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PBD I Exam 2 > Diseases of the Immune System IV > Flashcards

Diseases of the Immune System IV Flashcards

1
Q

cellular rejection

A

T cell response to transplant

CD8 and CD4

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2
Q

direct pathway of cellular rejection

A

T cells recognize antigens on donor MHC on APCs in graft

CD4 and CD8 response

**acute rejection

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3
Q

indirect pathway of cellular rejection

A

T cells recognize antigens of donor on own APCs

CD8 response not generated
-bc these CTLs recognize graft antigens presented by hosts APCs

**chronic rejection

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4
Q

humoral rejection

A

B cell response to transplant

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5
Q

hyperacute humoral rejection

A

preformed antidonor antibodies present in recipient

-ex/ multiparous women against paternal antigens from fetus

or blood transfusions

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6
Q

acute humoral rejection

A

exposure to antigens of donor graft stimulate antibody production

often attack vessels first - vasculitis

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7
Q

hyperacute rejection

A

within minutes or hours

in kidney - glomeruli have thrombi occlusion and fibrinoid necrosis

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8
Q

acute rejection

A

within days

in kidneys - vasculitis (humoral) and interstitial mononuclear infiltrate (cellular)

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9
Q

acute cellular rejection

A

CD4 and CD8

kidney - mononuclear cells in capillaries, glomeruli, tubules

endothelitis

respond well to immunosupressive therapy (cyclosporine)

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10
Q

acute humoral rejection

A

kidney - mainly damage to vessels
-proliferation of smooth muscles

deposition of C4d (from classical complement pathway)

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11
Q

chronic rejection

A

kidney - progressive renal failure with rise in creatinine over period of 4-6 months

dense obliterative intimal fibrosis in cortical arteries

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12
Q

increasing graft survival

A

unless identical twins - immunosuppressive therapy necessary

cyclosporine 
azathioprine
steroids
monoclonal anti-T-cell antibodies
rapamycin
mycophenolate mofetil

also, attempt to prevent costimulatory signals
-interrupt B7 CD28 interaction

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13
Q

cyclosporine

A

blocks NFAT

-no IL-2 production

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14
Q

transplantation of hematopoietic cells

A

from bone marrow

problems:
graft-versus host disease
immunodeficiency

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15
Q

graft-versus host disease

A

immune competent cells transplanted to immune crippled recipient
-transferred cells recognize host antigens

often with bone marrow transplant

depleting T cells in donor bone marrow can help to eliminate disease

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16
Q

acute GVH

A

within days or weeks
-involve immune system, skin epithelia, liver, intestines

rash, jaundice, bloody diarrhe

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17
Q

chronic GVH

A

cutaneous injury
fibrosis of dermis (may resemble scleroderma)

liver problems - jaundice
esophageal strictures

18
Q

graft-versus-leukemia effect

A

T cells in bone marrow transplant control leukemic cells

19
Q

primary immunodeficiency

A

genetic

most manifest in infancy

  • 6 months to 2 years
  • with recurrent infection
20
Q

secondary immunodeficiency

A

due to infection, cancer, malnutrition, therapy, etc.

21
Q

X-linked agammaglobulinemia

A

failure of B cell precursors to develop to mature B cells

heavy change rearranged first
-induce light chain rearrangement

mutation in Btk - no light chain rearrangement

seen mostly in males - around 6 months of age
-infections - haemophilis influenza, streptococcus pneumoniae, traphylococcus auresu

also susceptible to viral infections

22
Q

Btk

A

mutated in X-linked agammaglobulinemia

-no light chain formation in B cells

23
Q

clinical features of X-linked agammaglobulinemia

A

B cells decreased
-serum antibodies are all decreased

-pre-B cells in normal numbers

underdeveloped germinal centers

absent plasma cells

T cell responses normal

24
Q

Tx of x-linked agammaglobulinemia

A

immunoglobulin replacement therapy

-allows most to reach adulthood

25
Q

common variable immunodeficiency

A

hypogammaglobulinemia
-sometimes only IgG

normal B cells in blood - with no plasma cells
**contrast with X-linked agammaglobulinemia

26
Q

clinical features of common variable immunodeficiency

A

childhood or adolescence

hyperplastic B-cell areas of lymphoid tissues (no negative feedback by antibodies)

recurrent sinopulmonary pyogenic infection

recurrent herpesvirus infection

27
Q

isolated IgA deficiency

A

low levels of serum and secretory IgA

mucosal defense weakened
-infection of respiratory, GI, GU tracts

if transfused with normal IgA - can develop anaphylactic reaction to IgA

28
Q

hyper IgM syndrome

A

high IgM
no IgM, IgA, IgE

defect in ability of helper T cell to activate B cells

  • no class switching
  • mutation in CD40

hemolytic anemia
thrombocytopenia
neutropenia

recurrent pyogenic infections

29
Q

class switching

A

CD40 on B cells with CD40L on activated helper T cells

30
Q

Digeorge syndrome

A

T cell deficiency

failure development of 3rd and 4th pharyngeal pouches

  • no thymus (no T cells), parathyroid (tetany)
  • defects in heart and great vessels
31
Q

22q11 deletion syndrome

A

leads to Digeorge syndrome

32
Q

severe combined immunodeficiency

A

SCID

defects in humoral and cell-mediated immunity

infants with thrush, diaper rash, failure to thrive

recurrent infections - candida albicans, P. jiroveci, pseudomonas

Tx - bone marrow transplant necessary

33
Q

X-linked SCID

A

more common in boys

  • mutation in cytokine receptor (gamma-c)
  • defect in T cell development
  • defect in B cells - no helper T cells

also deficiency of NK cells

34
Q

autosomal recessive SCID

A

deficiency of adenosine deaminase (ADA)

35
Q

hassall corpuscles

A

seen in thymus of SCID with ADA deficiency

36
Q

lobules of undifferentiated epithelial cells resembling fetal thymus

A

seen in thymus of SCID with gamma-c deficiency (X-linked)

37
Q

Tx of SCID

A

bone marrow transplant

also gene therapy - retroviral gamma-c gene introduction

38
Q

wiskott-aldrich syndrome

A

immunodeficiency with thrombocytopenia and eczema

X-linked recessive

recurrent infections

progressive decrease of T cells

IgM low, IgG normal, IgE and IgA elevated

mutation in WASP

Tx bone marrow transplant

39
Q

genetic deficiency in complement

A

most common - C2
-SLE -like autoimmune disease

C3 - susceptible to infection

40
Q

neisseria infection

A

have thin cell walls

-recurrent infections with deficiency of C5,6,7,8,9

41
Q

hereditary angioedema

A

deficiency of C1 inhibitor

42
Q

parenteral

A

intravenous

PBD I Exam 2 (18 decks)

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