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Sem 2 - Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

Acute Inflammation is the response of living tissue to injury.

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2
Q

What are the characteristics of acute inflammation?

A
  • Innate,
  • immediate and early,
  • stereotyped (the same every time),
  • short duration -minutes/hours/few days.
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3
Q

What is the purpose of acute inflamation?

A

It is Initiated to limit the tissue damage

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4
Q

What are the two types of reaction involved in acute inflammation?

A
  1. Vascular and cellular reactions- accumulation of fluid exudate and neutrophild in tissues.

These reactions are controlled by a variety of chemical mediators derived from plasma or cells.

Acute inflamation is protective but can lead to local complications and systemic effects.

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5
Q

What are the causes of acute inflammation?

A
  • Microbial Infections eg pyogenic organisms
  • Hypersensitivity reactions (acute phase)
  • Physical agents
  • Chemicals
  • Tissue necrosis
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6
Q

What are the clinical features of acute inflamation?

A
  • Rubor (redness)
  • Tumor (swelling)
  • Calor (heat)
  • Dolor (pain)
  • Loss of function
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7
Q

What changes in tissue occur during acute inflammation?

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells.

There are inflammatory mediators of each step.

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8
Q

What are the vascular changes in acute inflammation?

A
  1. Transient vasoconstriction of arterioles (few seconds)
  2. Vasodilation of arterioles and then capillaries (increase in blood flow causing heat and redness)
  3. Increased permeability of blood cells causing excudation of protein rich fluid into tissues and slowing of circulation (swelling)
  4. Concentration of RBCs in small vessels and increased viscosity of blood = stasis
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9
Q

What is the first chemical mediator? (first 30 mins)

A

HISTAMINE

This is released from mast cells, basophils and platelets in response to many stimumi eg:

physical damage, immunological reactions, C3a, C5a, IL-1, factors from neutrophils and platelets.

It causes:

vascular dilation, transient increase in vascular permiability, pain

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10
Q

What chemical mediators cause a persistant response?

A

Many and varied chemical mediators, interlinked and of carrying important.

Incompletely understood eg leukotrienes and bradykinin

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11
Q

What is Starling’s law?

A

Fluid flow across vessel wall is determined by the balance of hydrostatic pressure and colloid osmotic pressure compairing plasma and interstitial fluid.

If there is increased hydrostatic pressure then fluid flows out if vessel.

If there is increased colloid osmotic pressure of interstitium then fluid flows out if the vessel.

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12
Q

Define oedema

A

Increased fluid in tissue space

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13
Q

How does fluid exudation occur in acute inflammation?

A
  • Arteriolar dilation leads to an increase in hydrostatic pressure.
  • Increased permeability of vessel walls leads to loss of protein into interstitum.

Therefore, net flow of fluid out of vessel which causes oedema.

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14
Q

What is transudate oedema?

A

Fluid loss due to hydrostatic pressure imbalance only. This is when fluid has a low protein content. (eg cardiac failiure of veous outflow obstruction)

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15
Q

What is exudate oedema?

A

Fluid loss in inflammation is an exudate. This is when there is high portein content.

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16
Q

What are the mechanisms of vascular leakage?

A
  • Endothelial contraction - gaps
  • Histamine, leukotrienes
  • Cytoskeleton reorganisation -gaps
  • -Cytokines, IL-1 and TNF*
  • Direct injury - Toxic burns, chemicals
  • Leuleukocyte dependant injury
  • -Toxic pxygen species amd enzymes from leucocytes*
  • Increased transcytosis -channels across endothelial cytoplasm.
  • VEGF
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17
Q

What plasma proteins are delivered to site of injury?

A

Fibrin - Make it a LOCALISED response to tissue.

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18
Q

What is a neutrophil leukocyte?

A

This is primary type of white bood cell in acute inflammation. Neutrophils are a type of granulocyte, also know as a polymorphonuclear leucocyte.

Neutrophil = polymorph

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19
Q

Other than neurophils, what other type of cells is involved in acute inflamation?

A

Macrophages also involved.

They are also involved in chronic inflammation.

20
Q

How does the infiltration of neutrophils occur?

A

(Before, stasis)

  1. Margination - stasis causes neutrophils to line up at the edge of the blood vessels along the endothelium.
  2. Rolling - Neutrophils then roll along the endothelium, stiking to it intermittently
  3. Adhesion -They then stick to more avidly
  4. Emigration. -This is then followed by emigration of neutrophils through the blood vessel walls.
21
Q

How do neutrophils escape from vessels?

A
  • Relaxation of inter-endothelial cell junctions
  • Digestion of vascular basement membrane
  • Movement.
22
Q

How do neutrophils move once they are in cells?

What does this result in?

A
  • Chemotaxis. (Movement along a concentration gradient of chemoattractants)
  • Emigration
  • Diapedisis (the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.)

These result in:

  • Receptor-ligand binding
  • Rearragment of the cytoskeleton
  • Production of pseudopod (a temporary protrusion of the surface of an amoeboid cell for movement and feeding.)
23
Q

What three chemotaxins mediate chemotaxis?

A
  • Bacterial peptides -attracted to areas of bacterial infection
  • LTB4 - leukotrienes
  • C5a - a complement protein so causes compliment activation.

Neutrophils have receptors on their surface for all of these receptors.

24
Q

What do neutrophils do?

A

Phagocytosis.

Contact, Recognition, Internalisation -forms a phagosome.

These processes are facilitated by opsonins (Fc and C3b)

Also cause cytoskeletal changes

Phagosome then fuse with lysosomes to produce a secondary lysosomes.

25
Q

What facilitates phagocytosis?

A

Opsonins - attatch to neutrophils and help it undergo phagicytosis.

Fc and C3b (compliment cascade) stick to surface of bacteria / tissues to allow them to be recognised or phagocytosed by neutrophils.

26
Q

What are the killing mechanisms of phagolysosomes?

A

Oxygen dependant

  • Produces superoxide and hydrogen peroxide
  • H2O2 -myeloperoxidases-halide system which produces HOCl-

Oxygen indipendant

  • Lysozymes and hydrolases
  • Bacterial permeability increasing protein (BPI)
  • Cationic proteins (‘defensins’)
27
Q

How are neutrophils, chemotaxis and phagocytosis linked?

A
  1. Neutrophils migrate to site of injury by chemotaxis
  2. Neutrophils phagocytose microorganisms
  3. Activated neutrophils May released toxic metabolites and enzymes causing damage to the host tissue.
28
Q

What are the groups of chemical mediators in acute inflammation?

A

Proteases (plasma protiens, produced in the liver)

  • kinins
  • Complement system C3a, C5a
  • Coagulation / fibrinolytic system

Prostaglandins / Leukotrienes

  • Metabolites of arachidonic acid

Cytokines / chemokines (produced by WBCs)

  • Many and vaired!
  • Interleukins
  • TNF alpha
29
Q

What are the chemical mediators in each step of acute inflammation?

A

Increased blood flow

  • Histamine
  • Prostaglandins

Vascular Permiability

  • Histamine
  • Leukotrienes

Neutrophil Chemotaxis

  • C5a
  • LTB4
  • Bacterial peptides

Phagocytosis

  • C3b
30
Q

How does the exudation of fluid combat injury?

A
  • Delivers plasma proteins to the area of injury inc.
    • Immunoglobulins
    • Inflammatory mediators
    • Fibrinogen
  • Dilutes toxins
  • Increases lympharic drainage
    • This delivers micro-organisms to phagocytes and antigens to the immune system
31
Q

How does infiltration of cells combat injury?

A

It removes pathogenic organisms and necrotic debris

32
Q

How does vasodilation combat injury?

A
  • It increased the delivery of blood (therefore proteins ect…) to the site of injury
  • It increases temperature
33
Q

How does pain and loss of function combat injury?

A

It enforces rest and therefore reduces the chance of further traumatic damage

34
Q

What are the local complications of acute inflammation?

