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RACP Immunology > Immnunology > Flashcards

Immnunology Flashcards

1
Q

Difference between Anaphylaxsis and anaphylactoid?

A

Identical signs and symptoms

Different activation of MAST

Anaphylaxsis - IgE mediated - preformed antigen made by B-cells then bound to MAST awaiting degranulation

VS.

Direct activation of MAST - Virus/Drugs/Hormones/Complement

  • No role for skin prick testing
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2
Q

What is Mepolizumab/Resilzumab

A

Anti IL-5 (Limiting interaction of IL-5 with IL-5 receptor, Which sits on the surface of Eosinophils)
Trade name - Nucala//Cinqair//Cinqaero
Indications:
Eosinophilic Asthma

Under Ix for:
Eosinophillic Eosphagitis

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3
Q

Widespread Urticaria, new welts on scratching?

A

Cutaneous mastocytosis - If given a mast cell degranulator like an opiod may release histamine +++

Dermatographism

Scabies

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4
Q

Adrenaline Receptors Role in anaphylaxsis?

A

Alpha-1 receptor
- Vasoconstrictior, increase BP, decrease odema

Beta-2 receptor

  • Bronchodilator
  • Reduces generation of mediators from MAST cells

(Also) B-2 - Increase HR, increase cardiac contraction

//

Relevant if have a beta-blocked patient

Dose - 0.01mL/kg of 1:1000 = 10mcg/kg
20Kg and under = EpiPen Junior (150mcg)
>20kg EpiPen (300mcg)

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5
Q

Glucagon, indication for anaphylaxsis?

A

In setting of refractory or

Adjunct IF BETABLOCKADE

Glucagon receptor in heart, cAMP, independent of adrenaline

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6
Q

STEM: 2 yo M p/w axillary abscess
PMHx cervical lymphadenitis age 7/12
Brother and Father recurrent abscess
Grows serratia marcesses

?Diagnosis

A

Chronic granulomatous disease
NADPH Oxidase (Phox)
Rare 1: 250,000
Failure to generate ROS

Pathognomic with liver abscess
Organisms are catalase positive of aspergillus (Or norcardia/burkholderia)

Rx
Bacterial prophylaxis - Bactrim
Fungal prophylaxsis - Itraconazole
Stem cell transplant

Natural Hx : 50% survival age 30

Association: Inflammatory bowel disease

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7
Q 
STEM:
11 month old with broad ulcer in nappy area
Very little pus
WCC 48
PMHx delayed cord separation
A

Leucocyte adhesion disorder
= Failure to exit endothelium to get to site of required action

LAD1 - CD 18 beta-integrin genes
LAD2 - CD 15
LD3 - KINDLIN3

Automsomal recessive

Recurrent bacterial
Peripharl leucocytosis
Absent pus formation
Delay cord separation

Rx
Aggresive Rx of infections
Stem cell transplant offered

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8
Q

Isoagglutins - Which class, what function?

A

Predominately IgM (So don’t cross placenta)
Anti-A and Anti-B
Develop by 12/12 in setting of cross reactivity

Test as raw function of ability to make IgM

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9
Q

ASOT Antibody
Which class
Which pathogen

A

IgG

Group A Streptococcus

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10
Q

In a protein losing state - which immunoglobulin levels are diminished?

A

IgG is most diminished
It has longest half life (23 days) so production is gradual and a loss of circulating antibody is apparent

Vs.
IgM/A (5 days) IgE (2days)
Which are rapidly replenished regardless of losing state

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11
Q

Relevant proportion of immunoglobulins circulating?

A

IgG - 75% (5g/L)
IgA 15% (0.3g/L)
IgM 5-10% (0.3g/L)
IgE 0.00002

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12
Q

In setting of low immunoglobulin:

How to determine protein losing state vs. primary immunodeficiency?

A

Do an albumin

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13
Q

Regarding interleukins:

Function/Origin of IL-2?

A

From dendritic cells
From T cells

For signalling T cells

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14
Q

Regarding interleukin:

Origin/Function of IL-12?

A

From antigen presenting cells

For Th1 Response
TNF - Alpha
Interferon Gamma

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15
Q

Macrophages love which cytokine?

A

Interferon Gamma - they turn into super macrophages

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16
Q

Immunologically: Th1 cells trigger what?

Release which cytokines
To stimulate what
And cause?

A

IL-2
IFN-gamma
LT

Stimulate Macrophages
And also IgG class 1 and 3
Which heavily stimulates complement

And also provide CD40L to b cells ro encourage maturation and isotype switching

Cause INFLAMMATION
TISSUE DAMAGE
Associated with auto-immunity

17
Q

Th2 response?

