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CPTP 3 > CPTP 3.13 Drugs used in Inflammation Allergy and Pain 1 > Flashcards

CPTP 3.13 Drugs used in Inflammation Allergy and Pain 1 Flashcards

1
Q

Through which route is emergency adrenaline given during anaphylaxis?

A

Intramuscular

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2
Q

What does 1:1000 solution mean in drug calculations?

A

1g in every 1000ml (revise drug calculations)

= 1000mg in 1000ml
= 1mg in 1ml

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3
Q

What are local hormones called? What do these include?

A 
Autocoids
  •  Histamine
  •  Eicosanoids
  •  Serotonin
  •  NO
  •  Kinins
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4
Q

Name the eicosanoids

A
  • Prostaglandins
    • Prostacyclins
    • Thromboxanes
    • Leukotrienes
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5
Q

Where are autocoids produces?

A

In the same tissue they act on, in many tissues (not specific glands)

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6
Q

Do autocoids have a systemic effect? Give an example

A

Only if large amounts are produced and are moved to the circulation.

Anaphylaxis is caused by a systemic-wide increase in histamine

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7
Q

Where are autocoids metabolised?

A

Metabolised locally and have a short duration of action

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8
Q

Where does most histamine synthesis occur? Which cells produce it and where is it stored?

A 
Where the body comes into contact with the environment:
  •  Lungs
  •  Skin 
  •  GI tract
  •  Brain (histaminergic neurones)
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9
Q

Which cells in the skin and lungs create histamine and where is it stored?

A

Produced by mast cells and basophils, and stored in their granules

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10
Q

Which cells in the GI tract create histamine?

A

Enterochromaffin-like (ECL) cells

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11
Q

What does histamine bind to? What does each of these receptors mediate?

A

H1-H4 receptors

H1: Inflammatory and allergic reactions
H2: Gastric acid secretion
H3: Presynaptic receptors (inhibit release)

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12
Q

What is the effect of Histamine on the following, and what receptor mediates this:

1) Lungs?
2) Vascular smooth muscle?
3) Vascular endothelium
4) Peripheral nerves
5) Heart
6) Stomach
7) CNS

What is the clinical manifestation of each?

A

Asthma:
1) Bronchoconstriction, H1

Erythema:
2) Vasodilation, H1

Oedema:
3) Contraction and separation of endothelial cells (creating fenestrations), H1

Pain & Itch:
4) One of many to sensitise multimodal nerves, H1

Minor/negligable
5) Increase in HR and contractility, H2

Peptic ulcers, heartburn
6) Increases gastric acid secretion, H2

Wakefulness
7) Neurotransmitter, H3

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13
Q

In histamine-mediated vasodilation, which vessels are affected?

A

The following dilate:
• Postcapillary venules
• Terminal arterioles

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14
Q

What molecules does H1 receptor stimulation lead to the increased expression of?

A
  • Release of cytokines
    • Release of eicosanoids
    • Expression of endothelial adhesion molecules
    • Activates NFKB (K=kappa)
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15
Q

What is NFKB?

A

A potent pro-inflammatory transcription factor, for innate immune responses

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16
Q

Which immune and inflammatory pathological processes are mediated by histamine?

A
  • Atopic dermatitis
    • Bronchospasm (Asthema)
    • Allergic rhinitus
    • Anaphylaxis
17
Q

What are hypersensitivity reactions?

Give examples

A

Allergic reactions due to IgE production against environmental agents (e.g. pollen)

  • Allergic asthema
  • Allergic rhinitis
  • Food or drug allergy
  • Anaphylactic shock
  • Urticaria (hives) or eczema
18
Q

What causes hypersensitivity? Describe this process.

A

Prior sensitisation to an allergen:
• Initial exposure causes B cells to produce ‘allergen-specific’ IgE antibodies
• These allergen-specific IgE antibodies bind to the surface of mast cells and basophils
• Subsequent exposure to the allergen binds to the IgE, causing crosslinking of mast cells
• The mast cells ‘degranulate’, releasing their mediators (i.e. histamine)

19
Q

How is urticaria and rhinitis most commonly treated?

What are other uses for this?

A

Antihistamines:
• H1 antagonists

Sedatives (first-generation antihistamines) and anti-emetics (for motion sickness)

20
Q

What is the difference between first and second generation antihistamines? Give the formulary example of each.

A

First generation (Chlorphenamine):
• Charge neutral at physiological pH
• Therefore readily cross blood-brain barrier
• Blocks histaminergic actions in the CNS (drowsiness)
• Less selective for H1 and may also bind:
> Cholinergic receptors
> a-adrenergic receptors
> Serotonergic receptors

Second-generation (Cetirizine):
• Ionised at physiological pH
• Therefore they cannot cross the BBB

21
Q

What IS anaphylaxis? (at last.)

A

Short for anaphylactic shock (type of shock) in response to massive histamine release. This is what happens:

  • Widespread increase in vascular permeability
  • Constriction of airways
  • Laryngeal oedema (which can cause suffocation)
22
Q

How is anaphylaxis treated?

A

Steps in order:

1) Stop administration of the antigen (food or drug)
2) Administer adrenaline IM (usually 0.5mg which is 0.5ml of 1:1000 solution)
3) Give the patient oxygen
4) IV fluids if hypotension still present
5) Administer parenteral H1 antagonist chlorphenamine
6) Administer glucocorticoid hydrocortisone

23
Q

What are the effects of adrenaline when administered to treat anaphylaxis? Which receptors are these effects mediated by?

A

a1 receptor:
• Vasoconstriction
• Combats hypotension/shock

B1 receptor:
• Increases HR and force
• Combats hypotension/shock

B2 receptor:
• Bronchodilator
• Decreases wheezing

24
Q

Why is a glucocorticoid administered during anaphylaxis treatment?

A

Some anaphylaxis events have a ‘biphasic response’ because as a result of the histamine release, a number of immune cells are recruited, which takes time to initiate due to gene transcription.

This can create a second ‘wave’ of anaphylaxis which can be prevented by glucocorticoids

25
Q

How do glucocorticoids have their anti-inflammatory effects?

A

They decrease the production of prostaglandins and leukotrienes

26
Q

What type of receptor is H1?

What states can it be in?

A

Gq protein coupled

It is in an equilibrium between active and inactive
• Active: GTP-bound
• Inactive: GDP-bound

They are ‘constitutively active’:
• In the basal state, where an agonist is not bound, the receptor tends towards ACTIVATION

27
Q

What does activation of Gq cause?

A
  • Activation of phospholipase C
    • IP3 and DAG release
    • PKC activated
    • Proteins are phosphorylated
    • Intracellular Ca2+ is released

This increase in intracellular Ca2 will create the symptoms of anaphylaxis:
• Bronchospasm through calmodulin
• Smooth muscle relaxation through NO synthesis causing ERYTHEMA

28
Q

Describe H1 receptor when bound to histamine, when bound to H1 antagonists, and when unbound.

A

(IMG 7) Unbound:
• ‘Constitutively active’ this means that in the basal state, the receptor is slightly active

Bound to histamine:
• When histamine binds, the equilibrium is shifted so that even more H1 receptors are active

H1 antagonists (antihistamines):
  •  Bind preferentially to the inactive confirmation of the H1 receptor, thus shifting the equilibrium to the inactive state
29
Q

What are H1 antagonists more accurately referred to as?

A

Inverse agonists

30
Q

Why are first generation antihistamines (such as the parenteral chlorphenamine) given in anaphylaxis rather than second generation ones?

A

The sedative effects are good for calming the patient down

These also help as their useful side effect is to reduce the pain and itching

31
Q

Describe the pharmacokinetics of antihistamines.

A

Administration:
• Well absorbed orally peak plasma conc. at 2 hours
• Also given topically (including sprays)
• Given parenterally for anaphylaxis

Metabolisation:
• Metabolised in the liver
• Can inhibit CYP450s

32
Q

What are the adverse effects of first generation antihistamines?

A
  • CNS depression (drowsiness)

* Dry mouth (anticholinergic effect)

CPTP 3 (21 decks)

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