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Pathology > Day 2- Lecture 1- Acute Inflammation > Flashcards

Day 2- Lecture 1- Acute Inflammation Flashcards

1
Q

What is the generalised cause of inflammation?

A

Injury of vascularised lung tissue. Inflammation delivers blood, cells and fluid (defensive materials) to a site of injury

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2
Q

Where are defensive agents found, and where do they target?

A

MOST defensive agents circulate in the blood in an inactive form, and when needed they leave the blood vessels into the tissues (without affecting blood flow), which are then activated

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3
Q

What controls the passage of leucocytes and fluid containing plasma proteins into the tissue space?

A

Controlled by chemical mediators- leads to delivery of fluid then leucocytes

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4
Q

List some causes of acute inflammation

A
  • Foreign bodies (splinters, dirt, sutures)
  • Immune reactions (leading to hypersensitivity reactions)
  • Infections and microbial toxins e.g. Pyogenic organisms (pus forming)
  • Tissue necrosis
  • Trauma (blunt and penetrating)
  • Physical and chemical agents (thermal injury e.g. Burns, frostbites, irradiation, environmental chemicals)
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5
Q

What are the clinical signs of acute inflammation?

A
  • Rubor: red
  • Calor: heat
  • Tumour: swelling
  • Dolor: pain
  • Loss of function
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6
Q

How does acute inflammation cause a change in tissues?

A
  • Changes in blood flow (vascular phase)
    -Exudations of fluid into tissues (vascular phase)
  • Infiltration of inflammatory cells (cellular phase)
  • Inflammatory mediators of each step*
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7
Q

What are the 3 steps of formation of the exudate?

A

1- Vasodilation of arterioles (small arteries)
2- Increased permeability of venules
3- Release of chemical mediators

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8
Q

What causes vasodilation of arterioles (small arteries) and what then happens to the flow of blood?

A

Vasodilation occurs by vasoactive mediators e.g. Histamine -> vasodilation causes flow to accelerate in the capillaries and capillary pressure rises causing an increased delivery of fluid and leucocytes to the area of injury

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9
Q

Why is there an increased permeability of venules and what is the consequence with regards to blood?

A

The wall become leaky so plasma can escape through tiny gaps between endothelial cells

This results in

  • Increased haematocrit (ratio of volume of red blood cells to blood) within the venules (so increases viscosity of blood)
  • Increased resistance to blood flow within the venules so the lumens of upstream vessels (e.g. Arterioles) dilate and blood flow slows down

Increased pressure within the vessels -> greater exudation of fluid into tissue spaces -> delivers more plasma proteins to the site of injury (tissues)

Slowing of circulation- leads to swelling

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10
Q

What chemical mediators are involves in vasodilation and where are they stored?

A

Histamine (stored in granules of mast cells, basophils and platelets)

Serotonin (stored in granules of platelets)

Prostaglandins (from many cells) and leukotrienes

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11
Q

What chemical mediators are involves in increased vascular permeability and where are they stored?

A

Histamine (stored in granules of mast cells, basophils and platelets)

Serotonin (stored in platelets)

Bradykinin (come from a plasma precursor called kininogen)

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12
Q

Chemical mediator: how does histamine work?

A
  • Belongs to a group called vasoactive amines (so is serotonin)
  • Important in early inflammation
  • Available immediately from pre-formed supplies and are already present in cells in the tissues and in platelets which are present at site of injury when vessels are damaged

Stimuli include:

  • Physical damage
  • Immune reactions
  • Complement proteins can cause the release of these vasoactive amines (C3a and C5a)
  • IL-1
  • Factors from neutrophils and platelets
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13
Q

In acute inflammation what does histamine do?

A
  • Produce pain
  • Arteriolar dilation
  • Venular leakage (increased permeability) -> histamine causes endothelial cells to contract and pulled apart to create gaps for plasma proteins to pass
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14
Q

Chemical mediator: how does prostaglandins work?

A

-Produced in inflammation by cell membrane phospholipids (derived from phospholipids)

Causes:

  • Vasodilation
  • Increased sensitivity to pain
  • Causes a fever
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15
Q

What inhibits the production of prostaglandins (and thromboxones which are also derived from phospholipids)?

A
  • Phospholipase A2 (inhibited by corticosteroids) produces arachadonic acid
  • Arachadonic acid can then be metabolised by cyclo-oxygenase to produce prostaglandins and thromboxanes
  • Enzyme cyclo-oxygenase can be inhibited by asparin and NSAIDs
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16
Q

Chemical mediator: how does bradykinin work?

