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nursing > 2450 wk 2 > Flashcards

2450 wk 2 Flashcards

1
Q

what are 2 processes, benefits, and types of inflammation

A 
biochemical and cellular
- decreases tissue damage
-captures removes invaders/debris
- promotes healing
acute (8-10 days) chronic (weeks months)
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2
Q

what are the signs/symptoms of inflammation

A

1&2 rubor & calor (vasodilation)

  1. tumor
  2. dolor
  3. impaired funx
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3
Q

3 lab values seen in inflammation

A

WBC,acute phase proteins, ESR

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4
Q

if inflammation is present rxn of WBC, and why this occurs

A

shift to left because of more immature netrophils released from bone marrow

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5
Q

when do acute-phase proteins peak, name 3 and process associated and where proteins released

A 
10-40 hrs after injury
an increase in c-reactive protein (CRP)
- in response to cytokines
-binds to invader and activates more mediators (i.e. cytokines and complement)
coag proteins (fibrinogen),
complement
from liver
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6
Q

what is ESR and describe process

A

erthryocyte sedimentation rate

  • faster sedimentation rate during inflammation
  • done in conjunction with CRP
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7
Q

5 tissue injury examples

A

infx, cell death/damage, shear stress, secretion, clotting

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8
Q

6 cells involved in inflammation

A

mast cells, basophils, neutrophils, eosinophils, monocytes/macrophages, cytokines

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9
Q

most important cell, location, when released & 2 associated processes

A

mast cell, connective tissue near blood vessels, released w/in seconds

  1. degranulation: release histamine and chemotactic factor
  2. synthesis of other inflamm. mediators synthesized from membrane lipids prostanoids, leukotrienes, platelet activating factor
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10
Q

rxn of histamine

A
  1. vasodilation (5-10min)
  2. increase vasc. permeability
  3. margination (pavementing) sticky leukocytes line up along vasc wall
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11
Q

rxn of chemotactic factors

A

substances at site of inflamm that attract white blood cells (neutrophils and eosinophils) by causing them to travel along a concentration gradient toward invader

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12
Q

describe arachnoid acid metab and 3 main products

A

membrane phospholipids–(activation PL A2) –>
PLATELET ACTIVATING FACTOR(PAF) & Arachidonic acid
Arachadonic acid–cox enzyme–>PROSTANOIDS
Arachadonic acid –lipoxygenase–> LEUKOTRIENES

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13
Q

3 prostanoids and rxn

A

prostaglandins, prostacyclin, thromboxanes

increase vasc permeability, bronchoconstrict, neutrophil chemotaxis, PAIN, platelet funxn

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14
Q

leukotriene rxn

A

increase vasc permeability, bronchoconstrict, platelet activation, slower & more powerful than prostanoids.

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15
Q

PAF rxn & character.

A

synthesized from phospholipids, arach acid not needed, increase vasc permeability, bronchoconstrict, platelet activation

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16
Q

basophil role and WBC %

A

mast cells come from basophil
less than 1% of WBC
contain histamine & other mediators that respond to inflamm and allergic rxns
remain in plasma

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17
Q

neutrophils: ETA, lifespan in plasma & tissue, % 4 axns

A

ETA:6-12 hrs after injury LIFESPAN: 10hrs, 4-5 days in tissue (40-75% WBC)

  1. MCF release
  2. Diapedesis
  3. Chemotaxis to injured site
  4. Phagocytosis
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18
Q

3 phases of phagocytosis

A 
adherence 
endocytosis (engulfment)
intracellular killing
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19
Q

2 types of adherence

A

opsonization: it is a free floating complement and antibody (opsonins) acts like glue and is strongest

inante receptors: Toll like receptors work in pairs/dimers, recognize blocks of antigens, slower

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20
Q

two methods of intracellular killing

A
  1. o2 dependent mechanism- increase uptake of o2 by phagosome and generates toxic oxidants ROS
  2. o2 independent mechanism: acidic pH of lysosomes, proteins/enzymes that damage wall cell membrane wall, phagocytic release of lactoferrin to bind with Fe so invaders can not reproduce
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21
Q

plasma protein that protect healthy tissue

A

protease inhibitor- inhibits enzymes

alpha antitrypsin: is released when the phagocyte dies (found in liver and lung)

