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Pharmacology > Analgesia ( 10% ) > Flashcards

Analgesia ( 10% ) Flashcards

1
Q
  1. Minimal or no tolerance is observed for which of the following opioid effects?
  • a. Analgesia
  • b. Repiratory depression
  • c. Cough suppression
  • d. Euphoria
  • e. Miosis
A

e. Miosis

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2
Q
  1. Chronic use of opioid analgesics leads to tolerance to all of the following effects except:
  • a. Euphoria
  • b. Miosis
  • c. Sedation
  • d. Laugh suppression
  • e. Nausea
A

b. Miosis

(also GI slowing does not develop tolerance)

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3
Q
  1. Codeine
  • a. Has a half life of six hours
  • b. Is excreted via the biliary system
  • c. Does not cross the blood brain barrier
  • d. Is commonly administered intravenously
  • e. Exerts its analgesic effect via conversion to morphine
A

e. Exerts its analgesic effect via conversion to morphine

T1/2 2-4 hours (TDS -QID dosing)

Metabolised in the liver, metabolites excreted in urine

Crosses the BBB

Used orally

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4
Q
  1. Naloxone
  • a. Has a half life of over 4 hours
  • b. Has a half life of less than one hour
  • c. Has a half life of between 2 and 3 hours
  • d. Has a half life of between 1 and 2 hours
  • e. Has a half life of between 3 and 4 hours
A

d. Has a half life of between 1 and 2 hours

  • Morphine 3 hours*
  • Fentanyl 1-2 hours*
  • Codeine 2-4 hours*
  • Methadone >24 hours*
  • Tramadol 5-7 hours*
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5
Q
  1. Pethidine
    * a. Causes raised CSF pressure
A

a. Causes raised CSF pressure

Hopefully you got this one right, sport.

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6
Q
  1. What do kappa receptors mediate?
  • a. Supraspinal analgesia, euphoria
  • b. Truncal rigidity
  • c. Hallucinations, dysphoria
  • d. Respiratory depression, dependence
  • e. Spinal analgesia, miosis
A

a. Supraspinal analgesia, euphoria

Mu - Supraspinal analgesia, resp suppression, euphoria, sedation, decreased GI motility, miosis, physical dependence

Kappa - Spinal analgesia, sedation, dyspnoea, dysphoria/euphoria, dependence, inhibition of ADH release

Delta - Spinal and supraspinal analgesia, inhibition of GI motility

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7
Q
  1. With respect to opioid receptors
  • a. Fentanyl works at kappa receptors
  • b. Both mu and delta receptors contribute to respiratory depression
  • c. Methadone is used for heroin withdrawal because its actions are predominantly at the delta receptors.
  • d. Opioid receptors are coupled to a tyrosine kinase mechanism of action.
  • e. Physical dependence and tolerance is caused by the rapid disintegration of receptors.
A

b. Both mu and delta receptors contribute to respiratory depression

this is the answer given by Nick, however I can only find that mu does this, and delta just does GI effects apart from analgesia. However none of the others seem right either (except maybe e), I didnt find anything on this)

  • a. Fentanyl works at mu receptors
  • c. Methadone is used for heroin withdrawal because its Long duration, and action at mu receptors
  • d. Opioid receptors are coupled to a GPCRs mechanism of action.
  • e. Physical dependence and tolerance is Mechanism not fully understood
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8
Q

Regarding the opioid receptor which is false

  • They are closely linked to the cAMP system
  • Analgesia at a supraspinal level results principally from kappa receptors
  • They are highly concentrated in the dorsal horn of the spinal cord
  • They may be involved in pain modulation
  • Sigma receptors are related to the hallucinogenic effects
A

Analgesia at a supraspinal level results principally from mu receptors

Kappa does spinal analgesia

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9
Q
  1. morphine
  • a. overdose can be reversed by flumazenil
  • b. is an antagonist at kappa receptors.
  • c. acts powerfully as an analgesic directly on the spinal cord
  • d. substitution for pentazocine may result in an abstinence syndrome
  • e. tolerance can result in dilated pupils in overdose.
A

c. acts powerfully as an analgesic directly on the spinal cord

  • a. overdose can be reversed by Naloxone
  • b. is an agonist at kappa receptors
  • d. substitution for pentazocine may result in an abstinence syndrome
    • analgesic/opiate - agonist at kappa receptors, antagonist at mu.
  • e. miosis does not develop tolerance - ie addicts still have small pupils
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10
Q
  1. The half life of naloxone is
  • a. 1-2 minutes
  • b. 2-4 minutes
  • c. 40-60 minutes
  • d. 60-90 minutes
  • e. more than 2 hours
A

d. 60-90 minutes

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11
Q
  1. the opiate associated with seizures when given in high dose to patients with renal failure is
  • a. morphine
  • b. pethidine
  • c. methadone
  • d. fentanyl
  • e. codeine
A

