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Immunology > Immunology case studies > Flashcards

Immunology case studies Flashcards

1
Q
  1. •What is the working diagnosis?
  2. •What are the clinical features found in this condition? (10 for complete answer)
A
  1. Anaphylaxis - systemic hypersensitivity reaction in which the response is so overwhelming as to one life-threatening.
    1. Mechanism: Type I hypersensitivity response
  2. Urticaria, angioedema, upper airway oedema, breathlessness and wheezing, flushing, dizziness, syncope, and hypotension, GI symptoms, rhinitis, headache, substernal pain, itch without rash and seizure.
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2
Q

What is the differential diagnosis to consider in collapse?

A
  • Myocardial infarction
  • Cardiac arrythmia
  • Acute asthmatic attack
  • Pulmonary embolus
  • Vasovagal attack
  • Epilepsy
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3
Q

•What immediate treatment would you instigate and why?

A
  • May require respiratory support
    • Intubation may be required for severe bronchoconstriction
    • Tracheostomy if develops upper airway tract obstruction
  • Oxygen by mask - improve oxygen delivery
  • Adrenaline IM (0.5mg for adult and may repeat)
    • Acts on B2 adrenergic receptors to constrict arterial smooth muscle
      • Increases blood pressure
      • Limits vascular leakage
      • bronchodilator
  • IV antihistamine (10 mg chlorpheniramine)
    • Acts to oppose the effects of mast cell derived histamine
  • Nebulised bronchodilators - improve oxygen delivery through bronchial dilatation
  • IV corticosteroids (hydrocortisone 200 mg)
    • Systemic anti-inflammatory agent
    • effects takes about 30 min to start, and does not peak for several hrs
    • Prevents rebound anaphylaxis
  • IV fluids
    • Increase circulating blood volume and therefore BP
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4
Q

What are the common causes of anaphylaxis?

A

–Foods

  • Peanuts
  • Tree nuts
  • Fish and shellfish
  • Milk
  • Eggs
  • Soy products

–Insect stings

  • Bee venom
  • Wasp venom

–Chemicals, drugs and other foreign proteins

  • Penicillin and other antibiotics
  • Intravenous anaesthetic agents, eg suxamethonium, propofol
  • Latex
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5
Q

What questions would you ask once he has stabilised?

A
  • What was he doing prior to the onset of symptoms
  • Does he have any know allergies
  • Has anything like this happened before
  • How is his general health
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6
Q

What is the likely allergen? Is the allergy to banana relevant?

A

Latex

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7
Q

What are the 2 types of latex allergy?

A
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8
Q

What symptom profile would you see in a type IV latex allergy?

A
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9
Q

Who does type I allergy to latex affect?

A
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10
Q

How would you confirm a diagnosis of allergy to latex?

A

Skin prick testing also an option - commercial latex extracts at a range of concentrations

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11
Q

How should we test for Type IV latex allergies?

A
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12
Q

What are the blood tests for latex allergy?

A
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13
Q

What long term management advice would you give for a latex allergy?

A
  • All patients with anaphylaxis should be referred to an allergist/immunologist
  • Given occupational implication, a plan of avoidance should be made in conjunction with occupational physician
  • Alert before any procedures
  • Avoid foods with cross reactivity
  • Use a medic alert bracelet
  • Carry a self-injectable adrenalin epipen
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14
Q

Is desensitisation an options for a severe latex allergy?

A

No, only for insect bites and air allergens

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15
Q

What disorders are associated with recurrent meningococcal meningitis?

A
  • Disorders associated with recurrent meningococcal meningitis:
    • Immunological:
      • Complement Deficiency – inc. risk of infection by encapsulated organisms:
        • Meningococcus
        • Pneumococcus, Neisseria gonorrhoeae, HiB
      • Antibody Deficiency – recurrent bacterial infections:
        • Especially upper and lower respiratory tract
    • Neurological:
      • Any disturbance of the blood-brain barrier
        • Occult skull fracture
        • Hydrocephalus
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16
Q

What other questions would you ask him?

A
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17
Q

•What immunological investigations would you request?

