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1Principles of Biomedicine - MD1 > 67 - Cellular and Molecular Aspects of Allergy > Flashcards

67 - Cellular and Molecular Aspects of Allergy Flashcards

1
Q

Where are mast cells often found?

A

Body sites in contact with external environment: skin, gut, lung Often close to blood vessels, nerves, glands

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2
Q

Things that can stimulate mast cells 1) 2) 3) 4) 5) 6) 7) 8)

A

EXTERNAL FACTORS 1) Polybasic drugs (vancomycin, morphine) 2) Mechanical stimulation 3) UV light, heat 4) Allergen (IgE-mediated) 5) Stings 6) Osmotic stimuli (hypertonic saline) INTERNAL FACTORS 7) Activated C’ 8) Neuropeptides

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3
Q

Unusual feature of ITAMS

A

No integral kinase activity. Activity arises when they cluster

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4
Q

Atopy

A

Genetic predisposition to overproduction of IgE against a specific antigen

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5
Q

Diseases associated with asthma

A

RSV, rhinovirus, strongly implicated as risk factors in development of asthma, if caught at an early age.

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6
Q

Mechanism of degranulation

A

Channels form in membrane, through which granule contents exit cell

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7
Q

Subunits of FceRI

A

Alpha1, alpha2 make up binding site, beta (4-pass transmembrane loop), 2xgamma

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8
Q

FceRI subunits with ITAMs

A

Beta and gamma1, 2

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9
Q

Pathways stimulated by FceRI stimulation 1) 2) 3)

A

1) MAPK 2) NF-kB 3) Phospholipase C

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10
Q

Immediate factors released by activated mast cells

A

Histamine Heparan sulphate Tryptase TNFa These are preformed mediators

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11
Q

How long does it take for mast cells to release preformed mediators?

A

~30-45 seconds

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12
Q

Phases of mast cell response 1) 2) 3)

A

1) Immediate (preformed mediators) 2) Rapid (arachidonic acid mediators) 3) Slow (transcription, translation of cytokines)

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13
Q

Rapid mediators released by mast cells

A

Cyteinyl leukotrienes PGD2

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14
Q

How long does it take for mast cells to release rapid mediators

A

Peak around 10-30 minutes

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15
Q

Slow mediators released by mast cells

A

IL-4, IL-5, GM-CSF

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16
Q

Timeframe for slow action of mast cells

A

Occurs over hours to days

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17
Q

Action of histamine stimulation of H1 receptors 1) 2) 3) 4) 5) 6)

A

1) Pain, itching 2) Bronchospasm 3) Mucus secretion 4) Vasodilation (hypotension) 5) Increased vascular lead (hypovolaemia) 6) Increased wakefulness (CNS activity)

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18
Q

Action of histamine stimulation of H2 receptors 1) 2)

A

1) Gastric acid secretion 2) Positive inotropic, chronotropic effect on heart (increases contractility, heart rate)

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19
Q

Cysteinyl leukotriene production

A

Glutathione-S-transferase converts LTA4 to LTC4

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20
Q

Cells producing cysteinyl leukotrienes

A

Macrophages, eosinophils, mast cells

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21
Q

Stimuli leading to LTC4 production 1) 2) 3)

A

1) Allergen 2) C5a 3) Platelet-activating factor

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22
Q

Mediators active at CysLT1 receptor

A

LTC4 and metabolites (LTD4, LTE4)

23
Q

Physiological roles of LTC4

A

None known

24
Q

Pathophysiological roles of LTC4 1) 2) 3) 4) 5) 6)

A

1) Hypotension during anaphylactic shock 2) Vasodilator in skeletal muscle 3) Diminished cardiovascular output 4) Hypovolaemia 5) Airway obstruction in asthma (mucus, oedema, airway smooth muscle shortening) 6) Nasal congestion in hayfever (mucus, oedema)

25
Q

*Arachidonic acid pathway

A
26
Q

What activates arachidonic acid pathway?

