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IMSE > IMSE II > Flashcards

IMSE II Flashcards

1
Q

LAD

____ protein DEFECTIVE. [component of adhesion receptors on [what cells: 3] ]
—Pathological consequence_________
—Laboratory Analysis manifestations ________

A

CD18
-Mono, Neutro, T-cell
-Abnormal VESSEL WALL adhesion + chemotaxis
–INC in Blood; [x] Infection site

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2
Q

Chediak Higashi Syndrome

____ _______ DEFECTIVE.
—Pathological consequence_________
—Laboratory Analysis manifestations ________

A

LYST, Phagosome-Lysosome
Recurrent pyogenic infection by Staph/Strep
Granulocytes/Platelets: Giant granules

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3
Q

Chronic Granulomatous Disease

________ DEFECTIVE for ____ killing.
—Pathological consequence_________
—Laboratory Analysis manifestations ________

A

Neutrophil’s inability to produce O2 REACTIVE FORMS
Bacterial
Abnormal Neutrophil Phagocytosis + Recurrent Infection
[X] NBT dye reduction

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4
Q

System that hinders Allogeneic Transplantation

A

Major Histocompatibility Antigens
Minor Histocompatibility Antigens
MHC Class I-related chain A [MICA]
ABO Blood group Antigens
Killer Immunoglobulin-like receptor System [KIR]

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5
Q

A system that hinders Allogeneic transplantation responsible for NK regulation

A

KIR system

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6
Q

transfer from a body part to another body part of same individual

A

Autograft

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7
Q

transfer from 1 twin to another twin

A

Syngeneic graft

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8
Q

transfer of cells/tissue between 2 individuals of the same species

A

Allograft

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9
Q

transfer of tissue bet. 2 individuals of different species

A

Xenograft

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10
Q

Pathways on how recipient’s immune system recognized foreign HLA proteins [2]

A

Direct Allorecognition
Indirect Allorecognition

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11
Q

Direct Allorecognition:
–MHC Type cells
–Requirements
– Response

A

MHC Class I

None

High frequency

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12
Q

Indirect
Allorecognition:
–MHC Type cells
–Requirements
– Response

A

MHC Class II

APC engulfment of MHC II foreign cells

Typical response

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13
Q

Hyperacute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention

A

Mins-Hrs after blood supply

HLA, ABO

Ischemia, Necrosis

INC. crossmatching sensitivity

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14
Q

Accelerated Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention

A

after Several days

Very low levels: Donor-specific Ab [pretransplant period]

Ischemia, Necrosis

Proper crossmatching

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15
Q

Acute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention

A

Days-Weeks

Interstitial cells

Parenchymal, Vascular Injury

Immunosuppressive drugs

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16
Q

Chronic Transplant Rejection Type
– Onset
– Mediator

A

Weeks after transplant

Prolonged cold ischemia
Reperfusion
Acute Rejection episodes

Immunosuppressive drugs toxicity

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17
Q

cellular-type rejection but may ALSO involve AB hence name also called as “Acute Cellular Rejection’

A

Acute Transplant Rejection Type

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18
Q

Chronic rejection addt’l pathological consequence

–caused by

A

Graft arteriosclerosis [progressive fibrosis + scarring, vessel lumen narrowing]

Smooth muscle proliferation

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19
Q

special type of transplant rejection exclusive for stem cell, liver, lung transplant

A

Graft-versus-Host Disease

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19
Q

Graft-versus-Host disease mediator

A

Mature T-cells in donor blood

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19
Q

2 TYPES of Graft-versus-Host disease

A

ACUTE
CHRONIC

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20
Q

2 types of Acute Graft-versus-Host disease

  1. _______
    [target of mature T-cell in donor’s graft]
  2. ________
    [target of mature T-cell in donor’s graft]
A

Mismatched Allogeneic Stem Cell Transplantation

-Mismatched HLA proteins

Matched Allogeneic Stem Cell Transplant

-Minor histocompatibility Ag

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21
Q

Occurs in first 100 days of stem cell/liver/lung transplant

Occurs in beyond 100 days of post-transplant

A

Acute Graft-versus-Host Disease

Chronic Graft-versus-Host Disease

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22
Q

Prevention for Chronic Graft-versus-Host Disease

A

Graft Irradiation
Graft removal of donor’s T-cell

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23
Q

3 IMMUNOSUPPRESSIVE AGENTS

A

Corticosteroids
Antimetabolic agents
Calcineurin inhibitors

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24
Q

act by blocking production/secretion of cytokines, inflammatory mediators, chemoattractants, adhesion molecules

