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A & P medic school > 4c human body defences > Flashcards

4c human body defences Flashcards

1
Q

First line of defence the body has against disease

A

Skin and mucous membranes

Both physical and chemical barrier

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2
Q

Innate immunity is

A

Nonspecific immunity, includes external physical and chemical barriers by skin and mucous membrane
Includes antimicrobial substances, NK cells, phagocytes, inflammation and fever

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3
Q

Epidermis defense against disease

A

Closely packed keratinized cells is a great physical barrier
Shedding helps remove microbes
Bacteria can rarely get through without break in skin

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4
Q

Mucous membranes defense

A

Produce mucous to trap microbes and foreign substances
Contain cilia to clear mucous after
Coughing or swallowing ejects or destroys them

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5
Q

Lacrimal apparatus defense

A

Makes and drains tears
Blinking spreads tears, washing eyes with movement
Tears have lysozyme

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6
Q

Lysozyme locations

A

Saliva, perspiration, nasal secretions, tissue fluid

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7
Q

Saliva defense

A

Washes microbes from teeth and mucous membrane of mouth. Flow reduces colonization

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8
Q

Flow of urine defense

A

Retards microb colonization

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9
Q

Vagina juice defense

A

Move microbes out by washing and is acidic

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10
Q

Defecation vomiting defense

A

Expels bacteria. Smooth muscle contracts vigorously in response to toxins

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11
Q

Chemical protection in skin and mucous membranes

A 
Sebum forms protective film, and unsaturated fats in it inhibit growth of some fungi and bacteria
Fatty and lactic acids make skin pH 3-5
Sweat flushes microbes 
Gastric juice pH 1.2-3 (2.0)
and has enzymes and mucous
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12
Q

Second line of defenses

A

Internal antimicrobial substances, phagocytes, NK cells, inflammation and fever

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13
Q

4 types of antimicrobial substances

A

Interferons
Complement
Iron-binding proteins
Antimicrobial proteins

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14
Q

Interferons

A

Alpha, beta, gamma IFN
Released by virus infected cells, diffuse to uninfected neighbours, and induce synthesis of antiviral proteins that interfere with virus replication.
Does not prevent them from entering cells

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15
Q

Complement system

A

Normally inactive proteins, when activated they enhance certain immune reactions

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16
Q

Iron-binding proteins

A

Reduce amount of iron for bacterial growth
Examples - transferrin (blood and fluid) lactoferrin (milk, saliva, mucus) ferritin (liver spleen red marrow) and hemoglobin (RBCs)

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17
Q

Antimicrobial proteins AMP

A

Short peptides, kill wide range of microbes, attract dendritic and mast cells. Microbes don’t develop tolerance to.

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18
Q

Antimicrobial proteins

A

Dermicidin (sweat)
Defensins and cathelicidins (by neutrophils, epithelia and macrophages)
thrombocidin (by platelets)

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19
Q

Natural Killer cells

A

Make up 5-10% of lymphocytes
Lack membrane molecules that identify B and T cells, but have ability to kill wide variety of infected cells and tumor cells
Attack any cells that display abnormal or unusual plasma membrane

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20
Q

Where are NK cells found

A

Spleen, lymph nodes, red bone marrow

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21
Q

How NK cells kill

A

Bind and release granules containing toxic substances
Perforin (a granule) inserts into plasma membrane and creates perforations for ECF to flow in and burst cell
Granzymes (a granule) Protein digesting enzymes that induce target to kill itself (but doesn’t kill microbes inside, phagocytes do)

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22
Q

Phagocytes

A

Neutrophils and macrophages (travel as monocytes and turn into an ultra robot enroute, called wandering macrophages)
There are also fixed macrophages which guard certain tissue

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23
Q

Where are fixed macrophages found

A

Histicocytes (connect tissue)
Stellate reticuloendothelial cells (kupffer cells) in liver
Alveolar in lungs
Microglial in nervous system
Tissue macrophages in spleen, lymph, red bone marrow

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24
Q

5 phases of phagocytosis

A 
Chemotaxis
Adherence
Ingestion
Digestion
Killing
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25
Q

Activities of phagocytic cells

A

Marignation (selectins on endothelial cells bind to integrins on neutrophil as it rolls by)
Diapedsis (squeezing between endothelial cells)
Chemotaxis (directed migration to site of damage) where it then undergoes 5 phases of phagocytosis

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26
Q

Chemotaxis phase

A

Chemicals from invading microbes, white blood cells, damaged tissue, or activated complement proteins attract phagocytes

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27
Q

Adherence phase

A

Phagocyte binding to material

Enhanced by complement proteins binding to invading pathogen

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28
Q

Ingestion phase

A

Phagocyte plasma membrane forms pseudopod to ingest.