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22
Q

eosinophils axn, WBC%

A

-granules contain proteins that are toxic to large parasites & respond in allergic rxn, limit inflamm by degrading inflamm molecules (histamines)
1-6% cop cells

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23
Q

monocytes/marcophages %, difference between mono and macro,& name in liver lung brain

A

3-8% of WBC
monocyte in blood, monocytes become macrophages
liver: kupffer in liver, alveolar macro in lung, and migroglia in brain

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24
Q

macrophage arrival, life span, funxn and what aids this funxn, mode of arrival

A

longer life span, arrive within 24 hrs of neutrophil, phagocytosis same as neutrophil & aided by cytokines, arrive by chemtoaxis neutrophil releases macro chemo fac

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25
Q

what are cytokines

A

protein products of many cell types, mostly lymphocytes and macrophages

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26
Q

how do cytokines funxn

A

act locally or systemically, induce synthesis of another inflamm mediator, can be pro-inflam or anti-inflamm or a chemokine (~40 that help with chemotaxis of leukocytes)

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27
Q

cytokine types

A

interleukins, interferons, tumor necrosis factor, transforming growth factor, colony stimulating factor

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28
Q

name and describe 3 interleukins

A

iL1 proinflam pyrogen, activates macrophage & lymphocytes many effects on neutrophils (local inflam)

iL 6 proinflam directly causes hepatocytes to produce proteins for inflamm

iL10 anti inflam decrease lymphocytic growth, decrease cytokine produxn

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29
Q

describe interferons

A

protexn from viral infxn, aid in phagocytosis, prescribed for viral infxn ie hepatitis

30
Q

describe 2 types of tumor necrosis factor

A

TNF a secreted by macrophages mast cells proinflamm adherence cytokine produxn, FEVER, liver proteins causes cachexia, risk of thromobosis shock

TNF b kills cells by aiding in phagocytosis

31
Q

transforming growth factor funx

A

stimulate cell growth eg fibroblast for healing tissue

32
Q

colony stimulating factor funx

A

stimulate blood cell growth (in bone marrow) blood cell type granulocytes

33
Q

define plasma protein system & name 3

A

the activation of many inactive proteins in blood through cascades during inflamm

  1. complement sys
  2. coag sys
  3. kinin sys
34
Q

complement sys funx

A
  1. opsonins
  2. chemotactic factor
  3. anaphlatoxins causing rapid degranulation
  4. membrane attack complex MAC, creates pores in out membrane of cell of invader
35
Q

complement pathway (3)

A
  1. classic activated by multiple antibodies which activates complement 1
  2. lectin pathway: activated by bacterial CHO: lectin + invaders mannose activates complement 1
  3. alternative activated by gram neg (-) bacteria and fungi which activates complement 3 this cascade converges with classical
36
Q

coag sys funx

A

1 traps blood cell and debris at site
2. repair and heals
3 fibrin major protein

37
Q

kinin system function

A

initiated by coag factor
bradykinin is major protein
vasodilation PAIN smooth muscle contrax, increase vasc permeability

38
Q

4 principle components of immune mechanisms

A
  1. humoral or antibody mediated immunity B-lymphocytes
  2. cell mediated immunity T-lymphocytes
  3. complement system (9 proteins 3 pathways)
  4. phagocytosis
39
Q

two classes of immunodefic

A
  1. primary congenital or inherited

2. secondary acquired later

40
Q

characteristics of humoral immunodeficiency

A

pyogenic (pus)
1 or all five immunoglobulins/antibodies
70% of primary immunodeficiencies involve humoral immunity

41
Q

2 primary humoral immunodeficiencies describe

A

common variable

  1. mature B cells to plasma cell blockage
  2. onset as young or middle aged adult (15-35)
  3. lack all antibodies/immunoglob pyogenic infx
  4. treatment I.V. Ig infusions q month Immunoglob G is most important and long lasting provides passive artificial immunity

selective IgA deficiency

  1. lacking initial defense in secretions/mucosal membranes
  2. most common IgM and IgG eventual compensate
  3. upper resp and GI infx
  4. more allergies
  5. no treatment but 50% outgrow by teen yrs
42
Q

2ndary humoral immunodefic.