A
  • Complement:
    • C3 and C4 levels
    • CH50 – a functional test of integrity of the classical complement cascade; a +ve result is NORMAL
    • AP50 – a functional test of integrity of the alternative complement cascade; a +ve result is NORMAL
  • Immunoglobulins:
    • Serum IgG, IgA and IgM
    • Protein electrophoresis
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18
Q

How would you manage this patient?

A
  • Management:
    • Vaccinations:
      • Meningovax - tetravalent meningococcal conjugate vaccine covering serogroups A, C, W-135, Y and the Men B
      • PCV-13 and 23vPneumovax vaccine
      • HIB vaccine
    • Daily prophylactic penicillin
    • High level of suspicion for infections
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19
Q

When should we suspect complement deficiencies?

A
  • Any deficiency of the complement pathway may be associated with recurrent meningococcal infection
    • In particular, deficiency of the alternative or final common pathway
  • Adults with sporadic meningococcal disease should be screened for complement deficiency
    • CH50 and AP50
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20
Q
  • 21yo student with arthralgia and rash
  • Facial rash, tender joints, HTN 165/95, pedal oedema
  • Blood test results

What further immunological tests would you request to help diagnosis and assess disease activity?

A
  • Complement testing:
    • Immune complexes bind to C1q and activate the classical pathway → complement consumption
    • Low levels of C4 and C3 indicate active SLE
    • ESR and dsDNA AB titre also reflect the activity of SLE
  • Further testing:
    • Urinalysis → proteinuria, microscopic haematuria
    • Urine microscopy → red cells and red cell casts
    • Renal biopsy → diffuse proliferative nephritis, immune complex and complement deposition
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21
Q

Describe the pathophysiology of SLE.

A
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22
Q
  • 21yo student with arthralgia and rash
  • Facial rash, tender joints, HTN 165/95, pedal oedema
A
23
Q
A

urticaria and agiodema

24
Q
A

Complement

25
Q
A

SLE

26
Q
  • Jack’s mother thinks he has too many infections for a 3yo and wants to know why
  • Presenting complaint – recurrent infections:
    • 3-year-old Caucasian male
    • Full term, normal delivery, normal pre and post-natal screen
    • Not breast fed – parental choice
    • Normal immunisation schedule.
    • Weight and height dropping from 50th centile to 10th centile
    • First infection aged 3 months
    • Cellulitis of gluteal region → responded to antibiotics
  • Infection history:
    • Recurrent ear infections
      • Age 5 months otitis media  oral antibiotics
      • 4 subsequent episodes of otitis media  oral antibiotics
      • ENT appointment pending (12 months waiting list), likely to require grommet
    • Age 15 months hospitalised for severe tonsillitis  tonsils removed
    • Recurrent chest infections
      • Age 8 months, 3 years, hospitalised for bronchiolitis/ pneumonia, resolved after intravenous antibiotics. Most recently Haemophilus Influenza isolated
  • Social hx:
    • 4th of 5 children, all under 10yo
    • 2 indoor cats, one indoor dog
    • Both parents smoke cigarettes

Family are frequent attenders to the GP practice

•What are the features that suggest Jack may have an immunodeficiency?

A
  • Features suggestive of immunodeficiency:
    • Severe infections (>1 hospitalisation/year) YES
    • Recurrent minor infections / failure to respond to conventional antibiotics YES
    • Evidence of early end-organ damage NO
    • Unusual organisms (Burkholderia cepacia, etc.) NO
    • Opportunistic organisms (CMV, PCP, candida, aspergillus) NO
    • Unusual sites of infection (deep muscle abscesses) NO
    • Concomitant problems (failure to thrive, FHx, hx of autoimmunity)YES
27
Q

What other factors can cause a 3 yr old to have too many infections?

A
  • Allergic rhinitis, sinusitis, asthma
  • Non-immunologic disorders – CF, local factors (i.e. foreign body), ciliary disorder)
  • Overestimation of infections
27
Q

What other factors can cause a 3 yr old to have too many infections?

A
  • Allergic rhinitis, sinusitis, asthma
  • Non-immunologic disorders – CF, local factors (i.e. foreign body), ciliary disorder)
  • Overestimation of infections
28
Q

What ix would you do for jack?

