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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
Hematopoietic cell transplantation (HCT)
the administration of hematopoietic progenitor cells from any source (blood, marrow, peripheral blood, umbilical cord blood) to reconstitute the bone marrow.
26
Autologous HCT (auto-HCT)
uses hematopoietic progenitor cells derived from the individual with the disorder
27
Allogenic HCT (allo-HCT)
uses hematopoietic progenitor cells collected from someone other than the individual with the disorder
28
Graft vs. Host Disease (GVHD)
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.
29
what happens when the T cells from the donor (graft) recognzie the recipient (host) cells as foreign?
GVHD
30
How do you minimize the complication of GVHD in allogeneic HCT
Transplants are done between donor and recipients that are HLA matched.
31
Do patients who undergo auto-HCT get GVHD
No!
32
Where else can GVHD be seen?
Liver transplants (lots of donor T-lymphocytes in liver) or transfusions of blood or platelets (why irradiate blood before transfusion)
33
Acute GVHD
First 100 days following allo-HCT | Direct cytotoxicity by CD8+ T cells and cellular injury via CD4+ recruitment via cytokines
34
Acute GVHD affects these areas most...
Skin, Liver, GI tract
35
Chronic GVHD
More than 100 days post allo-HCT | may follow acute GVHD or insidiously
36
Sx Chronic GVHD
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
Key prereqs of GVHD
Donor graft must contain immunocompetent T cells Recipient must be immunocompromised Recipient has HLA antigen foreign to donor T cells
38
Graft vs. Tumor reaction
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
HCT complications
immunodeficiency (opportunistic infections and development of secondary malignancies)
40
Why are patients receiving HCT immunodeficient?
receive myeloablative therapy in prep for the graft and to delay the repopulation of the recipients immune system
41
Common long term toxicities of allo-HCT
``` Chronic GVHD Infections Treatment related myelodysplasia/secondary leukemia secondary solid tumors Cardiac disease Pulmonary toxicity ```
42
Common long term toxicities of auto-HCT
``` Treatment related myelodysplasia/secondary leukemia secondary solid tumors Cardiac disease Pulmonary toxicity Infection ```
43
Amyloidosis
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
What is an amyloid?
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
what is unique about the physical configuration of amyloid?
Seen regardless of the chemical composition
46
What special stain is typically used to stain amyloid?
Congo red stain
47
Amyloidosis is not a single disease but...
a group of diseases having in common the deposition of similar appearing proteins
48
AL (amyloid light chain) amyloid
immunoglobulin light chains, amino-terminal fragments of light chains, or both Usually lambda, sometimes kappa secreted from monoclonal population of plasma cells
49
AA (amyloid associated) amyloid:
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
SSA production is increased in
inflammatory conditions as a part of the acute phase response
51
AA (amyloid associated) amyloid is associated with
chronic inflammation
52
beta- amyloid
derived by proteolysis of a larger precursor protein called amyloid precursor protein found in cerebral plaques and cerebral vessels of patients with Alzheimers.
53
Transthyretin (TTR)
normal serum protein binds and transports thyroxine and retinol. Mutation of TTR results in amyloid deposition.
54
TTR genetically determined disorders
heritable neuropathic and cardiomyopathic amyloidosis
55
TTR can deposit on the heart...
with aging (no mutation necessary)
56
B2 microglobulin
This normal serum protein cannot be filtered through dialysis membranes and can accumulate in patients on long term dialysis (>20 years).
57
Hemodialysis associated amyloidosis
B2 microglobulin cannot be filtered in dialysis. accumulates.
58
Amyloidosis results from
misfolding proteins, which become insoluble, aggregate and deposit as fibrils in the extracellular space.
59
What happens to misfolded proteins
Normally - degraded by proteosomes or macrophages | This fails in amyloidosis - accumulation
60
Normal proteins and amyloid
inherit tendency to fold imporperly and form aggregates in large amounts
61
Mutant proteins and amyloid
prone to misfolding, aggregate. | Defects in normal degradation process can lead to such accumulation
62
Can increased SSA produce amyloidosis?
Not alone, but if an enzyme is defective in breaking down AA then deposition of AA may occur.
63
Systemic amyloidosis
Involves several organ systems
64
Localized amyloidosis
Involves single organ
65
Primary amyloidosis
associated with clonal proliferative disorder of plasma cells producing light chain immunoglobulin (type of systemic)
66
secondary amyloidosis
complication of an underlying chronic inflammatory process | type of systemic
67
Hereditary/familial amyloidosis
A group of heterogenous, heritable form of amyloidosis with distinct pattern and organ involvement
68
Most common form of amyloidosis in US
primary amyloidosis (AL)
69
AL is usually associated with a monoclonal proliferation of _______
plasma cells | Sometimes multiple myeloma
70
AL amyloidosis occurs where?
``` Heart Kidney Peripheral nerve GI tract Respiratory tract (may affect other organs too) ```
71
Reactive Systemic Amyloidosis (AA amyloidosis, secondary amyloidosis) is often secondary to....
Rheumatoid arthritis Sometimes other connective tissue disorders and IBS
72
Rheumatoid arthritis corresponds with this type of amyloidosis
Reactive systemic/secondary/AA
73
Reactive Systemic Amyloidosis (AA/secondary) sites
Kidney Liver Spleen
74
Hemodialysis Associated Amyloidosis
depletion of beta-2 microglobulin which accumulates in patients with end stage renal disease (long term dialysis)
75
What disorder has a predilection for osteoarticular structures?
Hemodialysis Associated Amyloidosis
76
Familial mediterranean Fever
Auto inflammatory syndrome with autosomal recessive inheritance, associated with a mutation in gene that produces proteins that regulate inflammatory rxns.
77
Familial amyloidotic neuropathies
TRR mutations
78
Age related (senile) amyloidosis
Deposition of normal TRR. Ages 70s to 80s Heart typically involved - reactive cardiomyopathy and arrhythmia
79
Localized amyloidosis
Single organ or tissue without other involvement - nodular deposits in the lung, larynx, skin, bladder, tongue, orbit.
80
In localized amyloid - what is seen at periphery
infiltrates of lymphocytes and plasma cells.

IHO Week 5 (MJ) (4 decks)

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