Pseudopod surrounds and fuses around invader, called phagosome

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29
Q

Digestion phase

A

Phagosome enters cytoplasm and merges with lysosomes (phagolysosome)
Lysosome releases lysozyme to break down microbial wall and other digestive enzymes that degrade carbs proteins fats and nucleic acids

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30
Q

Oxidative burst

A

Par of digestion, phagocye forms O2- (superoxide anion) hypochlorite (OCl-) and hydrogen peroxide h2o2 in process called oxidative burst

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31
Q

Killing phase

A

Everything is degraded, if it can’t be it remains as residual bodies

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32
Q

4 + 1 inflammation

A 
Pain
Heat
Redness
Swelling
\+1 LOF
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33
Q

3 main stages of inflammation

A

Vasodilation and increased perm
Emigration of phagocytes from flood to ICF
Tissue repair

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34
Q

Histamine

A

Released by mast cells in CT, basophils, and platelets and also neutrophils and macrophages
Causes vasodilation and increased cap perm

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35
Q

Kinins

A

Polypeptides, from inactive precursor kininogens
Cause vasodilation, increased cap perm but also chemotactic properties.
E.G bradykinin

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36
Q

Prostaglandins

A

Released by damaged cells and intensify effect of histamine and kinin.
Stimulate emigration of phagocytes
Intensify and prolong pain caused by kinins

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37
Q

Leukotrienes

A

Produced by basophils and mast cells.

Cause increase perm, chemotactic properties for phagocytes

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38
Q

Complement

A

Different components of complement system release histamine, attract neutrophils, promote phagocytosis. Some can also destroy bacteria

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39
Q

Causes of pain in inflammation

A

Injury to neurons
Release of toxins from microbes
Kinins cause it
Prostaglandin gets the party wild and keeps the party going

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40
Q

Increased perm for clotting

A

Allows clotting factors through.
Fibrinogen ultimately converted to an insoluble, thick mesh of fibrin that localizes and traps invading microbes and blocks spread

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41
Q

Exudate

A

Fibrin, dead phagocytes, dead tissue, and serum

42
Q

Fever definition

A

Abnormally high temp that occurs from hypothalamus being reset.
Triggered by cytokines like interleukin-1 released from macrophages
Intensifies interferons, inhibits microbe growth, speeds up reactions that aid repair

43
Q

Adaptive immunity

A

Ability to defend self against specific invaders
Different than innate in:
Specificity for particular foreign molecules
Memory for most previously encountered antigens so that a second response is more rapid and vigorous

44
Q

Antigens

A

In adaptive immunity
Antigen means antibody generator
They are recognized as foreign and provoke immune responses

45
Q

B and T cells

A

Lymphocytes
Developed in red bone marrow and thymus from pluripotent stem cells that originate in red bone marrow
B cells mature in marrow
T cells come as pre-T and matured in thymus

46
Q

Immunocompetence

A

The mark of a mature T or B cell
They have distinct proteins inserted into their plasma membranes, some are antigen receptors (for recognizing specific antigen)

47
Q

Two types of adaptive immunity

A

Cell-mediated and antibody-mediated. Both triggered by antigens. Helper T’s help both

48
Q

Cell-mediated adaptive immunity

A

Cytotoxic T cells directly attack invading antigens

Called humoral since it happens in fluids

49
Q

Antibody mediated adaptive immunity

A

B cells turn into plasma cells which make antibodies (immunoglobulins)

50
Q

Cell mediated best against

A

Pathogens (virus, bact, fungi) (and also what antibody mediated attacks)
Cancer cells
Foreign tissue transplants
*Always involves cells attacking cells

51
Q

Clonal selection

A

Lymphocyte proliferates and differentiates in response to specific antigen.
Figures out how to fight invader, gets cloned many times (the huge number is what causes swelling of lymph)
Gives rise to effector and memory cells

52
Q

Effector cells

A

Clones of a lymphocyte that destroy antigens

Include helper T, active cytotoxic T, plasma cells

53
Q

Memory cells

A

Don’t actively participate, but if the same antigen is later noted clones more effector and memory cells
Same as effector, helper t, cytoxic t, plasma cells

54
Q

Antigens two important characteristics

A

Immunogenicity (ability to provoke immune response)

Reactivity (ability of antigen to react specifically with the antibodies or cells provoked.

