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YEAR 5: Immunopathology PM > Immuno: Case Studies in Immunology > Flashcards

Immuno: Case Studies in Immunology Flashcards

1
Q

Define anaphylaxis.

A

A systemic hypersensitivity reaction in which the response is so overwhelming that it can be life-threatening

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2
Q

Describe the mechanism of type I hypersensitivity reactions.

A
  • Cross-linking of IgE on mast cells by an antigen causes degranulation
  • The release of various mediators including histamines and leukotrienes results in increased vascular permeability, smooth muscle contraction, inflammation and increased mucus production
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3
Q

List some clinical features of anaphylaxis.

A
  • Conjunctival injection
  • Rhinorrhoea
  • Angioedema
  • Urticaria
  • Wheeze/bronchoconstriction
  • Laryngeal obstruction/stridor
  • Hypotension
  • Cardiac arrhythmias
  • Vomiting, diarrhoea, abdominal pain
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4
Q

What is the most common clinical feature of anaphylaxis?

A

Urticaria

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5
Q

Outline the management of anaphylaxis.

A
  • ABCDE approach
  • Respiratory support if necessary
  • Oxygen by mask
  • IM adrenaline (0.5 mg)
  • IV antihistamine (10 mg chlorpheniramine)
  • IV corticosteroid (200 mg hydrocortisone)
  • IV fluids
  • Nebulised bronchodiliators

NOTE: steroids take about 30 mins to start working but they are important in preventing rebound anaphylaxis

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6
Q

Describe the mechanism of action of adrenaline in anaphylaxis.

A
  • It stimulates beta-2 receptors causing constriction of arterial smooth muscle
  • This leads to increased blood pressure, limits vascular leakage and has a bronchodilator effect
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7
Q

Define positive trypase test

A

> 1.2 x baseline +2

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8
Q

List some common causes of anaphylaxis.

A
  • Foods: peanuts, fish, shellfish, milk, eggs, soy
  • Insect stings: bee venom, wasp venom
  • Chemicals, drugs and other foreign proteins: penicillin, IV anaesthetic, latex
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9
Q

What is latex?

A

Milky fluid produced by rubber trees (Hevea brasiliensis)

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10
Q

What are the two types of latex allergy and how do they typically present?

A

Type I Hypersensitivity

  • Acute onset of classical allergic symptoms soon after exposure (e.g. wheeze, urticaria, angioedema)
  • Spectrum of severity
  • Occupational exposure can lead to symptoms similar to asthma (e.g. lab workers)

Type IV Hypersensitivity

  • Causes contact dermatitis (very itchy, well demarcated rash)
  • Usually affecting the hands and feet (due to gloves and footwear)
  • Symptoms begin 24-48 hours after exposure
  • Not responsive to antihistamines
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11
Q

Which patient groups are particularly susceptible to type I hypersensitivity reactions to latex?

A
  • Patients undergoing multiple urological procedures
  • Preterm infants
  • Patients with indwlling latex devices (e.g. ventriculoperitoneal shunt)
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12
Q

What can a type I hypersensitivity reaction to latex cross-react with?

A
  • Avocado
  • Apricot
  • Banana
  • Passion fruit
  • Papaya

NOTE: basically quite a lot of fruit

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13
Q

Name and describe three types of test for hypersensitivity.

A
  • Specific IgE - this is a blood test that is preferentially used in patients with a history of anaphylaxis
  • Skin prick testing
  • Patch testing - patch is pasted onto the skin for 24-48 hours and eczema will be seen if there is a reaction
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14
Q

Describe the appearance of biopsy of urticarial tissue in anaphylaxis.

A
  • Infiltrating T cells
  • Granulomas
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15
Q

Which subset of patients should be referred to an allergist/immunologist?

A

All patients after anaphylaxis

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16
Q

For which types of allergies doees desensitisation work?

A

Insect venom and some sero-allergens (e.g. grass pollen)

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17
Q

List some disorders associted with recurrent meningococcal meningitis.

