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Unit 2 > BIOMED 10/24a Pharmacology > Flashcards

BIOMED 10/24a Pharmacology Flashcards

1
Q

sources of opiods

A

opium poppy

endogenous substances like opiods: endorphins, enkephalins, dynorphins

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2
Q

opioid receptors

A
  1. µ (mu)- analgesia, euphoria, resp. depression, addiction (most and best pain relief)
  2. k (kappa)- analgesia, euphoria, sedation (moderate affinity, not same as mu, cause hallucinations and warped perception)
  3. ∂ (delta)- analgesia, sedation
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3
Q

what do opiods when with?

A

ine

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4
Q

what are classifications of opiods?

A
  1. Strong agonists: fully bind to mu
    □ Used to treat severe pain, morphine, meperidine
  2. Mild-to-moderate agonists: partially bind to mu, may bind to kappa or delta
    □ Codeine, oxycodone
  3. Mixed agonist-antagonists:
    □ Nalbulphine (bind to kappa and partially block the mu), buprenorphine (partially binds mus but blocks kappa)
  4. Antagonists: bind and don’t allow opioids to bind, use with overdose
    □ Used to treat opioid overdose and addiction, naloxone
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5
Q

opioid mechanisms of action

A
  1. spinal effects
  2. brain effects
  3. peripheral effects
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6
Q

spinal effects of opioids

A

inhibition of nociceptive pathways

  • Presynaptic: decrease release of substance P
  • Postsynaptic: hyperpolarization
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7
Q

brain effects of opioids

A

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

  • Descending pathways
  • Affect mostly interneurons
  • Altered perception of the pain
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8
Q

peripheral effects of opioids

A

decrease excitability of sensory neurons

-Nociceptors decrease excitability

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9
Q

after pain comes from the ___, it is relayed by ___ to ____ of spinal cord and at each junction there are two main occurances

A

periphery
afferent nerves
dorsal horn

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10
Q

when pain enters the spinal cord, what happens at the junction when there are opioids present?

A
  1. Front end: presynaptic, opioid binds to receptors on sensory nerve and calcium cannot enter -> pain substances (substance P and glutamate) aren’t released because they release with calcium channels opening
  2. Post synaptic: creates opening of potassium channels such that potassium moves out and yields hyperpolarization (too negative) and goes farther away from threshold and AP is not relayed to the next portion inward (decrease awareness to CNS)
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11
Q

what are clinical considerations of opioid treatment for pain management

A
  • treatment is for moderate to severe pain that is consistent
  • alter perception of pain rather than eliminating painful sensations
  • route of admin
  • dosing schedule
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12
Q

what is the difference between oral and parenteral administration of drugs

A

oral - is taken by mouth and is subject to the first pass effect

parenteral - is taken by IV and goes straight to the target tissue

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13
Q

different dosing schedules of opioids

A
  • patient-controlled analgesia: patient can re-adminster at the end of the effective dose
  • fentanyl and other delivery vehicles (more localized) - delivery via patch, injection, and avoid respiratory depression
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14
Q

best dosing schedule of opioids?

A

IV - constantly matching the effect of the drug with the clearance of the drug

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15
Q

what are adverse effects and rehab concerns of opiods?

A
  1. Sedation - narcosis (sleep)
    - Patients will be nodding off and falling asleep most often
  2. Mood changes - dysphoria
    - Can become combative (acutely)
  3. Confusion
  4. respiratory depression
    - most severe
  5. orthostatic hypotension
  6. GI effects
    - decrease GI motility
    - can get some nausea and vomiting
  7. addiction, tolerance, dependence
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16
Q

adverse effects of opioids that cause addiction, tolerance, and physical dependence

A
  1. Addiction
    - Complex interaction of factors that leads to lack of control over drug use, onset of withdrawal should be avoided.
  2. Tolerance
    - The need to progressively increase the dosage of a drug to achieve a therapeutic effect when the drug is used for prolonged periods
    - Receptor downregulation and desensitization, G protein uncoupling
  3. Physical dependence
    - Onset of withdrawal symptoms when drug is abruptly removed
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17
Q

what is the treatment of opioid addiction?

