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Year 5 😊✌🏼 > Immunology Case studies > Flashcards

Immunology Case studies Flashcards

1
Q

What is atopy?

A

the tendency to develop IgE antibodies against innocuous antigens (allergens)

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2
Q

steps of allergy

A
  1. atopy
  2. sensitisation
  3. typical reaction hx and/or positive provocation
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3
Q

Tests for sensitisation

A

skin prick test

measure serum specific IgE

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4
Q

contents of granules in masst cells

A

histamine (h1-4R)
proteases e.g. tryptaase
proteoglycans
cytokines

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5
Q

sensitisation vs allergy

A

In allergy you have the sx, not just the presence of the IgE

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6
Q

Sx of allergic reactions

A

skin/mucosa:
- urticarial rash
- swelling
- angioedema
- erythema

respiratory:
- wheeze
- bronchoconstriction
- chest tightness
- cough
- haufever sx: runny nose, eye itching

CVS
- shock due to systemic vasodilatation
- compensatory tachycardia
- LOC
- empty ventricle syndrome
- palpitations

GI
- vomiting
- diarrhoea
- cramps

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7
Q

What causes swelling in allergy?

A

mast cell degranulation causes vasodilation -> leaky

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8
Q

Why does BP drop in allergic reactions?

A

systemic dilatation due to mast cell degranulation

you also get a compensatory tachycardia

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9
Q

What is anaphylaxis

A

severe allergic reaction that has an A, B or C problem + skin changes/angioedema.

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10
Q

Do you need a BP drop to diagnose anaphylaxis?

A

no

you just need an A, B or C problem.

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11
Q

What medications do we use to treat anaphylaxis?

A

adrenaline
fluids

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12
Q

How does adrenaline treat anaphylaxis?

A

vasoconstriction
bronchodilates
acts on beta1 receptors of immune cells and stop them from releasing

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13
Q

Why are antihistamines no longer used in anaphylaxis?

A

do not reverse the CV effects or bronchocontriciton

only helps with the rash

act still continues to progress

masks skin and resp manifestations even thought the reaction is still regressing

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14
Q

Why are steroids no longer used in anaphylaxis?

A

take a long time to work

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15
Q

biphasic reaction in anaphylaxis

A

de novo synthesis process

release immune mediators e.g. leukotrienes, prosstaglandins, prostacyclin, thromboxane

takes minutes to hours

therefore wait 6h before sending someone with/post anaphylaxis home

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16
Q

bispaahsic reaction

A

in anaphylaxis
in hayfever

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17
Q

how long do you keep someone in A&E post anaphylaxis

A

6h

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18
Q

Hospital discharge plan post anaphylaxislaxis

A
  1. avoidance advice
  2. educate on allergy
  3. action plan
  4. allergy referral

may give epipen depending on the allergen they react to e.g. yes in nuts, no in penicillin

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19
Q

what blood test level is useful in anaphylaxis?

A

tryptase

during reaction and baseline

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20
Q

What protein is associated with allergy to peanuts?

A

Ara h2

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21
Q

PR10

A

pollen protein

can be found in peanuts, hazelnuts and

this protein is denatured by heat so

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22
Q

Pollen food syndrome

A

allergy to PR10

avoid these nuts in and foods in raw forms but can have them in cooked forms

have haufever usually ?

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23
Q

Why do people need to have 2 EpiPens ?

A

They might need one an hour later (delayed reaction?)

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24
Q

Why do people need to have 2 EpiPens ?

A

They might need one an hour later (delayed reaction?)

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25
Q

What is the most appropriate first line treatment for anaphylaxis?

A

adrenaline

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26
Q

Which disorders are associated with recurrent meningococcal speticaemia/meningitis?

A
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27
Q

What immune deficiency is associated with meningococcal sepsis/meningitis?

A

complement deficiency
(recurrent infection with encapsulated organisms)

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28
Q

SPUR

A

serious
persistent
unusual
recurrent

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29
Q

What should you ask yourself if you think someone might have amn immune deficiency?

A

SPUR

serious
persistent
unusual
recurrent

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30
Q

Which immunological tests would you request in recurrent infection with encapsulated organisms?

A

complement - C3 and C4
CH50 (FUNCTIONAL TESTS)
AP50

serum Ig
protein phoresis ?

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31
Q

What are CH50 and AP50 tests?

A

functional tests of complement
downstream of C3 and C4

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32
Q

How do you manage someone with complement deficiency?

A
  • vaccination (MenACWY, MenB, pneumococcal vaccination, HiB vaccination)
  • daily prophylactic penicillin
  • tests family
    -…
33
Q

what infections are people with complement deficiency at risk of?

A

encapsulated organisms (meningococcus, pneumococcus, haemophilus)

particularly the final pathwaty and the common pathway

34
Q

Anti_CCP

A

seen in RA

35
Q

What disease should you screen people with SLE for?

A

APS

36
Q

Clinical criteria for APS

A
  1. intravascular thrombosis (arterial or venous)
  2. recurrent miscarriage
37
Q

tests for APS

A

anti-cardiolipin ab
beta2glycoprotein1 antibody
lupus anticoagulant test

clotting asset - prolonged AAPTT or dRVVT that doesn’t correct with normal pooled plasma but corrects with phospholipids

38
Q

What test should you do for monitoring patients with SLE?

