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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
what are cytokines
protein products of many cell types, mostly lymphocytes and macrophages
26
how do cytokines funxn
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)
27
cytokine types
interleukins, interferons, tumor necrosis factor, transforming growth factor, colony stimulating factor
28
name and describe 3 interleukins
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
29
describe interferons
protexn from viral infxn, aid in phagocytosis, prescribed for viral infxn ie hepatitis
30
describe 2 types of tumor necrosis factor
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
transforming growth factor funx
stimulate cell growth eg fibroblast for healing tissue
32
colony stimulating factor funx
stimulate blood cell growth (in bone marrow) blood cell type granulocytes
33
define plasma protein system & name 3
the activation of many inactive proteins in blood through cascades during inflamm 1. complement sys 2. coag sys 3. kinin sys
34
complement sys funx
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
complement pathway (3)
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
coag sys funx
1 traps blood cell and debris at site 2. repair and heals 3 fibrin major protein
37
kinin system function
initiated by coag factor bradykinin is major protein vasodilation PAIN smooth muscle contrax, increase vasc permeability
38
4 principle components of immune mechanisms
1. humoral or antibody mediated immunity B-lymphocytes 2. cell mediated immunity T-lymphocytes 3. complement system (9 proteins 3 pathways) 4. phagocytosis
39
two classes of immunodefic
1. primary congenital or inherited | 2. secondary acquired later
40
characteristics of humoral immunodeficiency
pyogenic (pus) 1 or all five immunoglobulins/antibodies 70% of primary immunodeficiencies involve humoral immunity
41
2 primary humoral immunodeficiencies describe
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
2ndary humoral immunodefic.
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
describe 5 immunoglobulins/antibodies
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
cell-mediated immunodeficiencies
invasion of viruses fungi cancer that are usually attacked by T cells
45
describe primary and 2ndary cell mediated immunodefic
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
describe Combined B & T cell deficiency
devastating complex difficult to Treat | severe combined immunodeficiency SCID genetically deficient in enzyme that results in few lymphocytes, Trx: adagen
47
primary complement system disorders
1. c3: unites entire complement cascade 2. c3b opsonin 3. c5-9 membrane attack complex
48
2ndry complement disorders
rheumatoid arthritis or lupus antigen-antibody complexes activate complement---> complement stores depleted malnutrition and liver disease can cause 2ndry complement disorders
49
primary phagocytosis disorder
chronic granulomatous disorder: defect in aerobic killing, less free radicals that aid in killing, minimal or no killing, chronic wounds
50
secondary phago. disorder
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
what mediates type 1 immediate hypersensitivity disorder, aka, what it causes 3 steps
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
describe sensitizing/priming stage
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
immediate hypersensitivity disorder subsequent allergen exposure process
- 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
define anaphylaxis, what type of hypersensitivity
histamine binding to H1 receptors triggers a # of inflamm responses which can lead to airway obstruction and shock, Type 1
55
Type II define and gives examples of type II hypersensitivity
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
type II damage process (4)
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
describe antigens and antibody for blood types
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
RH blood group
- 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
type III hypersensitivity process
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
possible complication of type III, areas involved
may used up complement and develop immune deficiency | areas: typically vessels joint & kidneys
61
what is raynaud's cryoglobulins
antigen-antibody complexes precipitate @ low temps (e.g. digits, nose)
62
type III rxns (2) signs and symptoms and causes
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
what is type IV: and what are the invaders, are antibody involved
T-Cell mediated disorders (invader goes intracellular and antibody cannot reach invader) - virus fungi, parasites, protozoa, chemicals, organics & self antigens - antibody not involved
64
two types of type IV t cell mediated disorders
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
what cells are involved with GVHD and signs and symptoms
CD4 helper t cell and CD8 T cytotoxic cells are activated, itching rash on palms or soles, desquamation (sloughing), bloody diarrhea
66
what is autoimmune disease
a disease process that involves the production of host antibodies to host tissue
67
what happens in tolerance
the immune system normally illiminates T and B cells that react to self-antigens
68
4 types of autoimmune disease
Diabetes Type I: Graves Disease Myasthenia Gravis Systemic lupus
69
what type hypersensitivity is Type I diabetes and what occurs
type II hypersensitvity antibodies to beta cells in the islets of langerhans of pancreas lack of insulin production
70
what type hypersensitivity is graves dz and what occurs
type II, antibodies to thyroid stimulating hormone receptors high levels of thyroid hormone
71
what type hypersensitivity is myasthenia gravis and what occurs
type II antibodies to postsynaptic ACH bulbar muscle weakness fatigue in face neck and proximal limbs
72
what type hypersensitivity is systemic lupus erythmeatosus and what occurs
``` 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 ```

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