b. pethidine

Also tramadol due to lowering of seizure threshold

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12
Q
  1. methadone is used in the treatment of narcotic addiction because
  • a. it does not produce constipation
  • b. it is a phenylpiperadine class narcotic agonist
  • c. it produces a short withdrawal when ceased
  • d. it produces predictable effects when given orally
  • e. it is a less efficacious analgesic than morphine
A

d. it produces predictable effects when given orally

Slow onset, long duration of action,

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13
Q
  1. Morphine
  • a. Is rapidly excreted
  • b. Has non-active metabolites
  • c. Excreted predominantly by enterohepatic circulation.
  • d. None of the above
A

None are right

  • a. Is rapidly excreted – 90% within 24 hours
  • b. Has active metabolites - M6G is active and has 6-13x the potency of morphine (M3G is inactive)
  • c. Excreted predominantly by renal circulation. Enterohepatic circulation plays a very minor role (10%)
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14
Q

Regarding aspirin

  • It is a selective inhibitor of COX II
  • It is a base.
  • It is slowly absorbed in the ileum.
  • It blocks the CNS response to IL-1
  • Its actions on platelet aggregation is reversible
A

It blocks the CNS response to IL-1

  • It is a non-selective inhibitor of COX I + II.
  • It is a Acid
  • It is slowly absorbed in the Stomach
  • Its actions on platelet aggregation is i**rreversible, so effect last until new platelets are formed (due to covalent bonds)
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15
Q

regarding NSAIDS

  • at high doses aspirin demonstrates first order kinetics
  • aspirin is a reversible inhibitor of COX
  • aspirin at doses < 2g/d reduces uric acid levels
  • all NSAIDS can be found in synovial fluid after repeated dosing
  • use of ibuprofen and aspirin together increases the anti-inflammatory effect
A

all NSAIDS can be found in synovial fluid after repeated dosing

  • at high doses aspirin demonstrates zero order kinetics
  • aspirin is a irreversible inhibitor of COX
  • aspirin at doses < 2g/d reduces uric acid levels
  • use of ibuprofen and aspirin together increases the anti-inflammatory effect
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16
Q

NSAIDS

  • Act by decreasing cAMP via inhibition of prostacyclin
  • Are not useful in reducing the slow releasing substances of anaphylaxis
  • May cause interstitial nephritis and hypokalaemia
  • Have anti-inflammatory action by inhibiting COX – 1
  • Are weak acids and are largely absorbed in the stomach
A

Are not useful in reducing the slow releasing substances of anaphylaxis

Are weak acids and are largely absorbed in the stomach

Top as per Nick, but absorption in stomach also true

  • Act by decreasing prostacyclin via inhibition of COX
  • May cause interstitial nephritis and hypokalaemia
    • ???? ? ATN
  • Have anti-inflammatory action by inhibiting COX 2
    • ​Cox 1 is homeostatic
17
Q

celecoxib

  • 5-10% protein bound
  • a sulphonamide
  • only indicated for acute inflammation
  • not inhibitory to COX-1
  • is primarily metabolized by the kidney
A

a sulphonamide

Apparenlty contains a sulphonamide moiety - this is the answer that was given as correct.

not inhibitory to COX-1

Celecoxib is considered to be COX 2 selective

  • Highly protein bound, as are all NSAIDs
  • only indicated for acute inflammation
    • Do not alter course of rheumatic disease; cannot find specific answer for this
  • is primarily metabolized by the liver (phase 1 and 2 reactions)
18
Q
  1. Indomethacin
  • a. Irreversibly inhibits COX
  • b. Is selective for COX-2
  • c. Causes less GI upset than aspirin
  • d. Is excreted unchanged
A

c. Causes less GI upset than aspirin

Non-selective COX inhibitor used in chronic conditions. Cannot find any further information in notes.

19
Q
  1. Regarding salicylates, which is NOT true?
  • a. Orally administerd, they are mostly absorbed in the small intestine
  • b. When urine is acid (pH 6), clearance of salicylates is above GFR
  • c. Salicylates are distributed to transcellular fluids including synovial and spinal fluid
  • d. Salicylates are more than 50% protein bound
  • e. Biotransformation of salicylates principally takes place in the liver
A

b. When urine is acid (pH 6), clearance of salicylates is above GFR

  • Clearance is increased in alkaline urine as it is in the ionised state. In acidic enviroment it is unionised and hence able to easily cross tissue barriers.*
  • Absorbed in stomach and proximal small intestine*
20
Q

OD of salicylates lead to all of the following except

  • Tinnitus
  • Marked hyperventilation
  • Increased metabolic rate
  • N & V
  • Metabolic alkalosis
A

Metabolic alkalosis.