A
  • Swelling
    • blocking of tubes and obstruction
      • eg bile duct, intestine
  • Exudate
    • compression
      • eg cardiac tanponade (heart cannot pump because of pressure in pleural space).
    • Serositis
  • Loss of fluid
    • eg burns
  • Pain and loss of function
    • especially if prolonged.
35
Q

What are the systemic effects of acute inflammation?

A
  • Fever -
    • ‘Endogenous pyrogens’ produced interleukin 1 and TNFa -
    • Prostaglandins: aspirin reduces fever
  • Leukocytosis
    • IL-1 and TNFa produce an accelerated release from bone marrow
    • Macrophages and T lymphocytes produce colony-stimulating factors
    • Bacterial infections -neutrophils, viral - lymphocytes
  • Acute phase response
    • Decreased apetite, raised pulse rate, altered sleep patters and changes in plasma conc of acute phase proteins inc:
      • C-reactive protein (CRP), a1 antitripsin, Haptoglobin, Fibrinogen, Serum amyloid A protein
  • Shock (a clinical syndrome of circulatory failure)
    • ​Caused by a spread of microorganisms and toxins and by the acute phase response
36
Q

What may happen after the development of acute inflammation?

A
  1. Complete resolution
  2. Continued acute inflammation with chronic inflammation = abscess
  3. Chronic inflammation and fibrous repair, probably with tissue regenerations
  4. Death
37
Q

What does the resolution of acute inflammation look like (morphology)?

A

Changes gradually reverse

  • Vascular changes stop so:
    • Neutrophils no longer marginate
    • Vessel permiability retuns to normal
    • Vessel calibre returns to normal

So…

  • Exudate drains to lymphatics
  • Fibrin is degraded by plasmin and other proteases
  • Neutrophils die, break up and are carried away or phagocytosed
  • Damaged tissue might be able to regenerate

If tissue architecture has been destoyed then complete resolution is NOT possible

38
Q

How does the resolution of acute inflammation work?

A
  • All mediators of acute inflammation have short half-lives.
  • May be inactivated by degridation
  • Inhibitors may bind
  • May be unstable
  • May be diluted in the exudate
  • Specific inhibitors of acute inflammatory changes
39
Q

Clinical examples of acute inflammation?

A
  • Bacterial meningitis
  • Lobar pneumonia
  • Skin blister
  • Abscess
  • Liver absess
  • Pericarditis
  • In serous cavities
40
Q

What is bacterial meningitis?

A

Acute inflammation the the maninges can cause vascular thrombosis and reduce cerebral pefusion.

Dangerous in brain! This is because of the increased pressure.

41
Q

What is lobar pneumonia?

A

Lungs fills with neutrophils / exudate becuase of the infection -They should be filled with air!

Caused by bacteria (Streptococcus pneumoniae).

Breathlessness, worsening fever, prostation, hypoxaemia over a few days, dry cough.

If treated, it can resolve completely.

42
Q

What are skin blisters?

A

Causes: heat, sunlight, chemical

Presents as painfun with profuse exudate

The collection of fluid strips pff the overlying epithelium

There are relatively few inflammatory cells so the exudate is clear (unless a bacterial infection develops)

There is either complete resolution or scarring

43
Q

What is an abscess?

A

Abscesses occur in solid tissues.

It is when the inflamatory exudate forces the tissue apart.

There is liquefactive neucrosis in the centre.

This may cause high pressure which results in pain

It may cause adjacent tissue damage and squash adaject structures.

44
Q

Serous What is acute inflammation in serous cavites?

A

This is when exudate pours into cavity.

It can be ascites (exudate in peritoneal), pleural or a pericardial effusion.

It results in respiratory or cardiac imparment

There is localied fibrin deposition

45
Q

What are some disorders of acute inflammation?

A

These are rare diseased (natural selection ensures that). But, they illustrate the importance of apparently small parts of this complex web of mechanisms.

For example:

  • Hereditary angio-oedema
  • Alpha-1 antitrypsin deficiency
  • Inherited complement deficiencies
  • Defects in neutrophil function
  • Defects in neutrophil numbers.

Sem 2 - Pathological Processes (13 decks)

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