Pathology 2 - Edema

Front 1

define inflammation?

Back 1

vascular and cellular response of local tissue to injury resulting in accumulation of fluid and leukocytes in extravascular tissues (a delivery system)

Front 2

what does inflammation consist of?

Back 2

hemodynamic and vascular events, inflammatory mediators from blood plasma (humoral) and cells (cellular), cellular infiltration

Front 3

what initiates inflammation?

Back 3

infectious agent, mechanical, chemical, or immunological injury

Front 4

what are two basic features of inflammation?

Back 4

nondiscering and stereotyped

Front 5

how is inflammation protective?

Back 5

destroys, dilutes, walls off agent of injury, set stage for repair of injured tissue by regeneration or repair

Front 6

how is inflammation harmful?

Back 6

hypersensitivity reactions (drugs, insect bites, toxins), chronic inflammation diseases (rheumatoid arthritis, immune complex glomerulonephritis, pemphigus vulgaris), fibrosis/scarring

Front 7

what occurs if there is a failure of response with inflammation?

Back 7

infections unchecked, wounds unhealed, permanent festering sores

Front 8

what are the cardinal signs of inflammation?

Back 8

heat (calor), swelling (tumor), redness (rubor), pain (dolor), loss of function (functio laesa)

Front 9

what does the suffix -itis indicate?

Back 9

inflammation of an organ

Front 10

what does the suffix -sis indicate?

Back 10

any abnormal process or condition affecting an organ

Front 11

what is the term for the inflammation of the spinal cord?

Back 11

myelitis

Front 12

what is the term for the inflammation of the vein?

Back 12

phlebitis

Front 13

what is the term for the inflammation of the lips?

Back 13

chelitis

Front 14

what is the term for the inflammation of the bone marrow?

Back 14

osteomyelitis

Front 15

what is the term for the inflammation of the cecum?

Back 15

cecitis or typhlitis

Front 16

what is the term for the inflammation of the oviduct?

Back 16

salpingitis

Front 17

what is the term for the inflammation of the lung?

Back 17

pneumonia/pneumonitis

Front 18

what is acute inflammation?

Back 18

exudative process designed to dilute (increase fluid in tissue space) and remove (via influx of inflammatory cells) injurious agents

Front 19

what is chronic inflammation?

Back 19

proliferative response, includes process of repair; scarring, neovascularization, reconstruction of damaged tissue

Front 20

what is the clinical course for acute inflammation?

Back 20

min-48hours

Front 21

what is the cellular response to acute inflammation?

Back 21

neutrophils

Front 22

what is the vascular response to acute inflammation?

Back 22

increased permeability and vasodilation

Front 23

what is the matrix of acute inflammation?

Back 23

edema and fibrin

Front 24

what is the clinical course for subacute inflammation?

Back 24

poorly defined, 3-7days

Front 25

what is the cellular response to subacute inflammation?

Back 25

neutrophils and macrophages and lymphocytes

Front 26

what is the vascular response to subacute inflammation?

Back 26

increased permeability, endothelial hypertrophy, hyperplasia

Front 27

what is the matrix of subacute inflammation?

Back 27

edema and fibrin

Front 28

what is the clinical course for chronic inflammation?

Back 28

7days-yrs

Front 29

what is the cellular response to chronic inflammation?

Back 29

macrophages, lymphocytes, plasma cells

Front 30

what is the vascular response to chronic inflammation?

Back 30

neovascularization

Front 31

what is the matrix of chronic inflammation?

Back 31

collagen (fibrous)

Front 32

what are the vascular events in acute inflammation?

Back 32

hemodynamic adjustments, increased vascular permeability, exudate (inflammatory edema) formation

Front 33

what occurs in tissues without adequate perfusion during acute inflammation?

Back 33

cannot support inflammatory response (lack of vascular events) and there is no inflammation in dead/avascular tissue)

Front 34

what hemodynamic adjustments occur in acute inflammation?

Back 34

(1) transient arteriolar vasoconstriction (inconsistent) (2) arterioles dilate first followed by adjacent capillaries resulting in (a) increased blood flow (active hyperemia; redness, heat) that brings in inflammatory mediators and leukocytes (b) local hemoconcentration and slowing of blood flow in capillaries and venules (passive hyperemia or congestion)

Front 35

what causes increased vascular permeability during acute inflammation?

Back 35

intercellular gaps form in post-capillary venules and endothelial cell injury

Front 36

what causes intercellular gaps to form in post-capillary venules?

Back 36

mast cell degranulation that causes endothelial contraction (receptor-mediated) via an immediate transient response caused by mediators (histamine, serotonin, bardykinin, kinins, leukotrienes, lymphokines, PAF, fibrinopeptides and delayed (4hrs) and prolonged (>24hrs) do to cytoskeletal reorganizaiont (IL1/TNF, hypoxia)

Front 37

what are the mediators of intercellular gaps in post-capillary venules?

Back 37

histamine, serotonin, bardykinin, kinins, leukotrienes, lymphokines, PAF, fibrinopeptides

Front 38

what causes direct endothelial injury resulting in increased vascular permeability?

Back 38

endotoxin, radiation, NO, O2, radicals, chemicals

Front 39

what type of process is the direct endothelial injury?

Back 39

necrosis

Front 40

in direct endothelial injury, toxins, burns, and chemicals occur where?

Back 40

immediate prolonged inflammation in any vessel type

Front 41

in direct endothelial injury, leukocyte-dependent injury (vasculitis, immune-mediated) occurs where?

Back 41

mostly post-capillary venules

Front 42

what are the patterns of vascular leakage responses?

Back 42

immediate transient (mins), delayed prolonged, immediate prolonged

Front 43

what causes and where does immediate transient vascular leakage occur?

Back 43

histamine on postcapillary venules

Front 44

what causes and where does delayed prolonged vascular leakage occur?

Back 44

damaged but not necrotizing effect on endothelial cells (UV radiation sunburn) all vessel types

Front 45

what causes and where does immediate prolonged vascular leakage occur?

Back 45

agents causing direct endothelial damage and death (burn) all vessel types

Front 46

when does exudate (inflammatory edema) formation occur?

Back 46

severe damage to vascular permeability; leakage of blood coagulation proteins (fibrinogen) into tissue space which polymerizes to fibrin

Front 47

when is exudate (inflammatory edema) formation seen clinically?

Back 47

when local lymphatic drainage is saturated and backs up

Front 48

how might exudate (inflammatory edema) formation be spread?

Back 48

lymphatics may also serve to spread inflammatory process to regional lymph nodes resulting in lymphadenitis then systemic inflammation

Front 49

what is permeability?

Back 49

fluids and proteins leak into surrounding extravascular tissues carrying acute phase proteins, complement, fibrinogen, fibronectin, antibodies

Front 50

the early vascular events of inflammation provide the physiologic basis for what?

Back 50

lewis triple response reaction, an example of mild acute inflammation

Front 51

what is the lewis triple response reaction?

Back 51

(1) red line appears (arteriole dilation) (2) red halo around line called a flare (hyperemia) (3) swelling around line, blanching of original mark (edema)