Acute inflammation

Question 1

Causes of acute inflammation

Answer 1

• Microbial infection
• Allergic reaction
• Physical causes
• Chemical causes

Question 2

Characteristics

Answer 2

Rubor – red – dilation of blood vessels

Calor – hot – peripheral inc in temp – due to inc blood flow

Tumor – swelling – mainly to oedema – some contribution from inflammatory cells

Tender – stimulation of nerve endings by pressure and chemical mediations

loss of function

Question 3

common examples

Answer 3

acute appendicitis and cellulitis

Question 4

Phases of acute inflammation

Answer 4

Initial reaction of tissue to injury

Vascular phase – dilation and increased permeability INC PERM

Exudative phase – fluid and cells escape from permeable venules ESC FROM PERM VEN

Neutrophil polymorph is the characteristic cell – weird nucleus so easy to spot – most common white blood cell – 70% of wbc are neutrophils

Question 5

Normal vs acute inflammation

Answer 5

Capillary beds start to occupy cells and fluid bc of the now open precapillary sphincter

Normal vs acute inf net flow – due to hydrostatic pressure the proteins escape the cell

No net flow – some hydrostatic pressure that relieves once some net flow is released by out flow is compensated by in flow – good balance

With net flow bc of permeable wall – this hydrostatic pressure compromises proteins to go to damaged area and fluid is secreted from the walls causing swelling in the tissue

Question 6

Features of exudate

Answer 6

Features of an exudate – the secretion

High protein content – 50 times more content

Proteins include immunoglobulins ( antibodies ) – may be important for destruction of invading organisms

Fibrinogen -> fibrin

• On extravascular contact
• Acutely inflamed organ surfaces commonly covered by fibrin

High turnover

• Continuously removed via lymphatics

Question 7

Exudate vs transudate

Answer 7

Exudate - acute inf processes

• Net flow out
• Inc vascular perm
• High protein content

Transudate – normal inf processes

• No net flow
• Normal vasc perm
• Low protein content

Question 8

What causes vascular permeabilty

Answer 8

• Produced by chemical mediators including histamine, bradykinin
• Involves stimulation of endothelial cell cytoskeleton by chemical mediators
• Confined to post capillary venules
• Transient intercellular gaps ( 0.1-0.4 microns ) appear
• Endothelial cells are not damaged in this process which is good, gaps go BETWEEN cells – tighten up again after inflammation

Question 9

Lymphatic system in inflmmation

Answer 9

• Lymphatics dilated
• Drain fluid from exudate
• Antigens carried to lymph nodes
• Recognised by lymphocytes

Question 10

Cellular component of acute inflammation

Answer 10

Neutrophil accumulation in the extracellular space is the diagnostic feature of acut inf

Neutrophils

• Kill orgs
• Degrade necrotic dissue
• Ingest offending agents
• Produce chem mediators
• Produce toxic oxygen radicals
• Produce tissue damaging enzymes

Question 11

pavementation and margination

Answer 11

Immune cells move out of blood vessels into inflamed area

And do, attaching to vessel walls through margination and moving along to find a gap through pavementation in a process called diapedesis

The vessel wall expresses certain molecules during inf time, proteins like selectins and integrins which inc in number and they interact with receptors on the immune cell membrane causing a higher affinity allowing them to move along and across to the inf site

Question 12

neutrophil chemotaxis

Answer 12

Neutrophil chemotaxis – smelling socks

Chemotactic compounds include:

Bacterial products

Some complement components

Products of neutrophil activity

How do neutrophils do it?

Movement – chemotaxis

Recognition of and adhesion to microorganisms

Phagocytosis

Intracellular killing of microorganisms

Question 13

Chemical mediators of acute inflammation

Answer 13

• The spread of acute inflammatory response following injury suggests chemical substances released from the injured tissues spread outwards into uninjured areas
• Derived from cells and extra cellular sources eg plasma
• These endogenous chemical mediators cause
• Vasodilation
• Emigration of neutrophils
• Chemotaxis
• Increased vascular permeability
• Itching and pain

Question 14

Plasma factors of acute inflammation

Answer 14

Plasma contains 4 enzymatic cascade systems – argents that get triggered

Complement system

The kinins

Coagulation factors

Fibrinolytic system

Question 15

Recognition and adhesion in acute inflammation

Answer 15

• Most microorganisms are not recognised for phagocytosis until they are coated in opsonins
• These opsonins bind to specific receptors on leuccocytes and greatly enhance phagocytosis
• Major opsnonins – IgG – C3b ( a fragment of C3 generated by complement activation ) – collectins – plasma proteins that bind to microbial cell walls

Question 16

Phagocytosis

Answer 16

Phagocytosis – process whereby cells such as neutrophils and macrophages ingest solid particles is termed phagocytosis

Question 17

what does acute inflammation tend to look like?

Answer 17

serous - protein rich fluid exudate

cattarhal - mucus hypersecretion

fibrinous - exudate contains plentiful fibrin

haemmorrhagic - extreme vascular injury

suppurative - production of pus

Membranous - epithelium coated by fibrin

Pseudomembraenous - superficial mucosal slough

suppuration

• formatio of pus - neutrophils, bacteria, cellular debris
• causative stimulus virtually always infective agent
• a collection of pus surrounded by a membrane of sprouting capillaries , neutrophils and occasional fibroblasts is called an abscess
• on draining , the absecc cavity collapses and is obliterated by organisation and fibrosis
• deep seated abcesses may drain along a sinus tract or fistula

ulceration

• an ulcer is a local defect or excavation of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue

Most commonly encountered

• inflammatory necrosis of the mucosa - mouth, stomach,intestine
• Chronic leg ulcers in those with circulatory disturbance

Question 18

Beneficial affects of circulation

Answer 18

• Dilution of toxins – allows them to be carried away by lymphatics
• Entry of antibodies – due to inc vasc permeability
• Fibrin formation – impedes movement of microorgansims
• Transport of drugs – eg antibiotics
• Delivery of nutrients and oxygem – aided by inc fluid flow
• Stimulation of the immune response – fluid exudate containg antigens reaches local lymph nodes

Question 19

Harmful affects of acute inflammation

Answer 19

Harmful effects of acute inflammation

• Digestion of normal tissues
• Swelling – eg laryngeal odema, brain swelling
• Inappropriate inflammatory response eg type 1 hypersensitivity

Question 20

Systemic affects of acute inflammation

Answer 20

Systemic effects of acute inflammation

Pyrexia – IL1-IL6 – cyotkytes – resets temp gage

Infectious agents can drive pyrogens to the brain that produce the drive forward and uptake the thermoregulatory mechanisms that push up the temperature which lead to a fever which means skin vasoconstriction and reduced heat dissipation

Elevation In temperature of even a few degrees may improve the efficiency of leukocyte killing and probably impairs the replication of many offending micro-organisms

Question 21

Is fever a good thing or a bad thing?

Answer 21

Is fevera good thing or a bad thing – fever is a good sign as it’s a sign that your body is recognising and taking actions to defeat infections – not dangerous but there is some exceptions like infants where it can trigger seizures, or sudden fevers which could indicate meningitis

Question 22

Symptoms of acute inflammation

Answer 22

Constitutional symptoms including malase, anorexia and nausea

Weight loss due to negative nitrogen balance, particularly when there is extensive chronic inflammation

Reactive hyperplasia of the reticuloendothelial system

Haematological changes

Increased erthrpocytes sedimentation rate

Anemia

Leukcytosis