Immunology 8 - case studies

Question 1

What is the most common clinical presentation of anaphylaxis?

Answer 1

Urticaria/angioedema

Question 2

Management of anaphylaxis in an adult

Answer 2

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

Question 3

What is IV hydrocortisone important for in anaphylaxis?

Answer 3

Prevents rebound anaphylaxis

Question 4

What are the 2 types of latex allergy?

Answer 4

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

Type IV contact dermatitis

Question 5

Risk factors for latex allergy

Answer 5

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

Question 6

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

Answer 6

Cross reactivity

Question 7

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

Answer 7

Anti-histamines

Question 8

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

Answer 8

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

Question 9

What investigation done to test for type IV latex allergy?

Answer 9

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

Question 10

For which allergens is desensitisation effective?

Answer 10

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

Question 11

Disorders associated with recurrent meningococcal meningitis?

Answer 11

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

Question 12

What kind of infections make you suspicious of an immunodeficiency?

Answer 12

SPUR
Serious
Persistent
Unusual
Recurrent

Question 13

Suggested complement deficiency, what investigations do you order?

Answer 13

C3, C4
CH50
AP50

Question 14

Normal C3
Normal C4
Absent CH50
Absent AP50

Answer 14

Indicates deficiency in final common pathway (C5-C9)

Question 15

Tests to investigate lupus nephritis?

Answer 15

Urinalysis –> proteinuria, microscopic haematuria
Urine microscopy –> red cells and red cell casts
REnal biopsy –> diffuse proliferative nephritis, immune complex and complement deposition

Question 16

What type of hypersensitivity is SLE?

Answer 16

Type iII (immune-complex mediated)

Question 17

Penicillin for CAP –> 3 days later:

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

Answer 17

Serum sickness

Question 18

How does penicillin cause serum sickness?

Answer 18

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

Question 19

Ix to confirm Dx of serum sickness

Answer 19

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

Question 20

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

Answer 20

Infiltration of macrophages and neutrophils

Deposition of IgG and IgM and complement

Question 21

Serum sickness type of hypersensitivity disorder

Answer 21

Type III

Question 22

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

Ddx?

Answer 22

CF
Foreign body
Atopy
Bruton's
SCID
HyperIgM

Question 23

Evaluation of lymphocyte immunodeficiency - which Ix?

Answer 23

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

Question 24

Treatment of Bruton’s agammaglobulinaemia

Answer 24

IVIG every 3 weeks indefinitely (HSCT is permanent cure)

Question 25

“punched out lytic lesions”

Answer 25

MM on radiology

Question 26

Why are MM patients susceptible to infection?

Answer 26

FUnctional antibody deficiency due to suppression of normal antibody production

Question 27

FEature on blood film of pt with MM

Answer 27

Rouleaux formation

Question 28

Why is ESR elevated in Multiple Myeloma

Answer 28

High protein content in plasma –> increases attractant charge

RBCs tend to clump together so they fall more quickly through plasma.

Question 29

How is recent childbirth significant in rheumatoid arthritis

Answer 29

In pregnancy predominantly Th2 immune response and once delivered, switch to Th1 immune response –> RA flare

Question 30

What immunoglobulin class is RF?

Answer 30

Predominantly IgM

Question 31

What is RF targeted against?

Answer 31

The Fc region of human IgG

Question 32

Polymorphisms in which enzymes increase generation of citrullinated peptides in patients who develop RhA

Answer 32

PADI enzymes (they deaminate arginine residues to citrulline)

Question 33

RA HLA associations

Answer 33

HLA DR 4 (AND DR1)

Question 34

What can affect the degree of CCP generation?

Answer 34

PADI type 2 and 4 polymorphisms

Question 35

PADI stands for?

Answer 35

peptidyl arginine deaminase

Question 36

PTPN22 is important in RA, what is its function?

Answer 36

suppresses t cell activation

In RA, the 1858T allele increases RA susceptibility

Question 37

1st line management of RA

Answer 37

DMARDs e.g. methotrexate, sulphasalazine, hydroxychloroquine

Question 38

What do you need to screen people for before starting on biologics?

Answer 38

TB ELISPOT, HBV, HCV, HIV

Question 39

Beyond DMARDs - state 4 diff drugs used to treat Rheumatoid arthritis

Answer 39

Infliximab (anti-TNFa)
Abatacept (CTLA-4 -Ig fusion protein)
Tocilizumab (Anti-IL-6 receptor)
Rituximab (anti-CD20, Depletes B cells but not plasma cells)