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BMED 4751 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

what are the 4 characteristics of acquired immunity

A
  1. specificity
  2. diversity
  3. memory
  4. self/nonself recoginition
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2
Q

what are the 2 types of acquired immunity

A
  1. humoral immunity

2. cellular immunity

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3
Q

humoral immunity is caused by the action of __

A

antibodies

fights off foreign invaders

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4
Q

humoral immunity is mediated by __

A

b cells

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5
Q

cellular immunity is responsible for detecting __

A

self vs. non-self cell

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6
Q

cellular immunity is mediated by __

A

T cells

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7
Q

what is an antigen

A

it binds to antibody or t cell receptor to initiate acquired immune response

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8
Q

what are examples of lymphocytes

A

B and t cells

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9
Q

what is a hapten

A

it is a low MW substance that binds to a high MW substance to initiate an acquired immune response. but upon subsequent exposure, you don’t need the high MW substance

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10
Q

__ non specifically enhances immune response to antigens

A

adjuvant

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11
Q

for an antigen to be recognized by the immune system __

A

it has to be displayed with an MHC

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12
Q

what reduces the chance of an organ rejection

A

if the donor and host have similar MHC molecules

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13
Q

MHC class I deals with

A

recognizing altered-self cells

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14
Q

MHC class I are recognized by

A

T cytotoxic cells

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15
Q

__ cells are found on every cell

A

MHC class I cells

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16
Q

MHC class II are recognized by

A

T helper cells

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17
Q

MCH class II are only found on __

A

antigen presenting cells

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18
Q

how do MHC class II cells work

A

antigen will bind to MHC class II cells presented on the foreign cell surface

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19
Q

how does acquired immunity achieve its high specificity

A

by the formation of antibodies and t cell receptors

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20
Q

how are b and t cells different

A

b cells don’t require antigen presentation by MHC cells in order to be activated

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21
Q

__ stimulate B cells to allow them to proliferate to form

A

T helper cells stimulate B cell proliferation

memory B cells and plasma cells (effector cells)

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22
Q

what do memory b cells and effector cells do

A

memory b cells –> express membrane bound antibodies

effector cells–> produce soluble antibodies

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23
Q

describe the structure of antibodies

A

made of 2 heavy chains and 2 light chains

24
Q

how can antibodies aid in the removal of pathogens

A
  1. agglutination - clump the particles together
  2. precipitation - complex of antibody and antigen become so large its no longer soluble
  3. neutralization - antibodies cover the active sites of foreign substance
  4. lysis - antibodies directly lyse the organism
25
Q

T cells require __ to become activated

A

antigen presentation via a MHC complex

26
Q

T helper cells recognize __

A

antigens presented on MHC class II molecules

27
Q

in AIDS, __ are destroyed

A

t helper cells

28
Q

what do T helper cells do

A
  1. stimulate b cell growth (humoral side)
  2. simulate Tc cells
  3. stimulate macrophages
  4. stimulate other Th cells
29
Q

Tc cells interact with __

A

antigens presented on MHC Class I molecules

30
Q

how are Tc cells activated

A

by T helper cells

31
Q

what do cytotoxic T lymphocytes do

A

they secrete perforins which lyse cells (acts like MAC)

32
Q

what is Type I hypersensitivity

A

it is IgE mediated

IgE binds to receptors on mast cells, resulting in sensitization of these cells

requires a second exposure

33
Q

Type II hypersensitivity

A

antibodies destroy cells that present a foreign antigen (blood transfusions)

34
Q

Type III hypersensitivity

A

auto immune disorder

35
Q

Type IV hypersensitivity

A

T cell mediated

doesn’t involve antibodies

ex. poison ivy

36
Q

after you cut yourself, the body does __ to prevent bleeding out

A
  1. constrict blood vessels
  2. form platelet plug
  3. blood coagulates
37
Q

what are platelets

A

non nucleated fragments of megakaryocytes

38
Q

platelets cannot __ because they are non nucleated

A

cannot proliferate

39
Q

platelets secrete __

A

factors stored in granules once activated

40
Q

what are the functions of platelets

A
  1. become platelet plugs

2. provide catalytic environment for the blood coagulation cascade

41
Q

describe platelet activation

A

they become activated by exposure to ECM or soluble factors

change shape when activated and spread out to form platelet plug and provide catalytic environment

