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Semester 2 Micro Practicals > When the immune system goes wrong (W24 and 25) > Flashcards

When the immune system goes wrong (W24 and 25) Flashcards

1
Q

Is autoimmunity the same as autoimmune disease?

A

No, autoimmunity (ie circulating autoreactive B and T cells) can be present without damge

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2
Q

Type 1 hypersensitivity: Definition, cells/antibodies involved and example?

A

“Allergy”: Immediate hypersensitivity caused by innocuous antigens

Cells: Mast cells, eosinophils, IgE

Eg: peanut allergy

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3
Q

Type 2 hypersensitivity: Definition, cells/antibodies involved and example?

A

Antibody dependent cytotoxicity

Cells: IgG, IgM

Acetylcholine receptors in Myasthenia Gravis, and TSH receptors in Grave’s Disease

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4
Q

Type 3 hypersensitivity: Definition and example?

A

Immune complex mediated

Eg: SLE

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5
Q

Type 4 hypersensitivity: Definition, cells/antibodies involved and example?

A

Delayed type hypersensitivity

Cells: T cells (CD4 Th1 cells), IL-2, IFN-gamma

Eg: T1DM, MS, Rheumatoid arthritic, Hashimoto’s Thyroiditis

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6
Q

What is the likely presentation

vitals of someone in anaphylactic shock?

A 
low BP
high HR
high RR
normal temp
inspiratory stridor, expiratory wheeze, urticarial rash, swollen nose and mouth.
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7
Q

What is a basic mechanism for Type 1 hypersensitivity reactions?

A

1st encounter with allergen–> binds to APC–> Th2 response–> IL-4–> B cells–> IgE–> released and binds to (“primes”) mast cells–> mast cell distribute all over body.

2nd encounter: binding of allergen to IgE on mast cells–> degranulation–> histamine, leukotrienes, cytokines

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8
Q

How do you treat anaphylaxis?

A

adrenaline= vasoconstriction
oxygen
SABA (eg salbutamol) to open airways

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9
Q

Are there delayed effects in a Type 1 hypersensitivity reaction?

A

Yes: due to eosinophils that come in later, and synthesise lots of mediators over a long period.

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10
Q

What is impetigo and what is it known as?

A

School sores, which arise secondary to scabies infestation–> scretch–> strep pyogenes and/or staph aureus

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11
Q

Pansystolic murmur secondary to sore throat or impetigo in indigenous teen. What is the condition and organism?

A

Rheumatic heart disease. rheumatic fever (mitral stenosis)

Strep pyogenes

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12
Q

Strep pyogenes: gram, catalase, growth on HBA and MAC, bacitraicin

A 
gram+ cocci,
catalase-
beta haemolysis
no growth on Mac
Bacitraicin sensitive
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13
Q

What is the Anti-streptolysin O test? (ASOT)

A

Test looks for antibodies to an S. pyogenes protein that lyses RBCs

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14
Q

Pansystolic murmur secondary to sore throat or impetigo in indigenous teen. What other body symptoms might be affected?

A

Rheumatic fever–> may also cause arthralgia

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15
Q

What is rheumatic fever?

A

Autoimmune disease that follows S. pyogenes infection–> antibodies to the M protein cross react with cardiac myosin–> cross link on mitral valve–> allows C’ fixation and further damage–> stenosis

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16
Q

How does tolerance break down in rheumatic fever?

A

molecular mimicry: similarity between M protein and cadiac myosin

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17
Q

Are there any organisms in the heart or joints with rheumatic fever?

A

No

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18
Q

Can S. pyogenes be normal flora?

A

Yes

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19
Q

How do you treat S pyogenes

A

Penicillin!

20
Q

What is the key differential diagnosis for Coeliac disease?

A

Giardia Lamblia

21
Q

What are the symptoms of Coeliac (8)?

A

weight loss, malaise, abdo pain, intermittent diarrhoea/ steatorrhoea, low BMI, mouth ulcers, anaemia, folate deficiency

22
Q

What are the biochemical tests for Coeliac?

A

anti-deaminated gliadin Abs (IgG and IgA), and anti-tissue transglutaminase antibodies (IgA)

23
Q

What does the jejunum of someone with coeliac look like? (3)

A

Blunted villi, elongated crypts, lymphocytic infiltrate

24
Q

What MHCs are associated with coeliac?

A

HLA DQ2 and HLA DQ8

25
Q

What is the pathogenesis of coeliac (briefly)?

A

Gluten ingested–> gliadin peptides–> gliadin deaminated by tgt–> deaminated gliadin binds to MHC–> CD4 T cell activation–> damage.

26
Q

What role to B cells/ antibodies play in coeliac pathogenesis?

A

They don’t cause significant pathology, but are useful for testing.

27
Q

How do you definitively diagnose Coeliac?

A

Jejunal biopsy

28
Q

Besides GIT symptoms, what else might coeliac present as?

A

osteoporosis
ulcers
angular chelitis
dermatitis hepatophormes

29
Q

What is the main serological screening test for SLE?

A

anti-nuclear antibody test

30
Q

Is SLE associated with high or low levels of C’?

A

LOW: C’ may be used up in forming immune complexes, or lower due to liver disease.

31
Q

What kind of hypersensitivity is coeliac?

A

Type 4: T cell mediated

32
Q

What are 2 potential SLE triggers?

A

UV light (ie being in the sun) and EBV (glandular fever)

33
Q

Why would a urine dip stick be performed when testing for SLE?

A

often get Lupus Nephritis

34
Q

What are the clinical manifestations of SLE?

A

Complexes can deposit anywhere in the vasculature: nephritis, arthritis, shin rashes, hair follicles–> alopecia, brain, lungss

35
Q

Is detection of anti nuclear antibodies sufficient to diagnose SLE

A

No, low predictive value, it’s only a screening test.

36
Q

What syndrome can Yersinia enterolitica cause?

A

Gastroenteritis. 5% of gastro in Aus.

37
Q

What is the gram stainof Y. enterolitica?

A

Gram- TINY rods

38
Q

What is CIN agar specific for?

A

Yersinia enterolitica

39
Q

What hypersensitivity syndrome can be caused by Y. enterolitica?

A

Rutter’s syndrome: reactive arthritis that occurs 1-3 weeks post Y.. enterolitica gastro.

40
Q

What bacteria can cause Rutter’s syndrome (reactive arthritis?)

A

Salmonella, Shigella. Campylobacter, Yersinia

41
Q

What syndromes can secondary reactive arthritis (Rutter’s syndrome) follow?

A

Gastroenteritis or sometimes urethritis.

42
Q

What HLA is associates with reactive arthritis?

A

HLA B27

43
Q

Where is Y. enterolitica often aquired from

A

Dairy products from sheep, cows, goats that haven’t been pasturised.

44
Q

What is the role if tissue trans glutaminase?

A

Deamidates free amino groups on particular
glutamine residues on gliadin peptides
Deamidation results in glutamine → glutamate which allows gliadin peptides to bind to HLA.

45
Q

What temperature does Y. enterolitica grow at?

A

25 degrees

Semester 2 Micro Practicals (5 decks)

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