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IHO Week 5 (MJ) > Immune Diseases 3 > Flashcards

Immune Diseases 3 Flashcards

1
Q

Autograft

A

self to self, such as a skin graft

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2
Q

Isograft

A

syngeneic, between identical twins

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3
Q

Allogrant

A

between genetically different individuals of the same species

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4
Q

Xenograft

A

Between two species (pig/porcine heart valve to human)

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5
Q

What is the major barrier to transplant success?

A

Rejection - immune system recognizes the graft as being foreign and attacks it.

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6
Q

What type of grafts are more likely to be compatible?

A

ABO and HLA compatible grafts

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7
Q

Cellular rejection

A

T cell mediated graft rejection that involves destruction of donated graft cells by recipient CD8+ cytotoxic T lymphocytes and delayed hypersensitivity reactions triggered by activated recipient CD4+ T hypersensitivies

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8
Q

The major antigenic differences between the donor and recipient that results in rejection of transplants are differences in ________

A

HLA alleles (highly pleomorphic)

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9
Q

Direct antigenic recognition pathway

A 
donor class I and II MHC antigens on APCS in the graft are recognized by the host CD8+ cytotoxic T cells and CD4+ helper T cells
CD4 - proliferate and produce cytokines which induce tissue damage by local delayed hypersensitivity 
CD8 - differentiate to CTLs that kill graft cells
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10
Q

Indirect antigenic recognition pathway

A

graft antigens are picked up, processed and displayed by host APCs and activate CD4+ T cells, which damage the graft by a local delayed hypersensitivity reaction and stimulate B lymphocytes to produce abs.

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11
Q

humoral rejection

A

antibodies produced against alloantigens in the graft mediate rejection

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12
Q

Important preformed anti-donor antibodies

A

anti-ABO blood groups (naturally formed)

anti-HLA antibodies (pregnancy, previous transfusion)

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13
Q

Hyperacute rejection is possible if…

A

preformed antibodies are present

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14
Q

The key immunologic factors affecting graft survival are (3)

A

ABO compatibility
matching HLA loci
absence of preformed anti-HLA antibodies

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15
Q

Hyperacute rejection

A

result of ABO incompatibility or preformed anti-HLA antibodies in the recipient, which bind to endothelial antigens, activate complement and result in vessel thrombi and ischemic necrosis (TYPE II HYPERSENS)

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16
Q

Onset of hyperacute rejection?

A

Minutes to hours after surgery

Very acute

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17
Q

Acute rejection

A

T cell mediated hypersensitivity reactions (host CD4+ T cells release cytokines, activating macrophages, CD8+ T cells)
or from antibody-mediated hypersensitivity reactions (host CD4 cytokines promote proliferation of B cells into plasma that produce anti-HLA abs to endothelial antigens)

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18
Q

Onset of acute rejection?

A

days to weeks

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19
Q

Chronic rejection

A

occurs over months or years and is often secondary to vascular injury, as a result of both cell-mediated and antibody-mediated hypersensitivity reactions.

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20
Q

Which type of rejection is the most common cause of renal graft failure?

A

Chronic

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21
Q

Current immunosuppression regimens usually control..

A

acute rejections

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22
Q

Two major complications of immunosuppression therapy in a transplant setting

A
  1. Increased susceptibility for opportunistic infection

2. Increased risk of malignancies

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23
Q

Opportunistic infections and transplant

A

CMV, pneumocystis and common community acquired infectious disease.

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24
Q

Malignancy and transplant

A

EBV and post transplant lymphoproliferative disorders (PTLD), squamous cell carcinoma of skin and Kaposi sarcoma.

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25
Q

Hematopoietic cell transplantation (HCT)

A

the administration of hematopoietic progenitor cells from any source (blood, marrow, peripheral blood, umbilical cord blood) to reconstitute the bone marrow.

