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Pathological Processes > Acute Inflammation Lecture > Flashcards

Acute Inflammation Lecture Flashcards

1
Q

What is inflammation?

A

Rapid response to injury of vascularised living tissue

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2
Q

What are the purpose of cell mediators? What are they?

A

Any molecule produced in a focus of inflammation and modulates inflammation

They deliver exudate and cells into the injured tissue from the blood Leucocytes take minutes to deliver, but exudate takes seconds

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3
Q

What is the rule of thumb for acute inflammation length?

A

After 2/3 days it becomes chronic

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4
Q

Why cant cartilage have inflammation? (eg. why does the cartilage appear as normal?)

A

Bc. inflammation can only occur at places with a blood supply. Cartilage doesn’t have one.

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5
Q

Causes of acute inflammation? FITPIT

A

FITPIT Foreign bodies Immune reactions Trauma Physical/Chemical agents Infections Tissue Necrosis

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6
Q

Clinical signs of acute inflammation? Real Dogs Take Cats

A

Rubor - Redness Dolor - Pain Tumour - Swelling Calor - Heat Loss of function - enforces rest and reduces further damage

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7
Q

What are prostaglandins?

A

Substances produced in inflammation from cell membrane phospholipids

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8
Q

What affect do prostaglandins have on the body?

A

Can make skin more sensitive to pain and fever

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9
Q

How do aspirins and NSAIDs block the action of prostaglandin, reducing pain and swelling?

A

They inhibit the cyclo-oxygenase cycle, which is the enzyme that produces prostaglandin from arachidonic acid.

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10
Q

How is the exudate formed during acute inflammation? (Long-step reaction?)

A
  • Firstly, brief moment of vasoconstriction followed by arteriole vasodilation
  • Vasodilation causes flow to capillaries to accelerate and capillary pressure rises, hence delivery of fluid and leucocytes to area of injury increases
  • Walls of venules become leaky and plasma escapes through gaps between endothelial cells
  • Increased haematocrit in venules and increased blood flow resistance in blood flowing out of tissue
  • Increased upstream pressure means blood flow out slows down and the pressure gradient results in fluid leaving the venules and delivering proteins to tissue
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11
Q

How are gaps created in venules, leading to leaky fluid?

A

Histamine causes endothelial cells to contract and pull apart, creating gaps for plasma proteins to pass

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12
Q

What group of chemical mediators does histamine belong to? Name another in this group

A

Vasoactive amines

Serotonin

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13
Q

Where are histamine and serotonin from? Where are they stored?

A

Formed before injury and already present in cells so immediately ready in injury

Histamine stored in granules of mast cells, basophils and platelets

Serotonin stored in granules of platelets

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14
Q

What does histamine do in acute inflammation?

A

Produces pain, arteriolar dilatation and venule leakage

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15
Q

What is Starling’s Law?

A

Theory that fluid movement is controlled by a balance between 4 factors:

  1. Capillary Pressure - Blood pressure in capillaries
  2. Interstitial Free Fluid Pressure - Pressure of interstitial fluid
  3. Plasma colloid oncotic pressure - Pressure exerted by plasma protein, drawing water towards it
  4. IF colloid osmotic pressure
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16
Q

Consequence of increased capillary hydrostatic pressure (vasodilation of vessels) AND interstitial osmotic pressure?

A

Increased fluid out of vessel

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17
Q

What can be said about the viscosity of blood if fluid leaves the vessel?

A

Increased viscosity (thicker) hence reduced flow of vessels known as stasis

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18
Q

Using Starling’s Law, explain what happens to the forces when acute inflammation occurs.

A

Membrane becomes leaky

Hydrostatic Capillary Pressure increases (due to vasodilatation) so more fluid leaves blood

Main force driving fluid back (colloidal osmotic pressure) reduced bc. proteins move into tissue raising osmotic pressure to same as blood (diffusion)

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19
Q

What do Lymph nodes do?

A

Drains tissues of excess fluid which takes microorganisms and pathogens to the immune system in the lymphatics

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20
Q

What are the 3 types of defensive proteins in exudate?

A
  • Opsonins - Coat foreign material making them easy to phagocytose
  • Complement - Locally assembled proteins that create a bacteria-perforating structure
  • Antibodies - Bind to microorganisms and act as opsonins
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21
Q

Exudate vs Transudate

A
  • Exudate - Protein full, in inflammation
  • Transudate - Protein-less, occurs due to increased CHP or reduced COP, vessels have same permeability as normal (no contraction of endothelial cells) and results in heart, hepatic and renal failure
22
Q

List all the chemical mediators that cause vascular leakage

A

Histamine

Serotonin

Bradykinin

Complement proteins C3a, C4a and C5a

23
Q

What are the 6 steps of neutrophil mechanism?

