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immune system function

identifies antigens/pathogens and destroys them.

host is recognized and spared

nonspecific immunity

( innate)

rapid response- limited microbed

stimulates and buys time for second line of defense (adaptive response to prepare)

specific immunity

( adaptive)

sepcific recognition, amplified response to invaders


involves b and t lymphocytes REMEMBERS AGENT

humoral and cell mediated


invaders which cause immune response

usually large molecules

macrophages breakdown through phagocytosis

binding sites ( epotopes/antigenic determinants) emerge on broken antigen units

the unique shape of the epitope recognizes by either receptors on immune cells or by antibodies


antigen presenting cell ( dendritic)


white blood cells


largest leukocyte

mature in tissues ( liver, lung, spleen)

become macrophages

activated wtih either inflammatory stimuli or antigens

involved in innate or adaptive response

experts at phagocytosis

capable of priming specific immunity


process and present antigen fragments to t cells for destruction


principle cells involved in adaptive ( specific) immunity

differentiate into t and b cells

constantly circulate but return to concentrate in lymphoid tissues ( lymph nodes, spleen, thymus)

cardinal features of immune cells

self recognition



self regulation


self recognition

keeps immune cells from destroying normal cells

healthy response against FOREING

major histocompatability complex


major histocompatability complex

unique set of proteins on cell surface that mark cells as " self"

this complex ( a protein) cradle antigens for presentation to t cells

human leukocyte antigen ( HLA)-= MHC controlled by chromosome 6

all play a role in immune function


refers to tissue compatability. determines whether organ transplant will be compatable

no two people have the same mhc except identical twins

mhc 1


proteins protect against viruses or cancers that are intracellular

the antigen is engulged by wbc ( macrophages) and broken down inside the cell...pieces present on cell surface conntected to mhc 1

this presentation allows immune system to look at and read whether " self" or " non self"

if judged foreign attracts cd8 t cells which KILL the antigen ( cell mediated)

mhc 2

proteins connect with antigens OUTSIDE the cell and present those to t lymphocytes

if read by immune system and judge foreign helper t cells multiply and stimulate b cells to produce antibodies
( specific to antigen, HUMORAL)


ability to exactly recognize invader

design and implement immune response targeted to that specific invader

not like inflammation ( where the response is the same equal for all antigens...inflamation is nonsepcific)

specific response for each pathogen


oncy lymphocytes stimulated by antigen they acquire memory
both t and b cells

remain in body a long time

allow for rapid response on repeated exposure to antigen

often so subtle we dont know its happening

self regulation

immune system carries out functions without direct input from other systems( brain doesnt need to say " hey start working"


ability to respond to different kinds of antigens daily


intercellular signalling molecules or chemical messangers of the immune system

keep immune system working together

very low molecular weight proteins

present in both immunitites

can persist all over

influence the actions of other cytokines- cascades

very short half life. protects against excessive immune response

released at cell to cell interfaces

signals sent to cytoplasm of cells- induced genes to respond

one cytokine often has the ability of acting on more than one cell type


administration of vaccine

active immunity

achieved by immunization or actually having disease- requires you to make antibodies

depends on a response to the antigen by the person's immune system

long lasting, once established

requires few days to weeks after first exposure to develop sufficient immune response to destroy pathogen

subsequent exposures reacts in hours to the same agent due to memory b and t cells and circulating antibodies

passive immunity

immunity transferred from another source, you dont need to produce your own antibodies they are given

maternal igG passes placenta and provides infant protection for first month of life

when an infant recieves immunity from antibodies through breast milk

only short term protection, weeks to months

can be artificially transferred if given antibodies produced from someone else ( immune serum globulin- pool of antibodies from many people)


antibody mediated


antibodies responsible for enhancing/ fostering antigen destruction

usually actiavated by bacteria bacterial toxins, free viruses, EXTRACELLULAR PATHOGENS

activate b lymph
two types of responses primary and secondary

primary immune response

first exposure to antigen

lagtime- before antibodies are detected in blood

allows for processing of antigen by apc( machrophages or dendritic)

allows for cd4 helper t cells to recognize antigen cradled on mhc2 protein on cell surface

helper t cells are activated and stimulate / direct the rest the immune system MASTER SWITCH

