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Anatomy and Phyisology > HLTH module 3: immunity > Flashcards

HLTH module 3: immunity Flashcards

1
Q

structures of the lymphatic system

A

lymph nodes, spleen, tonsils, intestinal lymphoid tissue, and lymphatic circulation

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2
Q

what does the immune system consist of?

A

the lymphoid structures, immune cells, tissues concerned with immune cell development, and chemical mediators

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3
Q

what structures remove foreign materials

A

lymphocytes and macrophages

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4
Q

what structures produce and develop immune cells?

A

the bone marrow and the thymus; all cells originate in the bone marrow and the thymus is significant during fetal development

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5
Q

role of thymus in immune cells

A

it programs the immune cells to ignore self-antigens

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6
Q

chemical mediators

A

include chemicals such as histamines and interleukins that can play a role in the immune reaction

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7
Q

anitgen

A

a foreign substance that stimulates immune response

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8
Q

antibody

A

specific protein produced in the humoral response to bind with an antigen

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9
Q

autoantibody

A

antibodies against self-antigens; body attacks itself

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10
Q

function of neutrophils

A

phagocytosis

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11
Q

function of basophils

A

releases histamine during anaphlylaxis

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12
Q

eosinophils

A

participate in allergic reactions and are defence against parasites

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13
Q

monocytes

A

migrate from the bloodstream to become macrophages

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14
Q

B lymphocytes

A

humoral immunity-activated cell that becomes an anti-body producing plasma cell or a B memory cell

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15
Q

what are T lymphocytes involved in?

A

cell-mediated immunity

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16
Q

memory T cells

A

remember antigen and quickly stimulate an immune response

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17
Q

helper T cells

A

activate B and T cells to control or limit specific immune responses

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18
Q

complement proteins

A

group of inactive proteins in the circulation that, when activated, stimulate the release of other chemical mediators, promoting inflammation, chemotaxis, and phagocytosis

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19
Q

prostaglandins

A

group of lipids with varying effects; some cause inflammation, vasodilation, and increased permeability

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20
Q

leukotrienes

A

group of lipids, derived from mast cells and basophils; causes contraction of bronchiolar smooth muscle and have a role in inflammation

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21
Q

cytokine examples

A

lymphokines, monokines, interferons, and interleukins

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22
Q

cytokines

A

produced by macrophages and activated T lymphocytes; stimulate activation and proliferation of B and T cells, communication between cells, and are involved in inflammation, fever, and leukocytosis

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23
Q

chemotactic factors

A

attract phagocytes to area of inflammation

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24
Q

what are antigens composed of?

A

usually a combination of complex proteins or polysaccharides, or glycoproteins

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25
Q

what are specific antibodies produced by?

A

B lymphocytes

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26
Q

major histocompatibility complex

A

antigen molecules present in genes (chromosome 6); has an essential role in activation and regulation of the immune response

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27
Q

autoimmune diseases

A

occur when the immune system no longer recognizes self from non-self and begins to attack its own cells and structures

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28
Q

mononuclear phagocytic system

A

occurs when monocytes develop into macrophages

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29
Q

where are macrophages present?

A

the liver, lungs, and lymph nodes

30
Q

what occurs after macrophages engulf materials?

A

they display the antigens on their cell membranes, allowing the lymphocytes to respond to this display and initiate the immune response

31
Q

what do macrophages secrete?

A

monokines and interleukins

32
Q

primary cell in the immune response

A

the lymphocyte

33
Q

where do T lymphocytes develop from?

A

stem cells held in the thymus

34
Q

what type of immunity are T lymphocytes involved in?

A

cell-mediated

35
Q

what do T lymphocytes do?

A

recognize antigens and create an army of more T and B lymphocytes to attack the invader

36
Q

two subgroups of T cells

A

CD4 (helper) and CD8 (killer)

37
Q

what secretes cytokines?

A

T lymphocytes

38
Q

B lymphocytes role

A

produce antibodies

39
Q

where do B lymphocytes come from?

