Chapters 4 And 5 In Health Problems (Midterm)

Front 1

Inflammation:

Back 1

a non specific response to any agent that causes cell injury

Front 2

What are agents of inflammation?

Back 2

- Physical: heat or cold
- chemical: (concentrated acid)
- Microbiologic (bacterium or virus)

Front 3

What are the local effects of inflammation?

Back 3

Local:
-Capillaries dilate to increase blood flow, so that
the leukocytes can reach the site before it gets worse.
When you see the warm and redness at the site.
-Capillary becomes more permeable so that the needed
fluid can move quicker from the blood cell to the site.
-Attraction of the leukocytes: must be signaled by the body,
do not go to the site automatically. You dont want all heading
want specific types.

Front 4

What are the hallmark signs of inflammation?

Back 4

redness, swelling, pain, tenderness, heat

Front 5

What are the systemic effects of inflammation?

Back 5

fever
leukocytes

Front 6

Blisters:

Back 6

accumulation of fluid.

Front 7

Acute inflammatory process:

Back 7

1. Polymorphonuclear leukocytes cells (killer cells, first there)
2. mononuclear cells come (second to site) ex: macrophage: clean up debris

- somtimes the body does not send the right leukoctyes
this leads to the severe inflammatory process (esp if in
blood stream) signs: fever, really sick

Front 8

Severe inflammatory process:

Back 8

-systemic effects become evident
- person gets ill, temp elevated
- bone marrow accelerates its production of leucocytes, number in bloodstream increases.
- liver produces: acute phase proteins, (C reactive protein) protects body from effects of inflammation

Front 9

Mild Inflammatory process:

Back 9

self limiting and subsides quickly

Front 10

What does the outcome of inflammation depend on?

Back 10

Amount of tissue damage

Front 11

What is the outcome of severe inflammatory process?

Back 11

Tissue damage
then replacement of damage cells
then Heal with scarring

Front 12

What is the outcome of mild inflammatory process?

Back 12

Self limiting
Subsides with tissue resolution

Front 13

What are the outcomes of inflammation?

Back 13

1. Resolution
2. Repair
3. Ares of destruction replaced by scar tissue
4. Mediators intensify inflammatory process
5. Mediators generate more mediators.

Front 14

Exudate:

Back 14

Fluid mixture of protein, leukocytes, and tissue debris
- proportions vary

Front 15

Serous exudate:

Back 15

primarily fluid

Front 16

Purulent exudate:

Back 16

largely inflammatory cells (pus)

Front 17

Fibrinous Exudate:

Back 17

rich in fibrinogen; coagulates and forms fibrin; produces stickly film on surface of inflamed tissue

Front 18

Adhesions:

Back 18

Bands of fibrous tissue that bind adjacent tissue together
- longtime inflammation

Front 19

Hemorrhagic exudate:

Back 19

increased RBCs

Front 20

Chemical mediators of Inflammation:

Back 20

chemicals that the body secreats to help
with the inflammatory process.

Front 21

What are examples of cell derived mediators?

Back 21

- mast cells
- histamine and serotonin
- prostaglandins
- leukotrienes

Front 22

What are examples mediators from blood plasma?

Back 22

bradykinin
complement

Front 23

Once the inflammatory reaction becomes specific what is it called?

Back 23

infection

Front 24

Infection:

Back 24

inflammatory process causes by disease- producing organisms

Front 25

cellulitis:

Back 25

infection in any place

Front 26

Abscess:

Back 26

cell breakdown that leads to production of pus

Front 27

Septicemia:

Back 27

overwhelming infection that gets in the blood stream

Front 28

Pathogenic:

Back 28

the ability of an organism to cause disease

Front 29

Virulence:

Back 29

more severe

Front 30

Host

Back 30

person invaded by an organism

Front 31

What factors influence an infection?

Back 31

the relationship between invading organism and defenses of the body

Front 32

What factors influencing the outcome of an infection?

Back 32

1. Virulence of organism:: ability of organism to do damage (MRSA) vs (VRA)
2. Numbers of invading organisms: : if the body is overwhelmed, this can cause a tip towards the antigen, then you get sick
3. Host resistance: : if immunosuppressant (HIV)

Front 33

Chronic Infection:

Back 33

- state in which the pathogenic organism and the host are evenly matched.
- relatively quiet, smoldering inflammation associated with repeated attempts of the body at healing
Predominant cells: Lymphocytes, plasma, cells, monocytes

Front 34

What are the two separate mechanisms that function together to protect

Back 34

Inflammatory reaction
Acquired immunity

Front 35

Acquired Immunity:

Back 35

: the body learns from a previous attack and becomes immune in the future
-:specific learned immunity to an antigen
-the next time the body knows how to
fight the antigen
-- the body picks up on identifiers

Front 36

What are the two types of acquired immunity?