A

It is a vasoactive peptide

Bradykinin:

  • Circulates in blood as part of kininogen (larger molecule)
  • Enzyme kallikrein cleaves kininogen to produce bradykinin
  • Produced quickly (in 1 min)
  • Causes vasodilation and a burning pain
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17
Q

What do the chemical mediators in acute inflammation cause-

A
  • Arterioles to dilate
  • Endothelial cells to contract, create gaps, leaky venules

HENCE: acute inflammation alters fluid exchange in the microcirculation

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18
Q

What are the four pressures with regards to ‘starling’s law’

A
  • Capillary pressure
  • Interstitial free fluid pressure
  • Plasma colloid oncotic pressure
  • Interstitial fluid colloid oncotic pressure
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19
Q

Explain the permeability of the endothelium?

A

Semi-permeable

  • Allow water and electrolytes to escape
  • Retain plasma proteins
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20
Q

In a normal capillary, what are the main forces drawing fluid in and out of the capillary?

A

HYDROSTATIC PRESSURE: main force driving fluid out of vessels

COLLOID OSMOTIC PRESSURE OF THE PLASMA PROTEINS: main force driving fluid into the vessels/blood

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21
Q

How is capillary pressure altered in acute inflammation?

A
  • The semi-permeable membrane becomes leaky
  • Hydrostatic pressure increased as arterioles dilate increasing capillary pressure
  • Colloid osmotic pressure of blood is reduced as plasma proteins escape into the tissue spaces (increases colloid osmotic pressure of the interstitium), raising the osmotic pressure to roughly equal that of blood- this occurs due to the increased permeability of vessel walls leading to a loss of protein and fluid out of the vessel (causes oedema)

RESULT: net flow of fluid (and plasma proteins) into tissue spaces

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22
Q

As well as delivering plasma proteins to the site of infection, what other function does the abundant tissue fluid have?

A

Excess fluid drains from the tissues in the lymphatics, taking microorganisms and antigens -> therefore present these to the immune system within the lymph nodes and returns to the venous system

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23
Q

What are the 3 types of defensive proteins in the exudate and what do they do?

A

OPSONINS: coat foreign materials and make them easier to phagocytose

COMPLEMENT: group of proteins that are assembled locally to produce a bacteria perforating structure

ANTIBODIES: bind to the surface of micro-organisms and also act as opsonins

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24
Q

What is an exudate?

A

A protein rich fluid (e.g. The fluid that develops in inflammation) -> oedema fluid has more protein than plasma

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25
Q

What is a transudate and when does it develop?

A

Fluid which is protein poor- it is an infiltrate of plasma and it occurs with normal vessels (i.e. There are no gaps caused by endothelial contractions) -> they are seen in conditions such as heart failure where there is an increase in hydrostatic pressure -> oedema fluid has same protein content as plasma

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26
Q

What is a neutrophil?

A

A type of leukocyte

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27
Q

Where are neutrophils found?

A

Blood and bone marrow

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28
Q

What does the presence of neutrophils indicate?

A

Indicates there is:

  • Invasion by bacteria or some other parasite
  • Tissue injury

(Chemicals and/or other inflammatory cells can trigger the release of neutrophils from blood vessels into tissue fluids)

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29
Q

Neutrophils are a end cell- what does that mean?

A

They cannot multiply - lifespan around 12-20 hours

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30
Q

What do neutrophils contain?

A

Thousands of granules containing bactericidal substances

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31
Q

What are the 6 stages that neutrophils capture and kill a bacterium in a tissue space?

A

1- Chemotaxis: summoned to site of injury
2- Activation: switch to higher metabolic level
3- Margination: stick to endothelial surface
4- Diapedesis: crawl through endothelium
5- Recognition-attachment: recognise and attach to bacteria
6- Phagocytosis: engulf the bacterium

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32
Q

STAGE 1: What is chemotaxis (stage 1)?

A

Directional movement of neutrophil towards a chemical attractant (chemotaxin)

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33
Q

STAGE 1: What triggers chemotaxis?

