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Foundations of Medicine > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

Define acute inflammation?

A

inflammation
-fundamental response
-dynamic, homeostatic mechanism
-you find a series of protective changes occurring in living tissue as a response to injury

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2
Q

Name the cardinal signs of inflammation?

A

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

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3
Q

List the causes of acute inflammation?

A

-micro-organisms
-trauma
-exposure to chemicals
-physical- extreme conditions
-dead tissue (cell necrosis irritates adjacent tissues)
-hypersensitivity

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4
Q

What is the microcirculation?

A

All over us

It is the capillary beds, fed by arterioles and drained by venules but also the extracellular compartment - fluid and molecules within it.

Also includes the lymphatic channels and lymphatic drainage channels.

Occurs in a dynamic balance- things move but in a way which is balanced

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5
Q

What happens in micro circulation?

A

fluid moves essentially from the vessels into the tissue

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6
Q

Pathogenesis of acute inflammation?

A

changes in vessel radius- alter the amount of flow through the vessel

change in permeability of the vessel wall-endothelium becomes more permissive or less permissive (exudation)

movement of neutrophils from the vessel to the extravascular space

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7
Q

Describe what happens with the local changes in vessel radius and blood flow?

A

1.transient arteriolar constriction
-transient constriction of the feeding arterials
-probably protective
2. local arteriolar dilation
-active hyperaemia
-see more blood in those vessels
-widen radius
3. relaxation of vessel smooth muscle that covers vessel wall

The triple response- goes red, redness about it and then swelling

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8
Q

How does increased permeability occur?

A

-happens in the vessels, in the microvascular bed
-caused by locally produced chemical mediators (small mols from cells) which increase permeability of endothelial cells (lining vessels) and make it leak
-When leaks, leaks fluid. Protein and fluid not held in vessel lumin- escape into adjacent tissue

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9
Q

Effects of increased permeability?

A

net movement of plasma from capillaries to extravascular space (exudation)

what is leaked is an exudate

exudate-exudate - fluid rich in protein - like plasma - includes immunoglobulin and fibrinogen

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10
Q

Effects of exudation?

A

oedema formed

oedema is accumulation of fluid in the extravascular space

explains swelling of tissue in acute inflammation because movement of fluid across membrane

swelling causes pain - reduce function

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11
Q

What is a further effect of increased permeability?

A

fluid loss-increased viscosity
increased viscosity-stasis
got all cells in blood and less plasma holding them up and the rate of flow slows (stasis)

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12
Q

What happens to flow in inflammation?

A

loss of normal laminar flow
red cells aggregate in the centre of the lumen
neutrophils found near endothelium

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13
Q

What are the phases of emigration of neutrophils?

A

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

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14
Q

Describe gingivitis?

A

gums are swollen and inflamed
associated with certain types of acute leukaemias

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15
Q

Describe acute pyelonephritis?

A

tubules inside kidney have blood and pus coming through

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16
Q

Describe bacterial endocarditis?

A

vegetations(mix of fibrin, neutrophils and micro organisms stuck on the atrial surface - of cusp)

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17
Q

What happens after acute inflammation?

A

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

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18
Q

What are the 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 to phagocytose
plasma proteins localise process
resolution and return to normal

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19
Q

Outcomes of acute inflammation?

A

resolution
suppuration (pus formation)
organisation (tissue repair)
chronic inflammation( inflammation doesn’t go away- associated with tissue damage)

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20
Q

Describe the role of the neutrophil?

A

mobile phagocytes
-recognise foreign antigen
-move towards it - chemotaxis
-adhere to organism

granules possess oxidants (eg H2O2) and enzymes (eg proteases)

release granule contents

phagocytose & destroy foreign antigen

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21
Q

Why is lung inflammation called pneumonia and not lung-itis?

A

inflammatory process in pneumonia doesn’t really sit in the lung tissue primarily but in air space within lung

22
Q

Consequences of neutrophil action?

A

neutophils die when granule contents released
produce a “soup” of fluid, bits of cell, organisms, endogenous proteins - pus
might extend into other tissues, progressing the inflammation

23
Q

Role fibrinogen (plasma protein) in inflammation?

A

Fibrinogen- coagulation factor
-floats around as blood plasma and under circumstances it coagulates to form fibrin (series of fibrogen mols all bonded together)
-when fibrinogen escapes from vessel due to increased permeability
-becomes in contact with what is around, including enzymes released by neutrophils-which are proteases
-protease chips off a bit of fibrinogen and makes it sticky and it then forms a polymer with other fibrinogen to produce fibrin
-clots the exudate and in doing so, localises the inflammatory process and its less easy for it to leak away into the adjacent lymphatics

24
Q

Role of immunoglobulins in the plasma?

A

immunoglobulins in plasma specific for antigen - humoural immune response

25
Q

List mediators of acute inflammation and describe functions?

A

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

26
Q

What are the collective effects of mediators?

A

vasodilatation- increasing blood flow into area

increased permeability- increases leakiness of the endothelium and then thereby increases the permeability of the endothelium to the flow of plasma and its contents across the membrane

neutrophil adhesion

chemotaxis- attracting neutrophils as transverse the tissue

itch and pain

27
Q

Give examples of the cell surface mediators?

A

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

28
Q

Give characteristics of histamine? (mols released from cells)

A

Histamine (causing vasodilation and increased permeability)
-sits in mast cells beside vessels, platelets and in basophils
-because of local injury (IgE mediated, histamine is released and has the effects of vasodilation and increased permeability
Causes smooth muscle to relax
-when histamine is released it acts to H1 receptors on endothelial cells

29
Q

Give characteristics of seratonin (mols released from cells)?

A

5-hydroxytryptamine (serotonin) (causing vasoconstriction)
-found pre formed in platelets
-when platelets begin to coagulate, the granules and platelets begin to fall apart and release the content.
-causes vasoconstriction

30
Q

Give characteristics of prostglandins (arachidonic acid metabolites via cyclo-oxygenase pathway)?

A

many cells (endothelium and leukocytes)

many promote histamine effects and inhibit inflammatory cells

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

prostglandins increase effectiveness of non-steroidal anti-inflammatory drugs. Counter acting

31
Q

Give characteristics of cytokines and chemokines? (eg TNFα, IL-1)

A

small molecules produced by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
pro-inflammatory and anti-inflammatory effects
different molecules have different effect
balance of effects
stimulate intracellular pathways and signalling

32
Q

Give characteristics of nitric oxide (molecule released from cells)?

A

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

33
Q

Give characteristics of oxygen free radicals?

A

released by neutrophils on phagocytosis
amplify other mediator effects

34
Q

What do molecules inside cells have the role of doing?

A

pattern associated molecular patterns
-microbial antigen
-genetically hard wired to recognise
-innate and adaptive immunity

danger associated molecular patterns
-substances released in response to stimulus

stimulate pattern recognition receptors on cell membranes to activate inflammatory response

35
Q

Give examples of intracellular inflammatory pathways and their functions?

A

NF-κB (nuclear factor kappa-B) pathway

MAPK (mitogen-activated protein kinase)

Stimulated in inflammation via surface receptors eg toll-like receptors (TLRs)
Regulates pro-inflammatory cytokine production and inflammatory cell recruitment

JAK-STAT (Janus kinase – signal transducer and activator to transcription) pathway
Direct translation of extracellular signal to molecular expression

36
Q

Describe the mechanism of the intracellular signalling pathway?

A

Microorganism floating around in our blood, releases an unpleasant product. And the unpleasant product works on the cell surface receptor.
After this happens, through a number of different pathways, you see activation of NF kappa B or the MAPK pathway.
Result is an inflammatory cytokine production occurring (in nucleus)

37
Q

Give the four enzyme cascades in blood plasma and what their function is?

A

blood coagulation pathways
-clots fibrinogen in exudate and interacts widely with other systems

fibrinolysis
breaks down fibrin, helps maintain blood supply and fibrin breakdown products vasoactive

kinin system
bradykinin: pain

complement cascade
ties inflammation with immune system
active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

38
Q

What are the general effects of mediators?

A

mediators have positive and negative effects
result is a dynamic balance
favours and inhibits acute inflammation
relative to need

39
Q

What are the immediate systemic effects of inflammation?

A

pyrexia - raised temperature
endogenous pyrogens from white cells
act centrally

feel unwell
malaise, anorexia, nausea
abdominal pain and vomiting in children

neutrophilia - raised white cell count
bone marrow releases/produces

40
Q

What are the longer term effects of acute inflammation?

A

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

41
Q

Describe suppuration as an outcome of acute inflammation?

A

pus formation
-dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris

pyogenic membrane surrounds pus
-capillary sprouts, neutrophils, fibroblasts
walls off pus

42
Q

Describe the differences between an abscess and a multiloculated abscess?

A

instead of pus discharging across epithelial surface, it forms other little abscesses in the tissue itself

43
Q

What is empyema?

A

Pus in a pleural cavity

44
Q

What is pyaemia?

A

discharge of pus into bloodstream

45
Q

Describe organisation?

A

the characteristic tissue reaction of organisation is granulation tissue.
Presence of granulation tissue indicates there is a process of healing and repair going on.
leads to fibrosis and formation of a scar.

46
Q

What is granulation tissue?

A

repair kit – for all damage
formed of
new capillaries - angiogenesis
fibroblasts and collagen
macrophages

47
Q

What is involved in dissemination/sepsis?

A

usually has a microbial cause

spread to bloodsteam - patient “septic”
bacteraemia - bacteria in blood
septicaemia - growth of bacteria in blood
toxaemia - toxic products in blood

48
Q

What are the equations to work out cardiac output and blood pressure?

A

Cardiac output

CO = SV x HR

cardiac output (CO)
stroke volume (SV)
heart rate (HR)

Blood pressure

BP = CO x SVR

blood pressure (BP)
cardiac output (CO)
systemic vascular resistance (SVR)

49
Q

Effects of systemic infection?

A

shock- cannot get enough oxygen delivered to tissues to make them function properly

clinical picture of early septic shock-
peripheral vasodilatation
tachycardia - high heart rate
hypotension - low blood pressure
often pyrexia
sometimes haemorrhagic skin rash

50
Q

Pathogenesis of septic shock?

A

systemic release of chemical mediators from cells into plasma
mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR
results in catecholamine release
tachycardia (increased heart rate) follows to maintain (CO) because
increased heart rate compensates - CO = SV x HR

bacterial endotoxin released

interleukin-1 released
acts on hypothalamus - pyrexia

activation of coagulation
disseminated intravascular coagulation
vasoactive chemical - vasodilatation
haemorrhagic skin rash

51
Q

What happens when compensation fails?

A

raised HR insufficient to maintain cardiac output
SVR low; so, BP falls
BP = CO x SVR
increasing heart rate insufficient (CO = SV x HR)
reduced perfusion of tissues
tissue hypoxia
loss of cell tissue and organ function

52
Q

Outcome of septic shock?

A

Foundations of Medicine (85 decks)

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