Acute Inflammation

Question 1

what is acute inflammation?

Answer 1

• “The immediate and early response to injury, designed to deliver leukocytes to the site of injury.”
• Inflammation is not a disease, but is often a manifestation of disease
• Inflammation can be beneficial but can also cause harm

Question 2

what are the 2 types if inflammation?

Answer 2

acute = initial & often transient series of tissue reactions to injury
chronic = subsequent & often prolonged tissue response following initial response

Question 3

nomenclature note:
a) what is it when words end with “itis”?
b) what is it when words end with “osis”?

Answer 3

a) inflammation of
b) disease or condition

Question 4

what are causes of acute inflammation?

Answer 4

• Microbial infections →e.g. bacteria & viruses
• Hypersensitivity reactions →Excessive immune response →tissue damage
• Physical agents →Trauma, radiation or heat injury
• Chemicals →Corrosives, acids or bacterial toxins
• Tissue necrosis →Secondary to ischaemia (dead tissue releases peptides which stimulate)

Question 5

what parts of microbial infection stimulate inflammation?

Answer 5

• bacterial exotoxins & endotoxins
• viral intra-cellular multiplication (leads to cell death & debris stimulate inflammation)
• organisms causing hypersensitivity

Question 6

what are cardinal signs of acute inflammation?

Answer 6

• redness (rubor) = due to dilation of vessels
• heat (calor) = due to increase blood flow
• swelling (tumor) = due to accumulation of fluids (also increase of inflammatory cells migrating to area)
• pain (dolar) = due to physical distortion of tissue & due to release of some chemical mediators
• loss of function

Question 7

what are stages of inflammation?

Answer 7

• release of chemical mediators
• vasodilation
• increased vascular permeability
• fluid accumulation
• cellular recruitment
• phagocytosis

Question 8

what are 2 major components of acute inflammation?

Answer 8

vascular changes (permeability & vasodilation) & cellular events (formation of cellular extrude)

Question 9

what are the vascular changes in acute inflammation?

Answer 9

increased vascular permeability & changes in vascular calibre

vasodilation - lasts from 15 mins to several hours
increased vascular permability = increased net flow of fluid out of vessels - called exudation

Question 10

what do neutrophil polymorphs do in acute inflammation?

Answer 10

they accumulate - they usually flow in middle of vessels:

margination - they marginate towards endothelial cells = loss of intravascular fluid & slowing
adhesion - also called pavementing - they stick to vascular endothelium
emigration - pass between endothelial cells & through basal lamina & into adventitia

Question 11

what is process of adhesion of neutrophils?

Answer 11

ligands on neutrophil surface engage with P-selectin on endothelial cells and PAF (platelet activating factor) dock with corresponding receptor on neutrophil & promote expression of other molecules which overall results in firm adhesion

Question 12

what are P-selectin & PAF?

Answer 12

they’re factors on endothelial cells that help adhesion of neutrophils
- the release of histamine & thromin (in original inflammatory stimulus) causes up regulation of P-selectin & PAF

(PAF = platelet activating factor)

Question 13

what are chemical mediators released by cell in acute inflammation?

Answer 13

• histamine
• lysosomal compounds
• leukotrines
• prostaglandins
• seratonin

Question 14

how does seritonin affect blood vessels?

Answer 14

vasoconstrictor = released by platelets

Question 15

what are prostaglandins?

Answer 15

• derived from arachadonic acid
• Some cause increased vascular permeability
• Some cause platelet aggregation
• Released by lots of cell types

Question 16

what are leukotrienes?

Answer 16

vasoactive properties - often made in neutrophils from arachidonic acid(a fatty acid in cell membrane)
(it’s a chemical mediator)
-some types attract immune cells to site of infection

Question 17

what are lysosomal compounds?

Answer 17

• Lots of different functions, such as vascular permeability
• Some can stimulate histamine release from mast cells
• Released by neutrophils

= lysosomes are membrane-bound organelles containing a variety of enzymes that have different functions

Question 18

what is histamine?

Answer 18

• released by mast cells - Released mainly by mast cells
• cause vascular dilation & permeability

Question 19

what are chemokines?

Answer 19

family of chemicals which attract more white blood cells to site of inflammation (they’re cytokines and help direct for chemotaxis)

Question 20

what are the 4 enzyme cascades in plasma? (part of cellular part of acute inflammation)

Answer 20

1. coagulation system (converts fibrinogen -> fibrin)
2. kinins (activated by coagulation factor - bradykinin = important peptide in mediating vasodilation)
3. fibrinolytic system
4. complement system

Question 21

what are the benefits of inflammation?

Answer 21

• dilution of toxins (mitigate effect of toxins on tissues)
• entry of antibodies (stimulates immune response, facilitates immune cells)
• transport of drugs
• fibrin formation
• delivery of nutrient & oxygen

Question 22

what are the harmful effects of inflammation?

Answer 22

• digestion of normal tissue (innapropriate overactive immune response)
• swelling (necessary by-product, if in neck you can get airway obstruction, anywhere in body it can end up with dangerous comprimise)
• innappropriate inflammatory response

Question 23

why are neutrophils good?

Answer 23

they can move = by contracting cytoplasmic microtubules = calcium ion dependant mechanism, chemotaxis in response to inflammatory chemicals

they can stick to opsonised microorganisms

they can phagocytose

they can kill them, once gobbled up - with variety of intra-cellular methods to produce microbicidal agents