Acute Inflammation

Question 1

Acute Inflammation

Answer 1

respond/protective changes to maintain intergrity, localised in site of injury
Redness that doesnt cease
Rubor tumor dalor (pain) calor (heat) + loss of function
takes place in microcirculation

Question 2

Flow (Q) is proportional to r (power of 4)

Answer 2

Poiseuille’s Law

Question 3

Control flow (fluid flux) across membrane
(hydrostatic and colloid osmotic pressures
compartments and physical constants)

Answer 3

Starling forces

Question 4

neutrophil move to endothelial aspect of lumen

Answer 4

Margination

Question 5

neutrophil attach to endothelial walls

Answer 5

Pavementing

Question 6

neutrophil squeeze between endothelial cells to ECF

Answer 6

Emigration

Question 7

Rouleux formation

Answer 7

RBCs aggregration

Question 8

Effects of exudation

Answer 8

oedema formation = swelling

Vasodilation and Increased Permeability
Increased blood - Increase HP inside - drives fluid pressure - leaks out
= Proteins and fluid leaking out of vessels
Decreased colloid pressure - conc inside lower

Question 9

Benefits of Acute Inflammation

Answer 9

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

Question 10

adhesion molecules appear on endothelial cells
ICAM-1 - help neutrophils stick
P-selectin - interacts with neutrophil surface

Answer 10

Cell surface mediators

Question 11

Causes vasoconstriction
Preformed in platelets
Released when platelets degranulate in coagulation

Answer 11

5-hydroxytryptamine (serotonin)

Mediators Molecules released from cells

Question 12

Increase conc of RBC as plasma protein pass between endothelial cells = Increase Viscosity = allows:

Answer 12

Stasis - blood pass slow - allows leucocyte - neutrophil - margination, pavementing, emigration

Question 13

mobile phagocyte
chemotaxis
adherence
release granules = pus

Answer 13

Neutrophils

Question 14

Form fibrin and clot exudate

Answer 14

fibrinogen (pp) - coag factor

Question 15

Blood coag

Answer 15

clots fibrinogen in exudate

Question 16

Pain

Answer 16

Bradykinin - Kinin System

Question 17

Active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

Answer 17

Complement cascade (C3a )

Question 18

preformed in mast cells beside vessels, platelets, basophils
released as a result of local injury; IgE mediated reactions
causes vasodilatation, increased permeability - H1 receptors on endothelial cells

Answer 18

Histamine (mediator)

Question 19

thromboxane A2 promotes platelet aggregation and vasoconstriction – the opposite effect to PGD2, PGE2, etc

Answer 19

Prostaglandins

Question 20

neutrophils especially

vasoactive - dynamic effect on vessels to increase permeability and constrict smooth muscle

Answer 20

leukotrienes

Question 21

decrease synthesis of arachidonic acid derived inflammatory mediators

Answer 21

Omega-3 FA

Question 22

cell memb - activated inflammatory cells

Reduce permeability by enhancing platelet granulation at site of injury

Answer 22

Platelet-activating factor (PAF)

Question 23

Small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
Attract inflammatory cells

Answer 23

cytokines and chemokines (eg TNFα, IL-1)

Question 24

smooth muscle relaxation (vasodilation), anti-platelet, regulate leukocyte recruitment to inflammatory focus

Answer 24

NO

Question 25

Released by neutrophils on phagocytosis | Amplify other mediator effects

Answer 25

Oxygen free radicals (H2O2, OH-, O2-)

Question 26

Breaks down fibrin, helps maintain blood supply | Fibrin breakdown products - vasoactive

Answer 26

fibrinolysis

Question 27

Pyrexia - fever Unwell - malaise (discomfort), anorexia, nausea, abd pain, vomiting in children T - temp increase - pyrogens - WBC - central

Answer 27

Immediate systemic effect of inflamm

Question 28

Lymphadenopathy - regional lymph node enlargement immune response weight loss - catabolic process anaemia

Answer 28

Longer term effect

Question 29

Pus (soup) | Pyogenic membrane surrounds pus (capillaries sprout)

Answer 29

Outcome of inflammation - suppuration Abscess - collection of pus under pressure “points” and discharges; collapses - healing and repair Empyema - pus in a hollow viscus - gall bladder, pleural cavity Pyaemia - discharge to bloodstream

Question 30

Granulation tissue characteristic Healing and repair =collagen - Leads to fibrOsis and formation of a scar

Answer 30

Outcome of inflammation - Organisation Granulation tissue -new capillaries - angiogenesis, fibroblasts and collagen, macrophages these happen if resolution fail new capillaries grow, macrophages and fibroblasts on the site of injury

Question 31

Spread to bloodstream - patient “septic”

Answer 31

DiSsemination bacteraemia - bacteria in blood septicaemia - growth of bacteria in blood toxaemia - toxic products in blood

Question 32

Clinical Features of Septic Shock

Answer 32

``` inability to perfuse tissues tachycardia - high HR hypotension periperal vasodilatation often pyrexia ``` ``` Outcome of septic shock rapidly fatal tissue hypoxia - cell death haemorrhage requires urgent intervention and support admit to hospital and intensive care ```

Question 33

Pathogenesis of septic shock

Answer 33

loss of systemic vascular resistance (SVR) results in catecholamine release bacterial endotoxin released - IL-1 - acts on hypothalamus - pyrexia activation of coagulation vasoactive chemical - vasodilatation haemorrhagic skin rash tachycardia (increased heart rate) follows to maintain cardiac output because (CO=SV x HR)

Question 34

Ideal outcome of Acute inflamm

Answer 34

resolution