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PAI (OSCE) > Case Study > Flashcards

Case Study Flashcards

1
Q

What is the molecular targets of opioid analgesics + outline mechanism of action

A

Target mu-opioid receptors

Cause excitable cell hyperpolarisation via activation of GPCRs leading to decreased cAMP formation

Closure of Ca<strong>2</strong>+ channels + opening of K+ channels reduce neurotransmitter release

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2
Q

Discuss common side effects of opioid medicines + explain pharmacological basis

A

Sedation

Respiratory depression

Pruritus

Nausea

Vomiting

Constipation

Urinary retention

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3
Q

Considering excipients in different brands of oxycodone SR tablets, describe mechansims used to control release from these formulations

A

Hypromellose = Hydrophilic swelling matrices

Ethylcellulose = membrane controlled system - release mechanism

Ammoniomethacrylate + hydrogenated castor oil = hydrohphobic matrix

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4
Q

What is multimodal analgesia + what are its principles?

A

Beneficial for post-management pain

Combinations of analgesics w/ different modes/site of action improve analgesia, reduce opioid requirements + reverse ADR of opioid

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5
Q

What types of medicines are used for multimodal analgesia in the management of post-operative pain?

A

Local anaesthetic techniques

Paracetamol

nsNSAIDs

COXIBs

Steroids

Ketamine

Alpha-2-agonist

Alpha-2-delta ligands

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6
Q

What is IV patient controlled analgesia?

A

Method of pain relief allowing patient to self-administer small doses of analgesic as required

Programmable infusion pumps that deliver opioid medications IV

Used for pain following trauma + cancer

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7
Q

Drugs used for IV PCA

A

Morphine

Fentanyl

Oxycodone

Tramadol

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8
Q

What are the dosing parameters in IV PCA to alter analgesia + what is their effect on plasma concentration?

A

Bolus dose - smallest amount capable of producing an appreciable analgesic effect. Provides minimal side effects. Optimal PCA Bolus dose for morphine = 1mg

Lockout interval - safety mechanism set to prevent further doses being delivered until the bolus dose has had time to achieve peak effect.

Background infusion - opioid will continue to be delivered regardless of patient’s sedation or respiratory level. Increases risk of respiratory depression

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9
Q

Describe the pathophysiology of opioid-induced nausea + vomiting?

A

Nausea is mediated by neural pathways, whereas, vomiting is initiated + coordinated by the vomiting centre + chemoreceptor trigger zone (CTZ)

After stimulation of vomiting centre, efferent pathways involve salivary, respiratory + vasomotor centres + cranial nerves mediate vomiting.

Activation of several centres lead to nausea + vomiting.

D2 receptors are located in the stomach, NTS, + CTZ. D2 receptors in the stomach mediate inhibition of gastric motility that occurs during nausea + vomiting, + they participate in reflexes that relax upper part of stomach + delay gastric emptying. Emesis is promoted by slow gastric emptying.

Serotonin act @ (5-HT3)-receptor = important neurotransmitter in afferent pathways from the stomach + small intestine, CTZ, area postrema + NTS.

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10
Q

What are the molecular targets for ondasetron + cyclizine?

A

Ondansetron = 5HT3 receptor antagonist

Cyclizine = piperazine-derivative antihistamine

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11
Q

Why have ondansetron + cyclizine been prescribed in combination?

A

Combination of anti-emetics with different mechanisms have better outcomes than use of single agents

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12
Q

Explain pharmacological effects of senna + docusate in managing opioid-induced constipation

A

Docusate - reduces surface tension of oil + water interface of the stool resulting in enhanced incorporation of water + fat allowing stool softening

Senna - sennosides A + B increase intestinal motility through release of active anthraquinones into the colon by colonic bacteria

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13
Q

What are potential serious complication of epidural administration of analgesics?

A

Neurological Injury

Epidural Haematoma

Epidural abscess/infection

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14
Q

Outline monitoring that is required whilst a patient is receiving epidural analgesia

A

HR + BP

Respiratory rate

Sedation score

Temperature

Pain score

Degree of motor + sensory block

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15
Q

How is inadvertent IV administration of levobupivacaine treated?

A

Lipid emulsion 20%

Due to partitioning of local anaesthetic within emulsion

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16
Q

Identify + describe features of bupivacaine that influence its action @ voltage-gated sodium channels

A

Amphiphilic molecule w/ hydrophobic aromatic ring, linking ester, weakly basic amine group

Incompletely protonated @ physiological extracellular pH

pH dependecy of membrane penetration, while protonation inside cell alters impact on VSNC function

They are weak bases

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17
Q

Why is levobupivacaine preferred to racemic bupivacaine?

A

Levo = S-enantiomer

It has lower affinity @ myocardial + nervous vital centres in studies => fewer CVS + CNS side effects

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18
Q

Recommendation for hypotension during epidural infusion

A

Cease/reduce epidural infusion rate

Fluid challenge

Vasopressors

19
Q

Describe pathways to paracetamol metabolism

A
20
Q

How does paracetamol cause hepatoxicity?

