Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 2 > Pharm: Analgesics & Anti-Inflammatories (10/24a) [Biomedical] > Flashcards

Pharm: Analgesics & Anti-Inflammatories (10/24a) [Biomedical] Flashcards

1
Q

Sources of Opioids

A

Opium poppy

Endogenous opioids
- endorphins, enkephalins, dynorphins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Opioid Receptors

A

µ (mu) — analgesia, euphoria, respiratory depression, addiction, fastest pain relief, strongest side effects

k (kappa) — analgesia, euphoria, sedation, psychotropic

∂ (delta) — analgesia, sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Opioid Classification

A

Strong agonists

  • used to treat severe pain
  • EX: morphine, meperidine

Mild-to-moderate agonists
- EX: codeine, oxycodone

Mixed agonist-antagonists
- EX: nalbuphine, buprenorphine

Antagonists

  • used to treat opioid overdose and addiction
  • EX: naloxone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Opioid Mechanism of Action - Spinal Effects

A

inhibition of nociceptive pathways

Presynaptic — decrease release of substance P

Postsynaptic — hyperpolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Opioid Mechanism of Action - Brain Effects

A

influence descending pain pathways, norepinephrine and serotonin, which inhibit pain pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Opioid Mechanism of Action - Peripheral Effects

A

decrease excitability of sensory neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Opioid - Mechanism of Action

A

Pain stimulus is sent from the periphery and relayed by afferent to dorsal horn in spinal cord

Presynaptic — at each junction the opioid binds to the receptors and blocks calcium channels, release of pain substances blocked

Postsynaptic — opioid binds to the nerve and creates opening of K+ channel and K+ flows out, causes that part of the synapse to become hyperpolarized and action potential can’t be triggered

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Opioid Clinical Considerations

A

Treatment of moderate-to-severe pain that is consistent

Alter perception of pain rather than eliminating painful sensation

Oral vs parenteral route of administration

Dosing schedule

  • Patient controlled analgesia
  • Fentanyl and other delivery vehicles (more localized)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Opioid Adverse Effects and Rehab Concerns

A

Sedation aka narcosis (most common)

Mood changes — dysphoria

Confusion

Respiratory depression — responsible for fatalities

Orthostatic hypotension

GI effects — decreased GI motility, nausea, vomiting

Tolerance and dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes opioid tolerance

A

Receptor downregulation and desensitization, G protein uncoupling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Opioid Addiction Treatment - Methadone

A

strong opioid agonist, similar in potency and efficacy to morphine

Mild withdrawal, Low success rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Opioid Addiction Treatment - Buprenorphine

A

mixed agonist-antagonist which partially stimulates mu receptors while acting as strong antagonist at kappa receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Opioid Addiction Treatment - Naloxone (Narcan)

A

nasal spray, used as rescue strategy

antagonist to all receptors but has high affinity for mu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

A

Used in the treatment of mild-to-moderate pain and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

NSAIDs - 4 primary therapeutic effects

A

Analgesia (pain)
Anti-inflammatory
Antipyretic (fever)
Anti-coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do NSAIDs work

A

Work by prostaglandin production inhibition

Prostaglandins — local hormones that regulate cell function
- inflammation, pain, fever, thrombus formation

17
Q

NSAIDs - Overall Mechanism of Action

A

When the cell is injured, cyclooxygenase break downs arachidonic acid→ leads to inflammation, pain, thrombus formation, etc

NSAIDs are responsible for cyclooxygenase (COX) inhibition

18
Q

NSAIDs Mechanism of Action - COX1 Inhibition

A

Protect stomach lining from gastric acid

Thromboxanes-platelet aggregation

19
Q

NSAIDs Mechanism of Action - COX2 Inhibition

A

Mediates:

local erythema & edema

pain, by ­increasing sensitivity of receptors

fever

20
Q

Risk Factors for NSAIDs — GI Complications

A

Typically no warning of severe complication

Risk factors:
- Age (>65), peptic ulcer, other drugs, multiple anti-inflammatories, systemic illness, cigarette smoking and alcohol

Clinical signs — silent mostly but can have pain, heartburn, nausea, melena (blood in stool), fatigue, severe is internal bleeding

21
Q

NSAIDs Adverse Effects

A

Gastrointestinal problems

Cardiovascular problems

  • Increase blood pressure
  • Increase blood clotting (COX2)

Hepatic and renal problems

NSAID toxicity — confusion, cranial nerve damage, tinnitus

Inhibit bone healing

Inhibit tissue healing?

22
Q

NSAIDs - COX2 Selective Inhibitors (Coxibs)

A

Inhibit synthesis of inflammatory prostaglandins produced by COX-2, while sparing the production of beneficial COX-1 prostaglandins that help regulate normal physiological function

Lower incidence of GI irritation

Preferred by patients at risk for prolonged bleeding and bruising (thromboxanes not inhibited)

Risk of heart attack and stroke

EX: Celecoxib (Celebrex), Etoricoxib (EFLAM, ETO, etc)

23
Q

NSAIDs - Aspirin

A

the prototypical NSAID, represents the major form of a group of drugs known as salicylates

Treatment of:

  • Pain and inflammation
  • Fever
  • Vascular disorders
  • Prevention of cancer (colorectal)
24
Q

Acetaminophen

A

Compared to NSAIDs

  • similar analgesic and antipyretic effects
  • no anti-inflammatory or anticoagulant effects
  • no upper GI tract irritation

Mechanism of action
- might only act in CNS (COX-3?)

Adverse effects — hepatotoxicity (liver damage at low doses)

Often combined with other meds (EX: cold meds)

25
Q

Topical Agents

A

Ointments

  • Contain menthol or capsaicin
  • EX: Bengay, Icy Hot, Tiger Balm
  • Adverse Effects — burning sensation

Sprays, creams and patches

  • Contain aspirin or other NSAIDs
  • EX: aspercreme, salonpas
  • Adverse Effects — rash
26
Q

2 types of anti-inflammatory drugs

A

NSAIDs — requires higher dose to get anti-inflammatory effects

Glucocorticoids

27
Q

Glucocorticoids

A

used in moderate to severe inflammation

ends in “-one” (EX: dexamethasone, hydrocortisone)

inhibits phospholipase, also immunosuppressant

28
Q

Glucocorticoids - Adverse Effects

A

Impaired tendon, ligament, bone, wound healing — due to effect on collagen

Catabolic effects

Adrenocortical suppression

Salt/water retention

Increased infections

Peptic ulcers

Hyperglycemia

Systemic vs localized administration
- max 3-4 injections per joint per year

Unit 2 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions