Acute Inflammation Flashcards

1
Q

Acute Inflammation

A

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

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2
Q

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

A

Poiseuille’s Law

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3
Q
Control flow (fluid flux) across membrane
(hydrostatic and colloid osmotic pressures
compartments and physical constants)
A

Starling forces

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4
Q

neutrophil move to endothelial aspect of lumen

A

Margination

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5
Q

neutrophil attach to endothelial walls

A

Pavementing

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6
Q

neutrophil squeeze between endothelial cells to ECF

A

Emigration

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7
Q

Rouleux formation

A

RBCs aggregration

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8
Q

Effects of exudation

A

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

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9
Q

Benefits of Acute Inflammation

A
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
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10
Q

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

A

Cell surface mediators

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11
Q

Causes vasoconstriction
Preformed in platelets
Released when platelets degranulate in coagulation

A

5-hydroxytryptamine (serotonin)

Mediators Molecules released from cells

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12
Q

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

A

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

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13
Q

mobile phagocyte
chemotaxis
adherence
release granules = pus

A

Neutrophils

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14
Q

Form fibrin and clot exudate

A

fibrinogen (pp) - coag factor

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15
Q

Blood coag

A

clots fibrinogen in exudate

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16
Q

Pain

A

Bradykinin - Kinin System

17
Q

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

A

Complement cascade (C3a )

18
Q

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

A

Histamine (mediator)

19
Q

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

A

Prostaglandins

20
Q

neutrophils especially

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

A

leukotrienes

21
Q

decrease synthesis of arachidonic acid derived inflammatory mediators

A

Omega-3 FA

22
Q

cell memb - activated inflammatory cells

Reduce permeability by enhancing platelet granulation at site of injury

A

Platelet-activating factor (PAF)

23
Q

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

A

cytokines and chemokines (eg TNFα, IL-1)

24
Q

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

A

NO

25
Q

Released by neutrophils on phagocytosis

Amplify other mediator effects

A

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

26
Q

Breaks down fibrin, helps maintain blood supply

Fibrin breakdown products - vasoactive

A

fibrinolysis

27
Q

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

A

Immediate systemic effect of inflamm

28
Q

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

A

Longer term effect

29
Q

Pus (soup)

Pyogenic membrane surrounds pus (capillaries sprout)

A

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

30
Q

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

A

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

31
Q

Spread to bloodstream - patient “septic”

A

DiSsemination

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

32
Q

Clinical Features of Septic Shock

A
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
33
Q

Pathogenesis of septic shock

A

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)

34
Q

Ideal outcome of Acute inflamm

A

resolution