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2. Foundations of Medicine PoD > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Define accute inflammation

A
  • fundamental response maintaining integrity of organism- dynamic homeostatic mechanism, occurs in higher organisms
  • series of protective changes occurring in living tissue as a response to injury
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2
Q

Cardinal signs of inflammation

A
  • rubor= redness, darkening of skin
  • calor = heat
  • Tumor= swelling
  • Dolor=pain
  • loss of function (protective mechanism)

all these explain sequence of pathological events taking place

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3
Q

aetiology (causes) of acute inflammation

6 + briefly describe each

A
  • micro-organisms - (bacteria, fungi, viruses, parasite); pathogenic organisms cause infection
  • mechanical - trauma - injury to tissue- all injuries even sterile (eg surgery)
  • chemical (upset stable environment)- acid or alkali (upset pH), bile and urine (irritation when in inappropriate place eg peritoneum)
  • physical (extreme conditions)- heat (sunburn), cold (frostbite), ionising radiation
  • dead tissue- cell necrosis irritates adjacent tissue
  • Hypersensitivity- several classes of reaction
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4
Q

process of acute inflammation

more of an overview

A
  • series of microscopic events localised to affected tissue
  • take place in the microcirculation
  • result in the clinical symptoms and signs of acute inflammation - the cardinal signs
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5
Q

microcirculation

brief summary, more in cardiovascular block

A
  • capillary beds, fed by arteruiles and drained by venules
  • extracellular compartment - fluid and molecules within it
  • lymphatic channels and drainage
  • dynamic balance (hydrostatic and colloid osmotic pressures)
  • fast to respond to stimuli
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6
Q

steps in acute inflammation (pathogenesis)

A
  1. changes in vessel radius - flow
  2. change in the permeability of the vessel wall - exudation
  3. movement of neutrophils from the vessel to the extravascular compartment
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7
Q

what does increased arteriolar radius cause

step 1

A

increased local tissue blood flow - results in abserved redness and heat

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8
Q

effect of rapid changes in vessel radius and thus, blood flow

step 1

A
  1. transient arteriolar constriction - few moments, probably protective
  2. local arteriolar dilatation; active hyperaemia
  3. relaxation of vessel smooth muscle - autonomic NS or mediator derived

Called the “Triple Response” - flush, flare, wheal

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9
Q

explain the increased permeability of blood vessels during acute inflammation

Go on to describe the effects of increased permeability

step 2

A
  • localised vascular response in microvascular bed
  • endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
  • locally produced chemical mediators

Effects:
* net movement of plasma from capillaries to extravascular space - process is exudation (has effect of its own (oedema))
* what is leaked in an exudate (fluid rich in protein - plasma - includes immunoglobulin and fibrinogen)

Further effects:
* fluid loss - increased viscosity (h)
* rate of flow (movement) slows - stasis
* stasis produces a change in flow characteristics in the vessel

key words: exudation, stasis

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10
Q

effects of exudation

stage 2

A
  • oedema formed (accumulation of fluid in the extravascular space)
  • explains swelling of tissue in acute inflammation
  • swelling causes pain and reduce function
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11
Q

How does normal laminar blood flow pattern compare with flow in inflammation

stage 2/3 (ish kinda just happens)

A

Normal:
* plasma - outside
* erythrocytes - middle
* WBC (neutrophils) - inside

Inflammation:
* WBC - outside (margination of neutrophils)
* erythrocytes - rouleaux formation (stacked up) - inside
* plamsa - everywhere?

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12
Q

summarise how blood flow changes in inflammation

stage 2/3 (ish kinda just happens)

A
  • neutrophil polymorphonuclear leukocyte is most important cell (neutrophil; polymorph; NPL)
  • loss of normal laminar flow
  • red cells aggregate in the centre of the lumen
  • neutrophils found near endothelium (outside)
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13
Q

Phases of emigration of neutrophils

stage 3

A
  1. margination - neutrophils move to endothelial aspect of lumen
  2. pavementing - neutrophils adhere to endothelium
  3. emigration - neutrophils squeeze/contort between endothelial cells - active process - to** extravascular tissues**
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14
Q

diapedesis

A

passive movement of (white) blood cells in acute inflammation

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15
Q

resolution of acute inflammation - what is the ideal outcome?