A
  • Bacterial products
  • Injured tissues
  • Substances produced by leucocytes
  • Spilled blood (clotted)
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34
Q

STAGE 1: What are the main chemical mediators of chemotaxis? (Molecules that are chemotactic)

A
  • Leukotriene B4 (from leukocytes)
  • C5a and C3a (from complement plasma precursors)
  • Chemokines (from leukocytes and other cells)
  • Bacterial products e.g. Endotoxins (from bacterial metabolism)
  • Blood clotting and fibrinolytic cascade both generate chemical mediators: fibrin is broken down by plasmin into fibrin degradation products-> both thrombin and fibrin degradation products are chemotactic
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35
Q

STAGE 1: Describe how complement components C3a and C5a are generated?

A
  • Function of complement - Form a tube (called the membrane attack complex) which punches holes into bacteria leading to death
  • Circulates in the blood as disassembled proteins
  • When assembled it generates (as by products) some powerful inflammatory mediators (including C3a, C5a and C3b)
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36
Q

STAGE 1: where are leukotrienes produced?

A

Produced in leucocytes- leukotriene B4 is the most powerful chemotactic agent

They also have vasoactive properties

37
Q

STAGE 1: Give some examples of cytokine and chemokines and explain what they are?

A

Examples: interleukins, tumour necrosis factor, interferons

  • Cytokines= polypeptides that are produced by many cells and act as messengers between cells (many are produced by macrophages - start to appear hours after injury)
  • Chemokines= a group of cytokines involved in chemotaxis

They have both local and systemic effects

38
Q

STAGE 1: give an example of a exogenous mediator of inflammation and a possible complication of this mediator?

A

Endotoxins- produced by gram negative bacteria

If released into tissue = inflammation
If released into blood = activation of numerous inflammatory responses at once (septic shock)

39
Q

STAGE 2: Describe how activation occurs and what is the consequence of activation?

A

Activated cells are stickier than normal cells and occur within 5 seconds of chemotaxin binding to the cell surface receptors

It leads to...
-Calcium and Sodium to enter the cell
-Water follows so cell swells
-Reorganises it's cytoplasm (triangular shape pointing to chemotactic stimulus)
After 5 to 10 seconds:
-Cell sends out pseudopodia
40
Q

STAGE 3: Describe margination, rolling and adhesion

A

Margination: due to flow changes (stasis) the neutrophils line up at the edge of blood vessels along the endothelium- they stick to the walls of the venules towards the chemotactic signal.

Rolling- roll along the endothelium wall whilst binding to selectins

Adhesion- become trapped and stop (neutrophils are trapped when their receptors bind to adhesion molecules called selectins and intergrins) -> when leucocyte adheres/sticks firmly is binds to intergrins such as ICAM1 (intercellular adhesion molecule 1)

Inflammatory mediators in chemotaxis- increase number of selectins and intergrins

41
Q

STAGE 4: Explain the process of diapedesis/emigration

A

-Leucocytes do not use endothelial gaps (that the exudate escapes from)
INSTEAD-
-Inter-endothelial cell junctions relax
-Produce collagenase which digests the basement membrane
-Move into tissue
-Once in extravascular space- leukocytes move towards their targets by pulling themselves along collagen fibres and other tissue structures

42
Q

STAGE 5: How do opsonins work?

A

Opsonins make it easier for phagocytes to recognise targets, attach to them and phagocytose them (so recognition is facilitated by opsonins)

43
Q

STAGE 5: Give some examples of opsonins?

A

They are plasma proteins:

  • IgG antibody: most important poisoning, but will not be present when Antimicrobial is encountered for the first time
  • C3b: fragment of complement which is released when complement is activated
44
Q

STAGE 5: If opsonins are not present how do the phagocytes recognise microbes?

A

Use the microbial surface antigens

45
Q

STAGE 6: What do neutrophils do and describe phagocytosis?

A

3 phases-

  1. Contact- get polymorph to the right place
  2. Recognition- polymorph distinguishes what needs to be phagocytosed
  3. Internalisation
  • Phagocyte (neutrophil) engulfs the microbe
  • Particle in phagocyte vacuole= phagosome
  • Lysosomes move towards phagosome- fuse- inject bactericidal substances int it leading to degranulation
  • Degranulation begins before particle is completely enclosed so some bactericidal enzymes can leak out to surrounding tissue space and kill bacterium and self body cells (can lead to local tissue injury)
46
Q

STAGE 6: What 2 mechanisms of killing are used in phagocytosis and give a brief explanation of each of them?

