Acute inflammation Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A
  1. Reddening - increased blood flow to area (hyperaemia due to dilation of capillaries)
  2. Swelling - exudation of fluid from dilated blood vessels into inflamed tissue
  3. increased heat - increased blood flow
  4. pain - due to chemical mediators and local pressor on nerve endings from exudate
  5. loss of function
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2
Q

What are the stages of acute inflammation?

A
  1. vascular phase
  2. exudative phase
  3. migration of leucocytes
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3
Q

What is the vascular phase?

A

Initial phase = transient (secs)
- arteriole constriction (‘white line’)
- smooth muscle response

Hyperaemia = (mins - days)
- arteriole and capillary dilation
- key chemical mediators are prostaglandins, endothelin and nitric oxide

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4
Q

What is the exudative phase>

A

Increased vascular permeability due to endothelial cell contraction, which is caused by histamine released by mast cells

Caused by:
Direct endothelial injury
Physical damage
Toxic agents
Infection
Enzymes
Oxygen free radicals

Result - escape (exudation) of protein-rich fluid from blood into surrounding tissue

Contents of fluid exudate
Water and electrolytes
Plasma proteins (albumin, globulin, fibrinogen)
Red blood cells
Platelets

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5
Q

What is the migration of leucocytes stage?

A

a) Margination / Pavementing
altered blood flow & loss of axial stream
expression of adhesion molecules (e.g. selectins, integrins)
b) Chemotaxis
Neutrophils move along a chemotactic gradient at ~2mm per hour, macrophages are slightly slower
Chemotaxins that attract & activate leukocytes:
bacterial products e.g. endotoxin
fibrin degradation products
complement derived factors
cytokines esp. lymphokines
tissue breakdown products
c) Emigration via intercellular junctions
motile cells force an opening
basement membrane is breached

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6
Q

What do neutrophils do in acute inflammation?

A

formed in the bone marrow
production time 7 days - half life in blood 6 hours
replaced twice a day
once they enter tissues do not return to the blood - most are lost through the mucous membranes of the body: gut, urinary and respiratory tract
have multilobed nuclei and fine cytoplasmic granules
- Phagocytosis of microorganisms or foreign material and fusion of phagosome with lysosomes to kill or degrade material
- Secretion and/or release of granules into exudate to enhance acute inflammatory response

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7
Q

How are neutrophils recruited?

A
  1. Neutrophils marginate in venules & capillaries
  2. Loosely adhere to endothelium and roll along inner blood vessel wall (mediated by selectins)
  3. At junction between endothelial cells, firmly adhere and emigrate from blood vessel into tissue (mediated by integrins)
  4. Migrate to site of damage along a chemotactic gradient
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8
Q

What do eosinophils do in acute inflammation?

A
  • formed in the bone marrow, similar life span to neutrophils
  • impart a greenish colour to the tissue
  • have bilobed nuclei and distinct granules in the cytoplasm
  • are prominent in parasitic infections, and local allergic reactions [IgE]
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9
Q

What do mast cells do in acute inflammation?

A

-heavily granulated mononuclear cells found in tissues
-tissue lifespan 4-12 weeks depending on location
-degranulate in tissue injury, releasing histamine, heparin, and 5-hydroxytryptamine (serotonin) – chemical mediators of vasodilation, chemotaxis and pain
-critical in initiation of acute inflammatory response

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10
Q

What are basophils?

A

also formed in the bone marrow
multilobed nucleated cells with large bluish granules in the cytoplasm
granules similar to those of both neutrophils and mast cells
important in IgE mediated injury to tissues (allergic reactions)

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11
Q

What are 5 different pyrogens?

A

Pyrogens act on the temp control centres in the hypothalamus of the brain to raise body temperature
1. Neutrophils - prime source when they begin to phagocytose, also eosinophils and macrophages
2. Gram-negative organisms - their cell walls contain pyrogens
3. Damaged tissue cells - necrosis releases pyrogens
4. Antigen-antibody complexes - may release pyrogens
5. Tumours - may release pyrogens particularly those which have metastasised - also the pyrexia caused by the central necrosis in such tumours

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12
Q

What is a summary of the sequence of events in acute inflammation?

