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YEAR 5: IMMUNO > Immuno: Case Studies in Immunology > Flashcards

Immuno: Case Studies in Immunology Flashcards

(52 cards)

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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

Diagnostic requirements for anti-phospholipid

A

1 clinical - reccurent miscarriage, thrombosis, livedo reticularis

1 laboratory - lupus anticoagulant, anti-cardiolipin, anti - beta-2-glycoprotein 1

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3
Q

Define allergy

A

Tendency to develop IgE antibodies against innocuous antigens (allergens)

sensitisation –> IgE binds mast cells + basophils once encountered

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4
Q

Describe the mechanism of type I hypersensitivity reactions.

A
  • Cross-linking of IgE bound to 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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5
Q

List some clinical features of anaphylaxis.

A

Skin:
* Angiodema
* Urticaria

Upper airway:
* Wheeze/bronchoconstriction
* Laryngeal obstruction/stridor

Other
* Conjunctival injection
* Rhinorrhoea

Cardiac:
* Hypotension
* Cardiac arrhythmias

GI
* Vomiting
* diarrhoea
* abdominal pain

skin manifestation most common

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6
Q

What is the most common clinical feature of anaphylaxis?

A

Urticaria

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7
Q

What factors increase risk of Rheumatoid arthritis due to increasing citrullination?

A

Smoking
Gingiviasis

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8
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 chlorphenamine)
  • 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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9
Q

Describe the mechanism of action of adrenaline in anaphylaxis.

A
  • alpha-1 receptors causing vasoconstriction, reduce edema
  • beta-1 increasing inotropy and heart rate
  • beta-2 receptors causing bronchodilation
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10
Q

Differentials for anaphylaxis

A

anxiety
vasovagal
asthma attack + skin flushing
asthma + urticaria
Drug side effect - levetiracetam, pencillins
Sepsis
PE
MI

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11
Q

what mediators are released on mast cell degranulation

A
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12
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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13
Q

What is latex?

A

Milky fluid produced by rubber trees (Hevea brasiliensis)

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14
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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15
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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16
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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17
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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18
Q

Describe the appearance of biopsy of urticarial tissue in anaphylaxis.

A
  • Infiltrating T cells
  • Granulomas
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19
Q

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

A

All patients after anaphylaxis

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20
Q

For which types of allergies doees desensitisation work?

A

Insect venom and some aero-allergens (e.g. dust mites, grass pollen)

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21
Q

List some disorders associted with recurrent meningococcal meningitis.

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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))
22
Q

History features which should make you consider immunological defiency

Study These Flashcards
A

Previous infections which are:
Serious
Persistent
Unusual
Recurrent

Family history

23
Q

Which people with nut allergies don’t need antihistamines?

Why

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A

PR-10 allergy

allergic to birch pollen so have mild reactions to other foods including nuts, fruit

cause itchy mouth, hoarse voice

managed with antihistamines

24
Q

Which investigation are typically usd to investigate complement deficiency?

Study These Flashcards
A
  • CH50
  • AP50
  • C3 and C4
25
Which tests to investigate immunological deficiency
Serum IgG, IgA, IgM protein electrophoresis
26
What does AP50 and CH50 test?
* AP50 - tests the alternative pathway - Factors B,H,I, Properidin * CH50 - tests the classical pathway C1,C2,C4 if both abnormal --> issue with common pathway i.e. C5-C9
27
What are the main aspects of management of complement deficiency?
* Vaccination (meningovax, pneumovax, Hib) * Daily prophylactic penicillin
28
Describe the mechanism of action of serum sickness.
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
29
How can serum sickness due to penicillin be investigated?
* 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)
30
Explain the following clinical manifestations of serum sickness: 1. Deterioration in renal function 2. Disorientation 3. Purpura
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
31
How should serum sickness be managed?
* Stop penicillin * Give corticosteroids * Ensure appropriate fluid balance
32
List some features of immunodeficiency.
* Severe infections * Persistant (difficult to treat) * Unusual (e.g. opportunistic, unusual sites of infection) * Recurrent * Concomitant problems
33
List some non-immunological causes of recurrent infections in children.
* Cystic fibrosis * Local factors (e.g. foreing body) * Ciliary disorders * Nephrotic syndrome - Ig loss in urine
34
What is the point of testing people with recurrent infections for antibodies against infections that they have been vaccinated for (e.g. tetanus)?
To see whether they are capable of mounting an antibody response
35
Which condition is characterised by a failure to produce any immunoglobulin?
X-linked agammaglobulinaemia - failure of pre-B cells to mature in the bone marrow leading to failure of production of antibodies
36
How is X-linked agammaglobulinaemia treated?
Immunoglobulin replacement therapy - every 3 weeks
37
What are some classic presenting features of multiple myeloma?
CRABS Bone pain and pathological fractures Hypercalcaemia symptoms
38
Which investigation is used to diagnose multiple myeloma?
Serum protein electrophoresis - shows a monoclonal band in gamma region (this can be stained to check whether it is composed of heavy or light chains)
39
how is urine analysed in multiple myeloma
urine electrophoresis - shows free light chans (Bence Jones proteins)
40
Why are patients with multiple myeloma prone to infections?
Suppression of normal antibody production by the "useless" malignant clone of cells results in a functional antibody deficiency NOTE: this is sometimes called immune paresis Most commonly high IgG which then suppresses IgA and IgM
41
How does multiple myeloma lead to aneamia?
* 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
42
Why is ESR elevated in multiple myeloma?
* 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 (Rouleaux formation) and clumped erythrocytes fall more quickly through plasma * This causes raised ESR
43
Which red blood cell abnormality may you see in the blood film of a patient with multiple myeloma?
Rouleaux formation NOTE: you may also see Bence-Jones protein in the urine
44
What are the key clinical features of rheumatoid arthritis?
Peripheral, symmetrical polyarthritis with stiffness lasting \> 6 weeks
45
When does rheumatoid arthritis commonly present and waht is a possible explanation for this?
Post-partum - Th2 cells predominate during pregnancy and this switches back to Th1 post-partum
46
What is Rheumatoid Factor?
* 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
47
How are citrullinated peptides implicated in rheumatoid arthritis?
* 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%)
48
Describe how specific HLA alleles can predispose to the development of rheumatoid arthritis.
* 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
49
Which PAD polymorphisms are associated with rheumatoid arthritis?
PAD 2 and PAD 4
50
What is the role of PTPN22 and which polymorphism is associated with rheumatoid arthritis?
* It is a lymphocyte-specific tyrosine kinase that suppresses T cell activation * 1858T allele increases susceptibility to rheumatoid arthritis, SLE and T1DM
51
Outline the management of rheumatoid arthritis.
* First-line: methotrexate * Other options: TNF-alpha antagonists, rituximab, abatacept (CTLA4-Ig fusion protein), tocilizumab (antibody against IL6 receptor)
52
List some risks of biological therapy for rheumatoid arthritis.
* TB - need to CXR and TB quantinterferon before starting * Opportunistic infections * Malignancy - non melanoma skin cancers * Reduced fertility

YEAR 5: IMMUNO (12 decks)

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