Back 36

Humoral Immunity
Cell-mediated immunity

Front 37

Humoral:

Back 37

Deals with production of antibodies. Antibodies have
been produced.

Front 38

Cell- mediated:

Back 38

formation of lymphocytes. That attack foriegn
material. This is how body detects organ transplants.

Front 39

Hypersensitivity:

Back 39

- someone who displays hypersensitivity usually processes some degree of immunity as well.
-

Front 40

Autoantibodies:

Back 40

- in autoimmune disease a patient forms antibodies against his or her own cells and tissues.
- these antibodies may injure or destroy the patients cells or tissue components

Front 41

cytokines:

Back 41

: general term for chemical messengers involved in response

Front 42

Lymphokines:

Back 42

: chemical messenger that is used to communicate between different cells in the immune system

Front 43

monokines:

Back 43

A monokine is a type of cytokine produced primarily by monocytes and macrophages.
Examples include interleukin 1 and tumor necrosis factor-alpha.

Front 44

Interferon

Back 44

: Interfers with the multiplication of viruses in the cell

Front 45

Interleukin:

Back 45

destroys bacterial cells

Front 46

tumor necrosis factor

Back 46

The primary role of TNF is in the regulation of immune cells. TNF is able to induce apoptotic cell death, to induce inflammation, and to inhibit tumorigenesis and viral replication.

Front 47

Where are precursor cells formed? and into which two groups?

Back 47

from stem cells in the bone marrow.
T lymphocytes
B lymphocytes

Front 48

T lymphocyte

Back 48

- thymus- dependent: precursor cells that migrated from the marrow to the thymus

Front 49

B lymphocyte

Back 49

bone marrow: precursor cells that remained within the bone marrow.

Front 50

Natural Killer Cells:

Back 50

can destroy target cells as soon as they are encountered

Front 51

Describe the lymphatic system development and amounts of types of cells.

Back 51

- before birth, precursor T and B lymphocytes migrate to the spleen, lymph nodes, and other sites and from masses of mature lymphocytes that will populate the various lymphoid organs.
- varying life spans
- lymphocytes to not remain localized but circulate between blood and lymphoid tissues.
T- lymphs = 2/ 3 of circulating lymphs
B- rest
- NK= 10 to 15%, major targets virus infected cells and cancer cells. (have no T or B targets)

Front 52

How do the lymphocytes recognize specific antigens?

Back 52

each programmed lymphocyte develops receptors on its cell membranes.

Front 53

What is the response process of lymphocytes to foreign antigens?

Back 53

-1st: recognition of the foreign antigen
-2nd: Poliferation of lymphocytes that have been programmed to
respond to the antigen. (What happened last time?) Overprodu
ction of a certian type of lymphocytes
-3rd: fight antigen and defeat (best case

Front 54

When appropriately stimulated B lymphocytes?

Back 54

proliferate and mature into antibody forming plasma cells

Front 55

When appropriately stimulated T lymphocytes?

Back 55

proliferate to form a diverse population of cells that regulate the immune response and generate a cell-mediated immune reaction to eliminate the antigen

Front 56

Explain the interaction of cell- mediated and humoral immunity.

Back 56

- initial contact with foreign antigen followed by week lag phase
- Once the body has reacted, some lymphoid cells retain memory
- memory passed on
- contact with same antigen again will provoke a faster, stronger response. of the sensitized lymphocytes or antibody forming plasma cells.

Front 57

Regulator T cells:

Back 57

helper t cells that regulate the immune system by establishing a balance between promoting and inhibiting the immune response
-maintain homeostasis

Front 58

Effecter T cells:

Back 58

Involved in delayed hypersensitivity reactions

Front 59

What do immune response genes do?