A

Oxygen dependant killing- oxygen derived free radials released into the phagosome leading to a respiratory/oxygen burst (superoxide and hydrogen peroxide)

Oxygen-independent killing- uses enzymes e.g. Phospholipases, proteases, nucleases and lysozymes

47
Q

STAGE 6: What is the main chemical mediator of phagocytosis?

A

C3b from the complement plasma precursor

48
Q

What is a chemical mediator?

A

Any molecule that is produced in a focus of inflammation and mediates the inflammatory response in some way

49
Q

What are the common responses to chemical mediators?

A

Mobile:

  • Contraction/relaxation of vascular smooth muscle cells
  • Contraction of venular endothelial cells
  • Movement along chemotactic gradient
  • Phagocytosis by neutrophils

-Secretion

50
Q

Why does evert chemical mediator have an inhibitor?

A

Otherwise inflammation would be ongoing and would spread around the body

51
Q

Why is there a limited duration for inflammation?

A
  • Mediators have short half lives (seconds to minutes)

- Effects last minutes to hours

52
Q

What 3 locations are endogenous mediators supplied by?

A
  • Plasma
  • Leucocytes
  • Local tissue
53
Q

What chemical mediators initiate pain?

A
  • Bradykinin (from plasma precursors- kininogen)

- Prostaglandins (from many cells)

54
Q

What are the 4 local complications of acute inflammation?

A

1- Damage to normal tissue, secondary to substances produced by neutrophils and released during the process of phagocytosis

2- Swelling can lead to obstruction of tubes e.g. Intestine and Fallopian tubes, and compression of vital structures secondary to the swelling produced by the inflammatory exudate

3- Loss of fluid- fluids accumulates in the tissue reaching a certain level preventing any further exudation. However, fluid can continuously leak from surface wound and for this reason extensive skin wounds e.g. BURNS result in a loss of a large amount of fluid

4- Pain and loss of function - especially if prolonged

55
Q

Although acute inflammation is produced locally, inflammatory mediators can enter the blind stream and have systemic effects->

List the 4 main systemic effects of acute inflammation?

A

1- FEVER
2- LEUKOCYTOSIS
3- ACUTE PHASE RESPONSE
4- SHOCK

56
Q

1- FEVER: why does it occur?

A

Set point of normal body temperature rises in anterior hypothalamus

57
Q

1- FEVER: what substance/substances cause it?

A
  • Exogenous bacterial pyrogens (endotoxins) stimulate macrophages to produce endogenous pyrogenic cytokines e.g. TNF or IL-1
  • These cytokines cause an increase in prostaglandins (also an endogenous pyrogen) within the anterior hypothalamus

Tip-
Endogenous- formed by body
Pyrogens- causing fever

58
Q

1- FEVER: what drugs could be used to reduce a fever?

A

Aspirin- inhibits cycle-oxygenated enzyme which produces prostaglandins

59
Q

1- FEVER: why are they useful?

A
  • Bacterias cannot survive in high temperatures

- Inflammation is more effective at higher temperatures

60
Q

2- LEUKOCYTOSIS: explain how this occurs?

A
  • Number of leucocytes (WBCs) in circulation increases
  • During a bacterial infection neutrophilia is seen
  • Macrophages and endothelial cells in injured tissues produce a colony of stimulating factors to stimulate the bone marrow to produce more neutrophils
61
Q

3- THE ACUTE PHASE RESPONSE: how does it occur?

A
  • Liver changes it’s pattern of protein synthesis - change in the level of some plasma proteins
  • Occurs within hours of injury
  • Albumin produced in smaller amounts by the liver
  • Other proteins are produced by larger amounts by the liver e.g. Fibrinogen (needed for blood coagulation), ceruloplasmin (free radical scavenger), C3 (protein of complement system), alpha-1-antitrypsin (a protease inhibitor), C reactive protein (CRP- an opsonin and a very good clinical marker of acute inflammation)
62
Q

4- SHOCK: how does it occur?

A
  • Bacterial products/ inflammatory mediators spread in blood stream around the body
  • Leads to inflammation throughout the body
  • Leads to shock: a dramatic drop in blood pressure due to widespread vasodilation and increased vascular permeability with resultant fluid exudation
  • Can often be fatal
63
Q

Why is there resolution in acute inflammation? And what is the mechanisms of resolution?

