acute inflammation Flashcards Preview

PRINCIPLES OF FUN > acute inflammation > Flashcards

Flashcards in acute inflammation Deck (42):
1

what is the definition of acute inflammation?

fundamental response maintaining integrity of organism ( dynamic homeostatic mechanism)
series of protective changes occurring in living tissue as a response to injury

2

what are the cardinal signs of inflammation?

rubor - redness
calor - heat
tumor - swelling
dolor - pain
loss of function

3

what is the aetiology of acute inflammation?

pathogenic organisms
mechanical trauma or injury to tissue (occurs in all injuries even those that are sterile)
Chemical - upset stable environment (acid or akali)
physical - extreme conditions such as heat, cold or ionising radiation
dead tissue - cell necrosis
HYPERSENSITIVITY

4

what is the process of acute inflammation?

series of events
localised to affected tissue
takes place in the microcirculation
result in the cardinal signs of inflammation

5

what is the microcirculation?

capillary beds, fed by arterioles and drained by venules
STARLING FORCES CONTROL FLOW ACROSS MEMBRANE
there is a dynamic balance, which is maintained by HYDROSTATIC AND COLLOID OSMOTIC PRESSURE and COMPARTMENTS AND PHYSICAL CONSTANTS
lymphatic channels and drainage
extracellular "space" and the fluid and molecules within it

6

what are the steps - pathogenesis - in acute inflammation?

changes in vessel radius - flow
change in the permeability of the vessel wall - exudation
movement of neutrophils from the vessel to the extravascular space

7

what changes take place locally in vessel radius and blood flow during acute inflammation?

transient arteriolar constriction
local arteriolar dilation - hyperaemia
relaxation of vessel smooth muscle
known as the triple response - flush,flare,wheal

8

what is the effect of increased arteriolar radius?

increased local tissue blood flow which results in observed redness and heat - active hyperaemia
poiseuille's law

9

what is increased permeability and what happens when it increases.

localised vascular response
microvascular bed
endothelial leak - fluid and protein not held in the vessel lumen
locally produced chemical mediators

10

what are the effects of increased permeability?

net movement of plasma from capillaries to extravascular space
process is called exudate
exudate is the name given to the fluid which leaks
exudate is rich in protein
fluid loss - which leads to increased viscosity and decreased flow (stasis)

11

what are the effects of exudation?

oedema formed
oedema is an accumulation of fluid in the extravascular space
causes swelling in acute inflammation
swelling causes pain - reduce function

12

what is the pattern of normal laminar flow?

neutrophils on the inside, eryhtrocytes on the outside, plasma contained within the cell

13

what happens to laminar flow in acute inflammation?

red cells aggregate in the centre of the lumen
neutrophils found near the endothelium
neutrophil polymorphonuclear leukocyte (NPL) is most important cell

14

what are the phases of neutrophil emigration?

margination - neutrophils move to endothelial aspect of lumen
pavementing - neutrophils adhere to endothelium
emigration - neutrophils squeeze between endothelial cells to extravascular tissues

15

how would acute inflammation be resolved?

inciting agent is isolated and destroyed
macrophages move in from blood and phagocytose the debris; then leave
epithelial surfaces regenerate
inflammatory exudate filters away
vascular changes return to normal
inflammation resolves

16

what are the benefits of acute inflammation?

rapid response to non specific insult
cardinal signs and loss of function provide transient protection of inflamed area
neutrophils destroy organisms and denature antigen for macrophages
plasma proteins keep the process localised
resolution and eventual return to normal function

17

what are the possible outcomes of acute inflammation?

resolution
suppuration
organisation
chronic inflammation

18

what do neutrophils do?

recognise foreign antigen
move to towards it - chemotaxis
adhere to organism
they release granule content which contain oxidants and enzyme
phagocytose and destroy foreign antigen

19

what are some consequences of neutrophil action?

die after granule contents released
produce a mixture of fluid, bits of cells, organisms, endogenous proteins - pus
pus may extend into other tissues, progressing the inflammation

20

what are the two plasma proteins involved in inflammation?

fibrinogen and immunoglobulins

21

what are the roles of plasma proteins in inflammation?

fibrinogen is a coagulation factor which forms fibrin and clots the exudate - localises inflammatory process
immunogloblulins are part of the humoural immune response

22

what are the mediators of acute inflammation?

molecules on endothelial cell surface membrane
molecules released from cells
molecules in the plasma

23

what are some collective effects of mediators?

vasodilatation
increased permeability
neutrophil adhesion
chemotaxis
itch and pain

24

why are cell surface mediators sticky?

adhesion molecules appear on endothelial cells e.g. to help neutrophils stick
P-selectin interacts with neutrophil surface

25

what molecules are released from cells during acute inflammation?

histamine - released is a result of local injury (IgE mediated). also causes vasodilatation and increased permeabilty
serotonin - released when platelets degranulate in coagulation, causes vasoconstriction
prostaglandins- promotes histamine effects and inhibits inflammatory cells
leukotrienes - neutrophils, vasoactive
omega-3-polyunsaturated fatty acids
platelet activating factor
cytokine and chemokines
nitroc oxide
oxygen free radicals

26

what four enzyme cascades interact in acute inflammation?

blood coagulation pathways
fibrinolysis
kinin system
complement cascade

27

what are the immediate systemic effects of inflammation?

pyrexia
feel unwell
neutrophilia - raised white cell count

28

what are some longer term systemic effects of inflammation?

lymphadenopathy
weight loss
anaemia

29

what is suppuration?

formation of pus which is then surrounded by a pyogenic membrane

30

what is an abscess?

collection of pus under pressure
single locule or multiloculated
points and discharges
collapses - healing and repair

31

what surrounds the abscess cavity?

an ingrowth of granulation tissue

32

what is a multiloculated abscess?

when pus bursts through the pyogenic membrane surrounding the original cavity to form more cavities

33

what is empyema?

when pus is in a hollow viscus, such as the pleural cavity

34

what is pyaemia?

pus discharge to the bloodstream

35

what is organisition?

an outcome of acute inflammation that is characteristic of granulation tissue, promotes healing and repair and leads to fibrosis and the formation of a scar

36

what is granulation tissue?

formation of new capillaries - angiogenesis
composed of fibroblasts, collagen and macrophages

37

what are some consequences of dissemination of acute inflammation?

spread to bloodstream -"septic"
bacteraemia - bacteria in blood
septicaemia - growth of bacteria in blood
toxaemia - toxic products in blood

38

what are the effects of systemic infection?

shock - inability to perfuse tissues

39

what are the clinical signs of early septic shock?

tachycardia
hypotension
peripheral vasodilation
pyrexia often
sometimes haemorrhagic skin rash

40

what is the pathogenesis of septic shock?

systemic release of chemical mediators from cells into plasma
decreased Systemic vascular resistance causes tachycardia because the heart rate is increased in order to maintain cardiac output
bacterial endotoxin is released
activation of coagulation - rash

41

what are the outcomes of septic shock?

rapidly fatal
tissue hypoxia = cell death
haemorrhage

42

summarise the outcomes of acute imflammation

resolution
suppuration
organisation
dissemination
chronic inflammation