55
Q

Immunologist definition

A

Antigens are substances with reactivity

Complete antigens have immunogenecity AND reactivity

56
Q

Small part of antigen responsible for triggering response

A

Epitopes or antigenic determinants

Most antigens have many, each induces production of a specific antibody or activates a specific T cell

57
Q

Chemical nature of antigens

A

Large, complex, usually proteins, but can be nucleic acids, lipo,glyco proteins and polysaccharides.
Large molecules with simply, repeating subunits(cellulose and most plastic)
Can use plastic in heart valves or joints

58
Q

Hapten

A

Reactivity but not immunogenicity.
Can only stimulate immune response if attached to larger carrier molecule
E.g poison ivy and penicillin

59
Q

Diversity of antigen receptors

A

Takes 35,000 genes and rearranges them (usually into 5-7 amino acids), can recognize a billion epiptopes doing this
Can also recognize epitopes not found in nature

60
Q

Major histocompatibilty complex (MHC)

A

Transmembrane glycoproteins also called human leukocyte antigens (HLA)
Class 1 in all but RBCs and on body cell wall
Class 2 on antigen presenting cells only on surface

61
Q

Urushiol

A

Substance on poison ivy, oxidized to quinone which is a hapten

62
Q

Hapten drugs

A

Hydralazine (antihypertensive), causes lupus

Halothane (anaesthetic gas) - life threatening hepatitis

63
Q

Antigen processing

A

Antigenic proteins broken down into peptide fragments, bind with MHC to tag for destruction
Exogenous and endogenous processing

64
Q

Exogenous processing

A

APC cells recognize exogenous intruders (dendritic cells, macrophages, B cells)
APC eats antigen, breaks it down, mixes with MHC-II, presents antigen to T cells in lymh tissue saying go kill this fucker

65
Q

Endogenous processing

A

Happens in a different order and with MHC-I but pretty similar to exogenous processing
For when virus make the cell shit bad stuff out, cancer, or toxins from bacteria

66
Q

B and T location

A

T cells leave lymph to look for baddies

B cells stay put in lymph, spleen, mucosa associated lymph

67
Q

Types of T cells in adaptive immunity

A

Helper T
Memory T
Cytotoxic T
Memory Cytotoxic T

68
Q

Types of B cells in adaptive immunity

A

B cell
Plasma Cell
Memory B
APCs and T cells are also adaptive immunity

69
Q

Characteristics of mature T and B cells

A

Immunocompetence (can recognize and respond to foreign antigens)
Immunotolerance (doesn’t kill you)

70
Q

Helper Ts

A

APC brings antigen and MHC-II to inactive helper T

71
Q

Cytoxic Ts

A

Infected body cell brings MHC-1 to inactivated cytotoxic T cell

72
Q

Cell-mediated

A

Pathogens, some cancer, tissue transplants (CD4 helper Ts telling CD8 cytotoxic to muck shit up

73
Q

Anti-body mediated

A

Extracellular pathogens (B cells to plasma cells)

74
Q

CD 4 T cells

A

Helper Ts
Remain inactive until exogenous antigen fragments associated with MHC-II and CD4 stimulate to activate T
Makes active and memory T s

75
Q

Active helper Ts

A

Produce cytokines
E.g interleukin-2 which is needed for all immune responses and prime trigger of T cell proliferation
IL-2 can be sostimulator for helper Ts or cytoxic Ts and NK cells
This is positive feedback

76
Q

Memory Ts

A

Chill out until next attack where they rapidly proliferate into helper and memory Ts

77
Q

Cytoxic T cells

A

CD8
Recognize those compatible with MHC-I
Attacks foreigners plus tumors and transplants
Activated by cytokines released from active helper Ts like IL-2

78
Q

Cytotoxic T cells killing mechanism

A

Like NK cells, but they are targeted
Bind then release granzymes which are protein digesting that trigger apoptosis
Or bind an release perforin which creates channels for ECF
Or granulysin which enters through channels and creates holes in plasma membrane
Or lymphotoxin which activates enzymes in target cell which fragment DNA
Also cyto t’s release gamma-interferone to attract phagocytes and macrophage inhibiting factor to keep phagocytes there.

