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SRNAanatomy > Immunity > Flashcards

Immunity Flashcards

1
Q

1st line of defense (MIN)

A

Intact skin
Mucous membranes
normal microbiota

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2
Q

2nd Line of defense (MINCAPFI)

A 
Mass cells and Basophils (inflammatory response)
Inflammation
Natural killer cells
Complement system
Anti-microbial substance
Phagocytes DEMMN(neutrophils, monocytes; eosinophils, 
      dendritic cells, and macrophages)
Fever 
Interferon
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3
Q

3rd line of defense

A 
Specialized lymphocytes T and B cells
Antibodies
T lymphocytes
Antigen presenting cells
B lymphocyts
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4
Q

Prevents microbes from entering airway

A

Epiglottis

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5
Q

Tears contain ______ which destroy cells walls, gram positive bacteria

A

Lysosomes.

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6
Q

Traps microbes in respiratory adn GI tract

A

Mucous

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7
Q

Phagocytes

A

Cells such as neutrophils, eosinophisl, dendritic cells, and macrophages.

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8
Q

Fever

A

Intensifies the effects of interferons, inhibits growths of some microbes, speeds up body reactions that aid repair.

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9
Q

***Interferons

A

Protect uninfected host cells from Viral infection

Interferes with viral replication

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10
Q

Granuloma -

A

Immune system walls off infectious organisms (fungal or tuberculosis Infections in the lungs). May calcify over time.

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11
Q

is ongoing inflammation. It can be

caused by foreign bodies, persistent pathogens, and autoimmune diseases.

A

Chronic inflammation.

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12
Q

Short term inflammatory response to an insult to the body

A

Acute inflammation

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13
Q

*****Repair and healing process

A

*****IFN-gama (activates macrophages)
TGF-B - (Stimulates fibroblast growth)
Angiogenic factors [VEGF, FGE-2} stimulates endothelial and fibroblast growth

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14
Q

Cellular injury –> Mast cell degranulation

A

Histamine is released

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15
Q

Cellular injury –> activation of plasma systems. Mast cell degranulation

A

Histamine is released

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16
Q

*****Mediators of Inflammation

A

Vasodilation: Prostaglandins, Histamine, Nitric Oxide
Vascular permeablity: Histamine, bradykinin, leukotrienes and , PAF
Pain: Prostaglandins, bradykinin

Systemic effects
Fever : Il-1 , Il-6, TNF alpha, prostaglandins
Acute phase reactants
Leukocytosis

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17
Q

Endogenous pyrogens

A 
Prostaglandin-E2 (PGE2) 
IL-1
IL-6
TNF-α
interferon-γ
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18
Q

Endotoxins of pathogens:

A

lipopolysaccharide (LPS) component of gram negative bacteria cell wall

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19
Q

Eosinophrils

A
  1. Fight PARASYTIC worms infction

2. Regulate and degrade substances.

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20
Q

Neutrophyils (PMN) most ABUNDANT

A

Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical

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21
Q

Natural Killer cells

A

Eliminate virus infected cells and tumor cells

DESTROY TUMOR/CANCER CELLS

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22
Q

Neutrophyils (PMN) most ABUNDANT

Both (shower and

A

Phagocytize microorganisms and cellular debris soon after injury FIRST RESPONDERS
Secrete chemical

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23
Q

Natural Killer cells

A

Eliminate virus infected cells and tumor cells
DESTROY TUMOR/CANCER CELLS
non-PHAGOCYTES, shower with citokines that destroy

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24
Q

Macrophages

A

Phagocytize microorganinsm and cellular debris
Secrete chemicals that promote tissue healing
Activate adaptive Immunity.

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25
Q

Production

What is arachidonic acid?

A

Cell membrane PHOSPHOTIDYLCHOLINE gives–>
Phospholipase A2 –> membrane protein Splits into Arachidonic acid and PAF
Arachidonic acid is a 20 carbon polyunsaturate fatty acid precursor to pro-inflammatory molecules
Arachidonic acid gives 2 cyclooxygenase (forms and gives us Prostaglandins 2) and 5-Lipoxygenas (which produces inflammatory leukotrienes)

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26
Q

Production of lipid vasoactive substance by mast cells.

A

Phospholipase A2 -membrane protein

Arachinoic acid precorse to cyclooxygenase (gives us Prostaglanding 2

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27
Q

Most NSAIDS are

A

cyclooxygenase

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28
Q

Too much ASA

A

Bleeding

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29
Q

Complement system (3) main action.