A

the bone marrow then proceed to the spleen and lymphoid tissue

40
Q

natural killer cells

A

destroy tumor cells and virus cells without any prior exposure and sensitization

41
Q

another name for antibodies

A

immunoglobulins

42
Q

anatomy of antibodies

A

each has a unique sequence of amino acids attached to a common base

43
Q

how do antibodies destroy antigens?

A

they bind to a specific matching antigen and through this, destroy it

44
Q

where are antibodies found?

A

the general circulation

45
Q

5 classes of antibodies

A

IgG, IgM, IgA, IgE, and IgD

46
Q

most common antibody in the blood

A

IgG

47
Q

how is the complement system activated?

A

when an anitgen-antibody complex binds to the first complement component (C1), a sequence of activating steps will occur

48
Q

result of the complement system?

A

destruction of the antigen by lysis

49
Q

two steps of the immune response

A

primary response (first exposure to the antigen) and secondary response (repeat exposure to the same antigen_

50
Q

4 types of acquired immunity

A

natural active, artificial active, natural passive, and artificial passive

51
Q

natural active immunity

A

acquired by direct exposure to an antigen

52
Q

activate artificial immunity

A

develops when a specific antigen is purposefully introduced into the body, stimulating the production of antibodies; ex. viruses

53
Q

passive immuntiy

A

occurs when antibodies are transferred from one person to another

54
Q

passive natural immunity

A

occurs when IgG is transferred from mother to fetus across the placenta or through breast milk; protects the infant for the first few months of life

55
Q

passive artificial immunity

A

results from the injection of antibodies from a person or animal into a second person; ex. rabies antiserum or snake antivenom

56
Q

herd immunity

A

a phenomenon in which a high percentage of the population is vaccinated or has experienced a prior infection of the disease, thus decreasing the chances of spreading the disease

57
Q

examples of autoimmune diseases

A

hashimoto thyroiditis, systemic lupus erythematosus, rheumatic fever, pernicious anemia, and hyperthyroidism

58
Q

what occurs in autoimmune reactions?

A

inflammation and tissue necrosis due to self-antigens not being recognized

59
Q

systemic lupus erythematosus

A

a chronic inflammatory autoimmune disease that affects a number of systems, creating a facial rash around the nose and cheeks

60
Q

discoid lupus erythematosus

A

a less serious version of SLE affecting only the skin

61
Q

who does SLE primarily affect?

A

women aged 10-50, higher in black, natives, asian, and hispanic individuals

62
Q

cause of SLE

A

not established but appears to be a combination of genetic, hormonal (estrogen levels), and environmental factors (UV light)

63
Q

what is SLE characterised by?

A

the presence of large number of circulating autoantibodies against DNA, platelets, RBCs, nucleic acid, and other cellular materials such as antinuclear antibodies

64
Q

why does skin inflammation occur in SLE?

A

due to immune complexes (especially those with anti-DNA antibodies) are deposited in CT’s, activating the complement system, inflammation, and tissue necrosis

65
Q

vasculitis

A

inflammation of the blood vessels and this occurs in SLE; also causes ischemia to cells, causing tissue necrosis

66
Q

common sites for vasculitis in SLE individuals

A

the kidneys, lungs, heart, brain, skin, joints, and GI tract

67
Q

diagnosis for SLE

A

vasculitis impacting at least four body areas

68
Q

clinical signs for SLE

A

skin rash and joint inflammation are initial symptoms which progress to kidney and lung involvement; later symptoms include chest pain, depression, anemia, hair loss, and oral ulcers

69
Q

diagnosis for SLE

A

looks for the presence of antinuclear antibodies in blood serum, as well as lupus erythematosus cells which are mature neutrophils containing nuclear materials; low RBC, leukocyte, lymphocytes, and platelets are also common

70
Q

SLE treatment

A

often treated by a rheumatologist and glucocorticoids and NSAIDS are often used to treat the inflammation and decrease the immune response

71
Q

how to prevent SLE flare ups?

A

avoidance of sun and excessive fatigue

Anatomy and Phyisology (72 decks)

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