A

Increase in cytosolic Ca2+ by stimuli produced in infection, allergic responses, other forms of inflammation

27
Q

CysLT1 receptor antagonist

A

Montelukast

28
Q

Arachidonic-acid-derived chemotactant

A

Leukotriene B4

29
Q

Glucocorticoid effect

A

Activates annexin-1, which inhibits phospholipase A2. This prevents arachidonic acid being cleaved from cell membrane

30
Q

Inhibitors of COX I and II 1) 2) 3)

A

1) Aspirin 2) NSAIDs 3) Coxibs

31
Q

Leukotrienes that are blocked by montelukast

A

LTC4, and LTC4 metabolites (LTD4, LTE4)

32
Q

PGD4 effect

A

Bronchoconstrictor released from mast cells

33
Q

When does arachidonic acid become available to mast cells?

A

When they are activated

34
Q

Minimum amount of time for a transcriptional response (in a mast cell)

A

45 minutes (at the shortest) to two or three hours

35
Q

Why is there a delay in mast cell production of lipid mediators?

A

Phospholipase A2 only de-esterifies membrane phospholipids to arachidonic acid upon mast cell activation.

36
Q

Cytokines released by mast cells that can be regulated with glucocorticoids

A

IL-1, TNFa

37
Q

Cytokines released by mast cells that aren’t well regulated by glucocorticoids

A

IL-4

38
Q

Endogenous inhibitors of mast cell activity 1) 2) 3)

A

1) PGE2 2) Adrenaline 3) Cortisol

39
Q

Pharmacological inhibitors of mast cell activity

A

Sodium cromoglycate Nedocromil sodium

40
Q

Effect of sodium cromoglycate and nedocromil sodium 1) 2) 3) 4) 5)

A

1) Moderate reduction in inflammation 2) Reduction in mast cell degranulation 3) Reduction in C-fibre activation 4) Reduction in eosinophil activation 5) Cause annexin-1 release

41
Q

Where are sodium cromoglycate and nedocromil sodium used?

A

For airway inflammation. Not orally-available

42
Q

MAB inhibitor of mast cell activation

A

Omalizumab. Prevents IgE binding to FceRI.

43
Q

Pros and cons of lack of oral efficacy of sodium cromoglycate and nedocromil sodium

A

Only active at mucosal sites (pro) Can’t reach deeper tissues (con)

44
Q

Alternate activity of H1 receptor antagonists

A

Have anti-muscarinic activity. Good for motion sickness treatment

45
Q

Effect of NSAIDs and COXII inhibitors on allergy

A

No net benefit for asthma or hayfever. May provoke symptoms in ~10% of asthmatics and hayfever sufferers.

46
Q

Example of a glucocorticoid used to treat asthma

A

Budesonide

47
Q

Indications for H1 receptor antagonists 1) 2) 3) 4) 5) 6)

A

1) Urticaria 2) Atopic dermatitis 3) Hayfever 4) Anaphylaxis and angioedema 5) Bites, stings 6) Motion sickness (anti-muscarinic activity

48
Q

Alternative name for H1 receptor antagonists

A

Antihistamines

49
Q

H1 receptor antagonists

A

Competitive, reversible antagonists of H1 receptors

50
Q

Three classes of antihistamines 1) 2) 3)

A

1) Sedative (promethazine) 2) Non-sedative (terfenadine, astemizole) 3) Newer non-sedative (cetirizine, loratidine)

51
Q

Why were newer non-sedative antihistamines produced?

A

Terfenadine and astemizole caused rare, sudden ventricular arrhythmias.

52
Q

Effect of antagonising LTC4

A

Modest bronchodilation Especially indicated for aspirin-induced or exercise-induced asthma

53
Q

LTC4 antagonist cotherapy

A

Administered with a glucocorticoid or beta2 adR agonist

54
Q

Reason for why colic pain is a feature of anaphylaxis

A

Increased gastric acid secretion from H2 stimulation by histamine in the GIT

1Principles of Biomedicine - MD1 (157 decks)

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