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Acute Inflammation Flashcards

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1
Q

What is acute inflammation?

A

An innate, immediate and early reaction that is initiated to limit tissue damage. Duration is normally a few minutes, hours or days.

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2
Q

What are the features of acute inflammation?

A
  • Reactions are vascular and cellular
    • accumulation of fluid exudate and neutrophils in tissue
  • Controlled by chemical mediators that are derived from plasma or cells
  • A protective mechanism but can cause local complications and systemic effects
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3
Q

What are the 6 causes of acute inflammation?

A
  • Microbial toxins and Infections
    • pyogenic (pus production) organisms
  • Hypersensitivity reactions/ Immune reactions
  • Physical and Chemical agents
    • thermal injury, irradiation, environmental chemicals
  • Trauma
    • blunt and penetrating
  • Tissue necrosis
  • Foreign Bodies
    • splinters, dirt, sutures
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4
Q

What are the clinical features of acute inflammation?

A
  • Rubor - redness
  • Calor - heat
  • Tumour - swelling
  • Dolor - pain
  • Loss of function
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5
Q

What changes in the tissue occur in acute inflammation?

A
  • Increase of blood flow
  • Exudation of fluid into tissues
  • Infiltration of inflammatory cells

All are controlled by chemical mediators

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6
Q

Outline the changes in blow flow that occur in acute inflammation

A
  1. Transient vasoconstriction of arterioles for a few seconds
    • unknown cause
  2. Vasodilation of arterioles then capillaries
    • caused by histamine
    • increases blood flow; rubor and calor
  3. Permeability of blood vessels increases
    • caused by histamine
    • exudation of protein rich fluid into tissues
    • circulation slows down due to swelling
  4. Concentration of RBC and WBC in small vessels increases
    • viscosity of blood is increased (stasis)
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7
Q

What is stasis?

A

slowing of the current of blood or fluid.

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8
Q

What is histamine?

A

A vasoactive amine that is released from mast cells, basophils and platelets in an early immune response.

Stimuli:

  • physical damage
  • immunological reactions
  • C3a, C5a, IL-1

Causes (early phase mediation):

  • vascular dilation
  • transient increase in vascular permeability
    • endothelial cells contract and pull apart
  • pain
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9
Q

Which chemical mediators are responsible for the prolonged response?

A

Overall there are many that are varied and interlinked with different degrees of importance.

  • Bradykinin
    • produces pain and increases vascular permeability
  • Leukotrienes
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10
Q

Outline the mechanism of exudation of fluid into tissues

A

Determined by a balance of hydrostatic pressure (blood pressure) and colloid osmotic pressure (concentration of protein in fluid).

  • Arteriolar dilation leads to an increase in hydrostatic pressure
  • Increased permeability of vessel walls leads to loss of protein into the interstitium
  1. Increase in hydrostatic pressure -> increased fluid flow out of the vessel
  2. Increased colloid osmotic pressure of interstitium -> increased fluid flow out of the vessel

The net flow of fluid out of the vessel leads to oedema.

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11
Q

What is the difference between transudate and exudate?

A

Transudate = oedema fluid has the same protein content of plasma

Exudate = oedema fluid has a higher protein content than plasma

Fluid loss due to only a loss in hydrostatic pressure is a transudate e.g. cardiac failure or venous outflow obstruction

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12
Q

What are the mechanisms of vascular leakage?

A
  • Endothelial contractions
    • gaps between cells caused by histamine and leukotrines
  • Cytoskeletal reorganisation
    • gaps between cells caused by cytokines, IL-1 and TNF
  • Direct injury
    • toxic burns or chemicals
  • Leukocyte dependant injury
    • toxic oxygen species and enzymes from leucocytes
  • Increased transcytosis
    • Vascular Endothelial GF (VEGF)
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13
Q

What is the purpose of exudation?

A

Delivers plasma proteins and immune cells to the site of injury.

  • Fibrin
    • involved in the clotting cascade and forms a plug
  • Neutrophil/ polymorph
    • WBC granulocyte
    • confirmation of inflammation under a slide
  • Macrophage
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14
Q

How do neutrophils infiltrate tissue?

A
  1. Margination
    • stasis -> neutrophils line at edge of blood vessels
  2. Diapedesis
    • roll/stick/roll/stick to endothelium (selectins)
  3. Adhesion
    • stronger sticking (integrins)
  4. Emigration
    • through blood vessel wall
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15
Q

How do neutrophils move?

