Dolor
NSAIDs: Non Steroidal anti-inflammatory drugs
(Aspirin)
a. Antithrombotic: inhibits platelets, clotting
b. Antipyretic: inhibits fever
c. Analgesic: inhibits pain
d. Anti-inflammatory: inhibits inflammation @ injury site
Side Effects of NSAIDs (Aspirin)
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
NSAIDs apart from Aspirin
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
Non-narcotic analgesic/antipyretic: Acetominophen
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
Drug Implications on Rehab:
Decrease Pain + Decrease Inflammation
=
Increased mobility & effort
Glucocorticoids
Glucose/ Adrenal Cortex/ Steroids
Normal physiology of Cortisol:
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)
Anabolic Steroids
ALL related to testosterone
take to increase muscle
DIFFERENT from glucocorticoids
Pharmacological use of glucocorticoids:
Anti-inflammatory effects through the inhibition of the phospholipase pathway.
Reasons to prescribe glucocorticoids:
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
Methods of Administering glucocorticoids
Topical Oral Injection Use of mist/drops -lungs -nasal -otic and ophthalmic
General Side effects of glucocorticoids
2° to overloaded normal metabolic effects
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”)
Examples of glucocorticoids used pharmacologically
Short 1/2 life (cortisone)
Intermediate 1/2 life (prednisone)
Long 1/2 life (dexamethasone)
Pharmacodynamics
How drugs exert their effects
Pharmacodynamics: Receptors
ALWAYS proteins (drug is ligand --> binds to protein) Intracellular Receptors (fat soluble) Membrane Receptors (water soluble)
Intracellular Receptors
Fat Soluble
Drug-receptor-binding will affect cell nucleus
Changes cell’s protein synthesis
Membrane Receptors
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
Drug-receptor interactions : Affinity
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
Drug-receptor interactions: Efficacy
drug produces an effect
i. agonist: drug binds – has normal effect
ii. antagonist: drug binds – block normal effect
Drug-receptor interactions: Selectivity
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
Drug-receptor interactions: Receptor Regulation
Cells often adjust #s of receptors
Reason for addictions
Dose-Response Terminology
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
What is TI?
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
Drug potency graph
More potent if lower dose gets you the same effect
A: most potent
D: lease potent
Efficacy Drug Graph
How big of an effect
Tallest= most effect
Shortest: least effect
