Patho Test Two Part 1

Front 1

cardiogenic shock

Back 1

results from heart failure
-follows myorcard. infarc., or surgery req. bypass
-CM= impaired mentation, edema, low card. output, dusky skin. low bp,

Front 2

hypovolemic shock

Back 2

burn victims
-loss of blood, plasma, or int. fluid
-begins when ICF vol. has decrease by 15%
-CM=poor skin turgor, thirst, oligneuria, rapid heart rate.

Front 3

nerugenic shock

Back 3

massive vasodialation that results from an imbalance between parasymp. and symp. stimulation of vascular smooth muscle.
-extreme vasodialation
-causes-trauma to spinal cord or meduulaa, dep. drugs, anest., sever stress or pain
-CM=low bp, bradycard., fainting

Front 4

anaphylactic shock

Back 4

sever shock, allergies
-similar to neruo shock: vasodia., peripheral pooling, decreased tissue perfusion and impaired celluar met.
-smoothc musc. contrict and cause resp. diff.,
-first signs: anxiety, breath diff., hives, burning.
-treatment: epinephrine administerd to cause vasoconst., antishist and steroids given to stop inflamation

Front 5

septic shock

Back 5

-full body is septic
most often cause by gram neg. bacteria
-CM= low bp, hypoxia, tachycardia, renal dysfun, jaundice, clot problems, and tachynpea
-treatment= mul. drug antimic. therapy, fluid resucitation and vasoactive medications.

Front 6

Immune system protects body from__?

Back 6

-internal threats (cancer or autoimm.)
-maintains the internal env. by removing dead or damaged cells
-protects us from challenges by antigens (anything foreign ((like w/ transplant))

Front 7

Natural Immunity

Back 7

-INNATE
-present at birth
-naturally resistant to (cowpox or canine distemper)

Front 8

Acguired Immunity

Back 8

-ADAPTIVE
- can be active or passive

Front 9

Active Immunity

Back 9

-produced by the host after exposure to an antigen or immunization
-long acting

Front 10

Passive immunity

Back 10

-does not involve the host's immune response - antibodies or t cells are transferred to the patient
-short acting

Front 11

two types of active imm?

Back 11

natural and artificial

Front 12

Acguired Natural active immunity

Back 12

-contact with antigen thru clinical infection
-chicken pox, measles, or mumps)

Front 13

Acquired active artificial immunity

Back 13

-immunization with live or killed vaccines

Front 14

types of acquired imm?

Back 14

active and passive

Front 15

acquired passive natural imm?

Back 15

-transplancental and or breast milk tranfer from mother to child

Front 16

acquired passive artifical imm?

Back 16

injection of serum from immune human
-injection of human gamma globulin, rabies, tetanus, snake bite)

Front 17

lines of defense

Back 17

1. inate: physical , mech, biochemical barriers
2. inflammatory
3. acguired

Front 18

2 types of immunity

Back 18

humoral and cell mediated

Front 19

Humoral

Back 19

-Cells= B lymphocytes
-products= antibodies
- have memory cells (remeber anitgen after contact)
-protection= bacteria, viruses (extracellular) respitory, GI pathogens
-matures in bone marrow
--produce and secret antibodies which bind to antigens

Front 20

cell mediated

Back 20

-cells- T lympoctues, macrophages
- products- sensitised T cells, lymphokines
-memory cells present
-protection- funguses, viruses (intracellular, chronic infectious agents, tumor cells
--attack the antigen directly

Front 21

Antigen

Back 21

substance that elicits an immune response; recognized by the body as self/ nonself.
-The presence of antigen starts imm. response.
-ex= infectious- viruses, bacteria, funig
ex= noninfectious- pollens, foods, bee venom, drugs, transfuions, transplants

Front 22

Histocompatability antigens

Back 22

HLA complex0 the more similar two people HLA makeup are the better sucess of transplants
-HLA antigens- distinguish self from non self

Front 23

Blood group antigens

Back 23

-provoke the strongest humoral immune response.
-ABO blood type consists of two types of antigens a and b

Front 24

A blood group

Back 24

- A antigen
-anti B antibodies

Front 25

B blood group

Back 25

-B antigen
-anti A antibodies

Front 26

AB blood group

Back 26

-AB antigen
-no antibodies

Front 27

O blood group

Back 27

-no antigen
-AB antibodies

Front 28

IF A gets B blood good immune response T/F?