A
  1. Methadone: strong opioid agonist, similar in potency and efficacy to morphine
    - Mild withdrawal
    - Low success rate
  2. Buprenorphine: mixed agonist-antagonist which partially stimulates mu receptors while acting as strong antagonist at kappa receptors
  3. Naloxone (Narcan) nasal spray – antagonist to all receptors but has high affinity for mu
    - Bumping off opioids from mu receptors and binding with them so opioids can’t bind
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18
Q

what type of drug is meperidine?

A

Strong agonist, associated with great pain relief but also problems

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19
Q

when should therapist schedule treatment session so that meperidine is reaching peak effects (effective dose is every 4 hrs)

A

1 hr after administration

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20
Q

what precautions should PT take into place when with a patient who is on meperidine?

A

-Orthostatic hypotension (BP in lying, then at 45o, then 90o)
>Bring reclinable wheelchair or stretcher
-Cognizance of respiratory rate

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21
Q

NSAID primary use

A

in the treatment of mild to moderate pain

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22
Q

4 primary therapeutic effects of NSAIDs

A
  1. Analgesia: pain relief
  2. Anti-inflammatory
  3. Antipyretic: fever resistant
  4. Anti-coagulation
23
Q

mechanism of action for NSAIDs

A

Work by prostaglandin production inhibition

  • Every cell produces and releases prostaglandins
  • When cell is injured, it releases a different type of prostaglandin and we associate with inflammation
24
Q

what is prostaglandin?

A

local hormones that regulate cell function (when injured)

  • inflammation
  • pain
  • fever
  • thrombus formation
25
Q

what is cyclooxygenase inihibition purpose?

A

COX breaks down arachadonic acid into prostaglandin, so when inhibited prostaglandins aren’t created

26
Q

COX1

A
  • associated with release of substances that protect the stomach from gastric acid
  • thromboxanes aggregate platelets to form a clot

-when inhibited, decreased clot formation and decreased protection of the stomach

27
Q

COX2

A

associate with negative consequences of injury

  • Mediates local erythema & edema
  • Mediates pain by ­ sensitivity of receptors
  • Mediates fever
28
Q

clinical applications of aspirin

A

Aspirin (acetylsalicylic acid): the prototypical NSAID, represents the major form of a group of drugs known as salicylates

29
Q

what is aspirin used to treat?

A

-Pain and inflammation
-Fever
-Vascular disorders
-Prevention of cancer
>Cholorectal cancer prevention
>Type of prostaglandin that’s a tumor promotor

30
Q

Risk factors for anti-inflammatory drugs or aspirin?

A
  1. GI complications
  2. Age (>65) - liver and kidneys are not working as efficiently to clear the drug (so we have more accumulation)
  3. peptic ulcer
  4. other drugs
  5. Drugs that mask the symptoms
  6. multiple anti-inflammatories
  7. systemic illness
  8. People who have a history of RA and an inflammatory component may be taking an NSAID for pain relief
  9. cigarette smoking and alcohol
31
Q

clinical signs of risk from aspirin?

A
  1. silent mostly but can have pain (Thoracic/in the back)
  2. heart burn
  3. Nausea
  4. Melena (tarry/bloody stool)
  5. Fatigue
32
Q

adverse effects of NSAIDs

A
  1. GI
  2. CV (Increased BP, Increased blood clots - COX2)
  3. Hepatic and renal problems
  4. NSAID toxicity
  5. inhibit bone healing
  6. inhibit tissue healing
33
Q

what is NSAID toxicity?

A
  1. Keep taking more NSAIDs and headache keeps getting worse
  2. Causes confusion
  3. Damage to cranial nerve 8 (loss of hearing)
  4. Ringing in the ears (tinnitus)
34
Q

do NSAIDs inhibit tissue healing?

