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Flashcards in Analgesics and pain Deck (132)
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1

What is an antipyretic analgesic?

An analgesic drug that also reduces fever by reducing body temperature

2

What "sets" the mean body temperature?

The hypothalamus

3

What happens when the core body temp is too low?

Body has to increase heat conservation by vasoconstriction and piloerection
Body also increases heat production by shivering and exercise

4

What happens when the core body temp is too high?

Body has to increase heat loss by vasodilation and sweating
Body has to decrease heat production

5

What is the difference between pyresis and hyperthermia?

In pyresis, the thermostat is changed, heat production and loss is in balance and patient feels cold.
In hyperthermia, the thermostat is not altered, heat production is greater than heat loss and patient feels hot

6

Describe the pathogenesis of fever

Occurs due to release of cytokines released in response to tissue injury and infection.
"Critical" endogenous mediators are IL-1B, IL-6 and TNF. They work directly on the hypothalamus to effect a fever (pyresis) response
The mediators cause an increase in prostaglandin synthesis
PGE2 raises the thermostat in the thermoregulatory centre in the hypothalamus through binding of E-prostanoid receptors.
Core temperature is sensed as too low so you feel cold
Increased heat gain

7

How are prostaglandins produced on perception of an inflammatory stimulus?

Phospholipase A2 produced within area of stimulus. This produces arachadonic acid from membrane phospholipids. This can either be converted into leukotrienes or phospholipids. Phospholipids are formed by enzymes called cyclooxygenases and a range of PGs are formed, with PGE2 being most important in pyresis

8

What is the function of COX-1 enzymes?

Maintain physiological levels of prostaglandins

9

Which COX enzymes are always present (constitutive) and which are inducible?

COX-1 and COX-3 constitutive
COX-2 inducible

10

When are COX-2 enzymes induced and what cells can they be produced by?

Induced during inflammation
Can be produced by macrophages, endothelial cells, synoviocytes
In the hypothalamus, microvascular endothelial cells are the most important at producing COX-2 during the fever response

11

What is the mechanism of action of anti-pyretics?

Inhibit COX enzymes so prostaglandins are not formed and therefore no action on the hypothalamus so body temp not changed

12

Which COX enzymes are inhibited by aspirin and ibuprofen?

COX-1 and COX-2

13

Which COX enzymes are inhibited by paracetamol?

COX-3 and COX-2 (weak)

14

Is the inhibition of COX enzymes by aspirin reversible or irreversible?

Irreversible

15

Is the inhibition of COX enzymes by ibuprofen reversible or irreversible?

Reversible, competitive

16

Is the inhibition of COX enzymes by paracetamol reversible or irreversible?

Reversible, non-competitive

17

Do NSAIDs and aspirin exert their effect centrally or peripherally?

Peripherally

18

Does paracetamol exert its effect centrally or peripherally?

Centrally - making it a more suitable (first-line) antipyretic in comparison to NSAIDs and aspirin

19

How can aspirin overdose be treated?

Bicarbonate ions - make urine alkaline, increases ionisation of aspirin and therefore increases excretion

20

How can paracetamol overdose be treated?

N-acetylcysteine

21

Describe stage 1 of general anaesthesia

Stage 1 is induction - analgesia begins
Patient is conscious but drowsy
Length varies depending on agent - much longer for ether than halothane
Ideally want to get through this stage as quickly as possible for patients comfort

22

Describe stage 2 of general analgesia

Responses to non-painful stimuli are lost but responses to painful ones are preserved
Coughing/gas reflexes are exacerbated so there is a risk of choking, breath-holding, vomiting and movement
Stage 2 therefore needs to be limited/avoided

23

Which is the desired phase of general anaesthesia for surgery?

Stage 3

24

Describe stage 3 of general anaesthesia

No response to painful stimuli
Patient has regular respiration
There is no/limited movement (possibly some muscle reflexes as muscle tone is preserved)
Breathing gets progressively shallower

25

Describe stage 4 of general anaesthesia

Medullary paralysis occurs. The medulla controls breathing and CV reflexes so control over respiration and vasomotor reflexes is lost
This can result in coma and death unless quickly treated
Aim is to maintain stage 3 as long as needed and not progress to stage 4

26

Give an example of a general anaesthetic that is used for rapid induction of unconsciousness

IV propofol

27

Give an example of a general anaesthetic that is used for maintenance of unconsciousness and production of anaesthesia

Inhaled nitrous oxide/halothane

28

Name a neuromuscular blocker used as a general anaesthetic and which stage is it relevant to?

Atracurium - stage 3 to stop spontaneous movements

29

Describe the lipid theory to how general anaesthetics work

As lipid solubility increased, potency of anaesthetic agent increased
Also noted that general anaesthetics had very diverse structures, suggesting they could not all affect a common receptor. This led to the theory that they act via disruption of the cell membrane (lipid bilayer)

30

Describe the protein theory to how general anaesthetics work

Flaws in the lipid theory suggested that rather than affecting the lipid membrane itself, general anaesthetics may act at specific membrane proteins within the membrane to bring about their effect. Suggested targets included GABA and NMDA receptors
General anaesthetic binding is thought to affect ion flow through the channels - either by increasing flow through GABA or blocking flow in the case of NMDA