A

Mechanisms of resolution-

  • Mediators of inflammation have a short half life so are degraded after their release (this reduces risk of inflammation extending to other tissue areas)
  • Mediators are present in quick bursts and are present only as long as the stimulus persists
  • Triggers for inflammation removed- leads to the return of normal vascular permeability (neutrophil no longer marginate, vessel permeability returns to normal)

Process:
1- Exudate is reabsorbed into the venules or is drained away by the lymphatics
2- Fibrin is degraded
3- Neutrophils undergo apoptosis and are phagocytised along with necrotic debris by macrophages
4- If damaged parenchymal cells can regenerate then tissue returns to normal (if not the inflammation occurs)

64
Q

Name and explain the 4 different types of exudate?

A

1- PUS/ABSCESS
Exudate is creamy/white as it is rich in neutrophils -> typical of infections with chemotactic bacteria

2- HAEMORRHAGIC EXUDATE

  • Contain enough RBCs to appear bloody to the naked eye
  • Indicative that both inflammation and vascular damage has occurred
  • Seen in destructive infections or when the exudate is a result of infiltration by a malignant tumour

3- SEROUS EXUDATE
-Contains plasma proteins but few leukocytes- suggests no infection by micro-organisms
-They are clear and seen typically in blisters (after a minor burn)
(Differ from plasma as do not contain fibrinogen, differ from transudate as do not contain plasma proteins)

4- FIBROUS EXUDATE

  • Significant deposition of fibrin (i.e. A blood clot without RBCs)
  • Occur in the pericardial or pleural spaces
  • Fibrin deposited means serosal surfaces can no longer slide smoothly over each other- results in friction between the surfaces and hence a rubbing sound
65
Q

Name 3 disorders or acute inflammation-

A
  1. Hereditary angio-oedema
  2. Alpha-1-antitrypsin deficiency
  3. Chronic granulomatous disease
66
Q

What is hereditary angio-oedema, and what are the signs and symptoms?

A
  • Rare
  • Autosomal dominant
  • Deficiency of C1-esterase inhibitor (component of complement system)

Results in..

  • Attacks of non-itchy cutaneous angio-oedema (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues)
  • Often experience recurrent abdominal pain due to intestinal oedema
  • Often a family history of sudden death which is due to laryngeal movement
67
Q

What is Alpha-1-antitrypsin deficiency, and what are the signs and symptoms?

A
  • Autosomal recessive- varying severity
  • Alpha-1-antitrypsin is a protease inhibitor which deactivates enzymes released from neutrophils at site of inflammation (deficiency means level of this protease inhibitor are low)
  • Patients develop emphysema as proteases released by neutrophils within the lung act unchecked and destroy normal parenchymal tissue
  • Liver disease also occurs- the hepatocytes produce an abnormal version of the protein which is incorrectly folded- it polymersises and cannot be exported from the ER -> leads to hepatocyte damage and eventually cirrhosis
68
Q

What is Chronic granulomatous disease, and what are the signs and symptoms?

A
  • Genetic condition
  • Phagocytes are unable to generate the free radical superoxide
  • Bacteria are phagocytised but phagocytes cannot kill them as cannot generate oxygen burst
  • Results in many chronic infections in first year of life
  • Numerous granulomas and abscesses affecting the skin, lymph nodes, and sometimes the lung, liver and bones
  • However- ineffective at eliminating infectious agents
69
Q

Is acute inflammation innate?

A

Yes (means you are born with it)

70
Q

What is acute inflammation?

A

The response of living tissues to injury-

  1. Vascular and cellular reactions: accumulation of fluid exudate and neutrophils in tissues that have been injured
  2. Controlled by a variety of chemical mediators derived from plasma or cells
  3. Protective, but can lead to local complications and systemic effects
71
Q

In the vascular stage of acute inflammation what is the first thing to happen to blood flow?

A

VASOCONSTRICTION OF ARTERIOLES (transient- only a few seconds)

Followed by vasodilation or arterioles and then capillaries which increases the blood flow to tissues (hence red and hot)

72
Q

What mechanisms cause vascular leakage?

A
  1. Endothelial contraction by histamine, serotonin, leukotrienes, bradykinin
  2. Cytoskeleton reorganisation by cytokines (IL-1) and tumour necrosis factor (TNF)
  3. Direct injury e.g. Toxic sun burns chemicals etc
  4. Leukocyte dependant injury- toxic oxygen species and enzymes from leukocytes
  5. Increased transcytosis (where fluid moves across the wall of non-leaky blood vessels)
73
Q

Why is fibrin an important plasma protein that leaks into tissues at site of injury?