A

nephrotic syndrome: loss of proteins in urine, secondary dz that affects kidneys, crucial loss of IgG IgA:but not IgM b/c too big

43
Q

describe 5 immunoglobulins/antibodies

A
  1. IgG most #, long term, cross placenta,
  2. IgA- mucous membranes
  3. IgM 1st to form, temporary, large, determines blood type
  4. IgE allergic and parasitic response
  5. IgD: receptor on B cell responds to all kinds of invaders and helps to process correct immunoglobulin
44
Q

cell-mediated immunodeficiencies

A

invasion of viruses fungi cancer that are usually attacked by T cells

45
Q

describe primary and 2ndary cell mediated immunodefic

A
  1. primary: very serious rarely survive infancy DiGeorge syndrome: small thymus/parathyroid gland, tetany due to low calcium from underdeveloped parathyroid, facial change low ears fishmouth, possible Trx: thymus or bone marrow transplant stem cell or gene replacement
  2. secondary: reciprocal relationship between virus/T cell funx/ cancer. HIV and Herpes Virus infect T cells
46
Q

describe Combined B & T cell deficiency

A

devastating complex difficult to Treat

severe combined immunodeficiency SCID genetically deficient in enzyme that results in few lymphocytes, Trx: adagen

47
Q

primary complement system disorders

A
  1. c3: unites entire complement cascade
  2. c3b opsonin
  3. c5-9 membrane attack complex
48
Q

2ndry complement disorders

A

rheumatoid arthritis or lupus antigen-antibody complexes activate complement—> complement stores depleted
malnutrition and liver disease can cause 2ndry complement disorders

49
Q

primary phagocytosis disorder

A

chronic granulomatous disorder: defect in aerobic killing, less free radicals that aid in killing, minimal or no killing, chronic wounds

50
Q

secondary phago. disorder

A
  1. steroids (corticosteroid) or immuno suppresants (cyclosporine) repress phagocytosis
  2. Diabetes mellitus causes alteration in chemotaxis, and HIV destruct T helper cells and monocytes and macrophages
51
Q

what mediates type 1 immediate hypersensitivity disorder, aka, what it causes 3 steps

A

aka allergic rxn, most common
mediated by IgE specific to antigen/allergen
1. sensitizing/priming stage :antigen presenting cell presents the antigen allergen
2. sensitized IgE resides on surface of mast cell and basophils
3.subsequent allergen exposure causes angioedema and uticaria

52
Q

describe sensitizing/priming stage

A

t cell recognition of allergen –> differentiation –> Th2 –> secretes cytokines –> stimulate B cell differentiation –> plasma cells –> IgE –> stimulate growth of mast cells (in skin mucousal membranes, near vessels and lymph) –> recruit and activate eosinophils

53
Q

immediate hypersensitivity disorder subsequent allergen exposure process

A
  • allergen binds to sensitized IgE
  • degranulation of sensitized mas cells (histamine)
  • release of mediators (histamine, prostaglandins, leukotrienes)
  • vasodilation, bronchoconstriction, edema, mucous secretion, possible bronchospasm (wheezy)
54
Q

define anaphylaxis, what type of hypersensitivity

A

histamine binding to H1 receptors triggers a # of inflamm responses which can lead to airway obstruction and shock, Type 1

55
Q

Type II define and gives examples of type II hypersensitivity

A

TISSUE-SPECIFIC rxn (IgM or IgG) (not allergy)