this triggers b cells to proliferate and differentiate into plasma cells

these plasma cells produce antibodies or memory cells

activation of this response takes 1-2 weeks detectable antibodies will continue to rise for several weeks

recovery from many infections occurs during primary response when antibodies have reached peak in blood

secondary immune response


secondary exposures

memory cells remain in body for a long time, ready for action

remember the invader and cause rapid reaction ( antibodies quick to area) on next exposure

antibodies rise sooner and reach a higher level due to memory cells

booster shot

plasma cells

formed by b cells

can secrete thousands of proteins called antibodies per second ( immunoglobulins)

these antibodies attach to foreign antigens

causing destruction of antigen by :
- clumping togehter
- lysis ( break down)
-facilitation phagocytosis
-activation of complement system


during an antibody mediated ( humoral) response

b lymph ( plasma cells) form antibodies to combat the antigen


first antibody type made by newborn


presence indicates in utero or newborn infection


found in saliva, tears, colostrum, bronchial, prostatic, vaginal, gi

pprotects against infection in mucosal tissue


found on b lymphocytes



only one that crosses the placenta from mother to infant

protects against bacteria, toxins and viruses


binds to mast cells and basophils


combats parasites

memory cells

created after initial exposure to an antigen, aquire memory

cell mediated immune response

invader living INTRACELLULARLY

invaders live inside body's cells ( antivodies cant penetrate the membrane)

both cd4 and cd8

antigens displayed on mhc1

cd8 induce apoptosis of infected cells-perforin secretion to punch holes in membrane

sensitized cd8 cells make clones that recognize other similarly infected cells and target those for destruction

activated t cells can also generate primary and secondary cell mediated immune responses ( humoral)

t cells also have memory

what is a complement

complements/enhances both innate adaptive defensives

a complex cascade of interdependent antimicrobial plasma proteins

circulated in blood in an inactivated form

when activated they can mark cells for destruction or promote inflammation

deposit protein fragment on pathogen ( tags) phagocytes then locate and destroy

immune system regulation

self regulation

when out of order
-inadequate response ( HIV)
-inappropriate response ( autoimmune)
- excessive response ( allergies)

innate immunity

( nonspecific)


protective in nature

eliminates cause of cell injury and necrotic cells

leads way for healing

physiological events similar regardless of cause location or extent of tissue injury

cardinal signs of inflamation

loss of function- functio laesa

systemic inflammation

generalized vasodilation due to infection

swelling, fever, bacterial count, high inflammatory cytokine levels

vascular stage

first stage of acute inflammation

begins with injury and results in momentary vaso constriction

followed immediately by vasodilation of arterioules and venules- which increasess capillary blood flow and results in redness and warmth

increase in vascular permeability- this causes protein rich fluid to move into the extravascular spaces creating an accumulation of fluid in the tissue ( results in swelling, pain and impaired function)

cellular stage

second stage of the acute inflammatory process


60-80 percent of total number of wbc

derive from myeloid stem cells in marrow and mature in the marrow


stain blue

precursors to mast cells

granules in the cytpolasm secrete histamine which is responsible for the symptoms of inflammation ( redness and swelling)


inolved in allergic responses and parasitic infections

present in chronic inflammation


most numerous leukocyte

first phagocytic cell to arrive at site of invasion ( within 90 minutes)

life spam-24-48 hours


immature neutrophils

increase when excessive demand for phagocytes


live 3-4x longer than granulocyte ( netrophils)

largest of all wbc

experts at phagocytosis

signal specific immune response to begin

predominant cell by 48 hours

play important role in chronic inflammation-( wall off material that cant be ingested)

event 1

cellular sequence of events during inflammation

margination ( pavementing)

as fluid seeps out through capillaries

blood becomes more viscous

wbc move to periphery of the vessels and adhere to capillary endothelium

event 2

cellular sequence of events during inflammation

emigration ( transmigration)

wbc move through vessel walls by ameboid action into the tissue spaces

event 3


damaged tissues

agents send out cytokines

oull wbc to damage areas

event 4


foreing agents engulfed and destroyed

done mostly by neuutrophils and macrophages

inflammatory mediators

responsivle for the signs and symptoms of inflamation
( histamine, bradykinin, prostaglandins, leuotrienes)