A
  1. Chemical signaling. Through NAFTATOXINS (tell white blood cells to kills bacteria , like smelling smoke)
  2. Starts putting protein molecule on the bacteria, so macrophages destroy. OPSONIZATION- Mark something so macrophages can attack and destroy.
  3. Punches holes in bacteria wall. (Membrane attack complex)
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30
Q

****________ bind to the cell membrane of the pathogen that activates it, labeling it for ___________

A

IgG & C3b; phagocytosis (opsonization)

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31
Q

Interferon α -

A

Produced by Monocytes, has Antiviral action, increases expression of MHC I can be used to treat Hep. B, C

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32
Q

Interferon β -

A

produced by Fibroblasts, has Antiviral action, increases expression of MHC I can be used to treat MS

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33
Q

Interferon γ -

A

produced by NK, Tc(CD8), Th(CD4)

Activates Macrophages, increases expression of MHC II, can be used in treatment of cancer

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34
Q

T-cell development in the Thymus (Cortex)

A

Step 1: Recognize foreign antigen

Step 2: Regonize self antigen

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35
Q

Where T cells are tested

A

Thymus

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36
Q

Where B cells are tested

A

Bone marrow

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37
Q

Thymic epithelial cells mechanism of action:

A

present MHC proteins to the untrained thymocytes
Thymocytes that succesffully bind to the protein MHC continue while those that cannot undergo APOPTOSIS (this is positive selection selecting those that binds)

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38
Q

CD 8 becomes

A

Cytotoxic T cells.

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39
Q

Which Ig Active against parasites; important mediators of allergic responses

A

IgE

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40
Q

IgE

A
  • Active against parasites; important mediators of allergic responses
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41
Q

Produced during the primary response to an antigen; are the largest Igs (pentamer)

A

IgM

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42
Q
  • Active against parasites; important mediators of allergic (attach mast cells and basophils) responses
A

IgE

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43
Q

Produced during the primary response to an antigen; are the largest Igs (pentamer)

A

IgM

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44
Q

IgM

A

Produced during the primary response to an antigen; are the largest Igs (pentamer)

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45
Q

Most abundant class of Igs; transported across the placenta

A

IgG

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46
Q

Has subclasses; one subclass is most abundant in body secretions

A

IgA

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47
Q

Has subclasses; one subclass is most abundant in body secretions

A

IgA

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48
Q

IgA

A

Has subclasses; one subclass is most abundant in body secretions

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49
Q

Serve as surface receptors on developing B lymphocytes

A

IgD

50
Q

Serve as surface receptors on developing B lymphocytes

A

IgD

51
Q

IgD

A

Serve as surface receptors on developing B lymphocytes

52
Q

Dendritic cells (CL -PM)

A

Capture Antigen from invading pathogen in epithelial tissue
Leave epithelium and migrate to lymphatic vessel
Presents Antigen to immature T cells
Mature T cells multiply and proliferate

53
Q

Type I hypersensitivity

A

IgE Medicated hypersensitivity
causes localized and systemic anaphylaxis, seasonal allergies including Hay fever, food allergies such as those to shellfish and peanus , hives and eczema

54
Q

Type II hypersensitivity

A

IgG - Mediated Cytotoxic Hypersensitivity.
Red blood cells destroyed by complement and antibody during a transfusion of mismatched blood type or during erythropoiesis fetalis

55
Q

Type III Hypersensitivity

A

Immune complex Mediated Hypersensitivity

Most COMMON FORMS of immune complex disease are seen in GLOMERULONEPHRITIS< RA, and SLE

56
Q

Type IV Hypersensitivity

A

Cell- Mediated Hypersensitivity

Most common forms are contact dermatitis, Tuberculin reaction, Autoimmune disease such as DM I, MS and RA

57
Q

**General Four MECHANISMS of Antibodies

A

Virus neutralization by blocking docking to host cells
Toxin neutrolization
Activate complement-mediated killing
Phagocytosis via opsinisation

58
Q

*****Class II MHC Distribution
Presents_____
Reacts with _______

A

B cells, APCs, and some epithelial cells
Exogenous antigens derived from extracellular organisms
CD4 on Th cells

59
Q

****Class I MHC Distribution –>
Presents_____
Reacts with _______

A

All nucleated cells and platelets
Endogenous antigens (8-10 amino acids)derived from INTRACELLULAR PROTEINS
CD-8 on Tc Cells

60
Q

ADCC

A

Antibody dependent CYtotoxic cell
Does not use CD8 or MHC
Binding to antiboeis
Has receptors for those antibodies.

61
Q

Epitomes

A

Specific regions for binding for antigen.

62
Q

Stages of B cell development in bone marrow.

A 
Stages
Stem cell 
Pro B cell (early, late)
Pre-B cells
Immature B cell
Naive B cell
Mature B cell
63
Q

1st step of complement system

A

IgE to bindg

64
Q

Dendritic Cells short version

A

Capture antigen from invading pathogen in epithelia tissue
Types of APCs
IN skin

65
Q

Antigen processing and presentation

A

Reaction when presented to pathogen

Autoimmune dysfunction.

