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Pathology Exam III > Immunopathology III > Flashcards

Immunopathology III Flashcards

1
Q

immunodeficiency disorder invovle ______ defects

A

adaptive or innate immune system

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2
Q

What are immunodefiency disorders divided into

A

primary and secondary types

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3
Q

what does immunodefieciency usually present as

A

freequence, severe, resistant infections
no symptoms free interval
unusual etiologic organism
severe, unexpected complications

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4
Q

primary immunodefiencies

A

generally rare, genetically determined defects of B and T lymphocytes

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5
Q

clinical manifestations of primary immunodeficiencyes

A

6mons - 2 years
repeated infection
failure to thrive

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6
Q

X-linked agammagloulinemia of bruton

A

failure of normal pre-B cells to undergo further differentiation, causes an absense of mature B cells

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7
Q

when does X-linked agammagloulinemia of bruton arise

A

after depletion of maternal Ab

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8
Q

x-linked agammaglouliemia may be viewed as a disorder of waht

A

opsonization

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9
Q

how do treat x-linked agammagloulinemia of bruton

A

parenteral immunoglobulin replacement

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10
Q

how is cellular immunity affected by x-linked agammagloulinema of bruton

A

intact, but susceptibiliiyt of enteric virus or protozoa from a lack of neutralizing IgA

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11
Q

common variable immunodefiency

A

fairly common, heterogenous group of disorders with sporadic and inferited forms

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12
Q

main feature of common variable immunodeficiency

A

hypogammaglobulinema, usuallyu all Ab classes but occasionally isolated IgG

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13
Q

who gets common variable immunodefiency

A

equal amoung men and women

happens in 2nd -3rd decades

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14
Q

mechanisms of common variable immunodeficiency

A

intrinsic B cell defect

abnormal T cell signal to B cell

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15
Q

what does lack of IgA in common variable immunodefiency cause

A

incrased entervoiral infection, chronic diarrhea

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16
Q

what disorders are increased in common variable immunodifern

A

AI disroders

lymphioids and gastric cacners

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17
Q

Selective IgA defiency is caused by

A

IgA being absent of IgA +B cells don’t mature

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18
Q

what is selective IgA deficiency assocaited with

A

family history
measles
toxoplasmosis

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19
Q

40% of people with IgA definecy have what

A

anti-IgA Ab

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20
Q

what do you have to keep in mind with blood transfusions and IgA defiency

A

can ahve an anaphylactic reaction if the transfused blood tehy are given contains IgA

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21
Q

hyper IgM syndrome

A

disorder characterized by failure of T cells to induce B cell isotype switching
activate macrophages to remove intracellular microbes

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22
Q

what do IgM-producing B cells normally do

A

activate transcription genes that encode for other Ig isotypes via signals between CD40 molecule on B cell and CD40 ligand on helper T cell

23
Q

how is IgG affected by hyper IgM syndrome

A

decreased or absent

24
Q

how is hyper IgM syndrome transmitted

A

x linked or autosomal recessive

25
Q

how are B and T cell populations affected by hyper IgM syndrome

A

normal

26
Q

how are B and T cell populations affected by hyper IgM syndrome

A

normal

27
Q

what type of infections tend to affect hyper IgM syndrome

A

pyogenic, intracellular organisms

28
Q

how do you get DiGeore syndrome

A

partial or complete interruption of 3rd and 4th pharygneal pouches

29
Q

what organs are affected by digeorger

A

hypoplasia of thymus nd parathyoirds

30
Q

what are features of digeorge

A

t celld efect
hypocalcemia
cardiac abnormaliies
cleft palate

31
Q

what mutation causes digeorger

A

deletion on 22q11

32
Q

who gets Digeorge

A

equally male and female

33
Q

how are immunoglobulins affected by DiGeorge

A

normal levels

34
Q

facial features of digeorge

A

low set ears
midline cleft
small mandible

35
Q

how is heart affected in digeorge

A

VSD

right subclaviar a derived form pulomary artery

36
Q

what causes more problems with digeore - hypoplasia or aplasia

A

aplasia

37
Q

SCID

A

boy in plastic buble

defieecnt in cellular and humor immune responses

38
Q

how is SCID transmitted

A

x linked

autosomal recessive

39
Q

what is the more rare from of SCID

A

combined T and defect

40
Q

what is the more common form of SCID

A

severe T cell defect

41
Q

x-linked SCID

A

mutation of common gamma chain subunit of cytokine receptors

42
Q

autosomally recessive SCID

A

adensonine deaminase deficeincy

failure of Class ii MHC expression

43
Q

clinical features of early onset SCID

A

thrush, diaper rash, failure to thrive

recurrent infection

44
Q

how do you treat early only SCID

A

bone marrow transplant

45
Q

how is Wiskott Aldrich transmitted

A

x linked

46
Q

what are the feautres of wiskott aldrich

A

immunodefiency, thrombocytopenia, eczema

47
Q

results of wiskott aldrich syndrome

A

Ab low or elevated
no Ab to polysacchride Ag
T cell deficent

48
Q

clinical features of wiskott aldrich

A

hemorrhagic diathesis
recurrent respiratio infection
increased lymphoid maligancies in survivors past age 10

49
Q

secondary immunodefiencyes

A

more common than primary
immune imparment in previously healthy people
can be reversible

50
Q

what are the mechanisms of T cell loss in HIV

A

apostosis in affected cells
apoptosis of infected cells
CTLs kill infected cells

51
Q

effect of T cell loss in HIV

A

lymphopenia of CD4+T cell
imparied specific B cell response to new Ag
altered macrophage fucntion with decreased MHC II expression

52
Q

AIDS defining neoplasma

A

kaposi’s sarcoma
B cell lymphoma
primary lymphoma of brain
invasive carcinoma of uterine cervix and anus

53
Q

what is the buzz word for jiroveci fugus

A

coffee bean

Pathology Exam III (10 decks)

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