fluids that have escaped blood vessels

destroyed wbc, rbc, fluid


mixture of rbc and plamasma


contains pus ( degraded wbc proteins, tissue debris)

odor and color depend on organism


watery, low protein

result when plasma enters site


form sticky meshwork

walls off infection


severe tissue injury causes damage to vessels

leak of rbc from capillaries

acute inflammation

occurs moments after injry

subsides quickly

self limiting

chronic inflammation

long term

self perpetuating

immune deficiency

deficient or underactive immune system


over active immune system

autoimmune disorders

loss of self recognition ability, immune system destroys host


acquired immunodeficiency syndrome

profound immunosuppression with association opportunistic infections



human immunodeficiency virus

selectively attacks cd4 t cells

deteriorating immune system


33 million people live with hiv/aids

women and young-50% of infections

not standard reporting

hiv transmision

exchange of blood/ body fluids that contain the virus or virus infected cells

( blood, semen, vaginal secretions, breast milk)

sexual mode of contact

most frequent for transmission

oral, anal, vaginal intercourse is risky

men/memn 53%

men/women 32- high risk

greater risk when mucosal surfaces not intact ( std)

blood to blood contact

needles, syringes contaminated with blood leads to direct route for transmission

.3 risk

perinatal contact

transmission from mom to child most common childhood infection

can occur in utero, during delivery, or thru breast milk

occupational contact

universal precautions

other std/sti

increased risk for hiv

increased severity of other stds

drug abuse

risk factors in essence

risk for infection exists when exposed to infected blood semen or vaginal secretions are deposited onto mucous membranes or into blood of another

risk factors no transmission risk

casual contact, mosquites or insects

hiv blood transfusion

screening after the 1980s

screened for p24 antigen


when a person converts from negative to positive

takes 1-3 months after exposure, can take up to 6 months

window period

time after infection before positive

there are no physical signs however person is highly contagious

hiv/aids pathogenesis

begins with hiv

retrovirus, infects cd4


most common form in us associated with aids


most common form in western africa

slower progression

step one viral replication

virus binds to cd4 cell

step two viral replication

uncoating and internalization-
virus uncoats itself

core content ( viral rna, and reverse transcriptase) enter cell

allows for more hiv production

step three viral replication

dna synthesis-
reverse transcriptase changes viral rna to viral dna

step four viral replication

viral dna enters nucleus of cd4 cells inserts into original dna

step five viral replication

viral dna transcribed, changed into messenger rna
provides instructions for building viruses

step six viral replication

use instructions
create proteins and exymes ( polyproteins) - these support new viral construction

step seven viral replication

polyproteins broken down to individual protein for new viruses

step eight viral replication

viral rna and proteins assembled to new viruses released from cd4 cell

acute phase hiv

primary infection

fever, fatigue, myalgias, sore throat, night sweat, gi, lymphadonopathy

incrased viral load, decreased cd4

1-4 weeks after exposure, lasts for 7-10 days

latent period hiv

chronic infection

no signs or symptoms

decreased cd4

10 years

overt aids

8-10 years to reach

cd4 lymph <200 respiratory gi wasting metabolic cancers
cd4 decrease load increases

2-3 years

viral replication results

cd4 cells killed ( million per day)

hiv copies released into blood ( billions)

invade next cd4 cell
overtime cant keep up viral load increases cd4 decreases

opportunistic infections

infections the immune system could normally get rid of , in hiv/aids causes greate damage

pneumosistis corinii pneumonia - most common

jiroveci coninii-humans

risk greatest when cd4 cells are at the lowest <200
mycobacterium tuberculosis

hypersensitivity disorders

excess or inappropriate immune system activation

results in injury and death

type 1 hypersensitivity disorder

antivodies involved are igE

b lymph

allergic reaction usually environmental cause
( inahaled, injected, ingested, skin contact)

type 1 hypersensitivity example

person exposed to ragweed
igE antivodies attach to mast cells
second exposure IgE primed mast cells -degranulate and release chemcials
- histamine, complement, ( stimulates inflammatory response) acetylcholine ( broncial smooth muscle contraction)

