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Vet Path. > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Cornelius celsius

A
  • calor, rubor, dolor, tumor
  • virchow added loss of function
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2
Q

Julius cohnheim

A

Revealed basis of inflammatory response

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3
Q

Characteristics of acute inflammation

A
  • vasc. Changes
  • inflammatory edema (plasma proteins & fluid)
  • leukocyte emigration ( mostly neutrophils)
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4
Q

Subacute inflammation characteristics

A
  • decline in vasc. Contrib. (Edema and hyperemia)
  • change in leukocytes (neutrophils @ inflamm. site & infiltrate mixed with mononuclear cells)
  • lasts few days- few weeks
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5
Q

Chronic inflammation characteristics

A
  • presence of lymphoc., macrophages
  • prolif. of small BV and fibroblasts
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6
Q

3 stages of acute inflammation

A

1) hemodynamic changes

2) vasc. Permeability changes

3) leukocytic exudation

(May have overlap)

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7
Q

3 types of hemodynamic changes

A

1) vasoconstriction of arterioles

2) vasodilation of arterioles

3) slowing of blood flow

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8
Q

Vasoconstriction

A
  • part of acute inflamm. response
  • inconsistent finding
  • usually disappears within 3-5 seconds
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9
Q

Vasodilation

A
  • believed to be caused by histamine, prostaglandins, and nitric oxide
  • initially involves arterioles
  • then opening of new capillaries & venule beds
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10
Q

Slowing of blood flow

A
  • started by increas. permeability of microvasculature
  • slowing disrupts laminar flow of blood -> cellular elements to move to periphery of vessels
  • pavementing occurs
  • leuk. exit BV and enter extravasc. space via emigration
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11
Q

3 types of vascular permeability changes

A
  • immediate transient perm. resp.
  • immediate prolonged perm. resp.
  • delayed prolonged perm. resp.
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12
Q

Exudation

A
  • increas. Vascular perm. W/ escape of plasma fluid and leukocytes
  • major & constant feature of acute inflammation rxns
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13
Q

Immediate transient permeability response

A
  • assc. w/ mild injury
  • immediate
  • elicited by histamine
  • increas. Perm. In venules
  • peak @ 5-10 mins
  • goes away within 30 mins
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14
Q

Immediate prolonged permeability response

A
  • assc. w/ severe inj.
  • immediate
  • lasts several days
  • peak @ few hrs
  • increas. perm. & vasc. Leakage in venules, arterioles, & capillaries
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15
Q

Delayed prolonged permeability response

A
  • delayed
  • lasts several hrs-days
  • mild to mod. Thermal injury, x ray & uv irrad., bact. Toxins, delayed hypersen. Rxns
  • increas. Permeability and leakage (MOA unkn.)

-venules & capillaries affected

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16
Q

Leukocytic exudation definition

A

Massing of leuk. (Esp. Neutr. & monocytes) @ inflammation sites

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17
Q

4 leukocyte exudation steps

A
  • margination and pavementing
  • emigration
  • chemotaxis
  • phagocytosis
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18
Q

Neutrophils are assc. w/ what type of inflamm?

A

Acute

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19
Q

Lymph. & macroph. assc. w/ what type of inflamm?

A

Chronic

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20
Q

Margination/pavementation

A
  • leuk. -> periphery of bloodstream
  • cellular elements fall out central column & roll along vasc. endoth.
  • leuk. Adhere to endothelial wall
21
Q

Emigration of leuk. Definition

A

Leuk. Escape bv & enter perivasc. Tissue

22
Q

Diapedesis definition

A
  • movement of leuk. between endothelial cells
23
Q

Emigration of leuk.

A
  • after stuck to endoth. wall, they insert pseudopods between junctions & escape via gap (diapedesis)
  • cross BM & enter perivasc. Tissue
  • erythrocytes may leave bv
  • neutr. 1st predominant, after 6-24 hrs, monocytes predom.
24
Q

Chemotaxis definition

A

Unidirect. migration of leuk. towards attractant

25
Q

Chemotaxis

A
  • influences may be exogenous or endogenous
  • granulocytes, monocytes, & some lymph. Respond to chemoattract.
  • primarily respond to bact. products & C5a, LTB4, and IL-8
26
Q

Pathophys. of chemotaxis

A
  • chemotactic agents bind to reansmembrane recept.
  • signal from binding -> activation of effector molecules in leuk., i.e.: Phospholipase C and Phosphoinositol-kinase
  • enzymes act on membrane lipids -> generate 2nd messengers
  • 2nd mess. Increase cytosolic calicum & activate enzymes that cause actin polymeriz.
  • actin regulatory proteins interact w/ leuk. cytoplasmic actin & myosin -> cell contract. And movement
27
Q

3 steps of phagocytosis

A
  • recognition
  • engulfment
  • killing/degrad.
28
Q

2 important opsonins in Recognition phase of phagocyt.