Back 28

false it would be bad

Front 29

RH system

Back 29

-is important in maternal/ fetal hemolytic disease.
-if the antigen is present they are RH pos
-85 pos and 15% neg.
-further in ch. 21

Front 30

anatomical barriers

Back 30

-physical barrier
-skin, mucous mem.,

Front 31

Biochemical barriers

Back 31

-sebaceous glands antibacterial and antifungal acids (ph 3-5) and helps to kill bacteri
-sweat, tears, and saliva
-normal flora

Front 32

if normal flora is killed by antibioticss we are more prone to get

Back 32

a secondary problem

Front 33

mechanical clearnace

Back 33

gets ride of foreign body by:
-skin sloughing, coughing, urinating

Front 34

normal flora

Back 34

the body has natural bacteria that prevents the growth of some invading bacteria (gut, vagina, and urinary tract)

Front 35

the inflammatory response is the __?

Back 35

2nd line of defense

Front 36

inflammatory response

Back 36

begins w/ in seconds of invasion
-promotes healing by surrounding afftected tissues w/ cells and fluid that isolate, destory and remove invaders

Front 37

Immune response

Back 37

3rd line
-slower than inflamm
-specific- acts on specific organisms
-can be induced by vaccine
- lymphocytes and anitbodies work to allow the body to adapt and respond to an insult.

Front 38

__ is the primary cell of the immune response?

Back 38

lymphocyte

Front 39

central lymphoid organs

Back 39

thymus gland and bone marrow

Front 40

peripheral lymhoid organs

Back 40

tonsils, gut, genital, skin, lymph nodes, and spleen

Front 41

memory cells

Back 41

-capable of remembering the antigen and acting faster if it invades the host again
-this creates what we call immunity

Front 42

modulators can __ or __ the imm. system

Back 42

amplify or suppress

Front 43

exogenous modulators

Back 43

trauma disease pollutants

Front 44

endogenous modulators

Back 44

age gender nutrition

Front 45

mature b cells are called

Back 45

plasma cells, they have encoutered antigen and developed specifictiy for that antigen

Front 46

Primary and secondary immune response

Back 46

Primary- (IGM) 4-8 days after exposure
Secondary- (IGG) occurs after 1-3 days after exposure, memory cells account for a more rapid production of anitbodies.q

Front 47

Immunoglobulins

Back 47

antibodies or immunoglobulins are serum glycoproteins produced by plasma cells in response to an antigen challenge.

Front 48

IGG

Back 48

crosses the placenta, resp. for secondary immune response (80-85%)

Front 49

IGA

Back 49

tears, saliva, and breast milk

Front 50

IGM

Back 50

responsible for primary imm. response
-forms antibodies to ABO blood antigens
-largest and first responder

Front 51

IGE

Back 51

causes symptoms of allergic reaction

Front 52

IGD

Back 52

information is limited
-function NK

Front 53

IGG crosses the placental membrane and provides newborns with __ for at least __?

Back 53

passive acquired imm.
3 months

Front 54

function of antibodies

Back 54

neutralize bacterial toxins
neutralize viruses
opsonize bacteria
activate components of the inflamm. response

Front 55

opsonin

Back 55

a substance that renders bacteria susceptible to phagocytosis

Front 56

direct effect on antigens

Back 56

-agglutination- clumping together insoluble antigens
-precipation- falling out of solution
-neutralization- inactivating

Front 57

indirect effect on antigens

Back 57

- enhancment of phagocytosis
- activation of plasma proteins that are capable of destroying the antigen

Front 58

molecular structure of anitbody

Back 58

4 chains 2 lite 2 heavy

Front 59

antigen-antibody binding

Back 59

-specificity is required for anitgen-antibody binding
-determine shape of the combining site
-the antigen fits into a binding site like lock and key

Front 60

secretory immune system

Back 60

antibodies present in tears, sweat, saliva, mucous, breast milk (IGA primary antibody

Front 61

cell mediated immunity

Back 61

initiated thorugh specific antigen recognition by t cells

Front 62

T cytoxic cells

Back 62

attack antigens directly and destroy foreign cells

Front 63

T Helper __ and T supressor __?

