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DEN 2026 - Pharmacology > NSAIDs and Paracetamol > Flashcards

NSAIDs and Paracetamol Flashcards

1
Q

What nerve and its divisions cause dental pain?

A

Maxillary and mandibular divisions of the trigeminal nerve

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2
Q

What 2 types of fibres are found in the dental pulp?

A
  1. High threshold (fast) mechanoceptors connected to Aδ axons
  2. Polymodal nociceptors (slow) which are bare nerve endings of C fibres
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3
Q

What type of pain is felt if high threshold mechanoceptors are stimulated?

A

Sharp pain

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4
Q

What type of pain is felt if polymodal nociceptors are stimulated?

A

Dull ache

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5
Q

What is the name given to 2 drugs working together?

A

Synergy

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6
Q

Why can synergistic drugs help control dental pain?

A

Drugs work at different levels to control pain

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7
Q

Describe the peripheral mediators of pain

A
  • Trauma or infection stimulates activity of phospholipase A₂
  • Increases arachidonic acid formation from cell membrane phospholipids
  • Phospholipids acted on by cyclooxygenases and lipoxygenases to create prostaglandins and leukotrienes
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8
Q

Give 5 methods of relieving pain

A
  1. Remove stimulus
  2. Interrupt nociceptive input
  3. Stimulate nociceptive inhibitory mechanisms
  4. Modulate central pain awareness
  5. Treat secondary factors contributing to pain
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9
Q

Name 2 ways which nociceptive input can be interrupted

A
  1. NSAIDs

2. Local anaesthetic

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10
Q

Name a method of controlling central pain awareness

A

Opiates

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11
Q

Name 5 drugs which can control pain (in ascending order of effectiveness)

A
  1. Paracetamol
  2. Codeine
  3. Dihydrocodeine
  4. Tramadol
  5. Morphine
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12
Q

Why is paracetamol not considered an NSAID?

A

It does not have anti-inflammatory properties

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13
Q

Give 2 ways paracetamol can be described

A
  1. Simple analgesic

2. Antipyretic

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14
Q

Why is paracetamol considered an antipyretic?

A

Inhibits hypothalamic heat-regulation centre

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15
Q

What is the likely mechanism of how paracetamol works as a simple analgesic?

A

Inhibits prostaglandin synthesis in the brain so inhibits pain via CNS inhibition of COX-3

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16
Q

What inactivates paracetamol?

A

Conjugation with glucuronide

17
Q

What occurs if paracetamol is consumed in overdose?

A

Supply of glucuronide is depleted leading to liver and renal toxicity

18
Q

Name 2 metabolites in which paracetamol is removed from the body

A
  1. Sulphate metabolite

2. Glucuronide metabolite

19
Q

What occurs if paracetamol is not conjugated?

A
  • It is oxidised by cytochrome P450
  • It conjugates with glutathione to form non-toxic mercapturic acid
  • If glutathione is absent, hepatic and renal damage can occur
20
Q

Describe aspirin as a drug

A

Irreversible non-selective inhibitor of cyclooxygenase (COX)

21
Q

For what COX does aspirin have greater affinity?

A

COX-1

22
Q

What are the 3 therapeutic doses of aspirin?

A
  1. Low (<300mg/d)
  2. Medium (300-2400mg/d)
  3. High (>2400mg/d)
23
Q

What is the function of each therapeutic dose of aspirin?

A
  1. Low - Anti-platelet
  2. Medium - Analgesic and antipyretic
  3. High - Anti-inflammatory
24
Q

Name 4 potential toxic side effects of aspirin

A
  1. Dyspepsia (gastric upset)
  2. Gastric ulceration and bleeding
  3. Analgesic nephropathy
  4. Increase bronchoconstriction in asthmatic patients
25
Q

Name 5 potential effects of aspirin if taken in overdose

A
  1. Tinnitus
  2. Hyperventilation
  3. Respiratory alkalosis
  4. Hyperthermia
  5. Coma
26
Q

What can occur in children is aspirin is taken in overdose?

A

Reye’s syndrome

27
Q

What is the major difference between aspirin and NSAIDs?

A

NSAIDs are reversible inhibitors of COX1 and COX2

28
Q

Name 4 main NSAIDs used in the UK

A
  1. Ibuprofen
  2. Naproxen
  3. Indometacin
  4. Diclofenac
29
Q

What 3 processes are prostaglandins produced by COX-1 involved in?

A
  1. Protection of gastric mucosa
  2. Platelet aggregation
  3. Renal blood flow autoregulation
30
Q

Why is it desirable to have NSAIDs with greater affinity to COX-2?

A

COX-2 is induced at sites of inflammation so if NSAID has greater affinity to these enzymes, it is more likely to reduce inflammation with less physiological side effects i.e. reduction of processes carried out by prostaglandins

31
Q

What are the 5 main uses of NSAIDs?

A
  1. Analgesia
  2. Anti-inflammatory
  3. Antipyretic
  4. Prolongation of labour
  5. Patency of ductus arteriosus
32
Q

How do NSAIDs work as antipyretics?

A

Block PG action on hypothalamus

33
Q

Name 5 areas of the body which can be adversely affected by NSAIDs

A
  1. GIT
  2. Kidney
  3. Cutaneous
  4. Liver
  5. Blood
34
Q

How can the GIT be affected adversely by NSAIDs?

A

Inhibition of mucosal prostaglandins can promote erosions and ulceration

35
Q

What 2 ways can the kidney be affected adversely by NSAIDs?

A
  1. Renal blood flow can decrease

2. Analgesic Nephritis

36
Q

Name 3 adverse affects of NSAIDs on cutaneous areas of the body

A
  1. Urticaria
  2. Rhinitis
  3. Asthma
37
Q

Name 6 possible drug interactions with NSAIDs

A
  1. ACE inhibitors and ARBs can cause loss of renal function
  2. Quinolone antibiotics can lead to convulsions
  3. Anticoagulants can lead to bleeding
  4. Antihypertensive drugs can reduce effect of NSAIDs
  5. Antidepressant drugs can lead to GI bleeding
  6. Lithium can cause high levels of toxicity as NSAIDs stop lithium elimination
38
Q

Name 6 situations where NSAIDs are contraindicated

A
  1. Patient with peptic ulcer disease
  2. Patient with history of GI bleeding
  3. Patient receiving anticoagulants
  4. Patient with renal impairment, heart failure or hypertension
  5. Used with caution in pregnancy
  6. Previous history of allergic reactions e.g. asthma
39
Q

Name 2 COS-2 selective inhibitors

A
  1. Rofecoxib

2. Celecoxib

DEN 2026 - Pharmacology (22 decks)

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