A
  1. Mixed results because this is time dependent
  2. Balance between degradation and production
  3. TBD!!
35
Q

COX-2 (fever, pain, inflammation) Selective Inhibitors (COXIBS)

A

Celecoxib (Celebrex) - caused death from hypertension and stroke, Etoricoxib (EFLAM, ETO, etc)(label warnings)
1. By inhibiting COX2 and not COX1, there is no anti-coag ability: more clots
2. Prostacyclin is produced and counters the COX1
-When it isn’t produced, there is increased vasoconstriction -> leads to hypertension and ability to counteract
-People died as a result of strokes and heart attacks right away
3. Inhibit synthesis of inflammatory prostaglandins produced by COX-2, while sparing the production of beneficial COX-1 prostaglandins that help regulate normal physiological function
4. Lower incidence of GI irritation
5. Preferred by patients at risk for prolonged bleeding and bruising (thromboxanes not inhibited)
Risk of heart attack and stroke

36
Q

Acetaminophen compared to NSAIDs

A
  • Similar analgesic and antipyretic effects
  • No anti-inflammatory or anticoagulant effects
  • No upper GI tract irritation
37
Q

mechanism of action of acetaminophen

A
  • Might only act in CNS (COX-3?)

- Doesn’t have the same effect on the prostaglandins as the others

38
Q

adverse effects of acetaminophen

A

hepatotoxicity

Initial metabolites is very toxic to the liver even in small doses

39
Q

is it good to have an allergy med that is combined with acetaminophen?

A

NO - reduces the effective dose of each drug

40
Q

topical agents that have acetaminophen

A
  1. ointments
  2. sprays, creams and patches
  3. adverse effects
41
Q

how do ointments work for reducing inflammation

A

contain menthol or capsaicin

and are a counter irritant for the pain

42
Q

how do sprays, creams and patches work for pain relief?

A
  • Contain aspirin or other NSAID’s
  • Salicylates
  • Salonpas - have salicylic acid in them
  • Work with repetition for results
  • Does reach down into the dermis
43
Q

what are adverse effects of topical agents for pain relief?

A

□ Ointment – burning sensation

Sprays - rash

44
Q

2 major categories of anti-inflammatory drugs

A
  1. NSAIDs

2. Glucocorticoids (steroidal)

45
Q

NSAIDs for anti-inflammatory properties

A

NSAID’s used in mild to moderate inflammation.

Takes higher dosage of active ingredient to be effective for anti-inflammatory effects

46
Q

Glucocorticoids for anti-inflammatory properties

A

used in moderate to severe inflammation

-ending in “one”

47
Q

glucocorticoids mechanism of action

A

Inhibits phospholipase (enzyme) so everything downstream doesn’t happen

  1. Phospholipase triggers ramp up of pro-inflammatory substances
  2. So, when it’s inhibited, the glucocorticoids are immunosuppressant
48
Q

adverse effects and rehab concerns for glucocorticoids

A
  1. Tendon, ligament, and wound healing (all because it has a negative affect on protein and collagen production)
  2. Catabolic effects
  3. Delay wound healing
  4. Adrenocortical suppression
  5. Salt/water retention
  6. Increased infections
  7. Peptic ulcers
  8. Hyperglycemia
  9. Systemic vs localized admin
49
Q

what does it mean to have adrenocortical suppression from glucocorticoids?

A
  1. Glucocorticoids are synthetic version of cortisol
  2. Cortisol in body gets shut down
  3. Front end loaded to put out the inflammation (dose packages)
  4. If you went through all of them at one time, BP drops tremendously and won’t be able to ramp up production
50
Q

what does salt/water retention from glucocorticoids yield?

A

Moon face

Need to monitor blood pressure with this

51
Q

why do people on glucocorticoids get infections more easily

A

no inflammatory substances circulating to help combat

52
Q

how many injections of glucocorticoids can one get a year

A

3-4 MAX

53
Q

how does acetaminophen differ from NSAIDs like aspirin and ibuprophen?

A

acetaminophen has pain and fever effects, but no effects on inflammation

54
Q

rehab concerns when pt is taking NSAIDs

A
  1. Are you taking anything?
  2. What are you taking?
  3. Was this prescribed to you or did you have it in your home?
  4. Consider age for age related consequences to organs
  5. Peptic ulcers?
  6. Antacids?
  7. Tums for calcium?
  8. Input from physician - how much and how often?

Unit 2 (31 decks)

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