66
Q 
How does Superantigen cause TSS?
Bind to MHC class II antigen
A

Kills all viruses (does not specifically target any particular cell)
STAPH AUREUS EXAMPLE: Toxic Shock syndrome.
The superantigen binds to all T-cells not specific one.–> RELEASE OF EXCESSIVE IL-2

67
Q

Toxic Shock syndrome can cause

A

Rash

Desquamation of hands

68
Q

2 types of adaptive immunity

A

Naturally acquired

Artificially Acquired.

69
Q

Mucosal immune Response
MALT such as Peyer’s patches (tonsils) of the small intestine generate ______immunity. Microfold cells (M cells) transport ________

A

IgA immunity.
antigen inside the body. Dendritic cells then take the antigen to the regional lymph nodes, where an immune response is mounted.

70
Q

Acute Inflammatory Response system
Cellular injury or pathogenic invasion leads
to:

A

mast cell degranulation
activation of plasma systems
Release of cellular produces

71
Q

Complement clotting kinin leads to

A 
Vasodilation
Vascular permeability 
Cellular infiltration
Thrombosis
stimulation of nerve endings
72
Q

Mediators of inflammation: What limit inflammation

A

IL-10 (inhibits cytokine production)
TGF-B (inhibits macrophage proliferation)
ECF-A (Attracts eosinophils)
Histaminage, arylsulfatase (destroy histamine and leukotrines)

73
Q

Mediators of inflammation: Vascular Permeability

A

Histamine
Bradykinin
Leukotrienes
PAF

74
Q

Intact skin forms a physical barrier to entrance of microbes

A

Epidermis of the skin

75
Q

Inhibit entrance of many microbes, but not as effective as intact skin

A

Mucous membranes.

76
Q

Traps microbes in respiratory and GI tract

A

Mucous

77
Q

Provide tears that wash away microbes: tears contain lysozyme which destroy cells especially GRAm POSITIVE BACTERIA

A

Lacrimal apparatus.

78
Q

Dilutes and washes microbes from mouth

A

Saliva

79
Q

Filters and traps microbes and dust in nose

A

Hairs

80
Q

Together with mucous form a ciliary escalator which traps and remove microbes from upper respiratory tract

A

Cillia

81
Q

Prevents microbe from entering ear

A

Earwax

82
Q

Washes microbes from urethra to prevent colonization

A

Urine

83
Q

Move microbes out of body

A

Vaginal secretions

84
Q

Expel microbes out of body

A

Peristalsis
Defecation
Vomiting
Diarrhea

85
Q

Component of First line defense: Chemical factors

SUP VEGS

A 
Sebum 
Urine
Perspiration
Vaginal secretion 
Earwax
Gastric juice
Saliva
86
Q

Both chemical and physical Factors of 1st line defense

A

Saliva
Urine
Vaginal secretions
Earwax

87
Q

Components of 2nd line of defense

A

Defensive cells
Inflammation
Fever
Antimicrobial Substances

88
Q

Components of 2nd line of defense : Defensive cells are

A

Phagocytes and

Natural killer cells

89
Q

Components of 2nd line of defense : Confine and destroys microbes initiate tissue repair

A

Inflammation

90
Q

Components of 2nd line of defense : Intensify the effects of interferons, inhibits growth of some microbes and SPEED UP THE BODY REACTION that aid repair

A

Fever

91
Q

Components of 2nd line of defense : Kill infected target cells

A

Kills infected target cells by releasing granules that contain PERFORIN and GRANZYMES –> PHAGOCYTES THEN KILL THE INFECTED MICROBES.

92
Q

Components of 2nd line of defense : Phagocytosis such a neutrophyills, eosinophils, dendritic cells and macrophages

A

Phagocytes

93
Q

Phagocytes are

A

neutrophils
Eosinophils
Dendritic cells
macrophages

94
Q

Antimicrobial substance : Complement system

A

Causes cytosis of microbes, promotes phagocytosis, and contributes to inflammation

95
Q

Interferons function?

A

Protect FROM VIRAL INFECTION.

96
Q

Inhibit growth of certain bacteria by reducing iron

A

Iron binding proteins.

97
Q

Describe arachadonic acid. Explain its role in the inflammatory response?

