immuno cases Flashcards

(45 cards)

1
Q

Check tmpt status before prescribing which drug?
why?

*Thiopurine s-methyltransferase

A

Azathioprine

a tempt deficiency = difficulty processig drugs with thiopurine.

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2
Q

Serum sickness is a ___ reaction?

A

type 3 reaction

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3
Q

what is rheumatoid factor?

A

an auto antibody – an IgM against the Fc portion of human igG

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4
Q

which polymorphisms are seen in rheumatoid arthirits?

A

PADI enzyme polymorphisms

also PTPN22

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5
Q

Etanercept and infliximab target ____ ?

A

TNF-alpha

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6
Q

what is the complete treatment of sever anaphylaxis?

A

○ ABC approach
○ Oxygen by mask
○ Nebulised bronchodilators- Salbutamol
○ IM Adrenaline (0.5 mg for adult- may repeat)
○ IV Antihistamines (10 mg Chlorpheniramine)
○ IV Corticosteroids (200 mg hydrocortisone)
○ IV Fluids

§ Intubation if severe bronchoconstriction

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7
Q

MOA of adrenaline?

A
Acts on beta-2 adrenergic receptors to constrict arterial smooth muscle
			§ Effects:
				□ Increased blood pressure 
				□ Limits vascular leakage
				□ Bronchodilator
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8
Q

why are steroids prescribed in anaphylaxis?

A

Important for preventing rebound anaphylaxis

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9
Q

list the 2 types of latex allergy

A

Type 1 Hypersensitivity

  • classical allergic symptoms and anaphylaxis
  • can cross react with some fruits and veg
  • immediate rxn

Type 4 hypersensitivity

  • contact dermatitis
  • usally just affects site of contact eg hands and feet rather thansystemic reaction
  • not due to latex but instead rubber additives
  • 24-48 hours after exposure
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10
Q

60% of occupational asthma in the UK is associated with ______ exposure?

which settings/jobs?

A

latex

Particularly laboratory workers, operating theatre staff and latex or manufacturing industry workers

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11
Q

Patient presents with a well demarcated rash often flaky 1.5 days after wearing a new pairof shoes

It is NOT responsive to antihistamines

ddx?

A

contact dermatitis t4 hypersensitivity rxn

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12
Q

patient has had an anaphylactic rxn to latex. has been stabilised. what ivx to do?

A
  1. Specific IgE Blood test

rather than a skin prick due to anaphylaxis risk

others; ?
in vivo skin prick
in vivio patch test

○ Biopsy
Infiltrating T lymphocytes
Granulomas

others;
 refer to an allergist
avoid latex
avoid cross reactive foods!
epipen
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13
Q

desensitisation therapies only works for ___?

A

insect venom and some aero-allergens (e.g. grass pollen)

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14
Q

what happens in Type I hypersensitivity response - anaphylaxis ?

A

Cross-linking of IgE on surface of mast cells
Causes mast cells to degranulate
Results in release of specific biological mediators including histamine and leukotrienes

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15
Q

what are the 2 most common clinical features of anaphylaxis?

the 3 following?

A

urticaria
angioedema

Upper airway oedema, SOB, Wheezing

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16
Q

what is involved in the rx / treatment of anaphylaxis - broad categories?

A
  1. Oxygen by mask
    Improve oxygen delivery
  2. Adrenalin im (0.5mg for adult and may repeat)
  3. Bronchodilator
  4. Intravenous anti-histamines (10mg Chlorpheniramine)
  5. Nebulised bronchodilators or salbutamol
  6. Intravenous corticosteroids (Hydrocortisone 200mgs)
  7. Intravenous fluids
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17
Q

what is the MOA of adrenaline?

A

Acts on B2 adrenergic receptors to constrict arterial smooth muscle
Increases blood pressure
Llimits vascular leakage

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18
Q

what is the MOA of bronchodilators?

A

Acts to oppose the effects of mast-cell derived histamine

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19
Q

what is the MOA of steroids in anaphylaxis?

A

Systemic anti-inflammatory agent.
Effect takes about 30minutes to start, and does not peak for several hours.

Important in preventing rebound anaphylaxis -

20
Q

what is the purpose of IV fluids in anaphylaxis?

A

Increase circulating blood volume and therefore increase blood pressure

21
Q

what is the purpose of nebulised bronchodilators in anaphylaxis?

A

Improve oxygen delivery through bronchial dilatation

22
Q

what is involved in the rx / treatment of anaphylaxis ?

A

Inhaled:
Oxygen
Salbutamol (bronchodilator)

Intramuscular: Adrenalin

Intravenous: Chlorpheniramine (anti-histamine) Hydrocortisone (anti-inflammatory)
Fluids

23
Q

what is latex fruit syndrome?

which are the culprit fruits?