A

urine dip every time in clinic

U&E

39
Q

red cell casts

A

feature of active, proliferative nephritis

40
Q

What drugs can be useful in SLE?

A

prednisolone
anifrolumab (in some)
azathioprine
hydroxychloroquine (pretty much everyone with lupus)
rituximab (deplete B cells, particularly good in renal disease)
belimumab
mycophenolate mofetil (steroid sparing)
adalimumab

you might use cyclophosphamide if they are very unwell, quite quick and effective

NOT
allopurinol
adalimumab)
colchicine (inhibits neutrophils)

41
Q

what disease is anti-dsDNA associated with?

A

SLE

most specific antibody

42
Q

What is RA?

A

peripheral symmetrical poly arthritis and stiffness persisting for more than 6 weeks

43
Q

What is rheumatoid factor?

A

antibody against Fc portion of IgG

you can also have IgM and IgA RF

60-70% sensitive and 60-70% specific

44
Q

what is anti-ccp?

A

ab against cyclic citullinated peptides

highly specific for RA (95%)

polymorphisms within OADU enzymes nay increase generation citrullinated residues in patients wh develop RAA

45
Q

Why is smoking associated with RA?

A

increases the amount of citrullinated proteins in the lung - this may play a role

46
Q

twin concordance for RA

A

30% identical
5% non identical

47
Q

what HLA are associated with RA

A

HLA DR4 subtypes Dw4, Dw14, Dw15
HLA DR1 also predisposes

48
Q

PADI type 2 and 4

A
  • certain polymorphisms increase citrullination of proteins
  • peptidularginine deiminase
49
Q

PTTPN 22

A

protein tyrosine phosphatase……
….

50
Q

Key cytokines in RA

A

TNF alpha
IL-6

51
Q
A

T-cells
B-cells
Macrophages (tif alpha)
synovial cells and fibroblasts (il-6)

52
Q

1st line management of RA

A

DMARDs

methotrexate
sulphasalazine, hydroxychloroquine, leflunomide

53
Q

What if DMARDs don’t work in RA?

A

specific biologics

biologic DMARDs and Jakinibs

TNF-alpha antagonists (infliximab, entarcept)
tocilizumab
rituximab
abatacept

54
Q

Why do you need to treat RA?

A

to prevent destructive joint disease.

55
Q

what to do before starting biologics?

A

make sure they are vaccinated
ask about TB exposure + CXR
screen for HIV, Hep B, Hep C

check if they had SA in the past - risk of it becoming a problem again

56
Q

/What cancers are people treated for RA at higher risk of?

A

non melanoma skin cancer

57
Q

most specific antibody for RA?

A

anti-ccp

58
Q

Ix in ?multiple myeloma

A

serum immmunoglobulins
serum protein electrophoresis (monoclonal band in gamma region)
urien electrophoresis (free light chains detected)

59
Q

R-ISS

A

multiple myeloma

staging

60
Q

Why are patient with myeloma more susceptible to infection

A

FUNCTIONAL ANTIBODY DEFICIENCY

even though their Ig is high, it is mainly monoclonal

only a small amount of polyclonal antibodies

61
Q

Why would you get anaemia in multiple myeloma?

A

seen in most patients with MM

mechanism:
- space limitation due to white cell precursors in bone marrow
- ???

62
Q

why is the ESR raised in multiple myeloma?

A

erythrocytes clump faster because there are more protein constituents in plasma which increases the attractant charge between the red cells

this makes them fall more quickly through the capillary/tube

therefore also Roleaux on blood film

63
Q

Roleaux on blood film

A

stack of RBCs

can be seen in multiple myeloma

add if seen anywhere else

64
Q

Why is calcium increased in multiple myeloma?

A

???

65
Q

median survival for multiple myeloma now

A

120 months / 10 years

66
Q

key question in mx of myeloma

A

are you eligible for a stem cell transplant

autologous done in multiple myeloma?

67
Q

What would suggest that aa child has a

A

unusual organisms
recurrent
……

68
Q

Reasons why children may have abnormally many infections?

A

CF
structural lung disease
asthma
ciliary disorders
foreign body
HIV
primary immune deficiency

69
Q

ix for ?immune deficiency

A

FBC
U&E
LFT
CRP
sweat test
CXR
Ig

check immune response to vaccination
FISH for immune deficiency down the line

70
Q

where is BTK important/

A

BTK is an important protein in development of B-cells

71
Q

What is BTK?

A
72
Q

BTK

A

over expression in BTK is associated with some haem malignancies e.g. CLL -> Ibrutinib can be used to specifically target it

also may be overactive in AID

73
Q
A

BTK controls the NLRP3 inflammasome

involved in secretion and production of IL-1beta (and IL-18)

74
Q

X-linked agammaglobulinaemia

A

failure of pre-B cells to mature in the BM
failure to produce IG

75
Q

Mx of X-linked agammaglobulinaemia

A

Ig replacement therapy
given every 3w IV at hospital or weekly SC at home
indefinite treatment

76
Q

murtaation in Bruton tyrossine kinase gene are a cause of which immunodeficiency?

A

XLA (x- linked agammaaglobinaemia)

77
Q

What causes CVID?

A

adult onset antibody deficiency syndrome

more details here xxx

78
Q

What causes selective IgA deficiency

A
79
Q

dendritic cell neoplasm types

A

???

Year 5 😊✌🏼 (53 decks)

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