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Year 2 - Clinical Pathology > Immunodeficiency > Flashcards

Immunodeficiency Flashcards

1
Q

what is the difference between primary and secondary autoimmune disease

A

primary - inherent defect usually genetic

secondary - immune system affect due to external causes or disease

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2
Q

describe the hierarchy of the immune system

A

immune syetem - innate and adaptive

innate - barrier and chemical, pathogen recognition, cellular (phagocytes and NK), complement

adaptive - hunoral (antibodies and B cells0 and cellular (B and T cells)

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3
Q

what are 5 causes of immunodeficiency

A 
breakdown of physical barriers - CF (lack of lung secretion) 
protein loss 
malignancy 
drugs 
infection (HIV/TB)
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4
Q

give 5 examples of drugs that have a secondary association with autoimmune disease

A 
steroids - suppress immune system 
DMARDS - anti rheumatic
Rituximab - against B cells 
anti-convulsants 
myelosuppressive
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5
Q

what is the role of neutrophils and macrophages in the innate immunity

A

neutrophils are short lived
macrophages are long lasting (start as monocytes then mature in bone marrow to macrophages)
east bacteria and fungi

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6
Q

what type of acid is found din a lysosome to form phagolysosome complex

A

hypochlorous acid

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7
Q

what quality about neutrophils and macrophages allow them to recognise pathogens associated molecular patterns (PAMPS)

A

the innate cells have pathogen recognition receptors unique to pathogens to differentiate from human cells

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8
Q

give an example of a PAMP

A

liposaccharide

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9
Q

give an example of a type of PRR and examples within that subset of recognition

A

TLR - toll like receptors are PRR

TLR3 - recognise viral RNA
TLR4 - liposacchrides
TLR5 - recognises flagellum

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10
Q

what is the role of MyD88 and IRAK4

A

released on phagocytosis after PRR activation on innate cells which release more inflammatory mediators

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11
Q

why is it strange to have normal levels of WBC’s during bacterial infection

A

should have increases in WBC to attack infection

which shows deficiency in B cell recruitment or activation which may infer an innate system issue

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12
Q

what is the clinical presentation of IRAK4 deficiency and how do you treat it

A

can recognise the bug but cannot cause an inflammatory response - recurrent infection strep/staph

prophylactic antibiotics or IV immunoglobin if severe

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13
Q

how do you differentiate between MyD88 deficiency and IRAK4

A

genetic testing

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14
Q

how do you create hypochlorous acid in the lysosome

A

O2 - superoxide via reduction (electron donation to O2)

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15
Q

what is a granuloma

A

collection of macrophages

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16
Q

what is the common problem associated with cells which causes chronic granulomatous disease

A

macrophages will eat pathogen but can’t destroy and NADPH complex can donate electron to produce lysosome acid

17
Q

what genetically in chronic granulomatous disease

A

X linked - affects men mainly

18
Q

what is the treatment of chronic granulomatous disease

A

haemopoitic stem cell transplant and prophylactic antibiotics

19
Q

how do you test to see if a phagocyte is dysfunction in producing effective hypochlorous acid

A

relays on reduction
eg test neutrophils - nitro blue tetrazolium reduction - healthy neutrophils go clear but purple mean they are dysfunctional

20
Q

which part of the immune system is complement within

A

innate

21
Q

what are the three types fo complement pathways

A

classical

alternative / MBL

22
Q

describe in terms of C proteins the classical compliant pathway

A 
antibody dependant (adaptive help)
antibody attaches to microbe 
C1 binds to this and cleaves C4 into C4a/b + C2 into C2a/b

then C4b and C2a bind to C4a2b (c3 convertase)

this cleaves C3 into C3a/b

C3a causes inflammation
C3b contends with c3 convertase = C4b2a3b (C5 convertase)

this cleaves c5 in c5a/b

c5b recruits c6/7/8 which then binds with C9 in microbe membrane

23
Q

what is the role of C3a C4a and C5a in complement

A

dilation of arterioles, release of histamine from mast cells and chemotaxis of phagocytes

24
Q

what is the role of C3b in complement

A

opsonisation of microbes to help phagocytosis

25
Q

what is the role of c5b C6 C7 C8 C9

A

form MAC complex which causes cytolysis of cell via perforation

26
Q

how do you test complement function

A

patients serum should Clyde sheep erythrocytes via classical pathway

27
Q

what would a deficiency in C2 or C4 cause

A

autoimmunity SLE or myositis

28
Q

what would a deficiency in MAC complex cause

A

repeated bacterial meningitis (N. meningitis)

29
Q

what Th cell tends to cause more atopic diseases

A

TH2

makes a lot of IgE

30
Q

what three ways to antibodies neutralise toxins

A

neutralise them
clump together
opsonise
activate complement

31
Q

what would a defect in Brutons tyrosine kinase cause

A

no b cell maturation in the bone marrow so no antibodies are made

32
Q

name 4 types of B cell defects

A

CVID
IgA deficiency
X linked hyper IgM syndrome
transient hypogammaglobulaemia of the infant

33
Q 
how do these drugs affect the immune system 
riturximab 
methotrexate 
ciclosporin/azathiprine
prednisolone
A

antibody against cd20 for B cell cancers

hits fast growing cells like neutrophils and macrophages

work of B/T cells

works on large part of immune

34
Q

what type of cell does HIV kill

A

CD4 cells

35
Q

what is SCID and what causes it

A

no T cells
defect in critical T cell receptors
loss of communication - MHC2 deficiency in B cells
metabolic - adenosine deaminase deficiency

36
Q 
what do problems in these types of cells cause 
phagocyte 
complement 
antibodies 
T cells
A

PRR - IRAK4 - recurrent pneumonia

recurrent bacterial meningitis

recurrent sinopulmonary infection

SCID, and HIV causes some complications with T cells

Year 2 - Clinical Pathology (67 decks)

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