Respiratory alkalosis and metabolic acidosis

21
Q

Regarding NSAIDS

  • They commonly cause psychosis
  • They may impair the hypotensive effects of ACE inhibitors
  • About 50% of patients develop adverse effects from aspirin
  • Misoprostol is contraindicated with NSAIDs
  • Sulindac is less gastro-irritative than aspirin
A

They may impair the hypotensive effects of ACE inhibitors

ACEi effects are partially mediated through reduced metabolism of bradykinin. ?NSAIDs inhibit bradykinin formation.

Misoprostol is used to prevent gastric ulcers in people taking NSAIDs

22
Q

Which of the following is true of aspirin

  • There is more of the unionized form in acid environment
  • It inhibits lipooxygenase
  • At normal analgesic doses it decreases plasma uric acid levels
  • In OD there is initial metabolic acidosis
  • It decrease the effect of tolbutamide.
A

There is more of the unionized form in acid environment

  • Such as the stomach. Unionised can cross tissues/lipid layers. Ionised cannot (hence why alkalinisation of urine is useful in increasing excretion).*
  • Inhibits cyclooxygenase*
  • In OD there is initial respiratory alkalosis due to direct stimulation of resp centres (12-24 hours), followed by increasing metabolic acidosis*
  • Increases the effects of tolbutamide by displacing it from albumin*
23
Q

aspirin

  • decreases plasma levels of phenytoin
  • increases the activity of spironolactone
  • will cause penicillin G level in plasma to reduce
  • inhibits the uricosuric effect of probenecid
  • toxicity will be enhanced by acetazolamide
A

inhibits the uricosuric effect of probenecid

inhibits uric acid secretion in low doses (inhibits reabsorption in high doses - same as probenacid)

toxicity will be enhanced by acetazolamide

  • Both create a metabolic acidosis + hyperventilation*
  • Will increase penicillin levels in plasma due to same effect as probenacid
24
Q

Celecoxib

  • Is a IIaIIIb antagonist
  • Has a high affinity for the COX 1 receptor
  • Inhibits PG synthesis in the stomach and SI
  • Has minimal antiplatelet action
  • Is beneficial in secondary stroke prevention
A

Has minimal antiplatelet action

  • Is a IIaIIIb antagonist - I dont know what this is.
  • Has a high affinity for the COX 2 receptor
  • Does not inhibit PG synthesis in the stomach and SI as this is mediated by COX 1
  • Is not beneficial in secondary stroke prevention as it does not have much antiplatelet action
25
Q

All are NSAIDS except

  • Sulindac
  • Piroxicam
  • Gemfibrozil
  • Ketorolac
  • Diflunisal
A

Gemfibrozil

26
Q

paracetamol

  • has no significant anti-inflammatory effects
  • has no pharmacologically active metabolites even in high doses
  • 25% is excreted unchanged.
  • half life is 12-14 hours.
  • increases uric acid levels significantly.
A

has no significant anti-inflammatory effects

  • Definitely has pharmacologically active metabolites even in high doses - NAPQI -> hepatic failure. Hence every tox patient getting a paracetamol level. Fuck you if you chose this answer, dumb cunt.
  • <5% is excreted unchanged - 95% -> phase 2 reactions
  • half life is 2 hours
  • does not increases uric acid levels significantly (cf NSAIDs which can)
27
Q

the toxic effect of paracetamol

  • can be avoided using cimetidine to inhibit cytochrome P450 system
  • are always evident with doses of 150mg/kg and greater
  • in chronic OD are less likely than in acute OD.
  • include neurotoxicity resulting in personality changes
  • occur because sulfation/glucuronidation pathways and metabolism are saturable
A

occur because sulfation/glucuronidation pathways and metabolism are saturable

These are the harmless metabolite pathways.

  • can be avoided using NAC to metabolise to glutathione, and hence provide enough substrate to avoid NAPQI formation.
  • begin to become evident with doses of 150mg/kg and greater
  • in chronic OD are more likely than in acute OD
    • ?due to chronic glutathione and substrate depletion
  • include neurotoxicity resulting in personality changes
28
Q

the main mechanism of colchicines is

  • inhibition of PMN
  • inhibition of synoviocyte phagocytosis
  • reduced formation of LTD4
  • inhibition of mononuclear phagocytes
  • decreasing the body pool of urate
A

inhibition of PMN

  • Inhibits polymorphonuclearcyte chemotaxis, polymerisastion, and mitosis*
  • Reduces release of LTD4*
29
Q

colchicine

  • arrests cell mitosis in anaphase
  • causes the release of HA from mast cells
  • inhibits the movement of melanin granules in melanophores
  • is mainly excreted in the urine
  • should never be administered IV
A

arrests cell mitosis in anaphase

Pharmacology (13 decks)

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