Review 1

Question 1

Clinical Trials Phase 1

Answer 1

Safety. <100 healthy subjects

Question 2

Clinical Trials Phase 2

Answer 2

Efficacy. Hundreds of patients with disease.

Compare to placebo or control group.

Question 3

Clinical Trials Phase 3

Answer 3

> 10,000 participants.

Random Double-Blind.

Question 4

Clinical Trials Phase 4

Answer 4

After FDA approval, post marketing.

You and me!

Question 5

Schedule I drugs

Answer 5

Med use- no
Abuse- high
Dependence- high
Ex.- Heroin, LSD, Marijuana

Question 6

Schedule II drugs

Answer 6

Med use- yes
Abuse- high
Dependence- high
Ex.- cocaine, meth, fentanyl, oxycodone, adderall

Question 7

Schedule III drugs

Answer 7

Med use- yes
Abuse- mid
Dependence- mid-low
Ex.- codeine, ketamine, testosterone

Question 8

Schedule IV drugs

Answer 8

Med use- yes
Abuse- low
Dependence- low
Ex.- Tramadol, Xanax, Ambien, Diazepam

Question 9

Schedule V drugs

Answer 9

Med use- yes
Abuse- low
Dependence- n/a
Ex.- lomitil, robitussin, lyrica

Question 10

1st order elimination

Answer 10

most common.
elimination proportional to concentration
constant half life

Question 11

2nd order elimination

Answer 11

elimination rate constant/independent of concentration.

Inconsistent half life

Question 12

How many half lives to “clear” a drug

Answer 12

5

Question 13

Specificity

Answer 13

binds to one receptor group but not another.

all alpha receptors no beta receptors

Question 14

Sensitivity

Answer 14

binds to a specific receptor type in a group.

only beta1 receptors, no beta 2 or 3

Question 15

Competitive Antagonist

Answer 15

Agonist and antagonist compete to bind to receptor.

Highest concentration wins

Question 16

Non-Competitive Antagonist

Answer 16

Near or irreversible binding to receptor
greatly diminishes/blocks agonist effect
increased agonist concentration can’t overcome it

Question 17

Partial agonist

Answer 17

“Doesn’t fit” the receptor exactly like natural ligand
Lower dose = agonist effect
Higher dose= antagonist effect

Question 18

Emax

Answer 18

maximal response.

receptors are saturated, may cause toxicity

Question 19

ED50

Answer 19

Effective dose to get 50% of expected response

Question 20

T/F: Lower ED50 is more potent

Answer 20

True

Question 21

TD50

Answer 21

Dose that is toxic for 50%

Question 22

Types of AE

Answer 22

Drug-Drug
Drug-Food
Allergies

Question 23

Types of Pain

Answer 23

Nociceptive, Neuropathic, Psychogenic

Question 24

2 types of nociceptive afferent neurons

Answer 24

unmyelinated C fibers (dull, burning, diffuse)

finely myelinated A delta fibers (sharp, intense, localized)

Question 25

Pathway of pain from source

Answer 25

Source of pain - dorsal root ganglia - dorsal horn+substantia gelatinose - spinothalmic tracts - brain stem - thalamus - cerebral cortex

Question 26

opioids MOA/AE

Answer 26

MOA- Bind opioid receptors in CNS to inhibit pain pathways AE- CNS: sedation, nausea, respiratory depression, cough suppression, miosis, truncal rigidity PNS: Constipation, urinary retention, bronchospasm, decreased GI motility, pruritis

Question 27

opioids PT concerns

Answer 27

Schedule therapy to maximize pain relief, increased fall risk, avoid heat and exercise in area of patch, drug seeking behavior.

Question 28

NSAIDS MOA/AE

Answer 28

MOA: Reversibly inhibit COX-1 and 2 enzymes. Decreased formation prostaglandin precursors. AE: GI (N/V, dyspepsia, ulcers, bleed) increased BP, nephrotoxicity, CV risk

Question 29

NSAIDS PT concerns

Answer 29

GI, bleeding and bruising risk, DDI with cardiac drugs, increased edema with CHF, HTN, decreased cartilage repair and synthesis

Question 30

Neuropathic pain

Answer 30

Pain associated with disease or injury to PSN or CNS

Question 31

Neuropathic pain causes

Answer 31

Diabetes, immune deficiencies, trauma, shingles, MS, ischemia, cancer, drugs

Question 32

Best treatments for Neuropathic pain

Answer 32

Gabapentin, Amitriptyline, Cymbalta, Lyrica

Question 33

Gold Standard for RA

Answer 33

Methotrexate

Question 34

Methotrexate MOA and AE

Answer 34

MOA: unknown, possibly impacts IL-1, TNF alpha, and leukotrine levels AE: N/V/D, alopecia, malaise, increased LFTs, hepatotoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression

Question 35

Biologic DMARD MOA:

Answer 35

Impacts mediators of inflammatory response.

Question 36

Sulfasalazine (biologic dmard) AE

Answer 36

nausea, rash, hepatitis, pneumonitis, bone marrow suppression

Question 37

Hydroxychloroquine (biologic dmard) AE

Answer 37

dyspepsia, nausea, abdominal pain, rashes, nightmares, visual disturbances

Question 38

BIO TNF inhibitors MOA and AE

Answer 38

MOA: bind to TNF-alpha receptors to modulate downstream effects on inflammatory process AE: HA, infection, antibody development, infusion reactions

Question 39

BIO Non-TNF inhibitor MOA and AE

Answer 39

MOA: impacts inflammation process AE: injection / infusion reactions, increased LFTs, antibody development

Question 40

BIO Janus kinase inhibitors MOA and AE

Answer 40

MOA: impacts various components of inflammation and antibody processes AE: infection, nasopharyngitis

Question 41

DMARDS PT concerns

Answer 41

Review labs DMARDS and Steroids=catabolic stay hydrated, rash, liver effeccts, bruising, fatigue, immunosuppression

Question 42

Corticosteroids MOA

Answer 42

MOA- decrease inflammation and suppress immune system

Question 43

Corticosteroids short term and long term AE

Answer 43

Short term- increased blood glucose, mood changes, fluid retention Long term- osteoporosis, Cushing's, thin skin, muscle wasting, adrenal suppression, immunosuppression, poor wound healing

Question 44

SLE treatment

Answer 44

NSAIDS, hydroxychloroquine, methotrexate, immunosuppresants

Question 45

OA oral, topical, and injection treatment options

Answer 45

Oral- acetaminophen, NSAIDS, Glucosamine chondroitin Topical options- NSAIDS Injections- Intra-articular hyaluronate, Intra-articular steroids (kenalog, depo-medrol)