Week 9 Flashcards

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1
Q

whats the difference between innate and acquired immunity?

A

Innate - doesnt require previous exposure to invading microbe

Acquired - the system remembers how to deal with a microbe it’s health with before

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2
Q

How does innate immunity work/

A
  • Neutrophils eat pathogen and send distress signal
  • Monocytes are triggered to turn into pathogen-eating macrophages
  • Eosinophils attack parasites
  • Basophils contain granules filled with histamine and other compounds
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3
Q

what is the primary physicall effects of the inflammatory response

A
  • Blood vessels dilate -> increasing blood flow
  • capillary wall permeability
  • red and warm due to increased blood flow
  • swollen tissues due to increased blood and proteins
  • painful due to pressure on nerve cells and due to the presence of pain mediators
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4
Q

WHat are the characteristics of inflammation?

A

pain
heat
redness
swelling

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5
Q

WHat is the purpose of nomal imfglammatory response?

A

protective response to eliminate initial cause of injury (bacteria/toxins) and consequences of injury such as dead cells and tissues

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6
Q

WHat is a mast cell?

A
  • Mast Cells are one of the primary facilitators of both inflammatory and immune responses.

• When Mast cells are damaged (or activated by antigens) they release their contents into the interstitial fluid.

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7
Q

what does a mast cell release?

A
• Mast Cells degranulation releases:
– Histamine
– Neutrophil chemotactic factor
– Eosinophil chemotactic factor
– and produces:
o Leukotrienes
o Prostaglandins
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8
Q

WHat does Histamine do?

A

Histamine is a vasoactive amine. It:
• Temporarily and rapidly vasoconstrictor large vessels
• Vasodilates post capillary venules
• Retracts the endothelial cells of the capillary walls.

Chemotactic factors attract WBC to destroy dead tissue and toxins, but importantly they release substances (histaminease) that limit the runaway effect of histamine.

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9
Q

What are Leukotrienes?

A

Slow‐reacting substances of anaphylaxis (SRS‐A)
• Similar effects to histamine (increased vascular permeability, WBC chemotactic)
• Stimulate slower but longer response than histamine

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10
Q

what are prostaglandins?

A
  • Synthesised in several forms (E, A, F, B).
  • Type E associated with inflammation
  • Act on smooth muscle (esp. post capillary venules)
  • Increase vascular permeability
  • Suppresses histamine release
  • Responsible for the long‐term pain of inflammation
  • Aspirin and some NSAIDs supresses PG‐E synthesis.
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11
Q

What is an antigen?

A

– Any substance that when introduced
into the tissues or blood induces the
formation of antibodies and reacts
only with its specific antibodies.

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12
Q

What is an antibody?

A
– A protein produced by certain cells in
the body in the presence of a specific
antigen; the antibody combines with
that antigen to neutralise, inhibit or
destroy it.
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13
Q

what is an allergen?

A

– An antigen that provokes a hypersensitivity reaction

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14
Q

Define anaphylaxis?

A

is a severe, life-threatening, generalised or systemic hypersensitivity reaction,
characterised by rapidly developing life-threatening airway and/or breathing
and/or circulation problems usually associated with skin and mucosal changes

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15
Q

What are the mechanisms of anaphylaxis?

A

• Prior sensitisation to an allergen

• Interaction of an allergen with
specific immunoglobin (IgE) antibodies

• Leads to activation of mast cells and release of preformed mediators stored in granules

• Mediators cause capillary leakage
and mucosal oedema resulting in shock and asphyxia

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16
Q

What are the physiological effects of mast cell mediators?

A

Capillary leakage
Mucosal oedema
Smooth muscle contraction

17
Q

What are some clinical signs of capillary leakage?

A

Urticaria (hives
Angiodema (facial swelling)
Hypotension

18
Q

What are some clinical signs of mucosal oedema

A

Laryngeal oedema
rhinitis
bronchospasm

19
Q

What are some clinical signs of smooth muscle contraction

A

bronchospasm

abdominal pain

20
Q

What are some common triggers of anaphylaxis?

A

Food
Insects
Drugs
Latex rubber

21
Q

WHat are the clinical features of anaphylaxis?

A

Cardiovascular - hypotension, lightheaded, syncope, dysrhythmias, angina

Respiratory - upper airway oedema, bronchospasm

Gastrointestinal - nasea, vomiting, diarrhea, cramping

CNS - headache, confusion, altered consciousness

22
Q

What type of reaction do cardiovascular problems tend to predominate with?

A

Insect stings/IV drugs

23
Q

What type of reaction do respiratory problems tend to predominate with?

A
  • foods
  • > milk/eggs
  • > seafood
24
Q

When should anaphylaxis be considered a differential?

A

any episode of severe, acute-onset
respiratory distress, bronchospasm
or cardiovascular collapse.

Typical cutaneous features may be absent in up to 20% of cases

25
Q

What does adrenaline do?

A

Beta 1 Adrenergic

  • Positive Inotrope- Raise blood pressure
  • Positive Chronotrope- increase heart rate
  • Beta 2 Adrenergic
  • Bronchodilatation
  • Beta Adrenergic
  • Increases Cyclic adenosine monophosphate (cAMP) production which decreases inflammatory mediator release
26
Q

what are some side effects of adrenaline?

A
– feeling of impending doom
– cardiac arrhythmias/palpitations
• SVT, VT, VF
– marked hypertension
• Transient “thumping” headache
• risk of intracerebral bleed
– increased myocardial oxygen demand
• May lead to angina/AMI
27
Q

When is adrenaline indicated for anaphylaxis?

A
• Two or more of R.A.S.H. (with or without confirmed antigen exposure)
– Respiratory distress
– Abdominal symptoms
– Skin/muscoal symptoms
– Hypotension or Altered conscious state

• Isolated hypotension (SBP < 90 mmHg)
– Following exposure to known antigen

28
Q

When do you not administer adreanline for anaphylaxis?

A
  • Isolated signs or symptoms without evidence of systemic involvement
  • Mild bronchospasm (treat as per asthma and continually reassess)
  • Isolated urticaria (hives) / skin flushing
  • Isolated swelling, eg. hand / leg
  • If in doubt consult with receiving hospital
29
Q

What is the pre-hospital management for anaphylaxis

A
• Full patient assessment
• Basic Care &amp; Cardiac monitoring
• Adult
– Adrenaline 500mcg IM / 300mcg IM
•AV CPG A0704

– Salbutamol
• AV CPG A0601 Asthma

– Nubulised Adrenaline
• AV CPG P0601 – Upper Airway Obstruction

– Normal Saline
• IV max 40 ml/Kg
• Consult for additional 20 ml/Kg

30
Q

What is the pre-hospital management for anaphylaxis for PAEDS

A
  • Full patient assessment
  • Basic Care & Cardiac monitoring
  • Paediatric

– Adrenaline 10 mcg/kg IM (1:1000)
• AV CPG P0704

– Salbutamol
• AV CPG P0602 Asthma

– Nebulised Adrenaline
• AV CPG P0601
• Transport

31
Q

What is the role of steroids in anaphylaxis?

A

Includes Hydrocortisone sodium succinate & Prednisolone
• Theoretically beneficial
• May prevent or shorten reactions but should never be relied upon as first line treatment
• Take up to 4-6 hours to be maximally effective
• Limited role in acute management

32
Q

What is the role of antihistamines in anaphylaxis?

A

• Includes Benadryl & Telfast
• Controversial in management of anaphylaxis
• Primary role in non life threatening allergic
reactions e.g. urticaria (hives)
• May prevent or shorten reactions but should never be relied upon as first line treatment