Back 59

- closely related to the HLZ complex on chromosome 6
- control the immune response by regulating T and B cell proliferation
- Influence resistance to infection and tumors
- Influence likelihood of acquiring an autoimmune disease

Front 60

IgG

Back 60

Principle antibodies
Crosses placenta protect newborn

Front 61

IgM:

Back 61

Pentamer
Fights fungus
Early immune response

Front 62

IgE:

Back 62

allergic reactions

Front 63

IgA:

Back 63

GI and respiratory tract
found in secretions saliva, tears, milk, mucous
dimer

Front 64

Antibodies:

Back 64

globulins produced by plasma cells
- can react only with specific antigen that induced its formation

Front 65

What are the three types of antibody mediated hypersensitivity reactions?

Back 65

Humurol
Type 1: anaphylactic
Type 2: cytoxic
Cell Mediated
Type 3: immune complex

Front 66

Type I: anaphylactic

Back 66

Immediate
- sensitizing antigen circulates throughout the body. Triggers widespread mediator release from Ig coated mast cells and basophils
- may lead to anaphylaxis: severe generalized IgE mediated reaction (fall in blood pressure, severe respiratory distress
- Need prompt epinephrine. or other agents

Front 67

Why do antihistamines work to relieve many allergic symptoms?

Back 67

Because histamine is one of the mediators released from IgE coated cells.

Front 68

What happens when there is again contact with the same antigen that triggered anaphylaxis?

Back 68

it will trigger a release of mediators (histamine) and related clinical manifestations.
Localized: hay fever, food allergy S
Systemic: bee sting, penicillin

Front 69

Atopic person:

Back 69

allergy-prone individual

Front 70

What are the three types of antibody mediated hypersensitivity reactions?

Back 70

Humurol
Type 1: anaphylactic
Type 2: cytoxic
Cell Mediated
Type 3: immune complex

Front 71

Type I: anaphylactic

Back 71

Immediate
- sensitizing antigen circulates throughout the body. Triggers widespread mediator release from Ig coated mast cells and basophils
- may lead to anaphylaxis: severe generalized IgE mediated reaction (fall in blood pressure, severe respiratory distress
- Need prompt epinephrine. or other agents

Front 72

Why do antihistamines work to relieve many allergic symptoms?

Back 72

Because histamine is one of the mediators released from IgE coated cells.

Front 73

What happens when there is again contact with the same antigen that triggered anaphylaxis?

Back 73

it will trigger a release of mediators (histamine) and related clinical manifestations.
Localized: hay fever, food allergy S
Systemic: bee sting, penicillin

Front 74

Atopic person:

Back 74

allergy-prone individual

Front 75

Allergen

Back 75

sensitizing antigen

Front 76

Type II: Cytotoxic

Back 76

- antibody combines to cell or tissue antigen resulting in complement- mediated lysis of cells or membrane damage
Ex: Autoimmune hemolytic disease, blood transfusions....

Front 77

Type III: Immune complex

Back 77

- Ag Ab immune complexes deposited in tissues activate complements; poly-morhponuclears attracted to sites, causes tissue damage
Ex: rheumatoid arthritis, SLE

Front 78

Type IV: Delayed hypersensitivity or cell mediated hypersensitivity

Back 78

- T Lymphocytes are sensitized and activated on second contact
- Lymphokines induce inflammation and activate macrophages
- Tuberculosis , fungal and parasitic infections

Front 79

Why suppress the immune system?

Back 79

- Prevent undesirable effects
- when directed against self ( autoimmune)
-organ rejection
-Rh hemolytic disease in newborns

Front 80

What are the main immunosuppressive agents?

Back 80

-Radiation
- Immunosuppressive drugs that impede cell division or cell function
- adrenal corticosteroid hormones: suppress inflammatory reaction, impair phagocytes, inhibit protein synthesis
- Gamma globulin preparations contain potent antibodies, that prevent the body from responding to the antigen

Front 81

What is the pathogenesis of autoimmune disease?

Back 81

1. Alteration of patients own self causing them to become antigenic. Immune reaction
2. formation of cross reacting antibodies against foreign antigens that also attack patients own antigens
3. Defection regulation by the immune response regulator T Lymphocyte.

Front 82

How do you treat autoimmune disease?

Back 82

Corticosteroids, cytotoxic drugs

Front 83

What are examples of autoimmune diseases?

Back 83

Systemic lupus erthematosus
( various organs)
Rheumatic fever
(joint and heart inflammation)
Glomerulonephritis
( inflammation in renal glomeruli)
- Blood: anemia, leukopenia, thrombocytopenia
Thyroiditis ( hyper and hypo thyroidism)