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Principles of Therapy > Theme 5 - Pain and inflammation > Flashcards

Theme 5 - Pain and inflammation Flashcards

1
Q

What is the main mechanism of action of NSAIDs?

A

Inhibition of prostaglandin synthesis

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2
Q

How do NSAIDs inhibit prostaglandin synthesis?

A

Act mainly peripherally by inhibiting COX1 & COX2 – enzymes

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3
Q

What does NSAIDs stand for?

A

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS

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4
Q

Name clinical uses of aspirin-like drugs

A

Anti-inflammatory, Analgesic (pain relief), Antipyretic (lowers fever)

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5
Q

What is the effect of aspirin on bleeding time?

A

Increased bleeding time

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6
Q

Which Gastrointestinal effects does aspirin have?

A

epigastric discomfort, nausea and vomiting, gastric ulcerations and bleeding

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7
Q

What effect does aspirin have on Urate excretion?

A

usual dose: decreases urate exretion

high dose: uricosuric effect

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8
Q

What effect does long-term use of aspirin have on the cardiovascular system?

A

The haematocrit is lowered and the cardiac output as well as work rate of the heart increased

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9
Q

What effect does aspirin have on the cardiovascular system of patients with carditis?

A

cardiac failure and pulmonary oedema

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10
Q

What can cause a sever reaction to aspirin?

A

Aspirin hypersensitivity

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11
Q

What happens indirectly to the respiratory system after an aspirin overdose?

A

induces the decoupling of oxidative phosphorylation in the skeletal muscles with a resulting increase in CO2-production that stimulates the respiratory centre which leads to hyperventilation

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12
Q

What happens directly to the respiratory system after an aspirin overdose?

A

direct stimulating effect on the respiratory center in medulla oblongata. This is a more potent stimulus than the indirect mechanism

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13
Q

What happens to the cardiovascular system after an aspirin overdose?

A

It is only after excessively high doses that the salicylates suppress the vasomotoric center resulting in circulatory collapse.

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14
Q

What happens to the acid-base status and water-electrolyte balance after an aspirin overdose?

A

respiratory alkalosis that will metabolically be compensated, severe: metabolic acidosis as well as a respiratory acidosis

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15
Q

What happens to the CNS after an aspirin overdose?

A

convulsions followed by generalised CNS suppression, increase in temperature metabolic rate

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16
Q

Which toxic effects develop during paracetamol overdose?

A

Fatal hepatic necrosis

Renal tubular necrosis

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17
Q

Where is aspirin absorbed?

A

Mainly upper GIT, partially in stomach

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18
Q

Where is aspirin hydrolysed?

A

GIT mucosa , liver, blood

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19
Q

What hydrolyses aspirin in GIT mucosa and blood?

A

esterases

20
Q

What is the nature of the hydrolysis of aspirin in the liver?

A

Vert fast, only present in plasma for short period of time

21
Q

What happens to aspirin after hydrolysis?

A

it becomes deacetylated

22
Q

What is the effect of the fast hydrolysis of aspirin in the blood?

A

A large portion of the pharmacological effects of aspirin must therefore be attributed to the mode of action of the deacetylated salicylate

23
Q

What does aspirin bind to in the plasma?

A

Plasma proteins (albumin)

24
Q

What does aspirin compete with for binding to proteins?

A

bilirubin or oral hypoglycemic drugs

25
Q

What is the effect of the competition for protein binding (aspirin)

A

This may give rise to undesirable and potentially dangerous interactions

26
Q

At body-pH is aspirin mostly ionised/unionised?

A

ionised

27
Q

What effect does the ionised property have on aspirin?

A

It cannot cross BBB

28
Q

Does the biotransformation of aspirin usually follow first-order or zero-order kinetics?

A

first-order

29
Q

When does aspirin follow zero-order kinetics?

A

In higher dosages when the liver’s biotransformation capacity is saturated

30
Q

What is the main excretory route of aspirin?

A

Kidneys

31
Q

What happens to aspirin when urine is at a low pH?

A

A large portion of the free aspirin is in the unionised form and back diffusion from the glomerular filtrate takes place readily

32
Q

What happens to aspirin when urine is at a high pH?

A

Up to 80% of the ingested drug can be excreted as free salicylate

33
Q

What is the treatment of paracetamol poisoning?

A
  • Prevent further GIT absorption (induce vomiting or perform a gastric lavage).
  • Take blood for a plasma level determination of paracetamol. Follow-up determinations are recommended.
  • Administer an “antidote”, if the patient presents within 12 hours after ingestion: methionine or N-acetyl cysteine.
  • Provide supportive treatment.
  • Treat liver failure.
34
Q

What is the treatment of aspirin poisoning?

A

activated charcoal, urine alkalinisation, haemodialysis

35
Q

List the central effects of morphine

A
  • Analgesia
  • Euphoria/dysphoria
  • Sedation/sleep
  • Suppression of: the cough reflex, respiratory centre, vasomotoric centre with hypotension, certain spinal reflexes and facilitation of others
  • Releasing of ADH resulting in oliguria
  • Decreased release of corticotrophin.
  • Miosis (“pin-point” pupils).
  • Nausea and vomiting by stimulating of the chemoreceptor trigger zone, followed by the reverse by suppression of the vomiting centre.
  • Tolerance
36
Q

List the peripheral effects of morphine

A
  • Decreased motility and increased tone of the GIT with closure of the sphincters leading to constipation.
  • Decreased glandular secretions of the GIT and pancreas.
  • Gall duct spasm and contraction of the sphincter of Oddi.
  • Increased tone of the detrusor muscle of the urinary bladder, but also increased tone of the sphincter such that urination becomes more difficult.
  • Constriction of bronchi – partially as a result of histamine release (only important in emphysema and asthma).
  • Dilatation of skin blood vessels (face, neck and upper chest). It causes an increase in skin temperature and sweat.
  • Pruritis – particularly of nose and cheeks (possibly as a result of histamine).
  • Contraction of erector pili muscles.
  • Lengthening of parturition and increased neonatal mortality.
37
Q

Name the clinical uses of morphine

A

 Relief of visceral and traumatic pain.
 Relief of anxiety in a severe crisis such as shock or myocardial infarctions.
 Control of diarrhea.
 Suppression of cough.

38
Q

What is the affect of morphine in high doses on pain?

A

elevate the pain threshold level

39
Q

What is the affect of morphine in therapeutic doses on pain?

A

lowers the anxiety component of pathological pain

40
Q

What is the difference in effect of morphine with and without pain?

A

With pain: euphoria

Without pain: dysphoria

41
Q

What is the effect of morphine on the GIT?

A

increases the non-propulsive peristalsis, causes constipation

42
Q

What is the effect of morphine on respiration in therapeutic doses?

A

suppresses respiration

43
Q

What is the effect of morphine on respiration in overdoses?

A

patient dies because he ceases breathing

44
Q

Describe the uses of opioid antagonist

A

Less addictive than morphine, saves the lives of patients with morphine overdose

45
Q

Describe the mechanism of action of opioid analgesics

A

They act as agonists on the encephalin and endorphin receptors. The neurons of both apparently have an inhibitory effect on other neurons of the central nervous system

46
Q

What happens when someone becomes tolerant to morphine?

A

Duration of effects decrease, absorption, distribution and excretion of morphine are not changed in tolerant persons

47
Q

What is the mechanism of action of corticosteroids?

A
  • Glucocorticoid binds to receptor inside cell = nuclear receptor (inside nucleus)
  • Involved in regulation of genes that induce specific mRNA synthesis which leads to synthesis of specific proteins
  • Acts on DNA transcription

Principles of Therapy (10 decks)

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