atopic hypersensitivity


common environmental allergens

hay fever, and allergic asthma

food allergies, and dermatitis less common

leads to sneezing, swelling and eye redness


nonatopic hypersensitivity

systemic response
more serious than the other two

lacks genetic component

not organ specific


immediate response
- vasodilation
-increased capillary permeability ( results in hypotension, or anaphylactic shock)
-blood pressure decreases due to leakiness
-smooth muscle contraction and bronchial constriction
-sense of foreboding
-itching palms, hives, swelling of eyelids, lips, tongue, feet, uvula, and larynx
-air hunger, stridor, wheezing

type 2 hypersensitivity disorder

cytotoxic reaction
antibodies involved are igG and igM attack antigens on cell surfaces

set of 20 plasma proteins
results in phagocytosis and cell lysis

usually involves antigens on rbc or wbc- transfusion reactions or certain drug reactions

incompatable blood

type two hypersensitivity disorder

blood gets coated with igG or igM
- targeted for destruction by macrophages
-complement activated and results in lysis
-transfused rbc

type o

no a or b antigens on rbc surface

a and b plasma

UNIVERSAL DONOR (no antigens present on cell surface of these rbc, no type of antibody present in a recipients blood would react with this donated blood)

type a

a antigens on rbc surface
b antibodies in plasma

transfuse with a or o

type b

b antigesn on rbc surface

a antibodies in plasma

transfuse with b or o

type ab

both a and b antigesn on rbc surface

neitgher a nor b antibodies

transfuse with abo


type three hypersensitivity

immune complex disorder

- formation if igG and igM antibody/antigen immune complezes

complexes accumulate in capillary walls

leads to activation of the chemical mediators of inflammation ( histamine)

neutrophils attracted to area
- attempt phagocytosis , cause immune complexes to release enxymes which cause further tissue damage

type three hypersensitivity example

strep throat infection, antigen binds with igG and igM in circulation to form immune complexes

complexes accumulate in glomerular basement

type four hypersensitivity

cell mediated

antibodies not involved-T CELLS INVOLVED
- react with antigens and release lymphokines ( draw macrophages to area) causing tissue damage

two sub types

direct cell mediated cytotoxicity

type 4 hypersensitivity sub type 1

when intracellular pathogens ( viruses) or extracellular agents ( fungi and protozoa)

cd8 cytolytic t cells directly kill antigen
- with some infection antigen itself not harmful
-cd8 cells cant tell difference so they kill all infected
--sometimes tissue damage that results is really due to cd8 response and not due to invader

delayed hyper sensitivity response

type 4 hypersensitivity sub type 2

occurs 24-72 hours after exposure of sensitized person to offending antigen ( delayed reaction)

cd4 t cells involved

example ( tb, poison ivy)

autoimmune disorders

inability of immune system to recognize self from nonself

immune response mounted against host tissue

leads to localized or systemic injury

can affect any tissue of body

immune unable to use HLA surface markers to determine foreign from host

autoimmune disorders-etiology

viruses, genetics, gender

if you have one auto disease more prone to others

often associated with abonormal stressors

major components of hematopoietic system

bone marrow- where blood is formed

blood cells- rbc, wbc, platelets

lymphoid tissue

puripotent stem cells

all blood cells derived from these

potential for proliferation and self renewal for life

source/resource for all blood cells

myeloid stem cells path

paths of differentiation

cells formed, maturation and differentiated in bone marrow

generates precursors to

lymphoid stem cell path

cells formed in marrow but generally mature to some lymph system ( thymus)

generates precursors to b and t cells

red blood cell

up to 1000x more numerous than other blood cells

non nulceated biconcave disks

transport oxygen to tissues via hemoglobin

binds some co2 in tissues and brings it back to lungs ( exhale)

adult hemoglobin

2 pairs ( 4 seperate) polypeptied chains ( alpha and beta)

heme component- pigmented iron containing portion, binds with o2

globin- protein

each hemoglobin molecule can carry 4 o2

with hemolysis iron and protein recycled
- heme changed to biliruibin and eliminated
-lack of iron means decreased hemoglobin synthesis