A
  • Diapedesis (outwards passed through intact capillaries)
  • Emigration
  • Chemotaxis: movement along concentration gradients of chemoattractants.
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16
Q

How do neutrophils escape from vessels?

A
  1. Relaxation of inter-endothelial cell junction
  2. Digestion of vascular basement membrane
  3. Movement
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17
Q

Which chemicals aid chemotaxis?

A

Chemotaxis = the movement along the gradients of chemoattractants

Chemotaxins:

  • Bacterial peptides
  • C5a
  • LTB4 (leukotriene B4)
    • from arachidonic acid in cell membranes

Neutrophils bind to chemotaxins through receptor-ligand binding and then rearrange their cytoskeleton to move as a pseudopod along the capillaries.

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18
Q

How do neutrophils phagocytose pathogens and cell debris??

A

After migrating through chemotaxis to the site of the pathogen neutrophils phagocytose by:

  1. Contact
  2. Recognition
    • opsonins: Fc (fixed component of Ig) and C3b
  3. Internalisation
    • cytoskeleton changes
    • phagosomes fuses with lysosome to produce secondary lysosomes
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19
Q

What are the two killing mechanisms of phagosomes?

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A

O2 Dependant:

  • superoxide and hydrogen peroxide
  • hydrogen peroxide-myeloperoxidase-halide system produces HOCl-

O2 independent

  • lysosomes and hydrolases
  • bactericidal permeability-increasing protein (BPI)
  • Cationic proteins (‘defensins’)

It is important that neutrophils can function at both high and low O2 conditions because of ischaemia/hypoxia

20
Q

How can activated neutrophils damage host tissue?

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A

During the processes of phagocytosis, activated neutrophils may release toxic metabolites and enzymes causing damage to the host tissue causing background tissue damage.

21
Q

What are the chemical mediators of acute inflammation?

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A

Protesases - plasma proteins produced by the liver

  • Kinases - bradykinin
  • Complement system - C3a, C3b and C5a
  • Coagulation/ fibrinolytic system
    • fibrin helps to keep the inflammation localised

Prostaglandins/ Leukotrienes

  • metabolites of arachidonic acid - dependant on the enzymes.
  • Come from the membranes of injured cells.

Cytokines or chemokines

  • proteins produced by red blood cells
  • IL-1 and TNF alpha
22
Q

Which chemical mediators increase blood flow?

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A

Histamine and prostaglandins

23
Q

Which chemical mediators increase vascular permeability?

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A

histamine and leukotrienes

24
Q

Which chemical mediators are involved in neutrophil chemotaxis?