A

Corticosteroids

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25
Q

interfere w/ lymphocytes’ maturation and kill proliferating cells

A

antimetabolic agents

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26
Q

blocks t-cells growth/diff. by impairing ____ synthesis

A

Calcineurin inhibitors
Cytokine

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27
Q

test for Phenotype in HLA Typing

A

Complement-dependent cytotoxicity test [CDC]

28
Q

test for Genotype in HLA Typing

A

PCR-based amplification

29
Q

study of antigens associated w/ tumors, immmune response to tumors, tumor’s effect on the host’s immune status, use of IS to help eradicate tumor

A

Tumor Immunology

30
Q

regulatory genes that promote cell division

A

Protooncogenes

31
Q

mutated protooncogenes

A

oncogenes

32
Q

a tumor that doesn’t invade surrounding tissue and normal body function is largely preserved

A

Benign tumor

33
Q

a tumor that invade surrounding tissue and body function is affected

A

Malignant tumor

34
Q

where malignant cells travel through the body

A

Metastasis

35
Q

Tumor dev’t stages

A

induction
In site
Invasion
Dessimination

36
Q

________– carcinogen exposure + cells exhibit _____.

A

Induction
Dysplasia

37
Q

neoplastic cells have formed but confined to the tissue of origin

A

In situ

38
Q

cancer cells proceed only to invasion [adjacent organs/tissues] if they are malignant, not benign.

A

Invasion

39
Q

traveling of malignant cells to the whole body through ____ and ______ _____.

A

Dissemination
blood, lymphatic vessels

40
Q

Reasons for tumor/MALIGNANT cell GROWTH

A

TUMOR CELLS are:
1.poorly immunogenic
2.lack MHC molecules
3.resistant
4.growth rate > immune response

  1. Soluble ag [released by tumor] may bind to T-cell receptor = no interaction w/ tumor cell
  2. Gene mutations
41
Q

higher amounts of antigens present in the tumor tissue than in normal tissue

they are tumor specific [True or False] [ if not, why?]

A

Tumor-associated antigens

False, tumor ag are also found in noncancerous human tissue

42
Q

differential diagnosis of tumor type can be done by:
_________
_________

A

tissue/cell morphology
tumor markers directly from tumor tissue

43
Q

Lab tests for tumor marker detection

A

1.Gross/Microscopic morphology of tumors
2. Antigen/Protein tumor markers detection
3. DNA/RNA molecular diagnostics
-Cytogenetic studies
-Nucleic acid amplification techniques [NAAT]
-Fluorescent in situ hybridization [FISH]

44
Q

Ideal tumor markers

A

Produced by tumor
Secreted into biological fluid

Inepensive
INC in significant levels while disease is still treatable
Antigen must be ABSENT w/o malignant disease

45
Q

Tumor marker class

A

Cell surface markers
Proteins

Oncofetal antigens
Carbohydrate antigens
Blood group antigens

Enzymes/Isoenzymes
Hormones

46
Q

EXAMPLES of:
1. Cell surface markers
2. Proteins
3, Enzymes/Isoenzymes
4. Hormones

A
  1. Estrogen/Progesterone receptors
    WBC CD markers
  2. Thyroglobulin [TG]
    IGs, Ig light chains [Bence Jones proteins]

3.
Prostate-specific antigen [PSA]
Alkaline phosphatase [ALKP]
Neuron specific enolase

  1. Human Chorionic Gonadotrophin
    Calcitonin
    Gastrin
47
Q

EXAMPLES of:
1. Oncofetal antigens
2. Carbohydrate Antigens
3. Blood group antigens

A
  1. AFP
    Carcinoembryonic antigen [CEA]
  2. CA 125
    CA 15-3
  3. CA 19-9 [Lewis antigens]
48
Q

DISEASE Associations of:
1. Cell surface markers
2. Proteins
3, Enzymes/Isoenzymes
4. Hormones

