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151 Cards in this Set
- Front
- Back
cardiogenic shock
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results from heart failure
-follows myorcard. infarc., or surgery req. bypass -CM= impaired mentation, edema, low card. output, dusky skin. low bp, |
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hypovolemic shock
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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. |
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nerugenic shock
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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 |
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anaphylactic shock
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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 |
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septic shock
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-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. |
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Immune system protects body from__?
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-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)) |
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Natural Immunity
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-INNATE
-present at birth -naturally resistant to (cowpox or canine distemper) |
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Acguired Immunity
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-ADAPTIVE
- can be active or passive |
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Active Immunity
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-produced by the host after exposure to an antigen or immunization
-long acting |
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Passive immunity
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-does not involve the host's immune response - antibodies or t cells are transferred to the patient
-short acting |
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two types of active imm?
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natural and artificial
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Acguired Natural active immunity
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-contact with antigen thru clinical infection
-chicken pox, measles, or mumps) |
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Acquired active artificial immunity
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-immunization with live or killed vaccines
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types of acquired imm?
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active and passive
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acquired passive natural imm?
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-transplancental and or breast milk tranfer from mother to child
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acquired passive artifical imm?
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injection of serum from immune human
-injection of human gamma globulin, rabies, tetanus, snake bite) |
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lines of defense
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1. inate: physical , mech, biochemical barriers
2. inflammatory 3. acguired |
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2 types of immunity
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humoral and cell mediated
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Humoral
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-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 |
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cell mediated
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-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 |
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Antigen
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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 |
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Histocompatability antigens
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HLA complex0 the more similar two people HLA makeup are the better sucess of transplants
-HLA antigens- distinguish self from non self |
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Blood group antigens
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-provoke the strongest humoral immune response.
-ABO blood type consists of two types of antigens a and b |
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A blood group
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- A antigen
-anti B antibodies |
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B blood group
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-B antigen
-anti A antibodies |
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AB blood group
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-AB antigen
-no antibodies |
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O blood group
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-no antigen
-AB antibodies |
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IF A gets B blood good immune response T/F?
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false it would be bad
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RH system
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-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 |
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anatomical barriers
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-physical barrier
-skin, mucous mem., |
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Biochemical barriers
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-sebaceous glands antibacterial and antifungal acids (ph 3-5) and helps to kill bacteri
-sweat, tears, and saliva -normal flora |
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if normal flora is killed by antibioticss we are more prone to get
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a secondary problem
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mechanical clearnace
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gets ride of foreign body by:
-skin sloughing, coughing, urinating |
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normal flora
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the body has natural bacteria that prevents the growth of some invading bacteria (gut, vagina, and urinary tract)
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the inflammatory response is the __?
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2nd line of defense
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inflammatory response
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begins w/ in seconds of invasion
-promotes healing by surrounding afftected tissues w/ cells and fluid that isolate, destory and remove invaders |
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Immune response
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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. |
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__ is the primary cell of the immune response?
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lymphocyte
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central lymphoid organs
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thymus gland and bone marrow
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peripheral lymhoid organs
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tonsils, gut, genital, skin, lymph nodes, and spleen
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memory cells
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-capable of remembering the antigen and acting faster if it invades the host again
-this creates what we call immunity |
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modulators can __ or __ the imm. system
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amplify or suppress
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exogenous modulators
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trauma disease pollutants
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endogenous modulators
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age gender nutrition
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mature b cells are called
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plasma cells, they have encoutered antigen and developed specifictiy for that antigen
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Primary and secondary immune response
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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 |
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Immunoglobulins
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antibodies or immunoglobulins are serum glycoproteins produced by plasma cells in response to an antigen challenge.
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IGG
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crosses the placenta, resp. for secondary immune response (80-85%)
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IGA
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tears, saliva, and breast milk
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IGM
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responsible for primary imm. response
-forms antibodies to ABO blood antigens -largest and first responder |
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IGE
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causes symptoms of allergic reaction
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IGD
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information is limited
-function NK |
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IGG crosses the placental membrane and provides newborns with __ for at least __?
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passive acquired imm.