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

Essentially; everything goes back to normal

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16
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 are
  • *neutrophils destroy organisms and denature antigen for macrophages
  • plasma proteins localise process
  • resolution and return to normal

Essentially; fast, easy to recognise, effecient, localised, returns to normal (no long-term effects)

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17
Q

4 (or 5) Outcomes of acute inflammation

A
  1. Resolution (ideal one)
  2. Suppuration
  3. Organisation
  4. Chronic inflammation

+ dissemination (potentially fatal)

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18
Q

Local effects of acute inflammation

A

local edema, redness, tenderness and pain, increased temperature, and restricted function.

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19
Q

what does itis mean

A

forming name of inflammatory disease

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20
Q

what do neutrophils do

(neutrophil polymorphonuclear leukocytes)

A
  • mobile phagocytes - recognise foreign antigen, move towards it - chemotaxis (recognise chemicals), adhere to organism –> vacuole formed
  • granules possess oxidants (eg H2O2) and enzymes (eg proteases)
  • release granule contents
  • phagocytose & destroy foreign antigen
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21
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 (not localised)
22
Q

role of plasma proteins in inflammation

A
  • fibrinogen (in plasma) - coagulation factor - forms fibrin and clots exudate - localises inflammatory process
  • immunoglobulins in plasma specific for antigen - humoural immune response
23
Q

what are the mediators of acute inflamation

don’t need to name directly, just where from

A
  • molecules on endothelial cell surface membrane
  • molecules released from cells
  • molecules in the plasma (–> activated when reach site of infection)
  • molecules inside cells
24
Q

what are the collective effects of mediators

brief overview

A
  • vasodilatation (inc vessel radius) - and constriction
  • increased permeability (dynamic balance)
  • cause/enable neutrophil adhesion
  • chemotaxis (form part of chemical gradient which neutrophil is attracted to)
  • itch and pain
25
Q

cell surface mediations that help neutrophils stick

A
  • adhesion molecules appear on endothelial cells
    eg ICAM-1 - help neutrophils stick
  • P-selectin - interacts with neutrophil surface
26
Q

List some molecules (mediators) released from cells

6

A
  • histamine
  • 5-hydroxytryptamine (serotonin)
  • prostglandins
  • cytokines and chemokines
  • Nitric oxids (NO)
  • Oxygen free radicals
27
Q

histamine as a mediator

A
  • preformed in mast cells beside vessels, platelets, basophils
  • released as a result of local injury; IgE mediated reactions
  • causes vasodilatation, increased permeability
  • acts via H1 receptors on endothelial cells
28
Q

Serotonin (5-hydroxytryptamine) as a mediator

A
  • preformed in platelets
  • released when platelets degranulate in coagulation
  • vasoconstriction
29
Q

prostglandins as mediators

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
  • latter: effectiveness of non-steroidal anti-inflammatory drugs
  • molecules provide target for treatment
30
Q

cytokines and chemokines

moleculer released from cells

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
31
Q

nitric oxide as a mediator

A
  • various cells
  • smooth muscle relaxation, anti-platelet, regulate leukocyte (lymphocyte) recruitment to inflammatory focus
32
Q

oxygen free radicals as mediators

A
  • released by neutrophils on phagocytosis (when they degranulate)
  • amplify other mediator effects
33
Q

does acute inflamation utilise innate or aquired ammunity

A

Innate only

(e.g. neutrophils, cytokines but not B/T cells) - I think???

