anaphylaxis Flashcards

this includes the anaphylaxis lecture notes

1
Q

define anaphylaxis

A

= a severe, potentially life-threatening allergic reaction that can develop rapidly.

It is a generalised or systemic hypersensitivity reaction.

Both of the following criteria should be met:

  1. Sudden onset and rapid progression of symptoms.
  2. Life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes
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2
Q

list some signs/symptoms of anaphylaxis

A

feeling lightheaded or faint

breathing difficulties due to bronchoconstriction– such as fast, shallow breathing, or wheezing

high heart rate (trying to overcompensate)

confusion and anxiety

Hives/urticaria (raised itchy red rash)

Swelling (angioedema) of eyes,lips,face,hands,feet

Central cyanosis - blue discolouration

Stomach pain

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3
Q

what type of hypersensitivity reaction is anaphylaxis? and why?

A

type 1 because its IgE mediated

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4
Q

explain how sensitisation to an antigen happens?

A

Initial exposure to antigen (sensitisation)

Antigen presenting cells present the antigen to T helper cells

T helper cells stimulate B cells to differentiate into plasma cells and produce IgE antibodies against this antigen

IgE binds to FceRI receptors on mast cells sensitising them to the antigen

if the Allergen/antigen is reintroduced it will react with these IgE antibodies

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5
Q

explain the steps of anaphylaxis (pathophysiology)

A
  1. Allergen/antigen reintroduced
  2. Reacts with specific IgE antibodies on mast cells and basophils
  3. IgE antibodies bind to high affinity receptors on the surface of mast cells and basophils

4.Triggers rapid release of the stored histamine and the rapid synthesis of newly formed inflammatory mediators

specifically, it is the Cross Linking of IgE antibodies and FceRI receptors on the cell surface causes rapid cellular degranulation and liberation of chemical mediators = (process is known as mast cell degranulation)

  1. the release of histamine and the mediators cause the symptoms of anaphylaxis
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6
Q

what are the mediators released in degranulation of mast cells during anaphylaxis?

A

histamine
protease enzymes,
proteoglycans and chemotactic factors.

Platelet activating factor (PAF),
leukotrienes
prostaglandins

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7
Q

what affects do the mediators released in degranulation have?

A
  • Smooth muscle spasm in resp + GI tracts
  • Muscle oedema
  • shock and asphyxia (deprivation of oxygen).
  • Vasodilation & Increased vascular permeability (which causes hypotension and hives)
  • Stimulation of sensory nerve endings
  • Increased mucous secretion and increased
    Smooth muscle contraction in airways
  • capillary leakage causes cardiac affects (vasodilation, Hypotension, cardiac arrhythmias, syncope and shock)
    increased vascular permeability can produce a shift of
  • fluid shift
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8
Q

what affect does histamine release have in anaphylaxis?

A

-activates H1 and H2 receptors

-Vasodilation, hypotension, and flushing are mediated by H1 receptors.

  • H2 receptors increase atrial and ventricular contractility, atrial chronotropy, and coronary artery vasodilation.
  • Histamine is what makes you itchy
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9
Q

what is a biphasic reaction?

A

two physical phases, or sets of effects that have time in between

eg. second anaphylaxis reaction 12 hours later

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10
Q

list some common triggers of anaphylaxis

A

Foods: peanuts, pulses, tree nuts (brazil nuts, almond, hazelnuts), fish and shellfish, eggs, milk, sesame

Venom: Bee stings, wasp stings

Drugs: antibiotics, opioids, NSAIDs, muscle relaxants (Baclofen, Diazepam), general anaesthetics

Contrast agents: (used in x-rays) eg. barium

Rubber latex

Non-immunologic (physical stimuli) eg. heat, cold, sunlight

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11
Q

what does ABCDE stand for in the guidelines of treatment for anaphylaxis?

A

Airway: look for and relieve airway obstruction. Remove any traces of allergen

Breathing: look for a treat bronchospasm and signs of respiratory distress

Circulation: colour, pulse, BP

Disability: assess whether responding or unconscious (AVPU)

Exposure: assess skin with adequate exposure, but avoid excess heat loss

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12
Q

what are the stages in the guidelines of treatment for anaphylaxis?

A
  1. ABCDE and decide anaphylaxis
  2. lay patient flat or sat down to help breathing
  3. call for help
  4. administer adrenaline - IM in the anterolateral aspect of the middle third of the thigh (adult dose 0.5mg)

5.give high flow oxygen

  1. monitor (pulse oximetry, ECG, BP)
  2. another dose of adrenaline if no affect after 5 mins
  3. can give antihistamine to stop skin symptoms. can administer IV fluids
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13
Q

how does adrenaline treat anaphylaxis?