3 months |
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function of antibodies
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neutralize bacterial toxins
neutralize viruses opsonize bacteria activate components of the inflamm. response |
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opsonin
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a substance that renders bacteria susceptible to phagocytosis
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direct effect on antigens
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-agglutination- clumping together insoluble antigens
-precipation- falling out of solution -neutralization- inactivating |
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indirect effect on antigens
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- enhancment of phagocytosis
- activation of plasma proteins that are capable of destroying the antigen |
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molecular structure of anitbody
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4 chains 2 lite 2 heavy
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antigen-antibody binding
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-specificity is required for anitgen-antibody binding
-determine shape of the combining site -the antigen fits into a binding site like lock and key |
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secretory immune system
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antibodies present in tears, sweat, saliva, mucous, breast milk (IGA primary antibody
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cell mediated immunity
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initiated thorugh specific antigen recognition by t cells
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T cytoxic cells
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attack antigens directly and destroy foreign cells
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T Helper __ and T supressor __?
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CD4 and CD 8
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natural killer cells
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-NK cells
-large lymphocytes -recognize and kill viruses, malignant cells, and trans. tissues. |
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cytokines
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-messengers of the imm. response
-"horomones of the imm. response" - comm. among macrophages and various subsets of lymphocytes |
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Interleukin
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-(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 |
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interferon
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inhibits viral replication
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there is a decline in the imm. sys. w/ advancing age
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higher incidence of tumors
increased levels of antobodies against self antigens age decreases size of thymus, by age 50 15 % decrease |
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Imm. system differs from inflammation by:
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antigen specific
has memory takes days to develop long term |
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Imflammaiton differs from Imm. sys by:
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non specific
no memory begins immediately short term 8-10 days |
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Purpose of the inflamm response
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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 |
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inflammatory response functions
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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 |
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Phases of the infl. response
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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 |
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clinical manifestations of inf. resp.
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local response (opposite of syst.)
redness, pain, heat swelling, loss of function (bc of edema) |
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causes of cell injury inthe inf. respo.
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temp extremes
radiation trauma allegens infection hypoxia |
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mast cells cue the infalm respo.
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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 |
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histamine
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bio chem mediator
-vasoactive amine-temporary, rapid, constriction. |
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netrophil chemotactic factor
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bio chem mediator
-attracts netrophils to the site which do the most work during early stages |
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eosinophil chemotactic factor
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biochem mediator
-attracts eosinophils to site |
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serotonin
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bio chem mediator
-relased by platlets -vasoactive -acts like histamine |
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leukotrines
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biochem mediator
syn. by mast cells -similar to histamine but slower acting and longer response (important in later stages in inf. resp.) |
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prostaglandins
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bio chem med
syn. by mast cells -increased vascular perm. -induce pain -aspirin-- blocks the synthesis of prostaglandins (inhibit infl. and pain) |
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aspirin
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inhibits syns.s of prostaglandins which inhibit inf. and pain
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platlet activating factor
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bio chem med
syn by mast cells -endotheial cells incrase vascular perm. causing leukocyte adhesion and platelts to be activated |
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Histamine receptor H1
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-responsible for promoting inflammation
-present in smooth musc. cells (esp. bronchial) -causes bronchoconstriction when stimulated |
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histamine receptor H2
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responsible for inhibiting inflam.
-present in parietel cells of the stomach -causes secretion of gastric acid when stimulated |
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pepsin blocks __ keeping __ from happening?
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H2, stomach ulcers from forming
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plasma protein systems
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complement
clotting kinin |
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complement system
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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. |
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clotting sys
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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) |
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kinin system
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-helps control vascular permeability
-primary kinin -brady kinin -causes vasodialation - causes smooth mus. contraction -incrases chemotaxis |
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cytokines
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affect neihbor cells and help them talk to one another
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interleukins
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cytokine
-send messages from one leukocyte to another to enhance inflamm. -produced in response to antigen stimulation or by products of inflammation |
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lymphokines
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biochemical mediators produced by T cells
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interferon
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-prevents viruses from infecting healthy cells
-has no effect on cells already infected |
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inflammatory response can be divided into 2 things
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vascular response and cellular response
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vascular response
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-after cell injury, arterioles in the area briefly undergo vasoconstriction
-after release of histamine and other chemicals by the injured cells, vessels dialate (vasodialation) |
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vasodialation
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-endothelial cell reaction
-incrased cap. perm. -movemtn of fluid from capp. into tiss. spaces |
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hyperemia
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high supply of blood
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cellular response level
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chemotaxis- pulls the leukocytes
-directional migration of WBCs along contraction gradient of chemotactic factors -mechanism for accumulating neutrophils and monocytes at site of injury |
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two classes of leukocytes
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-granuloctyes- neutrophils, eosinophils, and basophils
-monocytes/macrophages- monocytes (immature form in the blood), macrophages (mature cells in the tissues) |
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netrophils
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-1st leukocyte to arrive (6-12 hrs.)
