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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
Chemotaxis
- influences may be exogenous or endogenous - granulocytes, monocytes, & some lymph. Respond to chemoattract. - primarily respond to bact. products & C5a, LTB4, and IL-8
26
Pathophys. of chemotaxis
- 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
3 steps of phagocytosis
- recognition - engulfment - killing/degrad.
28
2 important opsonins in Recognition phase of phagocyt.
IgG & C3b
29
Engulfment phase of phagocyt.
- pseudopods wrap around particle -> phagosome - phagosome membrane fuses w/ lysosomal granules of leuk. -> expulsion of granule content into phagolysosome
30
4 intracellular events phagocytosis stimulates
- increased O2 consumpt. - glycogenolysis - incre. Glucose oxidation via oxygen monophosphate shunt - H2O2 prod.
31
2 categories of bactericidal mech. Caused by killing/degrad. Phase
- O2 dependent mech. - O2 independent mech.
32
O2 dependent bactericidal mech.
- triggered by activation of cytosolic and plasma membr. linked oxidases that -> O2 into H2O2 - toxic byprod. Of rxn -> kill ingest. Bact.
33
H2O2-myeloperoxidase-halide system
- 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
O2 independent bactericidal mech.
- 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
2 types of chemical mediators of inflamm.
- plasma deriv. - cell deriv. (Preformed or newly synth.)
36
3 types of preformed mediators
- histamine - serotonin - lysosomal enzymes
37
4 Newly synthesized cell mediators
- prostaglandins - leukotrienes - platelet activating factors - cytokines
38
3 plasma mediators
- complement syst. - kinin syst. - clotting/fibrinolytic syst.
39
Histamine
- from mast cell - increase.: arterial dilat. & venule perm. - early inflamm. resp. (IMMEDIATE TRANSIENT RESP.)
40
6 factors that release histamine
- IgE - Phys. Agents: trauma or heat, etc - C3a & C5a frag. - cationic proteins form neutroph. lysosomes - substance P (neuroproteins) - IL-1 & IL-8
41
Serotonin
- pre-formed - similar to hist. in rodents - released from mast cell granules & platelets
42
Kinins
- 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
C3a & C5a
- vasodilat. via stim. by histamine release - aka: anaphylatoxins
44
C5a
- chemotactic for eosin., neutr., basoph., & monocytes
45
C5b-9 complex
MAC (lyses bact.)
46
C3b
- opsonin
47
Prostaglandins
- 20 carbon fatty acid - enhance/reduce effects of biological processes - stim. by inflamm. stimuli - causes: vasodil., increas. Perm., fever, & pain
48
Lysosomal enzymes
- from neutr. - microbicidal - causes inadvertent tissue damage w/ oxyradicals - may increase vasc. Perm. & chemotaxis via C3 and C5
49
Cytokines
- 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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