Back 63

CD4 and CD 8

Front 64

natural killer cells

Back 64

-NK cells
-large lymphocytes
-recognize and kill viruses, malignant cells, and trans. tissues.

Front 65

cytokines

Back 65

-messengers of the imm. response
-"horomones of the imm. response"
- comm. among macrophages and various subsets of lymphocytes

Front 66

Interleukin

Back 66

-(1-10)
- Augments the imm. system in many ways.
--promotes maturation of b cells
--acts as inflamm. mediator
--activates t cells and macrophages
--enhances activity of NK cells

Front 67

interferon

Back 67

inhibits viral replication

Front 68

there is a decline in the imm. sys. w/ advancing age

Back 68

higher incidence of tumors
increased levels of antobodies against self antigens
age decreases size of thymus, by age 50 15 % decrease

Front 69

Imm. system differs from inflammation by:

Back 69

antigen specific
has memory
takes days to develop
long term

Front 70

Imflammaiton differs from Imm. sys by:

Back 70

non specific
no memory
begins immediately
short term 8-10 days

Front 71

Purpose of the inflamm response

Back 71

To increase the movments of plasma and blood cells from the circulation into the tissues surronding a site of injury
-mechanism of inflamm. basically same regardless of injuring agent

Front 72

inflammatory response functions

Back 72

establishes an env. suitable for healing and repair
1. blood vessels dialate, increaseing blood flow to the are of injury
2. vascular permablility increases (blood flow out of capp. into tissues) which leaks plasma forming exudate (edema and swelling)
3. Leukocytes (WBCs) adhere to the inner walls of vessels and migrate to the injury site

Front 73

Phases of the infl. response

Back 73

1. destory injurous agents and remove them
2. confine these agents in order to limit the effect on the host
3. stimulate and enhance the imm. response
4. promote healing

Front 74

clinical manifestations of inf. resp.

Back 74

local response (opposite of syst.)
redness, pain, heat swelling, loss of function (bc of edema)

Front 75

causes of cell injury inthe inf. respo.

Back 75

temp extremes
radiation
trauma
allegens
infection
hypoxia

Front 76

mast cells cue the infalm respo.

Back 76

activate the infl. resp. by releasing biochem. mediators
cellular bags of granuales located in conn. tiss. close blood vessels. This causes vasodialation and incrase capp. permeablity.
--in allergic response too many mast cells are turned on

Front 77

histamine

Back 77

bio chem mediator
-vasoactive amine-temporary, rapid, constriction.

Front 78

netrophil chemotactic factor

Back 78

bio chem mediator
-attracts netrophils to the site which do the most work during early stages

Front 79

eosinophil chemotactic factor

Back 79

biochem mediator
-attracts eosinophils to site

Front 80

serotonin

Back 80

bio chem mediator
-relased by platlets
-vasoactive
-acts like histamine

Front 81

leukotrines

Back 81

biochem mediator
syn. by mast cells
-similar to histamine but slower acting and longer response (important in later stages in inf. resp.)

Front 82

prostaglandins

Back 82

bio chem med
syn. by mast cells
-increased vascular perm.
-induce pain
-aspirin-- blocks the synthesis of prostaglandins (inhibit infl. and pain)

Front 83

aspirin

Back 83

inhibits syns.s of prostaglandins which inhibit inf. and pain

Front 84

platlet activating factor

Back 84

bio chem med
syn by mast cells
-endotheial cells incrase vascular perm. causing leukocyte adhesion and platelts to be activated

Front 85

Histamine receptor H1

Back 85

-responsible for promoting inflammation
-present in smooth musc. cells (esp. bronchial)
-causes bronchoconstriction when stimulated

Front 86

histamine receptor H2

Back 86

responsible for inhibiting inflam.
-present in parietel cells of the stomach
-causes secretion of gastric acid when stimulated

Front 87

pepsin blocks __ keeping __ from happening?

Back 87

H2, stomach ulcers from forming

Front 88

plasma protein systems

Back 88

complement
clotting
kinin

Front 89

complement system

Back 89

most important plasma prot. sys
-major role in direct destruction of cells (bacteria)
-cascade begins w/ act. of proenzyme
-produes compounds that opsonize bacteria and induce mast cell degranulation
-its components participate in every infl. resp.