-phag. bacteria, foreign materials, and damaged cells -short life span -die and removed as pus |
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monocytes
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-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 |
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macrophage
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-important in cleaning area before healing
-long life span -multiply -may stay in dam. tiss. for weeks -gradually take over place of neutralization |
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eosinophils
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-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 |
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basophils
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-function similar to mast cells, but found in blood instead of tissues
-carry histamine and heparin in their granules -realease during infl. |
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local manifestions of acute infl.
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-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 |
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exudate
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-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 |
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3 functions of exudate
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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) |
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serous exudate
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-watery, indicates mild inflm. (fluid in blister
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fibrinous exudate
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thick and clotted, indicates more sever or advaced infl. (lungs in patient w/ pneumonia)
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purulent exudate
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consists of pus large # of leukocytes, indicates persistant bacterial infection (cyst or absess)
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hemorrghic exudate
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bloody exudate
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systemic response of leukocytosis
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-fever
-induced by IL -1 relased from neutrophils and macrophages -endogenous pyrogen acts directly on the hypothalamus -increase in circulating plasma proteins |
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systemic response of anorexia
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-increased heart reate
-increase resp. rate ---major complication septicemia (whole body infection) ---causes CV problems and shock |
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repair
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the replacement of desroyed tissue with scar tissue
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debridement
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the cleanup of a lesion (dissolution of fibrin clots by fibrinolytic enzymes). Begins w/ phagocytosis
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reconstructive phase
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granulation tissue, epithelization. Occurs withing 3 days to 2 weeks. Fibroblasts- synthesize and secrete collagen
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maturation phase-
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continued scar formation and remodeling
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diabetes dys wound healing
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-dys would heal
infection common w/ uncontrolled diabetes (lack of circ and warm sugary env. for bacteria to grow in.) |
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hypoxemia dys wiould healing
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insuff. oxy, cant rebuild cells
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drugs dys wound healing
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anit inflm steroids
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hypovolemia dys. wound healing
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decreased blood volume
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nutriiton
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protein, iron, and calcium are essential for healing
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keloid/ hypertrophic scar
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reaised scar, too much collagen, found mostly in blacks
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elderly population wound healing
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-chronic illness
-immobility (Bed sores) -age -medications -dec. imm. sys. |
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Allergy
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immune response exaggerated against enviormental antigens
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autoimmunity
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immune response is misdirected against the host's cells own cells/ self vs. nonself
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alloimmunity
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immune response directed against beneficial foregin tissues such as transfusions or transplants
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immune defeciency
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immune response insuffiencient for protection due to a disesase or drugs such as chemo
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hypesensitivity
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pathologic immune response to an antigen after reexpossure
-immediate--minutes to few hours(anaphylactic) -delayed--several hours or at reexposure (poison ivy) |
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auto antibodies
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antibodies against self antigens
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Type I imm resp.
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anaphylactic
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Type II Imm. Resp.
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Cytoxic and Cytotylic (tissue specific)
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type III immm. resp.
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complex reaction
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type IV imm. resp.
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delayed hypersensitivity reactions (poison ivy)
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Allergy
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immune response exaggerated against enviormental antigens
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autoimmunity
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immune response is misdirected against the host's cells own cells/ self vs. nonself
|
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alloimmunity
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immune response directed against beneficial foregin tissues such as transfusions or transplants
|
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immune defeciency
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immune response insuffiencient for protection due to a disesase or drugs such as chemo
|
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hypesensitivity
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pathologic immune response to an antigen after reexpossure
-immediate--minutes to few hours(anaphylactic) -delayed--several hours or at reexposure (poison ivy) |
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auto antibodies
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antibodies against self antigens
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Type I imm resp.
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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 |
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Type II Imm. Resp.
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Cytoxic and Cytotylic (tissue specific)
-involevs binding of IgG or IgM antibodies -Graves disease |
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type III immm. resp.
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complex reaction
-local or systemic and immidealty or delayed (IgG or IgM) -serum sickness, raynaud phenomenon, arthus reaction |
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type IV imm. resp.
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delayed hypersensitivity reactions (poison ivy)
-cell mediated response |
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Enocrine autoimmune disease
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thyroditis and graves
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hematologic autoimm. diesease
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hemolytic and pernicious anemicas
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nervous system autoimm. disease
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masthenia griavis
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musculoskeleta autoimm. diesease
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rheumatoid arthiritis
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Systemic Lupus Erythematosus
|
most common auto imm. disorder
-system wide tissue damage -goes in remission |