A

1.
Breast cancer hormone therapy [prognosis]
WBC neoplasms [lineage/clonality]

2.
Papillary/Follicular THYROID Carcinoma
[well-differentiated]
Multiple MYELOMA
LYMPHOID malignancies

3.
PROSTATE cancer
BONE/LIVER cancer
NEURAL tissue neoplasms

  1. GERM CELL carcinoma
    MEDULLARY THYROID cancer
    PANCREATIC gastrinoma
    TROPHOBLASTIC tumors
49
Q

DISEASE Associations of:
1. Oncofetal antigens
2. Carbohydrate Antigens
3. Blood group antigens

A

1.
GERM CELL carcinoma
COLORECTAL carcinoma
HEPATOCELLULAR carcinoma

2.
Ovarian cancer
Breast cancer

  1. PANCREATIC cancer
    GI cancer
50
Q

transfer of antibodies, cytokines, or cells to patients who may not be able to mount an immune response

examples:

A

Passive immunotherapy

T cell
Antibody conjugates/immunotoxins

51
Q

patients are treated in a manner that stimulates them to mount immune responses to their tumors

examples:

A

Active immunotherapy

Bacillus Calmette Guerin
Cytokines
Cancer vaccines

52
Q

How do the bacteria evade the Immune System?

A
  1. Avoiding Ab [proteases’ destruction]
  2. Blocking Phagocytosis [M protein, No fusion of Granules and Phagosome]
  3. Inactivating complement casscade [Complement proteins’ disruption]
53
Q

2 Phenomenons in Type 1 Hypersensitivity

A
  1. TH2 SWITCH response [normal th1 + th2]
  2. HLA molecules [allergen rxn in HIGH RESPONSE]
54
Q

Type 1 Hypersensitivity

Time onset
Key reactant

A

Seconds-Minutes
IgE

55
Q

Diseases associated with Type 1 Hypersensitivity

A

Atopy
Anaphylaxis
Rhinitis
Asthma

56
Q

inherited tendency to respond to naturally occurring inhaled/ingested allergens w/ continued production of IgE.

A

Atopy

57
Q

most severe type of allergic response

A

anaphylaxis

58
Q

most common form of atopy/allergy

A

rhinitis

59
Q

caused by particles not greater than 2-4 um. Greek word _____, ______.

A

Asthma
Panting, breathlessness

60
Q

Diagnostic procedures for type 1 hypersensitivity

  1. ________________ test
    -all IgE or Total IgE. Uses ______ labels.
  2. ________________ test
    -Ag-specific IgE. Uses ______ labels.
A

Radioimmunosorbent Test [RIST]
radioactive labels

Radioallergosorbent Test [RAST]
–enzyme of fluorescent labels.

61
Q

Type I Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism

A

Anaphylactic/Atopic

IgE
Basophil, Mast cell

Allergen
NO
Release of inflammatory mediators

62
Q

Type II Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism

A

Cytotoxic

IgM/IgG
RBC,WBC, PLT

Cell-bound Ag
YES
Cell lysis

63
Q

Type III Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism

A

Immune Complex

IgM/IgG
Interstitial cells

Soluble Antigen
YES
Ag-Ab complexes deposition

64
Q

Type IV Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism

A

Delayed/Cell-Mediated

T cell [TH1]
APC, Macrophage, T-cell

Sensitized Antigen
NO
Cytokines release

65
Q

DISEASE EXAMPLE OF TYPE 1 HS

A

Anaphylactic:
Bee Sting
Food/Drug Allergens

Allergic/Atopic:
Asthma
Eczema
Hives
Hay Fever
rhinitis

66
Q

DISEASE EXAMPLE OF TYPE II HS

A

AIHA
HTR
HDN
ITP

Goodpasture Syndrome
Rheumatic fever

67
Q

DISEASE EXAMPLE OF TYPE III HS

A

Arthus reaction

Polyarteritis Nodosa
Poststreptococcal Glomerulonephritis

Serum Sickness
SLE

68
Q

DISEASE EXAMPLE OF TYPE IV HS

A

Contact Dermatitis
GHVD

PPD
Poison ivy

IMSE (3 decks)

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