34
Q

molecules inside cells as mediators- signalling

think patterns…

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
  • activate inflammatory response
35
Q

intracellular inflammatory pathways

probs neet to know but wouldn’t bother learning it all

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

What happens in the plasma during acute infection - (site for interaction of enzyme cascades)

A
  • blood coagulation pathways:
    -clots fibrinogen in exudate
    -interacts widely with other systems
  • fibrinolysis:
    -breaks down fibrin, helps maintain blood supply
    -fibrin breakdown products vasoactive
  • kinin system: bradykinin: pain
  • complement cascade:
    -ties inflammation with immune system
    -active components stimulate increased permeability, chemotaxis, phagocytosis, cell breakdown

happen simultaneously

37
Q

What are 3 immediate systemic effects of inflammation

explain each briefly

A
  • pyrexia (raised temperature) - endogenous pyrogens released 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
38
Q

Longer term effects of acute inflammation

3

A
  • lymphadenopathy (regional lymph node enlargement; “swollen glands”) - immune response
  • weight loss - catabolic process of inflammation
  • anaemia
39
Q

Outcome of acute inflammation: suppuration

A
  • pus formation - dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris (abscess)
  • pyogenic membrane surrounds pus - capillary sprouts (growths giving easier access into infected area), neutrophils, fibroblasts, walls off pus
40
Q

what is an abscess

A
  • collection of pus (suppuration) under pressure
  • single locule (1 blob), multiloculated (many like grapes)
  • “points” and discharges
  • collapses - healing and repair
41
Q

Explain the process/anatomy leading to pus discharge of an abscess

(suppuration)

A

Capillary sprouts grow into pyogenic membrane around abcess cavity. Ingrowth of granulation tissue (pyogenic membrane). Pus is discharged at weakest point, eouthelial surface (outside)

42
Q

what is a multiloculated abscess

A

pus bursts through pyogebic membrane and forms new cavities

43
Q

empyema

A

pus in a hollow viscus (e.g. gall bladder/pleural cavity)

44
Q

pyaemia

A

discharge of pus to bloodstream

45
Q

Outcome of acute inflammation: organisation

A
  • granulation tissue is characteristic
  • healing and repair
  • leads to fibrosis and formation of a scar
    • angiogenesis - new blood vessel formation

healing + fibrosis

46
Q

granulation tissue

A

repair kit/pathch for damage
Formed of: new capillaries (angiogenesis) fibroblasts and collagen, macrophages

47
Q

Outcomes of acute inflammation: dissemination

A
  • spread to bloodsteam - patient “septic”
  • bacteraemia - bacteria in blood
  • septicaemia - growth of bacteria in blood
  • toxaemia - toxic products in blood (but not necessarily pathogen/organism)
48
Q

effects of systemic infection

(sepsis)

A
  • shock - inability to perfuse tissues
  • clinical picture of early septic shock:
    -peripheral vasodilatation
    -tachycardia - high heart rate
    -hypotension - low blood pressure
    -often pyrexia (raised body temp; fever)
    -sometimes haemorrhagic skin rash
49
Q

Briefly summarise the pathogenesis of septic shock (compensation and then failure)

A
  1. release of chemical mediators into plasma
  2. cause vasodilation (loss of systemic vascular resistance)
  3. tachycardia - inc heart rate to compensate and maintain cardiac output
  4. bacterial endotoxin released - pyrexia
  5. activation of coagulation - vasodilation, haemorrhagic skin rash
  6. compensation fails - HR insffucuent to maintain CO
  7. reduced perfusion to tissues: tissue hypoxia (cell death), locc of cell tissue and organ function
  8. Haemorrhage
  9. Death
50
Q

Summarise the role of neutrophils in acute inflammation

A

The major role of the neutrophil in acute inflammation is to phagocytose microorganisms and foreign materials

51
Q

How can the process of acute inflammation be altered to the detriment of the patient

not sure if ans true but is LO, so made up this flashcard???

A

Compensation by inc HR —> tachycardia… lead to septic shock

52
Q

Endothelial cells

A

Cells lining blood vessels

2. Foundations of Medicine PoD (28 decks)

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