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ESA2 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What are the main clinical signs of acute inflammation?

A 
Rub or- redness
Tumor-swelling 
Calor-heat
Dolar-pain 
And loss of function
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2
Q

What changes occur in the tissue in response to acute inflammation?

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

Describe the changes in blood flow in acute inflammation:

A
  1. There will be transient vasoconstriction of the arterioles
  2. Vasodilatation of arterioles and then of capillaries–> increase in blood flow causing heat and redness
  3. Increase permeability of blood vessels causing an Exudation of protein rich fluid and slowing of circulation causing swelling
  4. Stasis of blood
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4
Q

Which mediators can cause vasodilation?

A

Histamine etc

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5
Q

What happens to the blood flow when arterioles vasodilator?

A

Flow accelaterws in the capillaries and capillary pressure rises

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6
Q

Why is vasodilation important in acute inflammation?

A

To increase the delivery of ,fluid to the area and leukocyte so to the site of injury

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7
Q

What happens to the walls of the venules following vasodilatstion of the arterioles?

A

They become leaky and plasma can escape through tiny gaps between endothelial cells.

This results in a higher haematocrit within the venules and increased resistance to blood flow within them, so blood outflow from the site of injury is reduced.

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8
Q

Why is an increase in pressure in the vessels important at the site of injury?

A

Allows greater Exudation of fluid into tissue spaces allowing the delivery of plasma proteins to the site of injury

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9
Q

Where is histamine stored?

A

In the granules of mast cells, basophils.

Serotonin is found in the granules of platelets

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10
Q

When is histamine released?

A

In response to stimuli such as physical damage, immune reactions and complement components

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11
Q

In acute inflammation what does histamine do?

A

Produced pain, arteriolar dilation and venular leakage

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12
Q

How does fluid leakage occur at venules?

A

Histamine causes the endothelial cells to contract and pull apart creating gaps which plasma protoens can pass through.

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13
Q

What can serotonin do which histamine cannot?

A

Stimulate fibroblasts

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14
Q

What other mediators are produced in acute inflammation other than histamine and serotonin?

A

Prostaglandins which also cause vasodilatation, increase the sensitive of the skin to pain and cause fever.

Leukotrienes and bradykinin

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15
Q

Overall, what do chemical mediators do in acute inflammation?

A

They dilate arterioles, venules are also under the direction of chemical mediators they become leaky as the endothelial cells contract and create gaps.

In this way acute inflammation throws off the equilibrium of fluid exchange in the microcirculation.

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16
Q

What are the four forces which affect starlings law?

A
  • Capillary pressure
  • Interstitial free fluid pressure
  • Plasma colloid osmotic pressure
  • Interstitial fluid colloid osmotic pressure
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17
Q

What is the main force forcing fluid out of blood and the main force forcing fluid back into blood?

A

The main force driving fluid out of the vessels is the hydrostatic pressure of the blood, the main force driving fluid back into the blood is the colloidal osmotic pressure of the plasma proteins

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18
Q

What are the main vascular changes which occur in acute inflammation?

A
  • The semipermeable membrane becomes leaky
    • The main force driving the fluid out of the vessels is increased (arterioles dilate increasing capillary pressure)
    • The main force driving fluid back into the blood is reduced as plasma
    proteins escape into the tissue spaces raising the osmotic pressure there so
    that it roughly equals that of blood
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19
Q

What are the Three main in types of defensive proteins present in the exudate?

A
  • opsonin
  • complement
  • antibodies
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20
Q

What do opsonins do?

A

coat foreign materials and make them easy to

phagocytise.

21
Q

What does complement do?

A

a group of proteins that are assembled locally to produce a

bacteria-perforating structure

22
Q

What is the difference between exudate and transudate?

A

The tissue fluid that develops in inflammation is an exudate, that is to say it is protein rich. In contrast, fluid which is protein poor is called a transudate. A transudate is an ultrafiltrate of plasma and it occurs in normal vessels. It is seen in conditions such as heart failure when there is increased capillary hydrostatic pressure.

23
Q

What is the primary leukocyte involved in acute inflammation?

A

Neutrophils

24
Q

In a healthy person, where are neutrophils only usually found?

A

In the blood and bone marrow

25
Q

What is the life span of a neutrophil?

A

12-20 hours

26
Q

Can neutrophils multiply?

A

No

27
Q

What 6 things must a neutrophil do in order to capture and kill a bacterium in a tissue space?

A
  1. Be summoned to the place of injury = chemotaxis
  2. Switch to a higher metabolic level = activation
  3. Stick to the endothelial surface = margination
  4. Crawl through the endothelium = diapedesis
  5. Recognise the bacterium and attach to it = recognition-attachment
  6. Engulf the bacterium = phagocytosis.
28
Q

What is chemotaxis?

A

It is the directional movement towards a chemical attractant. Using a chemotactic gradient.

29
Q

Give examples of chemotaxis:

A

Endotoxin, fresh blood, injured tissue, substances produces by leucocytes, complement fragments such as c5a

30
Q

What are the causes of acute inflammation?

A 
Microbial injections
Hypersensitivity reactions
Physical agents
Chemicals 
Tissue necrosis
31
Q

Describe the process of activation of neutrophils:

A

Within five seconds of the chemotaxin binding to the cell surface receptors, calcium and sodium ions rush into the cell, it swells and reorganises its cytoskeleton assuming a roughly triangular shape pointing in the direction of the chemotactic stimulus. Within 5-10 seconds the cell sends out pseudopodia. Activated cells are stickier than normal cells.