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A

C5a, LTB4 and bacterial peptides

25
Which chemical mediator is involved in phagocytosis?
C3b
26
How does the exudation of fluid combat injury?
1. Delivers plasma proteins to the area of injury * immunoglobulins * inflammatory mediators * fibrinogen (for fibrin production) 2. Dilutes toxins 3. Increases lymphatic drainage * delivers the microorganisms to phagocytes and antigens to the immune system
27
How does infiltration of cells combat injury?
Removes pathogenic organisms and necrotic debris
28
How does vasodilation combat injury?
Increased delivery of immune cells and fluid and increases the temperature
29
How does pain and loss of function combat injury?
Evolutionary mechanism: both enforce us to rest and reduces the chance of further traumatic damage.
30
What are the local complications of acute inflammation?
* Swelling * compression and tubes and obstruction * Exudate - depend on the location of exudate * compression (severity depends on the location of the exudate; finger vs heart- cardiac tamponade) * serositis (inflammation of the serous tissues of the body) * Loss of fluid * extensive burns * Pain and loss of function
31
What is cardiac tamponade?
Cardiac tamponade is also known as pericardial tamponade is when fluid builds up in pericardial sac and and results in compression of the heart
32
What is serositis?
Inflammation of the serous tissues of the body - the pericardial sac, pleural sac and peritoneum
33
What are the systemic effects of acute inflammation?
* Fever * caused by endogenous pyrogens: IL-1 and TNF alpha * prostaglandins * NSAIDs inhibit prostaglandin synthesis which is why they are effective at reducing a fever * Leukocytosis (increased levels of WBC) * IL-1 and TNF alpha cause an increased release of WBC from the bone marrow * Macrophages and T lymphocytes produce colony stimulating factors * Acute phase proteins: * C-reactive protein (CRP) CLINICALLY RELEVANT * alpha 1 antitrypsin * haptoglobin * fibrinogen * serum amyloid A protein * Acute phase response * decreased appetite * raised pulse rate * altered sleep patterns
34
What can happen if the acute phase response cannot manage a bacterial infection?
Shock - a clinical syndrome of circulatory failure Shock from a bacterial infection is called disruptive or septic shock, caused by widespread vasodilation and reduced resistance to flow.
35
What may happen after the development of acute inflammation?
* Complete resolution * inflammatory response is effective and the tissue can recover * Continued acute inflammation with chronic inflammation * abscess * Chronic inflammation and fibrous repair * Death
36
What is the morphology of resolution?
The changes that have occurred will gradually reverse: * neutrophils no longer marginate * vessel permeability returns to normal * vessel calibre (diameter) returns to normal All of these then cause... * Exudate to drain back into lymphatics * Fibrin to be degraded by plasmin and other proteases * Neutrophils die, break up and are carried away or are phagocytosed * Damaged tissue might be able to regenerate P.S. if the tissue architecture has been destroyed in the process of inflammation then complete resolution will not be possible.
37
How does the capillary hydrostatic pressure change in acute inflammation?
Capillary hydrostatic pressure increases - * After a brief moment of vasoconstriction, the arterioles vasodilate reducing the resistance of blood flow on a small level (think congested motorway and lane opens up. The flow would increase so the pressure would increase) * Walls of the venules become leaky so plasma escapes into the interstitial space causing an increase of haematocrit within the venules and increased resistance to blood flow.
38
What are the mechanisms by which chemical mediators of inflammation are resolved?
* All mediators have short half-lives * Degradation e.g. heparinase * Inhibitors e.g. various-antiproteases, lipoxins and endothelin * Unstable e.g. arachidonic acid derivatives * Dilution in exudate e.g. fibrin degradation products
39
What is bacterial meningitis?
Acute inflammation of meninges that can cause vascular thrombosis and reduce cerebral perfusion. Meninges become infected and inflamed reducing the space between the brain and the skull. Intracranial pressure increases and the brain is compressed which can cause blood vessels to necrose.
40
41
What is lobar pneumonia?
Acute inflammation and consolidation of a whole lung lobe. * mainly caused by Streptococcus pneumoniae Clinical course: * worsening fever, prostration (weakness), hypoxaemia over a few days. Dry cough and breathlessness * If treated it can resolve completely * young or the elderly will have complcations
42
What are the stages of lobar pneumonia?
1. Congestion (days 1 - 2) * blood vessels and alveoli fill with excess fluid 2. Red hepatisation (days 3 - 4) * exudate: RBC, neutrophil and fibrin fill airspaces and make them more solid * lung lobe has a liver like an appearance 3. Grey hepatisation (days 5-7) * still firm. RBC in exudate break down 4. Resolution (day 8 - 3 weeks) * Exudate is ingested, digested or coughed up
43
Describe a skin blister
Causes: * heat, sunlight and chemical Symptoms: * pain * profuse exudate * dehydration * exudate fluid is normally clear unless there is an infection (inflammatory cells are few unless there is an infection) Resolution or scarring depending on the degree of tissue injury
44
Describe an abscess
Normally occurs in solid tissues but can occur anywhere on the body. Inflammatory exudate forces the tissues apart. Liquefactive necrosis occurs in the centre of the abscess. There may be high pressure at the site of the abscess which will cause pain. This pressure can also squash adjacent structures.
45
What are liver abscesses normally caused by?
An ascending infection. Difficult to diagnose as there are no pain receptors so normally presents with systemic signs once the abscess has progressed.
46
When does acute inflammation occur in serous cavities?
* When exudate pours into the cavity * ascites (fluid in the peritoneum), pleural or pericardial effusion * Can cause respiratory or cardiac impairment * Causes localised fibrin deposition * when healing this can occur across the pleural surface and cause scarring
47
What is pericarditis?
Inflammation of the lining around the heart (the pericardium) that causes chest pain and accumulation of fluid around the heart (pericardial effusion). Causes: * specific cause unknown but likely due to a viral infection * complication of associated diseases * trauma

Pathological Processes (9 decks)

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