A

when some1 has an allergy to latex,

eating certain fruits* can cause an issue

because said fruits contain similar proteins - can lead to cross-reaction they are called cross-reactive foods

* Avocado
Apricot
Banana
Chestnut
Kiwi
Passion fruit
Papaya
Pear
Pineapple
24
Q

How would you confirm latex allergy? what might you see if positive?

A

In vitro IgE test:

Type I latex allergy
- Skin prick testing

Type 4 latex allergy

  • Patch tests: Eczema will be seen
  • Biopsy: Infiltrating T lymphocytes, Granuloma
25
when does desensitisation work ?
only works for insect venom and some aero-allergens (eg grass pollen).
26
What disorders are associated with recurrent meningococcal meningitis? what ivx would you do?
1.Complement deficiency encapsulated organisms 2. B cell/Antibody deficiency Recurrent bacteria infections, especially of upper and lower respiratory tract 3. Any disruption of blood brain barrier: Occult skull fracture Hydrocephalus ------ Tests: Complement C3 and C4 CH50 AP50 Immunoglobulins Serum IgG, IgA and IgM Protein electrophoresis
27
which test Measures haemolysis of antibody-coated sheep erythrocytes ?
CH50
28
Which test Measures haemolysis of rabbit erythrocytes?
AP50
29
what do the following mean: Results Normal C3 and C4 Absent CH50 Absent AP50
Indicates deficiency of component in final common pathway (C5-9) All components of the cascade need to be in place for the test to give a positive (normal) result
30
a patient is shown to have complete deficiency of C7 and recurrent meningococcal infection hwo to manage?
Meningovax, Pneumovax and HIB vaccines Daily prophylactic penicillin
31
adults with sporadic meningococcal disease should be screened for _____ ?
complement deficiency
32
a patient comes in with sx suggestive of SLE. what tests. would you do to confirm the diagnosis/disease activity?
ANA if +ve -> dsDNA, ENA, Cytoplasmic antibodies. Complement - because immune complexes can lead to complement activation and depletion
33
What is the predominant effector mechanism of SLE disease | in terms of the Gel and Coombs classification?
Type III response immune complex deposition
34
what is the associated mechanism in Serum sickness?
Drug eg penicillin can bind to cell surface proteins Acts as “neo-antigen”: stimulates very strong IgG antibody response Individual is “sensitised” to penicillin Subsequent exposure to drug/penicillin stimulates formation of immune complexes with circulating penicillin the production of more IgG antibodies you then get Immune complex deposition in small vessels -> vasculitis also arthralgia, purpura
35
what ivx is done to confirm serum sickness? findings?
Low serum C3 and C4 Specific IgG to drug/penicillin Biopsy features (skin, kidney): Infiltration of macrophages and neutrophils Deposition of IgG, IgM and complement
36
what are the signs/symptoms of serum sickness?
Develops fever Arthralgia of large joints Vasculitic skin rash Renal function starts to deteriorate Disorientation: Small vessel vasculitis affecting cerebral vessels may compromise oxygen supply to the brain
37
what causes pupura?
immune complex deposition Inflamed blood vessels are likely to leak results in local haemorrhage Also become plugged with clots
38
what si the mechanism of immune complex mediated renal function detrioration in serum sickness?
Deposition of immune complexes causes local complement activation and neutrophil and macrophage infiltration Results in inflammation of the glomeruli Results in increase in serum creatinine, proteinuria and haematuria
39
how dowe treat serum sickness?
stop drug Give corticosteriods fluids
40
why is there Rouleaux formation in multiple myeloma?
Normally, erythrocytes do not clump However, if protein constituents of plasma increase or change there is paraprotinaemia in MM / more serum free light chains So higher ESR
41
what ivx should one do in MM?
Immunoglobulins and electrophoretic strip, Urinary light chains (BJP), skeletal survey
42
what is rheumatoid factor?
an IgM antibody directed at the Fc region of human IgG
43
which is more specific in rheumatoid arthritis Anti-CCP or rheumatoid factor?
Anti-CCP
44
what are the genetic associations of Rheumatoid arthritis?
HLA DR4 present in 60-70% patients - only specific DR4 subtypes, ie Dw4, Dw14, Dw15 HLA DR1 Predisposing HLA class II molecules share common sequence at positions 70-74,in the alpha helix forming the wall of the peptide-binding groove PADI type 2 and 4 - Peptidylarginine deiminase polymorphisms increase citrullination of proteins - loss of B cell tolerance to CCP causes RA PTPN 22 - Protein tyrosine phosphatase non-receptor 22 - 1858T allele - suppresses T cell activation
45
how is Rheumatoid arthiritis treated?
DMARD - methotrexate Sulphasalazine, hydroxychloroquine, leflunomide ``` Others; TNFalpha antagonist Rituximab - anti-cd20 Abatacept - CTLA-4 – Ig fusion protein; stops T cell activation Tocilizumab - for IL6 ```