A

IgG & C3b

29
Q

Engulfment phase of phagocyt.

A
  • pseudopods wrap around particle -> phagosome
  • phagosome membrane fuses w/ lysosomal granules of leuk. -> expulsion of granule content into phagolysosome
30
Q

4 intracellular events phagocytosis stimulates

A
  • increased O2 consumpt.
  • glycogenolysis
  • incre. Glucose oxidation via oxygen monophosphate shunt
  • H2O2 prod.
31
Q

2 categories of bactericidal mech. Caused by killing/degrad. Phase

A
  • O2 dependent mech.
  • O2 independent mech.
32
Q

O2 dependent bactericidal mech.

A
  • triggered by activation of cytosolic and plasma membr. linked oxidases that -> O2 into H2O2
  • toxic byprod. Of rxn -> kill ingest. Bact.
33
Q

H2O2-myeloperoxidase-halide system

A
  • kills bact, fungi, viruses, & mycoplasma
  • reduced NADPH oxidase during phagocyt. -> liberation of H2OS from phagolysosome
  • H2O2 in presence of myeloperoxidase & halide ion -> hypochlorite
  • hypochlorite very effective in killing phagocytized org.
  • superoxide anion also toxic
34
Q

O2 independent bactericidal mech.

A
  • H+ ions from lactate or carbonic anhydrase -> decreas. in pH in phagolysosomes
  • lysozyme action attacks bact. cell wall via hydrolyzing muramic acid N-acetyl glucosamine bond in glycopeptide coat
  • lactoferrin: Fe binding protein in specific granules of neutr. are toxic
  • defensins: cationic arginine rich peptides toxic to microbes
35
Q

2 types of chemical mediators of inflamm.

A
  • plasma deriv.
  • cell deriv. (Preformed or newly synth.)
36
Q

3 types of preformed mediators

A
  • histamine
  • serotonin
  • lysosomal enzymes
37
Q

4 Newly synthesized cell mediators

A
  • prostaglandins
  • leukotrienes
  • platelet activating factors
  • cytokines
38
Q

3 plasma mediators

A
  • complement syst.
  • kinin syst.
  • clotting/fibrinolytic syst.
39
Q

Histamine

A
  • from mast cell
  • increase.: arterial dilat. & venule perm.
  • early inflamm. resp. (IMMEDIATE TRANSIENT RESP.)
40
Q

6 factors that release histamine

A
  • IgE
  • Phys. Agents: trauma or heat, etc
  • C3a & C5a frag.
  • cationic proteins form neutroph. lysosomes
  • substance P (neuroproteins)
  • IL-1 & IL-8
41
Q

Serotonin

A
  • pre-formed
  • similar to hist. in rodents
  • released from mast cell granules & platelets
42
Q

Kinins

A
  • from kininogens
  • lysis of cells -> kinin precurs.
  • Bradykinin: sust. & enhances histamine effects
  • pain mediator & contracts smooth m.
  • kallekrein: activates hageman fact.; fibrinolytic path.; and complement syst.
43
Q

C3a & C5a

A
  • vasodilat. via stim. by histamine release
  • aka: anaphylatoxins
44
Q

C5a

A
  • chemotactic for eosin., neutr., basoph., & monocytes
45
Q

C5b-9 complex

A

MAC (lyses bact.)

46
Q

C3b

A
  • opsonin
47
Q

Prostaglandins

A
  • 20 carbon fatty acid
  • enhance/reduce effects of biological processes
  • stim. by inflamm. stimuli
  • causes: vasodil., increas. Perm., fever, & pain
48
Q

Lysosomal enzymes

A
  • from neutr.
  • microbicidal
  • causes inadvertent tissue damage w/ oxyradicals
  • may increase vasc. Perm. & chemotaxis via C3 and C5
49
Q

Cytokines

A
  • proteins that mod. funct. of other cells
  • prod. by all cells, mainly lymph. & macroph.
  • roles in acute & chronic inflamm.
  • TNF & IL-1= Major inflamm. Cytokines (effect on endoth. Cells, leuk., and fibroblasts)

Vet Path. (10 decks)

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