42
Q

describe the steps of platelet plug formation

A
  1. platelets will adhere to the ECM
  2. They secrete factors for further platelet plug formation
  3. factors activate and attract more platelets which form an aggregate
  4. platelets express GPIIb/IIIa receptors for fibrinogen (fibrinogen allows platelets to stick together )
  5. platelets exhibit pro-coagulatory activity to further stabilize the plug
43
Q

how can you determine if platelet activation had occurred

A
  1. look at how adhered the platelets are

2. look at how spread out they are

44
Q

what are the parts of the coagulation cascade

A

intrinsic and extrinsic and common pathway

45
Q

how does the intrinsic pathway start

A

trauma to blood vessels

requires exposed ECM (which is negatively charged)

46
Q

describe the intrinsic pathway of the coagulation cascade

A
  1. factor 12 adsorbs to negatively charged surface and becomes activated
  2. factor 12a converts pre kallikrein to kallekrein and converts factor 11 to 11a
  3. kallikrein cleaves HMWK to form bradykinin
  4. ** bradykinin is an inflammatory mediator
  5. kallenkrien and factor 11a are bound to HMWK, which has high affinity for hydrophobic biomaterials (coagulation cascade will occur on hydrophobic biomaterials)
47
Q

describe the extrinsic pathway of the coagulation cascade

A
  1. initiated by the release of tissue factor
  2. **tissue factor is released form macrophages or endothelial cells
  3. tissue factor complexes with factor 7 to anchor to the surface between membrane
48
Q

which clotting pathway occurs first

A

extrinsic (occurs in about 15 seconds)

49
Q

describe the common pathway of the coagulation cascade

A
  1. platelets secrete and have receptors for factor 5
  2. factor 5 will bind to factor 10a on the platelet surface
  3. factor 10a will cleave prothrombin into thormbin
  4. thrombin will cleave fibronigen to fibrin
  5. ** fibrin binds with fibrinopeptide A and B which are chemotactic for neutorphils
  6. thrombin also activates factor 13a
  7. factor 13a crosslink fibrin which will help stabilize the platelet plug
50
Q

what are the ways to limit clot formation

A
  1. physiologic factors - high blood flow will prevent factors from being near each other
  2. heparin/antithormbin3 comples will bind to thrombins catalytic site and prevent the coagulation cascade
  3. thrombomodulin - bind to thrombin and prevent it from interacting with the rest of the cascade
  4. fibrinolysis - during clot formation, plasminogen gets trapped in the clot. TPA activates the plasminogen into plasmin which cleaves the fibrin fibers
51
Q

what about the endothelium make it anti-coagulant

A
  1. heparan sulfate make the endothelium very smooth which prevents adsorption
  2. thrombomodulin is found on the surface
  3. they secrete TPA to dissolve clots
52
Q

what about endothelium makes it pro-coagulant

A
  1. secretes cofactors in the extrinsic pathway

2. endothelium lining is disrupted, thus exposing the ECM which will start the intrinsic pathway

53
Q

__ is the movement of a part of a clot into general circulation

A

embolization

54
Q

problems with in vitro hemocompatability assays

A
  1. need to use anti-coagulants to preserve blood outside of the body
  2. must use pumps to circulate the blood
  3. need contorl surface (usually glass)
55
Q

problems with in vivo hemocompatability assays

A
  1. animals have different blood composition than humans

2. difficult to control blood flow near implant

56
Q

advantages of ex vivo hemocompatabiliy assays

A
  1. blood flow near implant can be controlled
  2. don’t need anticoagulants
  3. implants can remain in place for months

BMED 4751 (3 decks)

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