A

FBC

Immunoglobulins

Serum complement

HIV infections

  • Further investigations:
    • Flow cytometry (lymphocyte surface markers):
      • Quantify B cells
      • Quantify T cells (CD4+ and CD8+)
      • Examine abnormal populations
    • Specific ABs to known antigens to which one has been exposed (i.e. in vaccination):
      • Tetanus ABs
      • Antibodies to HiB
      • Antibodies to PCV-13
29
Q
  • CD4 and CD8 T cells present
  • B cells very low numbers
  • Specific responses to tetanus / HiB -ve

What does Jack have?

A

X-linked agammaglobulinaemia

30
Q

What is the tx for X-linked agammaglobulinaemia?

A
31
Q
  • Persistent back pain and generalised lethargy over last 12m
  • 3 episodes of pneumococcal pneumonia in last 2 years
  • Post-menopausal, on HRT
  • •Physical examination
    • –Swollen, tender hip with marked limitation of movement
    • –Clinically anaemic

What iiix would you ant?

A
32
Q

What is your differential diagnosis?

A
  • MM
  • Osteoporosis and Sjogren’s syndrome
  • Osteoporosis and SLE
33
Q

What is the diagnosis? What are the criteria to diagnose it?

A

MM

34
Q
A
35
Q

What does this urine electrophoresis show?

A

Free light chains

36
Q
A

punched out Lytic lesions

37
Q

Why is this patient susceptible to recurrent infections?

A
  • Recurrent infections because the suppression of production of normal immunoglobulin by the malignant cloneresults in a functional antibody deficiency = “immune paresis”
38
Q

Why is she anaemia?

A
  • Anaemia as expansion of malignant clones’…
    • Crowd out normal RBC and WC precursors in the bone marrow
    • Produce local cytokines which inhibit normal bone marrow function
39
Q

Why is the ESR elevated if the CRP is normal?

A
40
Q
A

rouleaux formation in MM

41
Q

When do you suspect myeloma?

A
42
Q

What test would you want to do?

A
43
Q

What fro you think she has?

A

Rheumatoid arthritis

44
Q

What are the characteristics of rheumatoid arthritis? What is the significance oh the patient’s recent pregnancy?

A
45
Q

What is rheumatoid factor? What type of antibody is it? How sensitive for RA is it?

A
46
Q

What is anti-CCP? How specific is ti?

A
47
Q

Describe the genetic predisposition of RA?

A
  • Genetic Predisposition in Rheumatoid Arthritis:
    • Genetic and environmental factors important
    • HLA DR→ DR1 and DR4 – peptide presentation on MHC II may be associated with disease pathogenesis:
      • DR4 is present in 60-70% of patients (only 20-35% of controls)
      • DR1 also predisposes to RhA
      • Predisposing HLA class II molecules share a common sequence at positions 70-74 (an area predicted to lie within the alpha helix forming the wall of the peptide-binding groove)
    • PADI Type 2 and 4:
      • PADI polymorphisms may increase citrullination of proteins  increased chance of RhA
    • PTPN22 (Protein tyrosine phosphate non-receptor 22) = lymphocyte-specific tyrosine kinase:
      • Normally, this suppresses T cell activation (i.e. problems here suggest T cell activation is important)
      • The 1858T allele increases susceptibility to rheumatoid arthritis, SLE and type 1 diabetes
48
Q

What is the pathophysiology of rheumatoid arthritis?

A
49
Q

How do we treat RA?

A
  • 1st line = DMARDs (disease modifying drugs) – methotrexate, Sulphasalazine, hydroxychloroquine, leflunomide
  • 2nd line = biologics:
    • TNF-alpha antagonists (inhibits downstream inflammation)
    • Rituximab (anti-CD20 which depleted mature B cells but not plasma cells)
    • Abatacept (CTLA4-Ig fusion protein binds to CD80 and CD86 and inhibits T cell activation)
    • Tocilizumab (antibody against IL6 receptor)
50
Q

What should you consider before subjecting a patient to immunosuppression?

A
51
Q
A

X-linked agammaglobulinaemia

52
Q
A

Tumour Necrosis Factor - alpha

Immunology (10 decks)

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