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Pharmacology Review > Review 1 > Flashcards

Review 1 Flashcards

1
Q

Clinical Trials Phase 1

A

Safety. <100 healthy subjects

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2
Q

Clinical Trials Phase 2

A

Efficacy. Hundreds of patients with disease.

Compare to placebo or control group.

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3
Q

Clinical Trials Phase 3

A

> 10,000 participants.

Random Double-Blind.

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4
Q

Clinical Trials Phase 4

A

After FDA approval, post marketing.

You and me!

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5
Q

Schedule I drugs

A

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

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6
Q

Schedule II drugs

A

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

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7
Q

Schedule III drugs

A

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

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8
Q

Schedule IV drugs

A

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

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9
Q

Schedule V drugs

A

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

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10
Q

1st order elimination

A

most common.
elimination proportional to concentration
constant half life

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11
Q

2nd order elimination

A

elimination rate constant/independent of concentration.

Inconsistent half life

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12
Q

How many half lives to “clear” a drug

A

5

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13
Q

Specificity

A

binds to one receptor group but not another.

all alpha receptors no beta receptors

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14
Q

Sensitivity

A

binds to a specific receptor type in a group.

only beta1 receptors, no beta 2 or 3

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15
Q

Competitive Antagonist

A

Agonist and antagonist compete to bind to receptor.

Highest concentration wins

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16
Q

Non-Competitive Antagonist

A

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

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17
Q

Partial agonist

A

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

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18
Q

Emax

A

maximal response.

receptors are saturated, may cause toxicity

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19
Q

ED50

A

Effective dose to get 50% of expected response

20
Q

T/F: Lower ED50 is more potent

A

True

21
Q

TD50

A

Dose that is toxic for 50%

22
Q

Types of AE

A

Drug-Drug
Drug-Food
Allergies

23
Q

Types of Pain

A

Nociceptive, Neuropathic, Psychogenic

24
Q

2 types of nociceptive afferent neurons

A

unmyelinated C fibers (dull, burning, diffuse)

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

25
Q

Pathway of pain from source

A

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

26
Q

opioids MOA/AE

A

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

27
Q

opioids PT concerns

A

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

28
Q

NSAIDS MOA/AE

A

MOA: Reversibly inhibit COX-1 and 2 enzymes. Decreased formation prostaglandin precursors.

AE: GI (N/V, dyspepsia, ulcers, bleed) increased BP, nephrotoxicity, CV risk

29
Q

NSAIDS PT concerns

A

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

30
Q

Neuropathic pain

A

Pain associated with disease or injury to PSN or CNS

31
Q

Neuropathic pain causes

A

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

32
Q

Best treatments for Neuropathic pain

A

Gabapentin, Amitriptyline, Cymbalta, Lyrica

33
Q

Gold Standard for RA

A

Methotrexate

34
Q

Methotrexate MOA and AE

A

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

35
Q

Biologic DMARD MOA:

A

Impacts mediators of inflammatory response.

36
Q

Sulfasalazine (biologic dmard) AE

A

nausea, rash, hepatitis, pneumonitis, bone marrow suppression

37
Q

Hydroxychloroquine (biologic dmard) AE

A

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

38
Q

BIO TNF inhibitors MOA and AE

A

MOA: bind to TNF-alpha receptors to modulate downstream effects on inflammatory process

AE: HA, infection, antibody development, infusion reactions

39
Q

BIO Non-TNF inhibitor MOA and AE

A

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

40
Q

BIO Janus kinase inhibitors MOA and AE

A

MOA: impacts various components of inflammation and antibody processes

AE: infection, nasopharyngitis

41
Q

DMARDS PT concerns

A

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

42
Q

Corticosteroids MOA

A

MOA- decrease inflammation and suppress immune system

43
Q

Corticosteroids short term and long term AE

A

Short term- increased blood glucose, mood changes, fluid retention

Long term- osteoporosis, Cushing’s, thin skin, muscle wasting, adrenal suppression, immunosuppression, poor wound healing

44
Q

SLE treatment

A

NSAIDS, hydroxychloroquine, methotrexate, immunosuppresants

45
Q

OA oral, topical, and injection treatment options

A

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

Pharmacology Review (2 decks)

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