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Pathological Processes - Alex's Cards (ESA2) > Session 2 Lecture Notes > Flashcards

Session 2 Lecture Notes Flashcards

1
Q

What is the definition of acute inflammation?

A

Response of living tissue to injury

  • it is innate, immediate and imitated to limit the tissue damage
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2
Q

What do vascular and cellular reactions to acute inflammation result in?

A

Accumulation of fluid exudate (mass of cells and fluid from vessels and/or organs) and neutrophils in tissues

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3
Q

Suggest some causes of acute inflammation

A
  1. Microbial infections
  2. Physical agents such as heat, light or radiation
  3. Chemicals
  4. Tissue necrosis
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4
Q

What are the 5 clinical signs of acute inflammation?

A 
Redness
Swelling
Heat 
Pain
Loss of function
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5
Q

What is the first immediate vascular phase reaction in acute inflammation?

A

Vasoconstriction of arterioles for a few seconds

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6
Q

After vasconstriction of arterioles what are the following steps in the vascular stage of acute inflammation?

A
  1. Vasodilation of arterioles and capillaries (increase in blood flow leads to increased heat and redness)
  2. Increased permeability of blood vessels (leads of excursion of protein rich fluid into tissues and slowing of circulation as blood has become more viscous)
  3. Increased concentration of RBCs and more viscous blood leads to stasis
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7
Q

What is stasis?

A

Slow blood flow

Occurs when blood is more viscous after fluid exudate

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8
Q

What is the first chemical mediator in acute inflammation?

Where is it released from?

A

Histamine
Released from mast cells, basophils and platelets
Can also be released from C3a, C5a and interleukin 1

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9
Q

What happens to blood vessels in acute inflammation and how does this lead to oedema?

A
  1. Arterioles dilate = increased blood flow to capillaries
  2. Increased blood flow = increased hydrostatic pressure and fluid movement into interstitium
  3. Blood vessels become more permeable so proteins move out into interstitium also increasing movement of fluid
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10
Q

What is the difference between exudate and transudate interstitial fluid?

A 
Exudate = only occurs in inflammation - the protein level is higher in interstitial fluid than in plasma
Transudate = protein level is equal to plasma
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11
Q

If a patient has an oedema of plural cavity - how can measuring protein levels help diagnose the cause?

A

If protein levels are high = oedema is due to pneumonia (inflammation of lungs)
If protein levels are low = oedema is due to heart failure (pulmonary oedema)

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12
Q

When would fluid loss be exudate and when would it be transudate?

A 
Exudate = when the fluid loss is due to inflammation and oedema has high protein content
Transudate = when the fluid loss is due to heart failure and hydrostatic pressure imbalance and oedema will have lower protein content
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13
Q

State 5 ways in which vascular leakage occurs - state whether the fluid moves between the cells or through the cells

A
  1. Endothelial contraction
  2. Cytoskeletal reorganisation
  3. Direct injury eg sunburn
  4. Leukocyte dependent injury (products of WBCs can injure cells)
    - these are all ways in which fluid moves BETWEEN cells
  5. Transcytosis - blood movements THROUGH cells
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14
Q

What is transcytosis?

A

The movement of macromolecules from fluid across/through a cell via endocytosis

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15
Q

During inflammation when fluid leaks into the interstitium - what plasma protein is key and what does it do?

A

Fibrin - it is involved in blood clotting cascade and creates a meshwork to localise the inflammation

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16
Q

What is the primary white blood cell involved in inflammation?

A

Neutrophil

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17
Q

What is another term used for neutrophil?

A

Polymorph

or Polymorphonuclear leukocyte

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18
Q

Describe the appearance of a polymorph

A

They come in multiple shapes and have multi lobed nuclei

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19
Q

What happens to the blood when it slows down and why does it slow down?

A

You get sludging of RBCs in the centre of the vessel

This is due to increased blood viscosity (as inflammation has caused exudation of fluid)

20
Q

In stasis describe the 4 movements of the neutrophils in/out the blood vessels

A
  1. Margination = they line up along endothelium
  2. Rolling = they roll along endothelium sticking to it intermittently
  3. Adhesion = they stick more stronger to endothelium
  4. Emigration = they move across blood vessel wall
21
Q

What is chemotaxis?

A

Cells move in response to a chemical signal down concentration gradient eg emigration of neutrophils across endothelium in response to infection

22
Q

How do neutrophils move across endothelium?

A

Relaxation of cell junctions and partial digestion of basement membrane

23
Q

What are chemotaxins and how do they work?