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26
Q

Autologous HCT (auto-HCT)

A

uses hematopoietic progenitor cells derived from the individual with the disorder

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27
Q

Allogenic HCT (allo-HCT)

A

uses hematopoietic progenitor cells collected from someone other than the individual with the disorder

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28
Q

Graft vs. Host Disease (GVHD)

A

Donor t cells recognize the recipients HLA antigens as foreign and react against them. Because host is immunocompromised the host in incapable of mounting a reaction against the grafted lymphocytes, thus allowing the graft lymphocytes to attack the host.

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29
Q

what happens when the T cells from the donor (graft) recognzie the recipient (host) cells as foreign?

A

GVHD

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30
Q

How do you minimize the complication of GVHD in allogeneic HCT

A

Transplants are done between donor and recipients that are HLA matched.

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31
Q

Do patients who undergo auto-HCT get GVHD

A

No!

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32
Q

Where else can GVHD be seen?

A

Liver transplants (lots of donor T-lymphocytes in liver) or transfusions of blood or platelets (why irradiate blood before transfusion)

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33
Q

Acute GVHD

A

First 100 days following allo-HCT

Direct cytotoxicity by CD8+ T cells and cellular injury via CD4+ recruitment via cytokines

34
Q

Acute GVHD affects these areas most…

A

Skin, Liver, GI tract

35
Q

Chronic GVHD

A

More than 100 days post allo-HCT

may follow acute GVHD or insidiously

36
Q

Sx Chronic GVHD

A

skill exhibits loss of skin appendages with dermal fibrosis
Chronic liver disease (cholestatic jaundice)
GI tract may exhibit fibrous strictures, malabsorption and chronic diarrhea
Obliterative bronchitis

37
Q

Key prereqs of GVHD

A

Donor graft must contain immunocompetent T cells
Recipient must be immunocompromised
Recipient has HLA antigen foreign to donor T cells

38
Q

Graft vs. Tumor reaction

A

if malignancy relapses and patient has received allo-HCT the tumor will have HLA antigens of the recipient and be recognized as foreign by the donor T-lymphocytes

39
Q

HCT complications

A

immunodeficiency (opportunistic infections and development of secondary malignancies)

40
Q

Why are patients receiving HCT immunodeficient?

A

receive myeloablative therapy in prep for the graft and to delay the repopulation of the recipients immune system

41
Q

Common long term toxicities of allo-HCT

A 
Chronic GVHD
Infections
Treatment related myelodysplasia/secondary leukemia
secondary solid tumors
Cardiac disease
Pulmonary toxicity
42
Q

Common long term toxicities of auto-HCT

A 
Treatment related myelodysplasia/secondary leukemia
secondary solid tumors
Cardiac disease
Pulmonary toxicity
Infection
43
Q

Amyloidosis

A

A group of disorders characterized by the deposition of amyloid in the extracellular space of tissues and organs, resulting in the tissue and organ dysfunction.

44
Q

What is an amyloid?

A

A group of pathologic proteins that share similar physical properties. Consists of linear, non-branching fibrils in a characteristic cross-beta pleated sheet configuration

45
Q

what is unique about the physical configuration of amyloid?

A

Seen regardless of the chemical composition

46
Q

What special stain is typically used to stain amyloid?

A

Congo red stain

47
Q

Amyloidosis is not a single disease but…

A

a group of diseases having in common the deposition of similar appearing proteins

48
Q

AL (amyloid light chain) amyloid

A

immunoglobulin light chains, amino-terminal fragments of light chains, or both
Usually lambda, sometimes kappa
secreted from monoclonal population of plasma cells

49
Q

AA (amyloid associated) amyloid:

A

Proteolysis of large precursor proteins in serum called SAA (serum amyloid-associated) protein that is synthesized in the liver and circulates in the serum
associated with HDL

50
Q

SSA production is increased in

A

inflammatory conditions as a part of the acute phase response

51
Q

AA (amyloid associated) amyloid is associated with

A

chronic inflammation

52
Q

beta- amyloid

A

derived by proteolysis of a larger precursor protein called amyloid precursor protein
found in cerebral plaques and cerebral vessels of patients with Alzheimers.

53
Q

Transthyretin (TTR)

A

normal serum protein binds and transports thyroxine and retinol. Mutation of TTR results in amyloid deposition.

54
Q

TTR genetically determined disorders

A

heritable neuropathic and cardiomyopathic amyloidosis

55
Q

TTR can deposit on the heart…

A

with aging (no mutation necessary)

56
Q

B2 microglobulin

A

This normal serum protein cannot be filtered through dialysis membranes and can accumulate in patients on long term dialysis (>20 years).

57
Q

Hemodialysis associated amyloidosis

A

B2 microglobulin cannot be filtered in dialysis. accumulates.

58
Q

Amyloidosis results from

A

misfolding proteins, which become insoluble, aggregate and deposit as fibrils in the extracellular space.

59
Q

What happens to misfolded proteins

A

Normally - degraded by proteosomes or macrophages

This fails in amyloidosis - accumulation

60
Q

Normal proteins and amyloid

A

inherit tendency to fold imporperly and form aggregates in large amounts

61
Q

Mutant proteins and amyloid

A

prone to misfolding, aggregate.

Defects in normal degradation process can lead to such accumulation

62
Q

Can increased SSA produce amyloidosis?

A

Not alone, but if an enzyme is defective in breaking down AA then deposition of AA may occur.

63
Q

Systemic amyloidosis

A

Involves several organ systems

64
Q

Localized amyloidosis

A

Involves single organ

65
Q

Primary amyloidosis

A

associated with clonal proliferative disorder of plasma cells producing light chain immunoglobulin
(type of systemic)

66
Q

secondary amyloidosis

A

complication of an underlying chronic inflammatory process

type of systemic

67
Q

Hereditary/familial amyloidosis

A

A group of heterogenous, heritable form of amyloidosis with distinct pattern and organ involvement

68
Q

Most common form of amyloidosis in US

A

primary amyloidosis (AL)

69
Q

AL is usually associated with a monoclonal proliferation of _______

A

plasma cells

Sometimes multiple myeloma

70
Q

AL amyloidosis occurs where?

A 
Heart
Kidney
Peripheral nerve
GI tract
Respiratory tract
(may affect other organs too)
71
Q

Reactive Systemic Amyloidosis (AA amyloidosis, secondary amyloidosis) is often secondary to….

A

Rheumatoid arthritis

Sometimes other connective tissue disorders and IBS

72
Q

Rheumatoid arthritis corresponds with this type of amyloidosis

A

Reactive systemic/secondary/AA

73
Q

Reactive Systemic Amyloidosis (AA/secondary) sites

A

Kidney
Liver
Spleen

74
Q

Hemodialysis Associated Amyloidosis

A

depletion of beta-2 microglobulin which accumulates in patients with end stage renal disease (long term dialysis)

75
Q

What disorder has a predilection for osteoarticular structures?

A

Hemodialysis Associated Amyloidosis

76
Q

Familial mediterranean Fever

A

Auto inflammatory syndrome with autosomal recessive inheritance, associated with a mutation in gene that produces proteins that regulate inflammatory rxns.

77
Q

Familial amyloidotic neuropathies

A

TRR mutations

78
Q

Age related (senile) amyloidosis

A

Deposition of normal TRR.
Ages 70s to 80s
Heart typically involved - reactive cardiomyopathy and arrhythmia

79
Q

Localized amyloidosis

A

Single organ or tissue without other involvement - nodular deposits in the lung, larynx, skin, bladder, tongue, orbit.

80
Q

In localized amyloid - what is seen at periphery

A

infiltrates of lymphocytes and plasma cells.

IHO Week 5 (MJ) (4 decks)

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