A

Stimulation of beta1-adrenoceptors: positive inotropic (force of heart contraction) and chronotropic (heart rate) effects on the heart

Stimulation of beta2-adrenoceptors: relaxes smooth muscle → reduces oedema and bronchodilators via stimulation of these receptors

decreases further release of mediators from mast cells and basophils by increasing c-AMP(cellular signal induction) and so reducing the release of inflammatory mediators

causes Vasoconstriction – increase in peripheral vascular resistance, increased BP and coronary perfusion. counters the vasodilation

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14
Q

how does IV fluid treat anaphylaxis?

A

help restore the circulating volume and therefore the stroke volume thus increasing the cardiac output

increases BP

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15
Q

how does Chlorphenamine treat anaphylaxis?

A

An antihistamine which blocks the Histamine 1 receptor

thus blocking the action of the histamine released during anaphylaxis

Used for skin symptoms

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16
Q

what treatment can be given to assist breathing during anaphylaxis?

A

Salbutamol

If Continuing respiratory deterioration: bronchodilator such as salbutamol

17
Q

why might a 2nd dose of adrenaline be needed during anaphylaxis?

A

Adrenaline has a short half life therefore a second dose may be required if the symptoms of not initially respond or get worse

18
Q

What confirmatory blood test will you need to take to determine if a reaction was anaphylaxis?

A

Serum mast-cell tryptase can be measured

Tryptase is released during mast-cell degranulation therefore high levels show mass degranulation and therefore anaphylaxis

levels peak at one hour after an anaphylactic reaction, remaining elevated for approximately six hours.

therefore measure ASAP after suspected reaction

19
Q

what are some theories for why there is an increased incidence of anaphylaxis in the UK?

A

Environmental changes →
Increase in air pollution
Changes in pollen patterns
Changes in distribution of stinging insects

The hygiene hypothesis - we live too clean so our immune systems are under stimulated.

Born by C section - exposed to less bacteria therefore more likely to have atopy

20
Q

what does ACID EGGT stand for (helpful acronym)

A

hypersensitivity reactions

A- type 1 is allergy
C - type 2 is cytotoxic
I- type 3 is Immune complex mediated
D - type 4 is delayed

E - type 1 is IgE
G- type 2 is IgG
G - type 3 is IgG
T - type 4 is T helper cells

21
Q

define hypersensitiity

A

= objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects’ and may be caused by immunologic (allergic) and non‐immunologic mechanisms’

22
Q

risk factors for hypersensitivity

  • medicine factors
A

Protein or polysaccharide based macromolecules

23
Q

risk factors for hypersensitivity

  • host factors
A

females > males UNKNOWN WHY
EBV, HIV
Pre drug reactions
Uncontrolled asthma

24
Q

risk factors for hypersensitivity

  • genetic factors
A

Certain HLA groups
Acetylator status

25
Q

what is non immunological anaphylaxis?

A

Previously called Anaphylactoid reactions
Due to direct mast cell degranulation.
Some drugs recognised to cause this
No prior exposure needed - not antigen/antibody mediated
Clinically identical to immunological

26
Q

clinical criteria for allergy to drug

A

does not correlate with pharmacological properties of the drug - is there an explanation?

No linear relation with dose (tiny dose can cause severe effects)

Reaction to similar to those produced by other allergens

Induction period of primary exposure

Disappearance on cessation

Re-appears on re exposure

Occurs in minority of patients on the drug

27
Q

describe type 1 hypersensitivity

(what antibody mediated it, give an example, explain the physiology)

A

IgE mediated

Prior exposure to the antigen

IgE becomes attached to mast cells or leukocytes, expressed as cell surface receptors

Re-exposure causes mast cell degranulation and release of pharmacologically active substances
- Histamine
- Prostaglandins
- Leukotrienes
- Platelet activating factor PAF

eg. anaphylaxis

28
Q

describe type 2 hypersensitivity

(what antibody mediated it, give an example, explain the physiology)

A

IgG mediated cytotoxicity

Antibody dependent cytotoxicity

Drug or metabolite combines with a protein

Body treats it as a foreign protein and forms antibodies (IgG, IgM)

Antibodies combine with the antigen and complement activation damages the cells

eg. drug induced lupus

28
Q

describe type 2 hypersensitivity

(what antibody mediated it, give an example, explain the physiology)

A

IgG mediated cytotoxicity

Antibody dependent cytotoxicity

Drug or metabolite combines with a protein

Body treats it as a foreign protein and forms antibodies (IgG, IgM)

Antibodies combine with the antigen and complement activation damages the cells

eg. drug induced lupus

29
Q

describe type 3 hypersensitivity

(what mediated it, give an example, explain the physiology)

A

immune complex mediated

Antigen and antibody form large complexes and activate complement

there is tissue deposition of IgG

Small blood vessels are damaged or blocked

Leucocytes attracted to the site of reaction release pharmacologically active substances leading to an inflammatory process

eg. serum sickness

30
Q

describe type 4 hypersensitivity

(what mediated it, give an example, explain the physiology)

A

T cell (lymphocyte) mediated + delayed

Antigen specific receptors develop on T-lymphocytes

Subsequent administration leads to local or tissue allergic reactions

Eg. contact dermatitis, stevens johnson syndrome