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Path - Immuno > immuno cases > Flashcards

immuno cases Flashcards

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
Q

when does desensitisation work ?

A

only works for insect venom and some aero-allergens (eg grass pollen).

26
Q

What disorders are associated with recurrent meningococcal meningitis?

what ivx would you do?

A

1.Complement deficiency
encapsulated organisms

  1. B cell/Antibody deficiency
    Recurrent bacteria infections, especially of upper and lower respiratory tract
  2. 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
Q

which test Measures haemolysis of antibody-coated sheep erythrocytes ?

A

CH50

28
Q

Which test Measures haemolysis of rabbit erythrocytes?

A

AP50

29
Q

what do the following mean:

Results
Normal C3 and C4
Absent CH50
Absent AP50

A

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
Q

a patient is shown to have complete deficiency of C7
and recurrent meningococcal infection

hwo to manage?

A

Meningovax, Pneumovax and HIB vaccines

Daily prophylactic penicillin

31
Q

adults with sporadic meningococcal disease should be screened for _____ ?

A

complement deficiency

32
Q

a patient comes in with sx suggestive of SLE. what tests. would you do to confirm the diagnosis/disease activity?

A

ANA
if +ve -> dsDNA, ENA, Cytoplasmic antibodies.

Complement
- because immune complexes can lead to complement activation and depletion

33
Q

What is the predominant effector mechanism of SLE disease

in terms of the Gel and Coombs classification?

A

Type III response

immune complex deposition

34
Q

what is the associated mechanism in Serum sickness?

A

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
Q

what ivx is done to confirm serum sickness? findings?

A

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
Q

what are the signs/symptoms of serum sickness?

A

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
Q

what causes pupura?

A

immune complex deposition

Inflamed blood vessels are likely to leak
results in local haemorrhage
Also become plugged with clots

38
Q

what si the mechanism of immune complex mediated renal function detrioration in serum sickness?

A

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
Q

how dowe treat serum sickness?

A

stop drug
Give corticosteriods
fluids

40
Q

why is there Rouleaux formation in multiple myeloma?

A

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
Q

what ivx should one do in MM?

A

Immunoglobulins and electrophoretic strip, Urinary light chains (BJP),

skeletal survey

42
Q

what is rheumatoid factor?

A

an IgM antibody directed at the Fc region of human IgG

43
Q

which is more specific in rheumatoid arthritis Anti-CCP or rheumatoid factor?

A

Anti-CCP

44
Q

what are the genetic associations of Rheumatoid arthritis?

A

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
Q

how is Rheumatoid arthiritis treated?

A

DMARD - methotrexate
Sulphasalazine, hydroxychloroquine, leflunomide

Others;
TNFalpha antagonist
Rituximab - anti-cd20
Abatacept - CTLA-4 – Ig fusion protein; stops T cell activation
Tocilizumab - for IL6

Path - Immuno (11 decks)

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