Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

semester 2 year 2 week 9-16 > immunology > Flashcards

immunology Flashcards

1
Q

signs of PID

A

large number, unusual organism, unusual places, not repose to treatment, failure to thrive or put on weight or loss weight, family history , unusual symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is most common PID?

A

B cell PID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

B cell PID includes?

A

THI, CVID, XLA, hyper lgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

THI?

A 
low lgG(+/- low lgA lgM) normalised over time
Dx retrospectively
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is most common immunological defects in human

A

selective lgA deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

selective lgA deficiency?

A

low lgA, normal lgG, lgM, mostly asymptomatic, recurrent sinopulmonar infection, severe reaction after receiving blood products( anti-lgA Ab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CVID?

A

more symptoms presentation : recurrent bacterial infection
low all lg ( lack of plasma cells differentiation)
ass with autoimmunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

XLA

A

absent B cell
BTK mutation: failure of pre-B into mature B
only in male infants( 5-6 mo)
Ass with autoimmunity, LN hypoplasia, neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is most common form of x linked PID

A

hyper lgM syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hyper lgM syndrome?

A

CD40 (ligand) defects required for B and T helper cell activation ( interaction required for isotope switching)
High lgM, others low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

types of T cell PID

A

disgorge syndrome, WAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DGS

A

defective pharyngeal pouch ( c22 q11.2 deletion)

thymus and PTH fail to develop, cardiac defects( hypoCa) developmental delay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Wiskott- Aldrich syndrome( WAS)

A

WAS gene mutation: organising actin cytoskeleton to form immunological synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical triad of WAS

A

Microthrombocytopenia, eczema, recurrent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what PID is associated with autoimmunity?

A

WAS, SVID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are some x linked PID

A

WAS, XLA, SCID, CGD( some)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SCID affects which part of immune system?

A

both ab and cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is most common form of SCID

A

x linked: T-B+ NK-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

other form of SCID

A

autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

problem in SCID?

A

stem cell failure to differentiate into T cells ( b,Nk cells affected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

presentation of SCID:

A

Prone to any microbial infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment for SCID?

A

haemotopoietic ell transplantation with IVIG

23
Q

mutation in X Linked SCID

A

Defects in gamma chain of IL receptor

24
Q

pathogenesis of SCID

A

main IL7: no T cell selection in thymus

also IL2: loss of t cell proliferation signals

25
Q

Ix for SCID?

A

Lack of thymus shadow ( no T cell fill it)
no tonsils, no LN
TRECs( T cell receptor excision circles)

26
Q

signs of phagocytic dysfunction?

A

recurrent infection with low virulence organism

poor wound healing

27
Q

CGD?

A

affect 5 componentes of NADPH oxidase (NCF) x linked or AR, defects in NADPH oxidase system to produce toxic oxygen metabolites for respiratory bursts and killing of organisms

28
Q

presentation of CGD

A

increased catalase +ve and certain fungi

29
Q

chediak hibachi syndrome?

A

AR
lysosome not use with phagosome
recurrent pyogenic infection by staph and strep

30
Q

complement deficiency

A

defects in complement cascade

31
Q

classical pathway deficiency

A

lead to immune complex disease( hypersensitivity type 3)

32
Q

alternative pathway and later pathway

A

increased tessera infection

33
Q

complement deficiency in C5-C9?

A

defects in MAC: leads to infection with Neisseria only

34
Q

Causes of secondary immunodeficiency?

A

HIV, extreme age, drug, malignancy, malnutrition

35
Q

mechanism of HIV

A

GP120 on T cell surface molecules CD4 on t helper cell –>apoptosis and destruction
indirectly affect cell mediated immunity, humeral immunity

36
Q

how to treat HIV

A

antiretroviral therapy: HAART

37
Q

What medications cause immune suppression?

A

glucocorticoids, alkylating agent’s, monoclonal ab, immunophlin binding agnets, inhibit nucleotide synthesis

  • allergy, autoimmune and inflammatory treatment
  • organ transplant
38
Q

normal function of immune system

A

defense against infection and tumours

39
Q

function of phagocytes, APC, PMNs

A

innate immunity , response to danger signals, capture pathogensis, display antigen and facilitate inflammation

40
Q

function of complement

A

proteins synthesized by liver, enhance function of phagocytes and abs in clearing microbes and damaged cells

41
Q

function of lymphoctes

A

adaptive immunity, recognise ags and ordinate immune response

42
Q

function of ab

A

proteins produced by plasma cells. recognise specific Ag and neutralise pathogens

43
Q

signs of PID

A

Increased rate and severity of infection

ass with autoimmunity, malignancy, chronic inflammation

44
Q

T cell PID

A

early onset
opportunistic infection n
viral, fugal and parasitic, failure to thrive
PJP, CMV,EBV, adeno, candida

45
Q

B cell PID

A

Later age
resp and sinupulmonary infection
pneumo, Hib, strep, GAS, Giardia, Psa

46
Q

phagocytic PID

A

any age, abscses, pyoderma, GI issue, catalase +ve organism( MSSA, Cepacia, nocardia, aspergilius)

47
Q

complement PID

A

Any age, fulminate sepsis, bacteremia Neisseria, pneumo

48
Q

Dx CGD

A

NBT, DHR test of superoxide production

49
Q

Tx CGD

A

Cotrimoxazole( bacterial prophylaxis) and itraconazole( fungal prophylaxis)
IFN, HSCT

50
Q

Presentation of CGD

A

adenopathy, HSM, gingivitis, stomatitis, perianal abscess, chronic diarrhoea, colitis, granulomata in organs

51
Q

presentation of XLA

A

Recurrent bacterial sinupulmonary infection( pneumonia, otitis, bronchitis, conjunctivitis, sinusitis), strep, pneumo, Hib,PsA, MSSA, recurrent enteroviral infection , recurrent Giardiasis

52
Q

complement disorder presentation

A 
sever sepsis( pneumonia, meningoccal infection) if C5-C9 (MAC)
Autoimmunity , GN, polymyositis( if C1-C3)
53
Q

Ix for complement disorder PID

A

Lab C3,C4 level
CH 50 classical activity
AH 50 alternative activitiy

semester 2 year 2 week 9-16 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions