Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology II > EXAM 2 Immune System > Flashcards

EXAM 2 Immune System Flashcards

1
Q

Innate Immunity Definition

A
  • natural or native
  • ready to attack before infection occurs
  • first 6-12 hours of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Epithelial cells

A

block microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phagocytic cells

A
  • neutrophils, monocytes/macrophages

- non specific, endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dendritic cells

A
  • initiate the innate response
  • during adaptive, DC progenitors sense pathogens and travel from bone marrow to non lymph tissue. Pathogens signal for them to mature, mature has high MHC II.
  • Strong APCs
  • Develop tolerance to own immune system. Used for immunotherapies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

NK cells

A
  • Early protection with activating/inhibiting receptors.
  • Infected cell will express less MHC I, inhibitory receptors on NK are not engaged, activated ligands are expressed.
  • NK is activated and infected cell is killed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

TLR

A
  • Toll Like Receptors
  • found on phagocytes, dendritic cells, epithelial cells
  • cytoplasm, endosymal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adaptive Immunity

A
  • acquired/specific
  • develops after exposure
  • more powerful than innate
  • B cells produce antibodies
  • 1-5 days after infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

B cells

A
  • humoral immunity/ antibodies
  • get help from antigen presenting cells that have MHC on them
  • Elimination of EXTRACELLULAR antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T cells

A
  • cell mediated immunity
  • T lymphocytes - effector T cells
  • Helper T produce cytokines
  • Cytotoxic directly kill via apoptosis
  • Elimination of INTRACELLULAR antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Generative lymphoid organs

A

Thymus for T cells and bone marrow for B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Peripheral lymphoid organs

A

Lymph nodes, spleen, mucosal, cutaneous lymphoid tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

“naiive” B and T cells

A

have not encountered an antigen yet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lymphocyte recirculation

A
  • most important for T cells - naiive T cells circulate through the peripheral lymphoid organs and effector T cells circulate to the site of infection.
  • B cells don’t do this because they produce antibodies that will get into blood and go to the infection site. B cells do not go anywhere.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CD

A

Cluster of differentiation - help T cells recognize antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

CD8+

A
  • Cytotoxic T cells
  • Class I MHC
  • On all nucleated cells
  • Any cells in the body can become infected and needs cytotoxic T cell to kill it. Help cytotoxic T cells recognize antigen
  • Kill infected cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CD4+

A
  • Helper T cell
  • Class II MHC
  • present in antigen presenting cells only (macrophages and dendritic cells)
  • Antigen presenting cells release cytokines which signals Helper T cells to grow and differentiate
  • Helps Helper T cells recognize antigen
  • Activate phagocyte to kill microbes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cytokines role

A
  • innate - TNF, IL1, IFNs and chemokines
  • Adaptive- by T helper cells –> IL2 and IL17
  • Colony stimulating factors (CSFs) by marrow cells, stimulate hematopoiesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Steps of Cell Mediated Immunity

A
  1. Dendritic cells capture microbial antigen from epithelia/tissues
  2. Transports them to lymph nodes
  3. In the process, dendritic cells mature and express MHC molecules and costimulators
  4. Naive T cells recognize MHC molecules
  5. T cells become activated, proliferate, and differentiate into effectors and memory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Steps of Humoral Immunity

A
  1. Naive B cells recognize antigens because of Helper T cells and other stimuli
  2. B cells are activated, proliferate, and differentiate into antibody secreting plasma cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

IgG

A
  • activate complement

- only one that can cross placenta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

IgM

A
  • Most prominent

- activate complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IgA

A
  • mucosal immunity

- prevents passage of foreign substances into the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IgE

A
  • mast cell and eosinophil activation

- allergies and parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type of Hypersensitivity that deals with antibodies

A

I, II, III

NOT IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type I Hypersensitivity (&steps)

A

Immediate Hypersensitivity (IgE)

  1. allergy introduced
  2. Helper T activated and stimulate B cells to make IgE (in genetically susceptible people)
  3. IgE binds to Fc receptor on Mast Cell
  4. Activated mast cell secretes mediators that cause rxn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Type I reaction

A
  • immediate (0-1 hr after exposure) - vasodilation, vascular leakage, smooth muscle spasm
  • late phase - leukocyte infiltration, epithelial damage, bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Type II Hypersensitivity (&steps)

A

Antibody-Mediated Hypersensitivity (IgG, IgM)

  1. Opsonization/phagocytosis
  2. Complement and Fc receptor mediated inflammation with antibodies
  3. Complement activates, by products cause neutrophils/ROS/inflammation
  4. Antibody-mediated cellular dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Autoimmune Hemolytic anemia

A
  • Type II
  • Rh antigen
  • opsonization and phagocytosis of red cells
  • hemolysis, anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Graves

A
  • Type II
  • TSH receptor
  • Antibody-mediated stimulation of TSH receptors
  • Hyperthyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Acute Rheumatic fever

A
  • Type II
  • streptococcal cell wall antigen, antibody cross-reacts with myocardial antigen
  • Inflammation, macrophage activation
  • Myocarditis, arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Insulin-resistant diabetes

A
  • Type II
  • Insulin receptor target
  • Antibody inhibits binding of insulin
  • Hyperglycemia, ketoacidosis
32
Q

Pernicious anemia

A
  • Type II
  • Intrinsic factor of gastric parietal cells are target
  • Neutralization of intrinsic factors, decreased absorption of VitB12
  • Abnormal erythropoiesis, anemia
33
Q

Type III Hypersensitivity (&steps)

A
  • Immune Complex Mediated Hypersensitivity
    1. Immune complex formation - antibodies are secreted into the blood and react with antigens, antigen-antibody complexes are formed
    2. deposition - complexes are deposited into various tissues
    3. Inflammation/tissue injury - about 10 days after antigen presented in blood -> fever, urticarial, arthralgia, LN enlargement, proteinuria
34
Q

Systemic Lupus Erythematosus

A
  • Type III
  • Nuclear antigen (circulating or planted in kidney) involved
  • Nephritis, skin lesion, arthritis
35
Q

Reactive Arthritis

A
  • Type III

- Bacterial antigens lead to acute arthritis

36
Q

Type IV Hypersensitivity (&steps)

A

NO ANTIBODIES INVOLVED

  1. CD4+ secrete cytokines that stimulate inflammation adn activate phargocytes
  2. Other helper T cells recruit neutrophils and monocytes which leads to further inflammation and tissue injury
  3. CD8+ directly kill tissue cells
37
Q

Rheumatoid arthritis

A
  • Type IV
  • Inflammation mediated by Help T cell cytokines; roles of antibodies and immune complexes?
  • Chronic arthritis with inflammation, destruction of articular cartilage
38
Q

Type I DM

A
  • Type IV
  • Antigens of pancreatic islet beta cells
  • T cell mediated inflammation, destruction of islet cells by cytotoxic T cell
  • chronic inflammation in Islets, destruction of beta cells, diabetes
39
Q

Contact dermatitis

A
  • Type IV
  • Various environmental chemicals such as poison ivy or oak
  • Inflammation mediated by Helper T cell cytokines
  • Epidermal necrosis, dermal inflammation, causing skin rash and blisters
40
Q

Characteristics of Autoimmune Diseases

A
  • Reaction to self-antigen or self-tissue
  • Primary or Secondary
  • Organ specific of systemic
41
Q

Immunologic Tolerance

A
  • The reason that we do NOT have autoimmune dz
  • autoimmune = lack of tolerance
  • “unresponsiveness to an antigen even though lymphocytes are exposed to that antigen”
42
Q

Central tolerance

A

T and B cells will be killed via apoptosis if they are recognized as self. B cells go through receptor editing

43
Q

Peripheral tolerance

A
  • Escape central and get caught = suppression and may be reversible.
  • Deleted via apoptosis.
  • regulatory T cells are suppressed - less prevention of immune reactions against self antigens. Apoptosis for T cells
44
Q

Anergy

A
  • during peripheral tolerance.

- lymphocytes recognize antigens but are unresponsive due to lack of co-stimulating signals.

45
Q

HLA gene

A

genetic susceptibility for autoimmune dz.

46
Q

Gateways to autoimmune dz

A
  • infection, tissue injury, and inflammation

- Entry of lymphocytes into tissues, activation of self-reacted lymphocytes, tissue damage

47
Q

SLE pathology

A
  • Systemic Lupus Erythromatosus
  • systemic AI dz.
  • Antinuclear antibodies (ANAs) bind to DNA, RNA, proteins and Smith (Sm) antigen.
  • deposition of immune complexes and binding of antibodies to cells and tissue = injury
  • elimination of self-reactive B cells and ineffective peripheral tolerance mechanism.
  • production of interferons amplifies response
48
Q

SLE clinical features

A

Butterfly rash, photosensitivity, usually in young women

49
Q

Sjogren Syndrome pathology

A
  • systemic AI
  • results from lacrimal and salivary gland destruction
  • Most have rheumatoid factor (IgM autoantibody) w/o having rheumatoid arthritis.
  • CD4+ react to an unknown self-antigen –> aberrant activation of both cellular and humeral (T&B)
50
Q

Sjogren Syndrome clinical features

A
  • women 50-60 y/o

- dry mouth and eyes

51
Q

Scleroderma pathology

A
  • chromic AI, widespread vascular damage, fibrosis in the skin and organs (GI, kidneys, heart, muscles, lungs).
  • Unknown external stimuli and/or genetic susceptibility
  • Major T and B cell activation
  • All leading to an increase of extracellular matrix of proteins; fibrosis of the skin and parenchymal organs.
  • CONSTANT ISCHEMIA/REPAIR
52
Q

Scleroderma clinical features

A
  • cutaneous fibrosis, especially on antebrachium.
  • Raynaud’s phenomenon.
  • dysphagia d/t esophageal fibrosis. GI malabsorption, intestinal pain and obstruction.
  • Pulmonary fibrosis - respiratory failure
53
Q

Recognition of allographs

A

graft antigens are recognized by T and B lymphocytes d/t differences in HLA alleles

54
Q

Rejection of allografts

A

T lymphocytes and antibodies against graft antigens are produced. Destroy tissue grafts

55
Q

Mechanism of allographs

A

foreign HA histocompatibility molecules on the endothelium and parenchymal cells of transplanted tissues trigger hosts’ immune system

56
Q

Direct pathway

A

host T cells recognize donor HLA on APC derived from the donor. dendritic cells most important

57
Q

Indirect pathway

A

Host T cells recognize donor HLA after processing and presentation on host APC CD4+ most important

58
Q

Acute T cell mediated rxn rejection of solid organs

A
  • within initial months after transplant

- cytokines secreted by the activated CD4+ - inflammatory reactions in the graft - activated macrophages - graft injury

59
Q

Chronic T cell mediated rxn rejection of solid organs

A

vascular lymphocytes reacting against alloantigens - secrete cytokines - inflammation. Mostly vascular, same mechanism as acute

60
Q

Hyperacute rejection

A
  • antibody-mediated reaction
  • Recipient has been previously sensitized to graft antigen (blood transfusion, pregnancy)
  • Circulating antibodies binds to graft endothelial HLA with an immediate (mins to days) complement
61
Q

Acute rejection

A
  • Within days or months of transplantation, not previously sensitized to transplantation antigens
  • Antibodies formed by the recipient - cause graft vasculature injury by inflammation and cytotoxicity
62
Q

Chronic rejection

A

Insidiously affect vascular components, unknown mechanism

63
Q

Hematopoietic transplant

A
  • Bone marrow transplantation
  • Using hematopoietic stem cells
  • Recipient is irradiated with or without chemo, to minimize rejection
64
Q

acute GVHD

A
  • days - weeks
  • Immunocompetent donor lymphs recognize host cells as foreignand induce T cell mediated injury
  • CLINICAL: host immune system, skin, liver, and intestine get affected
65
Q

chronic GVHD

A
  • Ongoing cutaneous and GI injury can resemble that seen in scleroderma
  • Recurrent and severe infection
66
Q

Immunodeficiency during transplantation

A
  • Due to lethal doses or irradiation/chemo
  • Opportunistic infection
  • Activation of previously silent infection
67
Q

Primary immunodeficiency

A
  • hereditary, manifest between 6mo-2yr

- Defects in innate OR adaptive immunities

68
Q

Secondary immunodeficiency

A

Due to infections, malnutrition, immunosuppression, autoimmunity, irradiation

69
Q

Most common Immunodeficiency syndrome

A

AIDS

70
Q

HIV transmission

A

Sexual (blood/mucosal), parenteral inoculation, vertical transmission

71
Q

HIV Life cycle

A
  • GP120 on HIV binds with CD4 on cell wall
  • HIV RNA released
  • Reverse transcriptase RNA–> DNA
  • Assembled into viron and released with phospholipid bilayer of host cell
72
Q

HIV Acute stage

A
  • death of memory CD4+ T
  • Infection established in lymphoid and presented to T cells
  • Spread via blood
  • Partial control of viral replication
  • 2-4 weeks after infection. Flu-like
73
Q

HIV Latent stage

A
  • asymptomatic establishment of chronic infection

- virus is concentrated in lymphoid tissue with low levels of viral replication

74
Q

AIDS

A
  • HIV chronic
  • marked by decreased levels of CD4+
  • Destruction of lymphoid tissues
  • prone to opportunistic illnesses
  • No Tx? 3 yr survival rate
75
Q

AIDS Sx

A
  • chills, fever, sweats, swollen lymph nodes, weakness, weight loss
  • CD4+ below 200 cells/mm

Pathology II (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions