Immunology 8 - case studies Flashcards

1
Q

What is the most common clinical presentation of anaphylaxis?

A

Urticaria/angioedema

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2
Q

Management of anaphylaxis in an adult

A
ABC (may need intubation/tracheostomy)
Mask O2, inhaled salbutamol
IM 1 in 1000 0.5mg adrenaline
IV 200mg hydrocortisone 
IV 10mg chlorphenamine
IV fluids
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3
Q

What is IV hydrocortisone important for in anaphylaxis?

A

Prevents rebound anaphylaxis

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4
Q

What are the 2 types of latex allergy?

A

Type I hypersensitivity (latex food syndrome), spectrum of sx

Type IV contact dermatitis

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5
Q

Risk factors for latex allergy

A

PREM
Indwelling latex devices e.g. VP shunt for hydrocephalus
Multiple urological procedures

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6
Q

Why are people with latex allergy prone to tropical fruit allergy? (latex-fruit syndrome)

A

Cross reactivity

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7
Q

What drug class does contact dermatitis not respond to? (type IV)

A

Anti-histamines

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8
Q

Ideal investigation for IgE specific to latex in patient who presented with anaphylaxis?

A

In vitro test i.e. blood test as skin prick has risk of anaphylaxis

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9
Q

What investigation done to test for type IV latex allergy?

A

Skin patch testing (taped to skin for 24-48 hrs)

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10
Q

For which allergens is desensitisation effective?

A

Insect venom and aero-allergens e.g. grass pollens

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11
Q

Disorders associated with recurrent meningococcal meningitis?

A
Complement deficiency (especially C5-C9) 
Anitbody deficiency 
ANy disturbance to BBB e.g. hydrocephalus, skull fracture
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12
Q

What kind of infections make you suspicious of an immunodeficiency?

A
SPUR
Serious
Persistent
Unusual
Recurrent
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13
Q

Suggested complement deficiency, what investigations do you order?

A

C3, C4
CH50
AP50

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14
Q

Normal C3
Normal C4
Absent CH50
Absent AP50

A

Indicates deficiency in final common pathway (C5-C9)

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15
Q

Tests to investigate lupus nephritis?

A

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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16
Q

What type of hypersensitivity is SLE?

A

Type iII (immune-complex mediated)

17
Q

Penicillin for CAP –> 3 days later:

Fever, arthralgia, vasculitic skin rash, proteinuria, haematuria, raised transaminases, disorientation

A

Serum sickness

18
Q

How does penicillin cause serum sickness?

A

Penicillin binds to cell surface proteins and is recognised as a neo-antigen: SENSITISATION. stimulates a strong IgG response

On next exposure –> IMMUNE COMPLEX FORMATION w circulating penicillin + mass IgG production –> complex deposits in glomeruli + skin + joints

19
Q

Ix to confirm Dx of serum sickness

A

C3+ C4 levels (LOW)
Specific IgG to penicillin
Biopsy of skin and kidneys

20
Q

What would biopsy of skin and kdineys show in serum sickness?

A

Infiltration of macrophages and neutrophils

Deposition of IgG and IgM and complement

21
Q

Serum sickness type of hypersensitivity disorder

22
Q

FTT +recurrent infections (tonsillitis, pneumonia, ROM, cellulitis):

Ddx?

A
CF
Foreign body
Atopy
Bruton's
SCID
HyperIgM
23
Q

Evaluation of lymphocyte immunodeficiency - which Ix?

A

CD4+ CD8+ T cells
Quantif B cells
IgM, IgG, igA
Specific antibodies to known antigens to which one has been exposed e.g. vaccination

24
Q

Treatment of Bruton’s agammaglobulinaemia

A

IVIG every 3 weeks indefinitely (HSCT is permanent cure)

25
"punched out lytic lesions"
MM on radiology
26
Why are MM patients susceptible to infection?
FUnctional antibody deficiency due to suppression of normal antibody production
27
FEature on blood film of pt with MM
Rouleaux formation
28
Why is ESR elevated in Multiple Myeloma
High protein content in plasma --> increases attractant charge RBCs tend to clump together so they fall more quickly through plasma.
29
How is recent childbirth significant in rheumatoid arthritis
In pregnancy predominantly Th2 immune response and once delivered, switch to Th1 immune response --> RA flare
30
What immunoglobulin class is RF?
Predominantly IgM
31
What is RF targeted against?
The Fc region of human IgG
32
Polymorphisms in which enzymes increase generation of citrullinated peptides in patients who develop RhA
PADI enzymes (they deaminate arginine residues to citrulline)
33
RA HLA associations
HLA DR 4 (AND DR1)
34
What can affect the degree of CCP generation?
PADI type 2 and 4 polymorphisms
35
PADI stands for?
peptidyl arginine deaminase
36
PTPN22 is important in RA, what is its function?
suppresses t cell activation In RA, the 1858T allele increases RA susceptibility
37
1st line management of RA
DMARDs e.g. methotrexate, sulphasalazine, hydroxychloroquine
38
What do you need to screen people for before starting on biologics?
TB ELISPOT, HBV, HCV, HIV
39
Beyond DMARDs - state 4 diff drugs used to treat Rheumatoid arthritis
Infliximab (anti-TNFa) Abatacept (CTLA-4 -Ig fusion protein) Tocilizumab (Anti-IL-6 receptor) Rituximab (anti-CD20, Depletes B cells but not plasma cells)