ILA 2 anaphylaxis Flashcards

1
Q

define anaphylaxis.

A

Anaphylaxis is a severe, potentially life-threatening systemic allergic reaction that occurs rapidly after exposure to an allergen. It involves the activation of the immune system, leading to the release of inflammatory mediators such as histamine, resulting in widespread symptoms affecting multiple organ systems.

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2
Q

descrine the pathophysiology of anaphylaxis and outline how this differs to a normal allergy reaction.

A

Same as allergy (hypersensitivity 1) however the effects are widespread around the body in constrast with allergies being localised, the effects are more severe, in contrast with an allergy which mostly aren’t life threatening.

sensitisation:
- allergen/antigen enters body
- it gets taken up and presented on the surface (MHC-II) of APC
- presented to naive T-cells skewing it to develop into Th2 cells
- the Th2 cells release IL-4 and IL-13
- this activates B-cells to make IgE specific to the antigen/allergen (the B cell will already be making some random antibodies so it will enter gene recombination to make IgE)
- IgE will bind to IgE receptors on basophils and mast cells (FceRI receptor)

mast cell degranulation
- IgE is now presented on the mast cells
- when the antigen/allergen binds to the IgE, it causes the IgE to crosslink
- this results in a chemical cascade within the mast cell/basophill
this causes the degranulation of the cell and the symphesis of new cytokines - Ca2+ and arachodonic acid is used in this
- the cytokines are released from the cell via vesicles
- this then leads to systemic differences in the body and organs

these are:
Histamine – vascular permeability and vasodilatation
Prostaglandin D – bronchoconstriction
Leukotrienes – bronchoconstriction and vascular permeability
Platelet-activating factor – bronchoconstriction and vascular permeability

How it differs with allergy response
* Systemic Effects: Unlike localized allergic reactions, anaphylaxis involves widespread activation of mast cells and basophils across the body.
* Severity: Massive release of mediators leads to life-threatening symptoms like severe hypotension, airway obstruction, and shock.
* Rapid Onset: Symptoms develop within minutes to hours, making it a medical emergency.
* Trigger Sensitivity: Small amounts of allergen can provoke a severe response.

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3
Q

what is the classic onset / presentation of anaphylaxis

A
  • Urticaria - hives
  • Itching
  • Angio-oedema, with swelling around lips and eyes (area of swelling in lower layer of skin or mucus membranes)
  • Abdominal pain
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4
Q

outline all possible symptoms which could present as a result of anaphylaxis

A

Skin and Mucosal Signs:
* Flushing: Redness of the skin.
* Urticaria (hives): Raised, itchy, and swollen areas of the skin.
* Angioedema: Swelling of the lips, tongue, face, or throat.
Respiratory Symptoms:
* Airway Obstruction: Swelling in the throat or tongue.
* Wheezing: A whistling sound during breathing due to bronchoconstriction.
* Shortness of Breath: Difficulty breathing.
* Increased Respiratory Rate: Tachypnea (rapid breathing).
Cardiovascular Symptoms:
* Hypotension: Low blood pressure leading to dizziness or fainting.
* Tachycardia: Increased heart rate.
* Shock: Reduced blood flow to organs causing weakness or collapse.
Gastrointestinal Symptoms:
* Nausea and Vomiting.
* Abdominal Cramps.
* Diarrhea.
Neurological Symptoms:
* Feeling of Doom: Anxiety or panic.
* Confusion: Due to low oxygen supply or shock.
General Symptoms:
* Itching or Rash: Diffuse and intense itching.
* Swelling: Often localized but can affect the airway.
* Collapse: Loss of consciousness in severe cases.

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5
Q

outline how adrenaline works as a treatment for anaphylaxis.

A
  • Intramuscular adrenalin, repeated after 5 minutes if required
    Rapidly counteracts symptoms
  • Alpha-adrenergic effects: Causes vasoconstriction, which reduces swelling, increases blood pressure, and reverses cardiovascular collapse.
  • Beta-adrenergic effects: Relaxes bronchial smooth muscles, improving breathing. Also reduces the release of further allergic mediators from mast cells and basophils.
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6
Q

outline how antihistamines works as a treatment for anaphylaxis.

A
  • Antihistamines, such as oral chlorphenamine or cetirizine
    While adrenaline addresses the acute, life-threatening aspects of anaphylaxis, antihistamines help manage the milder symptoms, such as itching, hives, or swelling.
    Blocks histamine receptors (H1 receptors), thereby reducing symptoms like rash, itching, and swelling.
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7
Q

outline how steroids works as a treatment for anaphylaxis.

A
  • Steroids, usually intravenous hydrocortisone
    Aren’t for immediate relief but prevent biphasic or delayed reactions
    Suppresses inflammation by reducing the activity of immune cells and cytokines involved in the allergic response.
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8
Q

define idiopathic anaphylaxis

A

anaphylaxis with no apparent trigger

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9
Q

H1 recpetor location and effect

A
  • smooth muscle, endothelium, CNS
  • allergy syptoms eg bronchoconstriction, itching, swelling
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10
Q

H2 recpetor location and effect

A
  • parietal cells, heart, smooth muscle cells
  • stimulates gastric acid secretion, mild vasodilation, increased heart rate
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11
Q

H3 recpetor location and effect

A
  • CNS, PNS
  • modulates neurotransmitter release, regulates sleep-wake cycles, apetite supression
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12
Q

H4 recpetor location and effect

A
  • immune cells, bone marrow
  • promotes immune cell activation, inflammation, itching and chemotaxis
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