Give 3 examples

A

Chemotaxins attract neutrophils
They act as ligands and bind to a receptor on the neutrophil which activates them - making them move towards more chemotaxins (at site of severe inflammation)
Examples: C5a, leukotriene B4 and bacterial peptides (only for bacterial infections)

24
Q

Describe the 3 stages in which neutrophils are able to phagocyte

A
  1. Contact - get the polymorphs where they need to be using chemotaxins
  2. Recognition - get the polymorph to recognise the antigen by opsonisation
  3. Internalisation - the antigen is internalised to become a phagosome which is then fused with lysosomes which break down antigen
25
Q

What are the 2 ways in which lysosomes kill phagosomes? Give an example of each

A

O2 dependent = superoxide and hydrogen peroxide (both particularly good at killing bacteria)
O2 independent = lysozymes and hydrolases

26
Q

State the 3 main groups of chemical mediators within acute inflammation and where they are produced

A
  1. Proteases (produced in liver)
  2. Leukotrines (released from mast cells)
  3. Cytokines (large proteins) and Chemokines (small proteins) - produced by WBCs
27
Q

Name three types of proteases (chemical mediators in acute inflammation)

A
  1. Complement proteins - C3a and C5a
  2. Kinins
  3. Fibrin
28
Q

Name a type of leuokotriene (a chemical mediator of acute inflammation)

A

Metabolites of arachidonic acid

29
Q

Name 2 types of cytokines/chemokines (chemical mediators in acute inflammation)

A

Interleukin-1

Tumour necrosis factor alpha

30
Q

Which chemical mediators in acute inflammation increase blood flow?

A

Histamine

Prostoglandins

31
Q

Which chemical mediators in acute inflammation increase vascular permeability?

A

Histamine

Leukotrienes

32
Q

Which chemical mediators in acute inflammation act as chemotaxins for neutrophils?

A

C5a
Leuokotriene B4
Bacterial peptides (if bacteria)

33
Q

Which chemical mediators in acute inflammation increase phagocytosis by neutrophils?

A

C3b

34
Q

Name 2 key local complications of acute inflammation

A
  1. Swelling - which can lead to blockage of tubes

2. Exudate can cause compression eg cardiac tamponade and can cause serositis (inflammation of serous membrane)

35
Q

Name 5 key systemic effects of acute inflammation

A
  1. Fever (pyrexia) = such as Interleukin-1 and tumour necrosis factor
  2. Leukocytosis (increase in no of WBCs in blood)
  3. Acute phase response (eg decreases appetite)
  4. Acute phase proteins (proteins that increase in plasma) - C-reactive protein is key
  5. Shock - syndrome of circulatory failure
36
Q

What plasma protein can you look for in the blood as a marker of acute phase inflammation?

A

C reactive protein - marker of bacterial infection

37
Q

During resolution of acute inflammation what happens to exudate?

A

Drained to lymphatics
Fibrin is degraded
Neutrophils due and are phagocytosed

38
Q

What happens in bacterial meningitis?

A

Inflammatory reaction causes swelling of meninges

Patients get compression of brain and/or thrombosis reducing cerebral perfusion

39
Q

What happens in lobar pneumonia?

A

Alveolar fill with exudate and patients becomes short of breath and can die

40
Q

What is pericarditis?

A

Inflammation of pericardium

41
Q

What happens in extradural haemorrhage?
What part of the skull is easily fractured?
What 2 blood vessels are commonly damaged?

A

Fracture particularly common at pterion
Damage to anterior and posterior middle meningeal artery
Blood moves out damaged vessel and accumulates in scull - causing compression and damaging sensors that control respiration and heart control

42
Q

What happens in a subdural haemorrhage?

A

Damage to head causes a hematoma (clotted blood) to form beneath dura (in subdural space)
Onset gradual

43
Q

What happens in a sub-arachnoid haemorrhage?

What is the name of the blood vessel interjunction this commonly occurs from?

A

Bleeding between brain and and arachnoid layer
Most commonly occurs as a result of damage to the Circle of Willis (links vessels of left and right side of brain)
Person feels a sudden shock as the blood travels to sub-arachnoid space

44
Q

What are the 2 types of stroke?

Which is fatal?

A
  1. Ischaemic (restriction in blood supply)

2. Haemorrhagic (bleed in brain stem which will be fatal)

45
Q

What causes a coronary thrombosis?

Where does the blood collect?

A

Caused by a blockage to coronary artery (such as left anterior descending) which leads to myocardial infarction
Blood flows from heart into pericardial sac

Pathological Processes - Alex's Cards (ESA2) (8 decks)

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