A
  • Complement deficiency (increases risk of encapsulated organisms)
  • Antibody deficiency (causes recurrent bacterial infections)
  • Neurological (disturbance of blood-brain barrier (e.g. hydrocephalus, occult skull fracture))

Inherited and aquired immunodeficiency

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18
Q

Which investigation are typically usd to investigate complement deficiency?

A
  • CH50
  • AP50
  • C3 and C4
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19
Q

What does AP50 and CH50 test?

A
  • AP50 - tests the alternative pathway
  • CH50 - tests the classical pathway

Functional tests for compliment
Deficiency in both = defect in final pathway C5-C9

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20
Q

What are the main aspects of management of complement deficiency?

A
  • Vaccination (meningococcus, pneumococcus, Hib)
  • Daily prophylactic penicillin
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21
Q

Investigations in SLE

A

Screen all lupus patient for APS antibodies

22
Q

What is lupus anticoagulant test

A

(for APS)
Prolonged APTT that does not correct with normal pooled plasma but corrects with phospholipids

APTT relies on phospholipids
because they have antibodies to phospholipids - prolonged - lab artefact

23
Q

Main interferon in SLE

A

Type 1 interferon

treated with antifrolumab

24
Q

General pathogenesis of SLE

A

Abberent cell removal
Overactive B cells
Leads to abnormal B cell reaction of nuclear proteins

25
Q

Describe the mechanism of action of serum sickness.

A
  1. Penicillin binds to cell surface proteins
  2. This acts as a neo-antigen, which stimulates a very strong IgG response
  3. This means that the individual is sensitised to penicillin
  4. Subsequent exposure leads to the formation of immune complexes with the penicillin and the production of more IgG antibodies
  5. Immune complexes deposit in joints, kidneys and skin causing arthralgia, glomeruloephritis and a vasculitic rash
26
Q

How can serum sickness due to penicillin be investigated?

A
  • Low serum C3 + C4 (suggests classical pathway activation)
  • Specific IgG to penicillin
  • Biopsy of skin or kidneys (showing infiltration of macrophages and neutrophils, deposition of IgG, IgM and complement)
27
Q

Explain the following clinical manifestations of serum sickness:

  1. Deterioration in renal function
  2. Disorientation
  3. Purpura
A
  1. Deterioration in renal function
    • ​​Deposition of immune complexes in the glomeruli leads to complement activation and inflammatory cell recruitment
    • This leads to glomerulonephritis resulting in a rise in creatinine, proteinuria and haematuria
  2. Disorientation
    • ​​Small vessel vassculitis affecting the cerebral vessels can compromise the oxygen supply to the brain
  3. Purpura
    • ​​Inflamed blood vessels are likely to leak resulting in local haemorrhage
28
Q

How should serum sickness be managed?

A
  • Stop penicillin
  • Give corticosteroids
  • Ensure appropriate fluid balance
29
Q

List some features of immunodeficiency.

A
  • Severe infections (hospitalisation)
  • Persistant (difficult to treat)
  • Unusual (e.g. opportunistic, unusual sites of infection)
  • Recurrent
  • Concomitant problems
    eg. failure to thrive,
30
Q

List some non-immunological causes of recurrent infections in children.

A
  • Prematurity
  • Allergic rhinitis, sinusitis, Asthma
  • Cystic fibrosis
  • Local factors (e.g. foreing body)
  • Ciliary disorders
31
Q

What is the point of testing people with recurrent infections for antibodies against infections that they have been vaccinated for (e.g. tetanus)?

A

To see whether they are capable of mounting an antibody response
eg. tetanus, HiB, PCV-13

32
Q

General investigations in suspected immunodeficiency?

A
  • FBC
  • Serum Immunoglobulins
  • HIV test

Immunologists will do the rest
(ie. antibody testing, Flow cytometry)

33
Q

Which condition is characterised by a failure to produce any immunoglobulin?

A

X-linked agammaglobulinaemia - failure of pre-B cells to mature in the bone marrow leading to failure of production of antibodies

Lack of Bruton’s Tyrosine kinase
(overactive in haematological malignancies eg. CLL)

34
Q

How is X-linked agammaglobulinaemia treated?