A
  1. Momentary vasoconstriction of the blood vessels in affected area
  2. Dilation of the blood vessels
  3. Exudation of fluid, rich in protein, into the tissues (effusion)
  4. Margination of leukocytes
  5. Emigration of leukocytes through the altered endothelium
  6. Induction of increased temperature
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13
Q

What are the functions of inflammatory effusion?

A

dilutes the agent
contains antibodies - which attack or coat (opsonise) the agent and facilitate phagocytosis by neutrophils and macrophages
may contain fibrin which immobilises the agent and provides a matrix for migration of inflammatory cells
contains chemotaxins that attract more inflammatory cells to the site
washes away the agent - if on a surface, e.g. skin and alimentary tract
brings the agent via the lymphatic vessels to the local lymph nodes - for further processing or antigen presentation

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14
Q

What are the fluid types?

A

serous
catarrhal
fibrinous
diphtheritic
haemorrhagic
purulent

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15
Q

What is serous inflammation?

A

Due to mild vascular injury in an organ or in vessels underlying a surface
- a clear to cloudy fluid with little protein present
- vesicles of the skin produce a serous fluid; many inflammations in joints are serous

Sequel - resolves when the irritant is overcome, or may progress to a more serious reaction

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16
Q

What is catarrhal inflammation?

A

This is a mild form and occurs on mucous membranes with goblet cells and/or mucous glands
varies from watery to gelatinous in consistency and cloudy to pinkish in colour
essentially a shedding of epithelium, mucus, neutrophils, some RBCs, and flecks of fibrin
common in mild forms of rhinitis, tracheitis, bronchitis, gastritis and enteritis
Sequel - resolves when the irritant is overcome, or may progress to a more serious reaction

17
Q

What is fibrinous inflammation?

A

Due to more severe endothelial injury resulting in the escape of fibrinogen from the blood and conversion to fibrin
is a yellowish coagulum on the surface of a tissue or within its substance
is common in lungs and on serous surfaces (e.g. thoracic, pericardial and peritoneal)
in hollow organs, it may coagulate within the lumen, forming a cast, it will peel off from the underlying tissue

Sequel - Fibrinous exudates may also resolve if the fibrin is digested by macrophages
- in pleural, pericardial and peritoneal cavities, organisation of the fibrin into fibrous tissue may occur producing adhesions between the visceral and parietal surfaces

18
Q

What is diphtheritic inflammation?

A

A more severe form of fibrinous exudate in which there is considerable necrosis of underlying tissues
firmly adherent to the underlying tissue: attempts at removal cause tearing of this tissue
commonly seen with internal surface fungal infections e.g. nose of the dog and guttural pouch of the horse, fungal toxins penetrating the underlying tissue causing coagulative necrosis
can be very haemorrhagic
Sequel - repairs by scar formation

19
Q

What is haemorrhagic inflammation?

A

A severe acute to peracute inflammation in which haemorrhage is the main component
- seen in the lymph nodes, lungs and intestine in severe inflammation
- sometimes occurring in all tissues

Sequel
if widespread, is most commonly associated with acute deaths e.g. acute viral, bacterial or toxic diseases
if strictly localised, e.g. bruising, then it may repair

20
Q

What is purulent (suppurative) inflammation)

A

Where pus (an admixture of dead and dying neutrophils with necrotic cells and a pyogenic agent) is the predominant feature

  • proteolytic enzymes released by the dying neutrophils lyse tissue cells producing a fluid
  • colour varies - white, yellow, green, brown - depending upon the agent

Sequel - the resolution of abscesses depends upon their location

21
Q

How do different abscesses resolve?

A

-if near to a surface, will rupture onto it
beneficial in the skin where it discharges to the exterior with or without the pyogenic organism
-detrimental if rupture is into a body cavity
-in deeper tissues, there is extensive fibrous capsule formation, the fluid becomes inspissated due to withdrawal of water content, macrophages digest the necrotic remains and fibrous tissue organises the interior, the end result being a fibrous scar