79
Q

Immunological surveillance

A

If a cell produces a tumor antigen it can be destroyed by cytotoxic Ts, NK, and macrophages
Usually to kill cancer from cancer causing viruses
Immunosuppresive drugs from transplants make you ONLY more prone to virus cancers

80
Q

Cell mediated vs humoral

A

Cell mediated is Ts humoral Bs

81
Q

Activation and clonal selection of B cells

A

Can respond to unprocessed antigen but much better if its processed
Antigen taken into B cell, bind with MHC-II self antigen and moved to cell membrane where T cells produce interleukin-2 and other cytokines that function as a costimulator to activate B cells
Turn into plasma cells or memory cells

82
Q

Plasma cells

A

A few days after exposure secrete hundreds of millions of antibodies till death 4-5 days later.
IL-4 and 6 (from helper Ts) helps proliferation, differentiation and secretion of antibodies from plasma cells
Each one recognizes only one antigen

83
Q

Antibody

A

Secreted by plasma cells. Work lock and key like.

Glycoproteins called immunoglobulins, usually 4 polypeptide chains

84
Q

Anti body polypeptide chains

A

Two heavy are identical to each other as are the two light chains
Disulfide bond holds each light chain to a heavy chain, and heavy chains together
Tips of H and L produce variable region where antigens bind
Remainder is called constant which differs between golf a m d and e and is a complement binding site and membrane binding site
IgM indicates recent invasion

85
Q

IgG

A

80-85%, longest lasting
Blood, lymph, intestines
Bacteria and viruses by enhancing phagocytosis, neutralizing toxins, and triggering complement system
CAN cross placenta

86
Q

IgM

A

5-10%, the biggest, found in saliva, reason for RBC ABO incompatability
First on scene
Activates complement, causes agglutination, and lysis of microbes

87
Q

Agglunation

A

Process of an antigen mixing with its corresponding antibody

88
Q

IgA

A

Predominant in normal secretions - tears, saliva, mucous, milk, intestinal secretions,
Prevents bacteria and viral attachement and invasion via mucous membranes
REDUCED during stress!

89
Q

IgD

A

Detector
0.2%
Found on B cell surfaces and antigen receptor, it activatesB cells

90
Q

IgE

A

Allergic response
Attaches to mast cells and causes histamine release
For parasytic worms
Systemic leads to anaphylaxis

91
Q

Complement system

A

Involves a group of 30+ inactive proteins produced in the liver and activated by IgG and IgM
They cause phagocytosis, inflammation, cytolysis and prevent excessive damage to body tissues

92
Q

C3 being activated

A

1 Inactivated 3 splits into C3a and C3b
C3b coats microbe (opsonization) which promotes attachment of phagocyte
C3b also splits C5 where C5b binds to C6 and C7 which attach to membrane of microbe
C8 C9 join the others and form a cylinder shaped membrane attack complex which inserts into plasma membrane
MAC creates channels resulting in cytolysis (blow it up with water)
C3a and C5a bind to mast cell for histamine release
C5a has chemotactic properties

93
Q

How can C3 be activated

A

Classic - antibodies binding to antigens activates C1 which activates C3
Alternative - Lipid-carb molecules on surface of microbes and complement proteins B D and P interact to activate C3
Lectin - Macrophages digest microbes and produce chemicals telling liver to make lectin which binds to carbs on surfaces and activates C3

94
Q

C3 inactivation

A

C3 is quickly broken down by proteins in blood and body cells to limit damage

95
Q

Immunological memory

A

First time IgM quickly peaks, then a bit later IgG.

Second exposure IgG skyrockets rapidly (secondary response)

96
Q

Self tolerance and recognition

A

T cells need to recognize MHC and (recognition)

lack reactivity from peptide fragments of own proteins (tolerance)

97
Q

Positive selection

A

Some Pre T cells express TCRs that interact with self MHC on epithelial cells in thymic cortex, if not they undergo apoptosis

98
Q

Negative selection

A

T cells interact with dendritic cells in thalamus, T cells survive if they do not respond to self antigens.
Negative selection occurs with deletion and anergy

99
Q

Deletion

A

Self-reactive T cells undergo apoptosis and die

100
Q

Anergy

A

Self reactive t cells survive but are unresponsive

only 1-5% percent survive this and deletion

101
Q

B cell tolerance

A

through deletion and anergy as well. Usually a b cell released that binds with a self-protein lacks a cofactor and undergoes anergy

A & P medic school (7 decks)

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