32
Q

Describe margination, rolling and adhesion of neutrophils in response to acute inflammation:

A

Margination is the process whereby leucocytes assume marginal positions in the vessels.
Leucocytes stick to the walls of venules as they heed the chemotactic ‘call’. They roll along the wall but then become ‘trapped’ (adhesion), stop and crawl out of the vessel.
Leucocytes are trapped when their receptors bind to adhesion molecules (called selectins and integrins) on the endothelium.

33
Q

What is diapedesis?

A

Where Leucocytes ‘dig’ their way out of the venules, they don’t use the endothelial gaps through which the exudate escapes.
They produce collagenase which digests the basement membrane. Diapedesis takes a number of minutes, in the order of 3-9 minutes.
Once in the extravascular space the leucocytes move towards their target by pulling themselves along collagen fibres of other tissue structures.

34
Q

Describe the recognition-attachment phase of neutrophils:

A

Opsonins are substances which make it easier for phagocytes to recognise targets, attach to them and then phagocytise them.

35
Q

How do neutrophils phagocytose things?

A

During phagocytosis the membrane of the phagocyte forms a crater shape around the particle that is to be phagocytised.

This crater then develops into a cup which surrounds the particle.

The edges of the cup come together and the apposed plasma membranes fuse. The particle is then within an intracellular vacuole which is called a phagosome.

They then degranulate

36
Q

What are the two ways that neutrophils can kill organisms?

A

-Oxygen-dependent – using oxygen derived free radicals which are released into the phagosome. This mechanism of killing is called the oxygen burst or respiratory burst.

-Oxygen-independent – using enzymes, e.g., proteases, phospholipases,
nucleases and lysozyme.

37
Q

What are the main roles of inflammatory mediators?

A 
Vasodilation
Increased vascular permeability 
Chemotaxis 
Phagocytosis
Pain
38
Q

Name some of the local complications which can be caused by acute inflammation:

A
  • damage to normal tissue
  • obstruction of tubes due to due to swelling
  • loss of fluid
  • pain and loss of function
39
Q

What are the 4 main systemic effects of acute inflammation:

A

1- Fever
2-leucocytosis
3-the acute-phase response
4- shock

40
Q

Why does fever occur in acute inflammation?

A

Macrophages when they are stimulated to do so by exogenous (bacterial) pyrogens (particularly endotoxin) produce pyrogenic cytokines, e.g., TNF, interleukin-1.

These cytokines cause an increase in synthesis of prostaglandin E2 within the anterior hypothalamus which increase body temperature.

41
Q

What is leucocytosis?

A

In leucocytosis the number of circulating leucocytes increases.

Neutrophilia is seen during bacterial infection. Macrophages and endothelial cells in injured tissues produce colony stimulating factors and these stimulate the bone marrow to produce more neutrophils.

42
Q

What is the acute phase response in acute inflammation ?

A

The acute phase response is a change in the levels of some plasma proteins that is seen because the liver changes its pattern of protein synthesis. It occurs within hours of injury.

The acute phase response is produced by cytokines released during inflammation. The sleepiness and lack of appetite that are seen in serious injury are a result of the acute phase response.

43
Q

What causes shock in acute inflammation?

A

If bacterial products or inflammatory mediators spread around the body in the blood stream inflammation can occur throughout the body. This results in shock. Shock is a dramatic drop in blood pressure due to widespread vasodilatation and increase in vascular permeability with resultant fluid exudation.

44
Q

How is acute inflammation brought to an end?

A

Th mediators of acute inflammation have short half lives and are degraded shortly after release.

Normal vascular permeability returns, there is cessation of emigration of neutrophils and resolution of acute inflammation begins.

The exudate is reabsorbed and drained away via the lymphatic system and neutrophils under go apoptosis

If the damaged parenchymal cells can regenerate then the tissue will return to normal, however if regeneration cannot occur or damage has been extensive a fibrous scar will form.

45
Q

What are the 4 types of exudate?

A
  • pus/abscess, creamy white colour rich in neutrophils
  • haemorhaggic exudate, contains rbs so appears bloody to naked eye
  • serous exudate, contain plasma proteins but few leucocytosis. Found in blisters.
  • fibrinous exudate, significant amount of fibrin, eg blood clot without the cells. In pericardial surfaces or pleural spaces means serosal surfaces no longer glide over each other easily.
46
Q

Briefly describe hereditary Angio-oedema:

A
  • This is an extremely rare autosomal dominant condition in which sufferers have an inherited deficiency of C1-esterase inhibitor (a component of the compliment system)
  • Patients have attacks of non-itchy cutaneous angio-oedema and also recurrent abdo pain due to intestinal oedema
  • sudden death due to laryngeal involvement
47
Q

What is alpha1-antitrypsin deficiency?

A

This is an autosomal recessive disorder in which there are low levels of alpha-1 antitrypsin, a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation.

Patients with the disorder develop emphysema as proteases released by neutrophils act unchecked and destroy normal parenchymal tissue.

Liver disease also occurs as the hepatocytes produce abnormal version of the protein which is incorrectly folded. It polymerises and This causes hepatocyte damage and eventually cirrhosis.

48
Q

What is chronic granulomatous disease?

A

In this genetic condition phagocytes are unable to generate the free radical superoxide. Bacteria are phagocytised but the phagocytes cannot kill them as they can’t generate an oxygen burst.

This results in the formation of chronic infections in the first year of life.

ESA2 (7 decks)

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