Front 90

clotting sys

Back 90

coagulation
-traps bacteria in injured tissue
-interacts w/ platelets to prevent hemorahging
- mesh is formed from fibrin
--clotting casade-- intrsinsic and extrinsic converge at factor X (ten)

Front 91

kinin system

Back 91

-helps control vascular permeability
-primary kinin
-brady kinin
-causes vasodialation
- causes smooth mus. contraction
-incrases chemotaxis

Front 92

cytokines

Back 92

affect neihbor cells and help them talk to one another

Front 93

interleukins

Back 93

cytokine
-send messages from one leukocyte to another to enhance inflamm.
-produced in response to antigen stimulation or by products of inflammation

Front 94

lymphokines

Back 94

biochemical mediators produced by T cells

Front 95

interferon

Back 95

-prevents viruses from infecting healthy cells
-has no effect on cells already infected

Front 96

inflammatory response can be divided into 2 things

Back 96

vascular response and cellular response

Front 97

vascular response

Back 97

-after cell injury, arterioles in the area briefly undergo vasoconstriction
-after release of histamine and other chemicals by the injured cells, vessels dialate (vasodialation)

Front 98

vasodialation

Back 98

-endothelial cell reaction
-incrased cap. perm.
-movemtn of fluid from capp. into tiss. spaces

Front 99

hyperemia

Back 99

high supply of blood

Front 100

cellular response level

Back 100

chemotaxis- pulls the leukocytes
-directional migration of WBCs along contraction gradient of chemotactic factors
-mechanism for accumulating neutrophils and monocytes at site of injury

Front 101

two classes of leukocytes

Back 101

-granuloctyes- neutrophils, eosinophils, and basophils
-monocytes/macrophages- monocytes (immature form in the blood), macrophages (mature cells in the tissues)

Front 102

netrophils

Back 102

-1st leukocyte to arrive (6-12 hrs.)
-phag. bacteria, foreign materials, and damaged cells
-short life span
-die and removed as pus

Front 103

monocytes

Back 103

-2nd type of phag. cell
-attracted to the site by chem. factors
-arrive w/ in 3-7 days after onset of inf.
-largest blood cells
-when they enter tissue they become macrophages

Front 104

macrophage

Back 104

-important in cleaning area before healing
-long life span
-multiply
-may stay in dam. tiss. for weeks
-gradually take over place of neutralization

Front 105

eosinophils

Back 105

-released in large quantities during an allergic reaction (IGE)
-release chemicals that act to control the effects of histamine and serotonin
-phagocytosis of allergen antibody complex
-acts dirctly against parasites by dissolving membrane

Front 106

basophils

Back 106

-function similar to mast cells, but found in blood instead of tissues
-carry histamine and heparin in their granules
-realease during infl.

Front 107

local manifestions of acute infl.

Back 107

-swelling- occurs as exudate accumulates
-pain- cause by pressure exerted by sweeling and the presence of mediators such as prstaglnadings and bradykinin
-heat and redness are the result of vasocilation and increased perfusion

Front 108

exudate

Back 108

-consist of fluid and leuk. that move from the circulation to the site of injury to fac. tissue repair and healing
-nature and quant. depend on the type and severity of the injury and the tissues involved

Front 109

3 functions of exudate

Back 109

1/ dilute toxins produced by bacteria and dying cells
2/ carry plasma proteins, including antibodies, and leukocytes to the site
3/ carry away toxins, dead cells and debris
-occurs via channels thorugh epi. (sinuses) or through lymph nodes (stimulating B and T cells)

Front 110

serous exudate

Back 110

-watery, indicates mild inflm. (fluid in blister

Front 111

fibrinous exudate

Back 111

thick and clotted, indicates more sever or advaced infl. (lungs in patient w/ pneumonia)

Front 112

purulent exudate

Back 112

consists of pus large # of leukocytes, indicates persistant bacterial infection (cyst or absess)

Front 113

hemorrghic exudate

Back 113

bloody exudate

Front 114

systemic response of leukocytosis

Back 114

-fever
-induced by IL -1 relased from neutrophils and macrophages
-endogenous pyrogen acts directly on the hypothalamus
-increase in circulating plasma proteins

Front 115

systemic response of anorexia

Back 115

-increased heart reate
-increase resp. rate
---major complication septicemia (whole body infection)
---causes CV problems and shock

