Immuno - case studies Flashcards

1
Q

2 types of latex allergy

A

Type I - spectrum of severity from wheeze + urticaria –> anaphylaxis

Type IV - CONTACT DERMATITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Immediate management of anaphylaxis - 7 points

A
  1. Airway management
  2. O2
  3. IM adrenaline 500mcg
  4. IV fluids
  5. IV chlorpeniramine +
  6. hydrocortisone
  7. Inhaled salbutamol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Specific pt groups at risk of Type I allergy to latex

A

PREM
Indwelling latex devices (eg for hydrocephalus)
Multiple urological proedures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why is tropical fruit allergy significant in latex allergy

A

Cross reactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Eg of latex containing products in healthcare setting

A
BP cuff
Gloves
Catheters
Face masks
Bandages
Steth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

For which allergens is desensitisation actually useful? state 2

A

Insect venom

Grass pollen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Disorders associated with recurrent meningococcal meningitis

A

Complement deficiency
Antibody deficiency

Any disruption to BBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What kinda infections make you suspicious of an immunodeficiency?

A
SPUR 
Serious
Persistent
Unusual 
Recurrent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Suspected complement deficiency - what Ix are ordered?

A

C3
C4
CH50
AP50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complement components in classical pathway

A

C1
C2
C4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Complement components of the alternate pathway

A

Factor B H I (from bacterial cells wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Complement components of the final common pathway

A

C5-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Normal C3
Normal C4
Absent CH50
Absent AP50

What does this indicate?

A

Deficiency in final common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tests to investigate lupus nephritis?

A

Urinalysis (proteinuria + haematuria)

urine microscopy - red cells + casts

Renal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SLE - what kinda hypersensitivity disorder is it?

A

Type III: immune complex mediated

antinuclear antibodies bind to bare cells. these complexes activate complement + attract WBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

wtf is adalimumab

A

humanised anti-TNFalpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MOA of cyclophosphamide?

Which cells are most affected

A

Alkylates guanine

- affects B cells>T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Rituximab - which cells does it deplete?

A

mature B cells (but not plasma cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MMF - which cells does it affect?

A

T cells>B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Azathioprine - which cells does it affect

A

T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Penicillin for CAP –> 3 days later:

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

A

Serum sickness

22
Q

WTF is the pathophysiology behind serum sickness

A

Penicillin 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

23
Q

Clinical features of serum sickness

A

Arthralgia
Renal dysfunction
Purpuric rash

(immune complex deposition in small vessels)

24
Q

Ix to confirm Dx of serum sickness

A
  • complement levels - LOW due to immune complex activation
  • specific IgG to penicillin
  • Skin and kidney biopsies
25
Q

Serum sickness: Type of hypersensitivity disorder

A

Type III

26
Q

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

Ddx?

A
CF
DM
Bruton's 
SCID
Hyper IgM
Cytokine deficiency

having ATOPIC DISEASE

27
Q

Evaluation of lymphocyte immunodeficiency - which Ix?

A

T-cells (CD4 + 8)
B-cells
IgM, IgA, IgG

28
Q

Ix for suspected phagocyte deficiency

A

NBT
Neutrophil count
Leukocyte adhesion markers

29
Q

Treatment of Bruton’s

A

Immunoglobulin replacement every 3 weeks

30
Q

Why are multiple myeloma patients susceptible to infections

A

The mass clonal proliferation of one plasma cell –> suppresses production of normal Ig

31
Q

Why are multiple myeloma patients often anemics?

A

Crowding out of normal RBCs in bone marrow by plasma cells

Tumour releases cytokines which inhibits normal bone marrow function

32
Q

Why is ESR elevated in Multiple Myeloma

A

High protein content in plasma –> increases attractant charge

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

33
Q

X-ray lesions in multiple myeloma

A

lytic lesions “punched out”

34
Q

How is recent childbirth significant in rheumatoid arthritis

A

In pregnancy, Th2 cells tend to predominate and then return to Th1 post-partum

35
Q

Which class of Ig is rheumatoid factor? what does rheumatoid factor target

A

Rheumatoid factor is an IgM which targets Fc portion of human IgG

36
Q

what does anti-CCP stand for

A

anti-cyclic citrullinated protein

37
Q

what is CCP? how are they formed?

A

arginine residues are converted to citrulline residues by PADI enzymes

38
Q

What can affect the degree of CCP generation?

A

Polymorphisms in PADI enzymes - type 2 and 4

39
Q

2 HLA associations with Rheumatoid arthritis?

A

DR1

DR4 (Dw4, 14, 15)

40
Q

PADI stands for?

A

Peptidylarginine deiminase

41
Q

PADI enzymes are important cosssss whyyyy

A

PADI enzymes act to turn arginine residues into citrulline residues

Polymorphisms (type 2 and 4) lof PADI –> more citrulline resiudes –> more likely to develop RA

42
Q

PTPN22 is an enzyme important in rheumatoid arthritis. what is its function?

A

PTPN22
- suppresses T cell activation

In RA, the 1858T allele increases RA susceptibility

43
Q

Genetic predisposition to Rheumatoid arthritis

A
  • HLA DR1 + 4
  • PTPN22 - 1858T allele
  • PADI enzyme (PMs type 2 + 4)
44
Q

1st line tx of rheumatoid arthritis

A

DMARDs inc methotrexate

45
Q

If methotrexate is not tolerated - which DMARds are used for rheumatoid arthritis

A

Sulphasalazine

Hydroxychloroquine

46
Q

name 2 anti-TNFalpha agents

A

infliximab

Adalimumab

47
Q

Tocilizumab - MOA? use?

A

Anti-IL6 receptor

Rheumatoid arthritis

48
Q

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

A

Infliximab (anti-TNFa)
Abatacept (anti-CTLA4)
Tocilizumab (anti-IL6)
Rituximab (depletes B cells, anti-CD20)

49
Q

Natalizumab - MOA? use?

A

MOA: anti-alpha4 intern

Use: relapsing remitting MS

50
Q

Use for basiliximab

A

prevention of transplant rejection