A

IgG Immunoglobulin replacement therapy - every 3 weeks

IV or SC
in hospital or trained to do it at home
Lifelong

includes Antibodies against pneumococcus and haemophillus

35
Q

Why do XLA patients have predisposition to autoinflammatory disease

A

BTK tyrosine kinase (deficiency in XLA) also acts as an inhibitor to inflammasome

So unregulated immune responses

36
Q

What are some classic presenting features of multiple myeloma?

A

CRABS

Bone pain and pathological fractures

Hypercalcaemia symptoms

37
Q

Which investigation is used to diagnose multiple myeloma?

A

Serum protein electrophoresis - shows a monoclonal band (this can be stained to check whether it is composed of heavy or light chains)

Kappa : Lambda ratio of ligh chains in serum

38
Q

Why are patients with multiple myeloma prone to infections?

A

Suppression of normal antibody production by the malignant clone of cells results in a functional antibody deficiency

NOTE: this is sometimes called immune paresis

39
Q

How does multiple myeloma lead to aneamia?

A
  • Expansion of malignant clone of cells into the bone marrow crowds out normal red and white cell precursors
  • Cytokines produced by the myeloma cells inhibit normal bone marrow function
40
Q

Why is ESR elevated in multiple myeloma?

A
  • Normally, erythrocytes don’t clump together because the repellent negative surface charge is greater than the attractant charge of plasma constituents
  • If the protein constituents of plasma change, it increases the attractant charge, causes erythrocytes to clump together and clumped erythrocytes fall more quickly through plasma
  • This causes raised ESR
  • Often normal CRP
41
Q

Which red blood cell abnormality may you see in the blood film of a patient with multiple myeloma?

A

Rouleaux formation

NOTE: you may also see Bence-Jones protein in the urine

42
Q

What are the key clinical features of rheumatoid arthritis?

A

Peripheral, symmetrical polyarthritis with stiffness lasting > 6 weeks

43
Q

When does rheumatoid arthritis commonly present and waht is a possible explanation for this?

A

Post-partum - Th2 cells predominate during pregnancy and this switches back to Th1 post-partum

44
Q

What is Rheumatoid Factor?

A
  • Antibody directed against the Fc portion of human IgG
  • Assays mainly look for IgM but there are also IgG and IgA variants
  • 60-70% sensitive and specific
45
Q

Better test than rheumatoid factor?

A

Anti-CCP

46
Q

How are citrullinated peptides implicated in rheumatoid arthritis?

A
  • Arginine residues are deiminated to form citrulline by PAD enzymes
  • Polymorphisms in PAD that increases the level of citrullination may predispose to rheumatoid arthritis
  • Loss of tolerance to citrullinated peptides results in the production of antibodies against CCP
  • Anti-CCP antibodies are highly specific (95%)
47
Q

Describe how specific HLA alleles can predispose to the development of rheumatoid arthritis.

A
  • HLA-DR4 (60-70%) and HLA-DR1
  • These predisposing classes have a common sequence at positions 70-74 (this area encodes the peptide-binding groove)
  • Peptide presentation by these HLA molecules may be involved in disease pathogenesis
48
Q

Which PAD polymorphisms are associated with rheumatoid arthritis?

A

PAD 2 and PAD 4

49
Q

What is the role of PTPN22 and which polymorphism is associated with rheumatoid arthritis?

A
  • It is a lymphocyte-specific tyrosine kinase that suppresses T cell activation
  • 1858T allele increases susceptibility to rheumatoid arthritis, SLE and T1DM
50
Q

Outline the management of rheumatoid arthritis.

A
  • First-line: methotrexate (DMARD)
  • Other options: TNF-alpha antagonists, rituximab, abatacept (CTLA4-Ig fusion protein), tocilizumab (antibody against IL6 receptor)
51
Q

List some risks of biological therapy for rheumatoid arthritis.

A
  • TB
  • Opportunistic infections
  • Malignancy - skin protection

YEAR 5: Immunopathology PM (12 decks)

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