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Year 5 😊✌🏼 > Immunology Case studies > Flashcards

Immunology Case studies Flashcards

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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
What is the most appropriate first line treatment for anaphylaxis?
adrenaline
26
Which disorders are associated with recurrent meningococcal speticaemia/meningitis?
27
What immune deficiency is associated with meningococcal sepsis/meningitis?
complement deficiency (recurrent infection with encapsulated organisms)
28
SPUR
serious persistent unusual recurrent
29
What should you ask yourself if you think someone might have amn immune deficiency?
SPUR serious persistent unusual recurrent
30
Which immunological tests would you request in recurrent infection with encapsulated organisms?
complement - C3 and C4 CH50 (FUNCTIONAL TESTS) AP50 serum Ig protein phoresis ?
31
What are CH50 and AP50 tests?
functional tests of complement downstream of C3 and C4
32
How do you manage someone with complement deficiency?
- vaccination (MenACWY, MenB, pneumococcal vaccination, HiB vaccination) - daily prophylactic penicillin - tests family -...
33
what infections are people with complement deficiency at risk of?
encapsulated organisms (meningococcus, pneumococcus, haemophilus) particularly the final pathwaty and the common pathway
34
Anti_CCP
seen in RA
35
What disease should you screen people with SLE for?
APS
36
Clinical criteria for APS
1. intravascular thrombosis (arterial or venous) 2. recurrent miscarriage
37
tests for APS
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
What test should you do for monitoring patients with SLE?
urine dip every time in clinic U&E
39
red cell casts
feature of active, proliferative nephritis
40
What drugs can be useful in SLE?
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
what disease is anti-dsDNA associated with?
SLE most specific antibody
42
What is RA?
peripheral symmetrical poly arthritis and stiffness persisting for more than 6 weeks
43
What is rheumatoid factor?
antibody against Fc portion of IgG you can also have IgM and IgA RF 60-70% sensitive and 60-70% specific
44
what is anti-ccp?
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
Why is smoking associated with RA?
increases the amount of citrullinated proteins in the lung - this may play a role
46
twin concordance for RA
30% identical 5% non identical
47
what HLA are associated with RA
HLA DR4 subtypes Dw4, Dw14, Dw15 HLA DR1 also predisposes
48
PADI type 2 and 4
- certain polymorphisms increase citrullination of proteins - peptidularginine deiminase
49
PTTPN 22
protein tyrosine phosphatase...... ....
50
Key cytokines in RA
TNF alpha IL-6
51
T-cells B-cells Macrophages (tif alpha) synovial cells and fibroblasts (il-6)
52
1st line management of RA
DMARDs methotrexate sulphasalazine, hydroxychloroquine, leflunomide
53
What if DMARDs don't work in RA?
specific biologics biologic DMARDs and Jakinibs TNF-alpha antagonists (infliximab, entarcept) tocilizumab rituximab abatacept
54
Why do you need to treat RA?
to prevent destructive joint disease.
55
what to do before starting biologics?
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
/What cancers are people treated for RA at higher risk of?
non melanoma skin cancer
57
most specific antibody for RA?
anti-ccp
58
Ix in ?multiple myeloma
serum immmunoglobulins serum protein electrophoresis (monoclonal band in gamma region) urien electrophoresis (free light chains detected)
59
R-ISS
multiple myeloma staging
60
Why are patient with myeloma more susceptible to infection
FUNCTIONAL ANTIBODY DEFICIENCY even though their Ig is high, it is mainly monoclonal only a small amount of polyclonal antibodies
61
Why would you get anaemia in multiple myeloma?
seen in most patients with MM mechanism: - space limitation due to white cell precursors in bone marrow - ???
62
why is the ESR raised in multiple myeloma?
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
Roleaux on blood film
stack of RBCs can be seen in multiple myeloma add if seen anywhere else
64
Why is calcium increased in multiple myeloma?
???
65
median survival for multiple myeloma now
120 months / 10 years
66
key question in mx of myeloma
are you eligible for a stem cell transplant autologous done in multiple myeloma?
67
What would suggest that aa child has a
unusual organisms recurrent ......
68
Reasons why children may have abnormally many infections?
CF structural lung disease asthma ciliary disorders foreign body HIV primary immune deficiency
69
ix for ?immune deficiency
FBC U&E LFT CRP sweat test CXR Ig check immune response to vaccination FISH for immune deficiency down the line
70
where is BTK important/
BTK is an important protein in development of B-cells
71
What is BTK?
72
BTK
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
BTK controls the NLRP3 inflammasome involved in secretion and production of IL-1beta (and IL-18)
74
X-linked agammaglobulinaemia
failure of pre-B cells to mature in the BM failure to produce IG
75
Mx of X-linked agammaglobulinaemia
Ig replacement therapy given every 3w IV at hospital or weekly SC at home indefinite treatment
76
murtaation in Bruton tyrossine kinase gene are a cause of which immunodeficiency?
XLA (x- linked agammaaglobinaemia)
77
What causes CVID?
adult onset antibody deficiency syndrome more details here xxx
78
What causes selective IgA deficiency
79
dendritic cell neoplasm types
???

Year 5 😊✌🏼 (53 decks)

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