Call And Message DR Pepper
(CAMDRP)

A
  • Chemotaxis
  • Activation
  • Margination
  • Diapedesis
  • Recognition-attachment
  • Phagocytosis
24
Q

Explain Chemotaxis of Neutrophils

A

Chemotaxis is directional movement towards a chemical attractant

Examples: Bacterial peptides, C5a, LTB4

Creates pseudopods on neutrophils = Extensions of cytoplasm towards the attractant

25
Q

Explain Activation of Neutrophils

A

Chemotaxin bind to cell, causing Calcium and Sodium influx, cell swells and assumes triangular shape pointing to chemotaxin due to cytoskeleton change

Cell sends out psuedopodia and are stickier than normal

26
Q

Explain Margination of Neutrophils

A
  • Leucocytes assume marginal positions on vessel walls to heed chemotactic call
  • Cells roll along wall and then become trapped (adhesion) by receptors binding to selectins and integrins on endothelium
27
Q

What is the difference between Selectins and Integrins

A

Selectins are what stick to neutrophils when they just roll

When neutrophils stick to integrins such as ICAM-1, they firmly stick (intercellular adhesion molecule 1)

28
Q

Explain Diapedesis of Neutrophils

A

Neutrophils dig through endothelial wall

Produce collagenase to digest basement membrane

Takes 3-9 mins

Once in space, they pull themselves to target via collagen fibres

29
Q

Explain Recognition-Attachment of Neutrophils

A

Opsonins help phagocytes recognise targets

Examples are igG and C3b complementary protein

30
Q

Explain Phagocytosis of Neutrophils

A

Engulfs antigen

Phagosome

Degranulation by bactericidal enzymes - These can sometimes leak out of cell and kill body cells, causing further injury (phagosome not closed yet)

Orgamisms killed by two mechanisms:

  • Oxygen - O2 free radicals into phagosome, called oxygen or respiratory burst
  • Using enzymes (oxygen-independent)
31
Q

Which mediators are responsible for vasodilatation?

A

Histamine, Serotonin and Prostaglandin

32
Q

Which mediators are responsible for increased vascular permeability?

A

Histamine, Serotonin and Bradykinin

33
Q

What is bradykinin made from?

A

From the plasma precursor Kininogen

34
Q

Which mediators are responsible for Chemotaxis?

A

Leukotriene B4, C5a, C3a, chemokines and bacterial products

35
Q

Which single mediator is responsible for phagocytosis?

A

C3b

36
Q

Which mediators are responsible for pain? Why do we get pain?

A

Bradykinin and Prostaglandin

To alert us of a problem and to ensure we rest well

37
Q

List some local complications of acute inflammation

A
  • Damage to normal tissue by products and substances of phagocytosis and neutrophils
  • Swelling can cause blocking of tubes eg. fallopian or intestinal, and compression of structures
  • Fluid builds up in tissue to a pressure extent, but fluid can continuously leak from surface wound, hence burns lead to loss of fluid
  • Pain and loss of function
38
Q

Fever is a systemic effect of inflammation. What is fever? What stops it? Why is it important?

A
  • Fever - Macrophages stimulated by exogenous pyrogens to produce pyrogenic cytokines TNF or IL-1, that produce Prostaglandin E2 in hypothalamus, causing fever

REMEMBER: Aspirin inhibits prostaglandin formation and hence inhibits fever

Fever is good to kill bacteria w/ temp and better for inflammation

39
Q

Leucocytosis is a systemic effect of acute inflammation. What is it?

A

Increase in circulating leucocyte no.

Macrophages and endothelial cells produce stimulating factors to stimulate bone marrow to make more neutrophils

40
Q

The Acute Phase Response is a systemic effect of acute inflammation.

A

Liver produces diff. levels of proteins

Low albumin, high fibrinogen, C3 etc.

Produced by cytokines released during inflammation

Leads to sleepiness and lack of appetite in injury

41
Q

Shock is a systemic effect of acute inflammation. What is shock? Why does it happen?

A

Inflammation can occur around the body due to spreading of the mediators, causing shock

Dramatic drop in blood pressure due to widespread vasodilatation, and leads to excessive exudate formation, often fatal

42
Q

What is hypovolaemic shock?

A

Shock when body loses 20% of blood or fluid

43
Q

How is acute inflammation resolved?

A

Short-lived mediators stop being produced

Normal vascular permeability returns, cessation of neutrophil emigration

Exudate reabsorbed into venules or drained into lymphatic, fibrin degraded, neutrophils undergo apoptosis and phagocytosed

Tissue will regenerate or scar will form

44
Q

What is Pus/Abscess

A
  • Type of exudate
  • Creamy white bc rich in neutrophils, typical of infection by chemotactic bacteria
45
Q

What is Haemorrhagic exudate?

A

Lots of RBC to appear bloody, indicates vascular damage, seen in destructive infections or tumour

46
Q

What is Serous Exudate?

A
  • Contains plasma proteins but few leucocytes, suggesting no infection
  • Clear, seen in blisters
  • Differ from plasma bc dont contain fibrinogen
47
Q

What is Fibrinous Exudate?

A
  • Significant deposit of fibrin
  • Take away smooth sliding surfaces of serous membranes if build up there
  • Can be heard as a rubbing sound
48
Q

Clinical examples of acute inflammation?

A

Liver Abscess

Acute Appendicitis

Lobar Pneumonia

49
Q

What is Hereditary Angio-Oedema?

A

Extremely rare autosomal dominant condition

Inherited C1-esterase deficiency

Non itchy oedema attacks

Abdominal pain

Often have family history of sudden death due to larynx

50
Q

What is Alpha-1 Antitrypsin Deficiency?

A

Autosomal recessive

Deactivates enzymes released by neutrophils

Develop emphysema as proteases from neutrophils arent checked

Liver disease occurs and cirrhosis

51
Q

What is Chronic Granulomatous Disease?

A

Phagocytes cant produce superoxide

Can’t generate oxygen burst

Chronic infections in first year of life

Granulomas and abscesses affecting skin, lymph, lungs, liver and bones occur but cant rid of infections

52
Q
A

Pathological Processes (2 decks)

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