A

20- Carbon polyunsaturated fatty acid precursor to pro-inflammatory molecules (Cyclooxygenase and 5-Lipooxygenase)

98
Q

Precursor of Arachidonic acid

A

Phospholipase A2

99
Q

T Cell development in the THYMUS (MEDULLA)

A

The surviving thymocytes move to the thymic medulla where they encounter antigen-presenting cells (APCs) . These APCs present self-antigents from other body ceslls. Thymocytes that bind with the self-antigens undergo apoptosis, as this indicates that they will attack body cells. This is called NEGATIVE SELECTION (selection for cells that don’t bind)

100
Q

T-cell development in the thymus MEDULLA is the one with the _________ for cells that _____ bind

A

Negative selection, don’t

101
Q

Effects of Histamine on Target cells : H1

A 
Target cells  (SENM)
Smooth muscle cell; endothelial cell; Neutrophil ; Mast cell

Effect of histamine:( Smooth muscle cell) Contraction –> Bronchoconstriction

Effect of histamine on Endothelial Cells:
Contraction (Retraction at endothelial junction)–> Edema and vasodilation

Effects of histamine on Neutrophils:
Increased chemotaxis –> Neutrophil migration

Effects of histamine on Mast cell
Prostaglandin synthesis –> Enhanced Inflammation.

102
Q

Effects of Histamine on Target cells : H2

A

Target Cell:
Parietal cell of stomach mucosa
Effect of histamine –> secretion of gastric acid

LENM
Lymphocyte : Decreased activity
Eosinophils: decreased activity
Neutrophil: Decreased chemotaxis
Mast cell: Decreased granulation.
103
Q

Explain mast cell degranulation

A

Degranulation is a cellular process that releases antimicrobial cytotoxic or other molecules from secretory vesicles called granules found inside some cells. It is used by several different cells involved in the immune system, including granulocytes (neutrophils, basophils, and eosinophils) and mast cells.

104
Q

Inflammatory Phases 2 fates

A

Cellular injury –> Acute inflammatory –> healing

Cellular injury –> Acute inflammatory –> Chronic inflammatory –> Glanuloma formation –> Healing

105
Q

Actions of PGD2 (VIBE)

A

Vasodilation
Increased capillary permeability
Bronchoconstriction (smooth muscle contraction)
Enhanced inflammation

106
Q

Actions of PAF (VEBEF VI)

A 
Vasoconstriction
Enhanced Inflammation
Bronchoconstriction
Eosinophils chemotaxis 
Platelet activation (VI) at low PAF
107
Q

Actions at H1 receptor

A

GTP converted to cGMP–> increasing level (cell activation)

108
Q

Actions at H2 receptor

A

ATP converted to cAMP –> increasing level –>Cell INACTIVATION

109
Q

Degranulation immediate response

1. Histamine –> vascular effects

A

Vasodilation–> Increased permeability –> Exudation

110
Q

Degranulation immediate response

2.Neutrophil chemotactic factor

A

Neutrophils attracted to site –> Phagocytosis

111
Q

Degranulation immediate response

3. Eosinophils chemotactic factor

A

Eosinophils attached to site –>Phagocytosis

112
Q

Synthesis long term response

Leukotrienes and Prostalginding E- series

A

Vascular effects–> Dilation and increased permeability–> EXUDATION

113
Q

T cells and B cells can be activated only by

A

exposure to a specific antigen at a specific site in a plasma membrane.

114
Q

When an antigen is bound to a Class II MHC protein, it can activate a ________ cell.

A

B helper Cells

115
Q

Class II MHC molecules are found on which of the following?

A

Lymphocytes and APCs

116
Q

When an antigen is bound to a Class I MHC molecule, it can stimulate a ________ cell.

A

CYTOTOXIC T cells

117
Q

Cell mediated immune response in order: Several cycles of mitosis occur.

  1. Antigen is engulfed and presented by a macrophage.
  2. Cytotoxic T cells migrate to focus of infection.
  3. T cells with specific receptors recognize the antigen.
  4. T cells differentiate into cytotoxic T cells or T memory cells.
  5. Cytotoxic T cells release perforin and/or lymphotoxin.
A

B) 2, 4, 1, 5, 3, 6

Antigen is engulfed and presented by a macrophage
T cells with specific receptors recognize the antigen
Several cycles of mitosis occur.
T cells differentiate into cytotoxic T cells or T memory cells.
Cytotoxic T cells migrate to focus of infection.
Cytotoxic T cells release perforin and/or lymphotoxin

118
Q

Immunity that results from antibodies that pass through the placenta from mother to fetus is called ________ immunity.

A

Naturally acquired passive

119
Q

The first line of CELLULAR DEFENSE Against PATHOGENS

A

Phagocytes

120
Q

Most of the lymph returns to the venous circulation by way of the

A

THORACIC DUCT

121
Q

Lymphatic tissue is found in the greatest quantity in

A

A) the adult spleen.

SRNAanatomy (25 decks)

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