A

Large doses of paracetamol cause acute hepatic necrosis as a result of lack of glutathione + binding of the excess reactive metabolite to vital cell constituents

21
Q

Describe mechanism of action of NSAIDs + binding to their molecular target

A

Inhibit COX enzymes needed for conversion of arachidonic acid to cyclic endoperoxides

Inhibit prostaglandin + thromboxane production

22
Q

Common side effects of NSAIDs + explain pharmacological basis

A

GI Tract

  • Irritation, erosion + ulceration
  • Reduction of prostaglandins => lack of inhibition of gastric acid production, reduced mucus secretion + mucosal wall vasoconnstriction

Renal Impairment

  • PGI2 + PGI3 are vital to renal vasculature smooth muscle tone + renal perfusion
  • Analgesic nephropathy can occur
  • Electrolyte imbalance

NSAID - Induced Asthma

  • Increase leukotrienes + reduced PGE2-mediated bronchodilation

Altered platelet function

  • Don’t inhibit platelet function

CVS

  • Increase BP
23
Q

Strategies to prevent GI side effects of NSAIDs

A

H2 receptor antagonists

Misoprostol

PPI

24
Q

How do COXIBs differ from NSAIDs

A

COXIBs more selective to COX-2 enzyme than 1.

Inhibit prostaglandin synthesis

25
Q

How does mood influence pain?

A

Pain impacts mood + mood influences pain

26
Q

What are symptoms of a sprain?

A

Pain around affected joint

Bruising

Tenderness

Swelling

Inflammation

27
Q

Treatment for a sprain (injury)

A

RICE

28
Q

Signs + symptoms of dysmenorrhea

A

Pain @ lower abdomen

Radiate to thighs + lower back

Co-symptoms include:

  • N + V
  • Diarrhea
  • Constipation
  • Headache
  • Dizziness
  • Disorientation
  • Hypersensitivity to sound, light, smell, touch
  • Fainting
  • Fatigue
29
Q

How do prostaglandins contribute to symptoms of dysmenorrhea?

A

Prostaglandins regulate ovulation, endometrial physiology + menstruation etc

COX enzymes have a role in pathology + angiogenesis, apoptosis + proliferation, tissue invasion + immunosuppression

30
Q

How are the absorption characteristics when ibuprofen is administered as different salt formulations?

A

Speed absorption

Provide better analgesia

Flux across lipophilic membrane is increased by formation of ion-pairs

31
Q

Where is the epidural space?

A

Anatomic space that is the outermost part of the spinal cord.

It is space within canal lying outside dura mater (arachnoid mater, cerebrospinal fluid + spinal cord).

It contains a lymphatic spinal nerve roots, loose fatty tissue, small arteries + a network of large thin-walled blood vessels called epidural venous plexus

32
Q

Why did anaesthetist annotate the drug chart to ensure that enoxaparin was not administered on the day of surgery?

A

Enoxaparin = a LMW heparin

Anticoagulant used to prevent venous thromboembolism

33
Q

Outline the benefits of using epidural analgesia over parenteral analgesic regimens

A

Provides better pain relief @ rest + movement after all types of surgery

Decrease incidence of N+V + sedation

  • However, higher incidence of pruritis, urinary retention + motor block*
  • Improved pain relief led to increase PaO2 levels + decrease incidence of pulmonary infections + complications*
34
Q

What type of epidural drugs are prescribed?

A

Fentanyl = opiod

Levobupivacaine = LAs

35
Q

Outline the monitoring that is required whilst a patient is receiving epidural analgesia

A
36
Q

How is inadvertent IV admin of levobupivacaine treated?

A

Lipid emulsion 20%

Liquid emulsion helps to partition LAs within emulsion itself

37
Q

Identify and describe structural features of bupivacaine that influence its action at VGSC

A

Amphiphilic molecule witha hydrophobic aromatic ring, linking ester, weakly basic amine group,

which is incompletely protonated @ physiological pH, pH dependency of membrane penetration while protonation inside cell alters VGSC function

38
Q

Calculate the proportion of bupivacaine + lidocaine ionised @ physiological pH (7.4)

A
39
Q

Explain the clinical onsequences of the difference in physicochemical properties of lidocaine + bupivacaine

A

Lidocaine has a faster onset of action than bupivacaine as it is more unionised @ physiological pH + will teach its target site more quickly than the drug which is less so

40
Q

Why is levobupivacaine preferred clinically to bupivacaine?

A

It has lower affinity @ myocardial + CNS vital centres which leads to fewer CVS + CNS side effects

Levobupivacaine has lower affinity + strength of inhibitory effect onto the inactivated state of cardiac Na+ channels than racemic parent 1R-bupivacaine

It has longer duration of action

41
Q

What would you recommend for hypotension during an epidural infusion?

A

Stop epidural or reduce infusion rate

Fluid challenge

Vasopressors

42
Q

Why would a patient on epidural suffer from hypotension?

A
  1. Epidural - due to sympathetic blockage produces vasodilatation. Compensated for by an increase in cardiac output
  2. Fluid loss - consequence of surgery
  3. Ramipril = witheld around time of surgery
43
Q

Describe the pharmacokinetic + pharmacodynamic differences between tramadol + other opioids?

A

Tramadol is a weak mu-opioid receptor agonist

Inhibits noradrenaline + serotonin reuptake + 5-HT release

Less pronounced opioid side effects (e.g. constipation) but more pronounced side effects (e.g. nausea)

PAI (OSCE) (5 decks)

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