rbc life cycle

120 days


fully saturated bright red


not fully saturated with o2-blue purple color

fetal hemoglobin

present from 3rd-9th month gestation

alpha chains substituted for gama chains that allow for a greater affinity for oxygen( 6 months after birth changes to adult)


mature rbc

enter blood stream before they are fully mature ( reticulocyte)


precursors to rbc come from pluripotent stem cells

1% of rbc in immature stage



hormone released by the kidneys that stimulates the production of rbc

governed by tissue oxygen needs

red blood cell destruction

normal lifespan 120 days

normally the rate of production and destruction are equal ( 1% made 1% destroyed)

macrophages in liver, spleen, bone marrow, and lymph tissue destroy rbc

amino acids are saved from globin chains

iron saved from heme


break down


insoluble plasma, unconjugated ( indirect) (what heme is first converted to )

travels to liver where it is changed to soluble (bile) ( direct/conjugated)

too much unconjugated bilirubin builds up when levels exheed liver's ability to remove it ( jaundice)

red blood cell count

total number of rbc in 1 mm of blood


reticulocyte count

provides an index of rate of red blood cell production

normally 1% of rbc


MALES 14-16.5 FEMALES 12-15


percentage or rbc in plasma

varies with quantity of extracellular fluid ( increases with dehydration)

MALES 40-50 FEMALES 37-47

rbc indicies

help to differentiate/classify type of anemia

mean corpuscular volume


reflects the volume of size of rbc

falls with microcytic anemias, grows with carcocytic anemias


rbc of normal size

mean corpuscular hemoglobin concentration

refers to concentration of hemoglobin in each cell

accounts for the color of rbc


rbc of normal color


decreased color


low number of circulating rbc

low level of hemoglobin

or both

anemia possible etiology

excess blood loss

excess rbc destruction ( hemolysis)

decidient rbc production

anemia cosequences

decreased o2 carrying capacity

tissue hypoxia ( if not treated)

anemia manefestations

depend on its severity, the rapidity of its development, underlying pathologic conditions and the age and health status

if onselt is slow, body compensates for the drop in o2 carrying capacity of the blood with an increase in plasma volume ( heart works harder, it does this to increase blood flow to tissue) cardiac output( more blood pumped out tachycardia) and resporatory rate( take in more o2)

pallor of skin and nailbeds
- redistribution of the blood from cutaneous tissues or lack of hemoglobin
-body aims to pump blood to vital organs -skin pale

tissue hypoxia signs and symptoms

weakness and fatigue

hemolytic anemia

blood breakdown

premature destruction of rbc

retention of iron-good

results in increased erythropoiesis ( kidneys try to compensate)

hemolytic anemia indicies and labs

normocytic rbc

normochromic rbc

increased reticulocyte count ( premature destruction of erythrocytes reticlocytes released)

hemolytic anemia clinical manifestations

typical of anemia ( fatique and weakness)

bilirubinema ( jaundice)

hemolytic anemia causes

extrinsic ( acquired) - things outside tbc itself ( drugs, bacteria, toxins)

intrinsic ( inherited)- conditions hwere there are defects in rbc membrane or hemoglobinopathies ( sickle cell)

blood loss anemia

if blood loss is rapid circulatory shock and collapse

-bp decreases, pulse incresase, resporatory rate increases

can lose gradually 50 percent without symptoms

if bleeding is controlled and iron is god 3-4 weeks to replenish

external bleeding equals loss in iron

chronic blood loss

does not affect blood volume

usually causes iron deficiency anemia

normally free of symptoms until <8

microcytic hypochromic rbc involved

sickle cell anemia

hemoglobin is altered in sickle cell , caused by mutation of beta chain aa substituted for valine

mostly affects african americans

.1-.2 in us affected by sickle cell disease

8% heterozygous affected by trait

inherited by ressessive inheritance

40% abnormal hbs heteroxygote

80-95% hbs in sickle cell disease ( homo)


the higher the concentration the higher the risk of sickeling

it polymerizes when deoxygenated creating a semisolid gel that make erythrocyte rigid
- distorts shape and causes structural damage to rbc membrane

can return to its normal shape with oxygenation but if episode of deoxy repeated they are permanentrly sickled

infants dont experience until they are 8-10 weeks because of fetal hemoblobin

sickle cell trait has less hbs generally asymptomatic

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