A

IL4
IL5
IL13

Allergy phenotype

IL4 isotype switches to IgE
IL 5 activates eosinophils?

18
Q

Th17 does what?

A

Release IL 17
Neutrophil recruitment
Autoimmune disease

19
Q

What do T-Reg cells do?

A

TGF -beta
IL-10

Regulates and dampens immunity response

20
Q

What does TFH cell do?

A

T-Follicular-Helper

Helps B-Cell high affinity response(plasma or memory)

Lives in germinal centre of lymphoid gissue

B cell has MHC2 molecule
Binds to Tfh cell( an activated cd4 distinct from thr other Th cells)
TFH PROVIDES CD40L AND IL21 and Il4 to

21
Q

Toculizimab?

Indications?

A

Anti IL6
Refractory Systemic JIA, refractory polyarticular JIA, Rheumatoid arthritis

TB absolute contraindication

22
Q

Anakinra
Canakinumab
Rilonacept

All target?

A

Targeting IL-1 components
Anakinra IL-1 Receptor antagonist

Indicated for rhematoid arthritis/stills

23
Q

Pathophysiology of Herediatry angioedema?

A

Deficiency of C1 Esterase inhibiotr
Too much C1 Action
Too much bradykinin

Angioedema

24
Q

Fingolomod?

A

Multiple Sclerosis Rx
Inhibits leucocyte movement

Orally active anti-leucocyte
Keeps lympocytes sequestered in their lymph nodes and unable to leave

If sick just stop meds, short half life, preveent sepsis

Target is Sphingosin-1-PO4

Small molecule (Not MAB)

25
Q

Natalizumab?

A

Anti leucocyte trafficing monoclonal antibody for multiple sclerosis

Targets alpha-4-beta-1 (VLA4)
Blocks adhesion of activate T-cells to blood/brain barrier

26
Q

What does CXC or CC signify in immunology?

A

Chemokine - guides migration of cells around body

27
Q

What are Toll-Like Receptors?

A

Highly confined
German ‘Toll” = “wow/cool”

So when german scientists knocked out innate cell immunity in drosphillia to give a fuzzy green (fungally infected) fly they were like “Super Cool” - Sehr Toll.

TLR1-9, we got the same, recognise pathogen associated molecular patterns, - cell membrane bound (for extracellular) and endosome membrane bound for RNA/DNA (for intracellular viral)

28
Q

Pro Inflammatory Cytokines? From innate immnity

A 
IL-1beta
TNF alpha
IL 6
CXCL8
IL 12
29
Q

Membrane attack complex?

A 
C5b
C6
C7
C8
C9

Punches holes

30
Q

Alternative complement pathway - key molecules?

A

Activated by pathogen surface

THEN C3, B, D
-Always ticking over - needs regulation

Gets to C3 Convertase then common
C3a, C4a, C5a (chemo attracts)
C3b opsonises
C5b-C9 (MAC)

31
Q

Eculiziumab

A

Blocks C5 in C5a

Risk of can’t form MAC

Risk of Nisseria

32
Q

TMA, Renal failure, organ failure?

ADAMTS13?

Shiga Toxin?

A

If -ve then not TTP

If -ve then not infection induced - HUS

So then aHUS - genetic deficiency in Complement Factor H, or I

33
Q

Avacopan?

A

Blocks C5 receptor
Orally active

Use in place of prednisolone for vasculitis (In trial, in adults)

34
Q

How many different TCRs possilbe?

A

10^23 - aka almost any protein segment you could place in front of it.

35
Q

TCR Structure

A

alpha chain, beta chain - DIMER by disulphide bond

Variable region pokes out
Constant region close to membrane

-RANDOM RECOMBINATION of 5x GENES - Shuffled like card, VDJ

36
Q

T-Cell - How big and what does it recognise

What does it attach to?

A

10-16 peptides

Presented by ANTIGEN PRESENTING CELL, extracellular place on MHCII - to CD4

CYTOSOLIC PROTEIN processed onto MHC1 = presented to CD8

Only in setting of danger

APC - DC(dendritic cells), B cells, Macrophage

37
Q

Thymic Purging of self recognising?

A

Thymic epithelial cells contain IRE - which is a transcription factor to express most self peptides - e.g. insulin (just this and pancreas)

If strong binding (as 70% do) then apoptosis

After this selection, and some maturation, naive CD4 and CD8 leave to begin immune surveillance.

38
Q

Immunoglobulin, levels, dosage, halflife

A

IGG 10g/l serum, 400mg/kg dose, 21-28 day half life

RACP Immunology (2 decks)

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