Front 116

repair

Back 116

the replacement of desroyed tissue with scar tissue

Front 117

debridement

Back 117

the cleanup of a lesion (dissolution of fibrin clots by fibrinolytic enzymes). Begins w/ phagocytosis

Front 118

reconstructive phase

Back 118

granulation tissue, epithelization. Occurs withing 3 days to 2 weeks. Fibroblasts- synthesize and secrete collagen

Front 119

maturation phase-

Back 119

continued scar formation and remodeling

Front 120

diabetes dys wound healing

Back 120

-dys would heal
infection common w/ uncontrolled diabetes (lack of circ and warm sugary env. for bacteria to grow in.)

Front 121

hypoxemia dys wiould healing

Back 121

insuff. oxy, cant rebuild cells

Front 122

drugs dys wound healing

Back 122

anit inflm steroids

Front 123

hypovolemia dys. wound healing

Back 123

decreased blood volume

Front 124

nutriiton

Back 124

protein, iron, and calcium are essential for healing

Front 125

keloid/ hypertrophic scar

Back 125

reaised scar, too much collagen, found mostly in blacks

Front 126

elderly population wound healing

Back 126

-chronic illness
-immobility (Bed sores)
-age
-medications
-dec. imm. sys.

Front 127

Allergy

Back 127

immune response exaggerated against enviormental antigens

Front 128

autoimmunity

Back 128

immune response is misdirected against the host's cells own cells/ self vs. nonself

Front 129

alloimmunity

Back 129

immune response directed against beneficial foregin tissues such as transfusions or transplants

Front 130

immune defeciency

Back 130

immune response insuffiencient for protection due to a disesase or drugs such as chemo

Front 131

hypesensitivity

Back 131

pathologic immune response to an antigen after reexpossure
-immediate--minutes to few hours(anaphylactic)
-delayed--several hours or at reexposure (poison ivy)

Front 132

auto antibodies

Back 132

antibodies against self antigens

Front 133

Type I imm resp.

Back 133

anaphylactic

Front 134

Type II Imm. Resp.

Back 134

Cytoxic and Cytotylic (tissue specific)

Front 135

type III immm. resp.

Back 135

complex reaction

Front 136

type IV imm. resp.

Back 136

delayed hypersensitivity reactions (poison ivy)

Front 137

Allergy

Back 137

immune response exaggerated against enviormental antigens

Front 138

autoimmunity

Back 138

immune response is misdirected against the host's cells own cells/ self vs. nonself

Front 139

alloimmunity

Back 139

immune response directed against beneficial foregin tissues such as transfusions or transplants

Front 140

immune defeciency

Back 140

immune response insuffiencient for protection due to a disesase or drugs such as chemo

Front 141

hypesensitivity

Back 141

pathologic immune response to an antigen after reexpossure
-immediate--minutes to few hours(anaphylactic)
-delayed--several hours or at reexposure (poison ivy)

Front 142

auto antibodies

Back 142

antibodies against self antigens

Front 143

Type I imm resp.

Back 143

anaphylactic
-gastrointestinal--foods cuase vomit diarrhea
-urticarie/hives- localized release of histamine causes edem and rash
-conjuctivits or asthma
-atopic individuals- prone to allergies higher concentraitons of IgE

Front 144

Type II Imm. Resp.

Back 144

Cytoxic and Cytotylic (tissue specific)
-involevs binding of IgG or IgM antibodies
-Graves disease

Front 145

type III immm. resp.

Back 145

complex reaction
-local or systemic and immidealty or delayed (IgG or IgM)
-serum sickness, raynaud phenomenon, arthus reaction

Front 146

type IV imm. resp.

Back 146

delayed hypersensitivity reactions (poison ivy)
-cell mediated response

Front 147

Enocrine autoimmune disease

Back 147

thyroditis and graves

Front 148

hematologic autoimm. diesease

Back 148

hemolytic and pernicious anemicas

Front 149

nervous system autoimm. disease

Back 149

masthenia griavis

Front 150

musculoskeleta autoimm. diesease

Back 150

rheumatoid arthiritis

Front 151

Systemic Lupus Erythematosus

Back 151

most common auto imm. disorder
-system wide tissue damage
-goes in remission