A

Crucial in blood clotting- it causes a sticky meshwork to localise inflammation (particularly important for serosal surfaces)

74
Q

Neutrophils are a type of granulocyte, also known as polymorphonuclear- what does this mean?

A

They have multi-lobed nuclei

75
Q

Macrophages are different form of granulocyte- how is it different to a neutrophil?

A

Different type of WBC, bigger and involved in both acute and chronic inflammation

76
Q

Give a brief overview of neutrophil chemotaxis and phagocytosis?

A
  1. Neutrophils migrate to site of injury by chemotaxis (move towards chemicals along chemical gradient which have been produced by inflammation)
  2. Neutrophils phagocytise microorganism
  3. Activated neutrophils may release toxic metabolised and enzymes causing damage to the host tissue
77
Q

Give an overview of the chemical mediator families of acute inflammation?

A

Proteases include:

  • Kinins
  • Complement system
  • Coagulation/fibrinolytic system

Prostaglandins and leukotrienes
-Metabolites of arachanoid acid

Cytokines and chemokines (produced by wbc) are varied (IL-1, TNF)

78
Q

What are the key chemical mediators for increasing blood flow, altering vascular permeability, neutrophil chemotaxis and phagocytosis?

A
  1. Vasodilation- histamine, serotonin, prostaglandins
  2. Vascular permeability- histamine, leukotrienes, serotonin, bradykinin
  3. Neutrophil chemotaxis- C5a, C3a, Leuketriene B4, bacterial peptides
  4. Phagocytosis- C3b
79
Q

What are the 2 main hallmarks of acute inflammation?

A

Exudate of oedema FLUID

Infiltrate of inflammatory CELLS

80
Q

How does exudation of fluid combat injury?

A
  • Delivers plasma proteins to the area of injury (immunoglobulins, inflammatory mediators, fibrinogen)
  • Increases lymphatic draining- fluid goes through lymph nodes where the immune system is located and delivers micro-organisms to phagocytes and antigens to the immune system
  • Dilutes toxins
81
Q

How does infiltration of cells combat injury?

A

Removes pathogenic organisms and necrotic debris (mainly polymorphs/neutrophils but also macrophages)

82
Q

How does vasodilation combat injury?

A
  • Increases delivery of exudate

- Increases temperature

83
Q

How does pain and loss of function combat injury?

A

Enforces rest, reducing change of further traumatic injury

84
Q

Explain bacterial meningitis

A
  • Acute inflammation of meninges can cause vascular thrombosis and reduce perfusion
  • Triggered by various different bacterium
  • Inflammation of meninges- little exudate so can cause significant swelling and can damage the brain and blood vessels

Image: on notes

85
Q

Explain lobar pneumonia

A
  • Caused by streptococcus pneumoniae
  • The alveoli contain exudate (meant to contain air!)

Clinical course:

  • Worsening fever, prostration, hypoxaemia over a few days
  • Dry cough and breathless

If treated can completely resolve

86
Q

Explain skin blisters

A

Caused by heat sunlight or chemicals

Predominant features:

  • Pain
  • Profuse exudate

Collection of fluid strips off the overlying epithelium-> very few inflammatory cells so the exudate is clear unless the bacterial infection develops where it may lead to resolution or scarring

87
Q

Explain an abscess

A

Occurs in solid tissues e.g. Skin

Inflammatory exudate forces the tissue apart- there is liquefactive necrosis in the centre

It may cause tissue damage and squash adjacent structures

Example: liver abscess

88
Q

What is the problem with acute inflammation in serious cavity

A

The exudate can pour into the cavity (ascites, pleural or pericardial effusion)

Can lead to respiratory or cardiac impairment due to a localised fibrin deposition

Example: pericarditis (inflammatory exudate)

89
Q

What are the key characteristics of acute inflammation?

A
  • Rapid, stereotyped response of living tissue to any injury
  • Macroscopic: redness, swelling, heat, pain and loss of function
  • Microscopic: vascular dilation, exudate leaks into tissues, neutrophils emigrate
  • Changes controlled by many short-lived chemical mediators
  • Neutrophils: fast acting, short-lived phagocytes, engulf and degrade bacteria, dead tissue etc
  • Phagocytosis enhanced by opsonisation
  • Bacterial killing largely oxygen dependant
  • Defects in the system lead to severe susceptibility to infection

Pathology (8 decks)

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