  • cell damage b/c of abnorm antigen-antibody complex on specific tissue
  • antigens on blood cells in a mis-matched transfusion (alloimmunity-response to donor tissue IgM attackss the donor cells)
  • autoimmune disease: antibody binds to target cells: no anergy to own cells
  • drugs (drug’s small protein hapten) may bind(adsorb) to cell membranes and intiate rxn
  • Group A beta-hemolytic strep protein mimics heart and kidney cells, after infection antibodies attack heart and kidney cells
56
Q

type II damage process (4)

A
  1. complete-mediated (MAC) lysis
  2. phagocytosis by extravascular macrophage
  3. antibody-dependent cell-mediated cytotoxicity
  4. Receptor blockage, myasthenia gravis (block receptor for ACH causes weakness)
57
Q

describe antigens and antibody for blood types

A

A: A antigen and B antibody (IgM)
B: B antigen and A antibody
AB:AB antigen no antibody (universal recip)
O: No antigens AB antibody (universal donor)

58
Q

RH blood group

A
  • No antibodies to RH antigen but can make IgM and IgG antibodies
  • Affects RH(-) Moms who had first RH+ baby which can harm the 2nd RH+ baby b/c she has RH IgG antibodies that will cross placenta
59
Q

type III hypersensitivity process

A

immune complex mediated disorders (involves IgM and IgG)

  • antigen-antibody complex form in blood and deposit in tissues
  • complement cascade triggered and result in chemotaxis of neutrophils to site
  • neutrophil destruction of antigen-antibody complex (cause tissue damage
60
Q

possible complication of type III, areas involved

A

may used up complement and develop immune deficiency

areas: typically vessels joint & kidneys

61
Q

what is raynaud’s cryoglobulins

A

antigen-antibody complexes precipitate @ low temps (e.g. digits, nose)

62
Q

type III rxns (2) signs and symptoms and causes

A
  1. systemic: uticaria, edema, fever, pain
    causes: drugs, snake or spider venom, autoimmune disesase lupus rheumatoid arthritis
  2. localized: arthus rxn
    causes: bug bites, hyper acute host-versus-graft disease (4-10hrs) immediate death to donated tissue, allergy testing dz
63
Q

what is type IV: and what are the invaders, are antibody involved

A

T-Cell mediated disorders (invader goes intracellular and antibody cannot reach invader)

  • virus fungi, parasites, protozoa, chemicals, organics & self antigens
  • antibody not involved
64
Q

two types of type IV t cell mediated disorders

A
  1. direct cell mediated cytotoxicity
    - Tcytotoxic cell kill antigen presenting target cells
    - hepatitis manifestations due to Tc destruction of liver cells, not the invading virus
    - acute HVGD months or years later
  2. delayed type hypersensitivity disorders
    - TB skin test
    - contact dermatitis (delayed type)
    - graft versus host disease
65
Q

what cells are involved with GVHD and signs and symptoms

A

CD4 helper t cell and CD8 T cytotoxic cells are activated, itching rash on palms or soles, desquamation (sloughing), bloody diarrhea

66
Q

what is autoimmune disease

A

a disease process that involves the production of host antibodies to host tissue

67
Q

what happens in tolerance

A

the immune system normally illiminates T and B cells that react to self-antigens

68
Q

4 types of autoimmune disease

A

Diabetes Type I:
Graves Disease
Myasthenia Gravis
Systemic lupus

69
Q

what type hypersensitivity is Type I diabetes and what occurs

A

type II hypersensitvity antibodies to beta cells in the islets of langerhans of pancreas lack of insulin production

70
Q

what type hypersensitivity is graves dz and what occurs

A

type II, antibodies to thyroid stimulating hormone receptors high levels of thyroid hormone

71
Q

what type hypersensitivity is myasthenia gravis and what occurs

A

type II antibodies to postsynaptic ACH bulbar muscle weakness fatigue in face neck and proximal limbs

72
Q

what type hypersensitivity is systemic lupus erythmeatosus and what occurs

A 
type III (most common, complex and serious) (antigen-antibody complex in blood) antibodies to nucleic acids and other selfcomponents: 
-will see vasculitis, renal dz, rash, arthritis

nursing (15 decks)

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