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Pathological Processes > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

Response of living tissue to injury initiated to limit the tissue damage.

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2
Q

Outline the main causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions
Physical agents e.g heat 
Chemicals
Tissue necrosis
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3
Q

What are the signs of acute inflammation?

A 
Rubor - redness
Tumor - swelling
Calor - heat
Dolor - pain
and loss of function
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4
Q

What changes in tissues occur as a result of acute inflammation?

A

Changes in blood flow (vascular phase inflammation), exudation of fluid into tissues, infiltration of inflammatory cells

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5
Q

What is the first stage in vascular inflammation?

A

Transient vasoconstriction of arterioles

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6
Q

Describe the stages of vascular inflammation

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilation of arterioles and then capillaries (heat and redness)
  3. Increased permeability of blood vessels (exudation of protein rich fluid and slowing of circulation due to swelling)
  4. Concentration of RBC’s in small vessels and increased viscosity of blood = stasis
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7
Q

What is histamine?

A

Chemical mediator involved in acute inflammation. Released from mast cells, basophils and platelets in response to stimuli e.g. physical damage

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8
Q

How does acute inflammation cause oedema?

A

Arteriolar dilatation leads to increase in hydrostatic pressure. Increased permeability of vessel wall leads to loss of protein into interstitium. Net flow of fluid out of vessel = oedema (excess of fluid in interstitium)

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9
Q

What is the difference between transudate and exudate?

A

Transudate has the same protein content as plasma, exudate has more protein than plasma (only in inflammation).

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10
Q

How is a transudate formed?

A

Fluid loss due to hydrostatic pressure = low protein content e.g. cardiac failure or venous outflow obstruction

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11
Q

Describe the mechanisms involved in vascular leakage

A
  • Endothelial contraction
  • Cytoskeletal reorganisation
  • and Direct injury
  • Leukocyte dependant injury (toxic oxygen species and enzymes from leucocytes)
  • Increased transcytosis - channels across endothelial cytoplasm
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12
Q

What is a polymorph?

A

Primary type of white blood cell involved in inflammation. Neutrophils are a type of granulocyte, also known as a polymorph.

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13
Q

Describe neutrophil infiltration

A
  1. Stasis causes neutrophils to line up at the edge of blood vessels along the endothelium (MARGINATION)
  2. Neutrophils then ROLL along endothelium, sticking intermittently
  3. Then they ADHERE more avidly
  4. Neutrophils EMIGRATE through vessel wall
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14
Q

Why does neutrophil infiltration occur in inflamed tissue?

A

Surface receptors of endothelial cells change to support rolling and adhesion.

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15
Q

How do neutrophils escape from vessels?

A
  • Relaxation of inter-endothelial cell junctions
  • Digestion of vascular basement membrane
  • Movement
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16
Q

How do neutrophils move?

A

Diapedesis and emigration; chemotaxis

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17
Q

What is chemotaxis?

A

Movement along concentration gradients of chemoattractants

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18
Q

Give an example of a chemotaxin

A

C5a, LTB4, bacterial peptides etc

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19
Q

What are the 3 stages of phagocytosis?

A

Contact, recognition, internalisation

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20
Q

How do phagocytes kill pathogens?

A
  • O2 dependant (produces superoxide and hydrogen peroxide)

- O2 independent (lysozyme and hydrolases)

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21
Q

How might an activated neutrophil cause host tissue damage?

A

May release toxic metabolites and enzymes

22
Q

What are the main chemical mediators of acute inflammation?

A
  • Proteases (plasma proteins, produced in liver)
  • Prostaglandins/ leukotrienes
  • Cytokines/ chemokines
23
Q

Which chemical mediators are responsible for increased blood flow in acute inflammation?

A

Histamines and prostaglandins

24
Q

Which chemical mediators are responsible for increased vascular permeability in acute inflammation?

A

Histamine, leukotrienes

25
Q

Which chemical mediators are responsible for neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

26
Q

Which chemical mediator is responsible for phagocytosis in acute inflammation?

A

C3b

27
Q

How does the exudation of fluid combat injury?

A
  • Delivers plasma proteins to area of injury (immunoglobulins, inflammatory mediators, fibrinogen etc)
  • Dilutes toxins
  • Increases lymphatic drainage (increasing delivery of micro-organisms to phagocytes and antigens to immune system)
28
Q

How does the infiltration of cells combat injury?

A

Removes pathogenic organisms and necrotic debris

29
Q

How does vasodilation combat injury?

A

Increases delivery, increases temperature

30
Q

How does pain and loss of function combat injury?

A

Enforces rest, reduces chance of further traumatic damage.

31
Q

Describe the local complications of acute inflammation

A
  • Swelling = blockage of tubes e.g. bile duct, intestine etc
  • Exudate = compression/ tamponade or serial inflammation
  • Loss of fluid e.g. burns
  • Pain or loss of function
32
Q

What are the four main effects of systemic acute inflammation?

A

Fever
Leucocytosis
Acute phase response
Shock

33
Q

Why does fever occur in acute inflammation?

A
  • Macrophages are stimulated by exogenous pyrogens (from bacteria)
  • Release pyrogenic cytokines e.g. TNF, interleukin-1
  • Cytokines cause an increase in synthesis of prostaglandin E2 within anterior hypothalamus
  • Hypothalamus increases body temperature
34
Q

How does aspirin reduce fever?

A

Inhibits cycle-oxygenase (enzyme which produces prostaglandins)

35
Q

What happens in leucocytosis?

A

The number of circulating leucocytes increases.

36
Q

Why is neutrophilia seen during bacterial infections?

A

Macrophages and endothelial cells in injured tissues produce colony stimulating factors that stimulate the bone marrow to produce more neutrophils.

37
Q

What is the acute phase response?

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.

38
Q

How is the acute phase response produced?

A

By cytokines released during inflammation.

39
Q

Which symptoms following injury are caused by the acute phase response?

A

Sleepiness, raised pulse, and lack of appetite

40
Q

Which proteins increase in the blood during inflammation?

A
  • CRP (bacterial)
  • A1 antitrypsin (protease inhibitor)
  • Haptoglobin
  • Fibrinogen
41
Q

What is shock?

A

The result of bacterial products or inflammatory mediators spreading around the body in the blood stream. Inflammation occurs throughout the body causing a massive drop in blood pressure due to vasodilation and an increase in vascular permeability with resultant fluid exudation.

42
Q

How does acute inflammation resolve?

A

Changes gradually reverse and the vascular changes stop.

  • Neutrophils no longer marginate
  • Vessel permeability returns to normal.
  • Therefore, exudate drains to lymphatics
  • Fibrin is degraded by plasmin and other proteases
  • Neutrophils die, break up and are carried away or phagocytosed
  • If tissue architecture has not been destroyed, may regenerate
43
Q

What are the four main types of exudate?

A

Pus/abscess
Haemorrhagic
Serous
Fibrinous

44
Q

Describe the exudate in an abscess

A

Creamy/ white as it is right in neutrophils. Typical of chemotactic bacterial infections.

45
Q

Describe haemorrhage exudate

A

Contains enough RBC’s to appear bloody. Indicative of vascular damage as well as inflammation. It is seen in destructive infections or when the exudate is a result of infiltration by a malignant tumour.

46
Q

Describe serous exudate

A

Serous exudate contains plasma proteins but few leucocytes suggesting there is no infection by micro organisms. They are clear and typically seen in blisters e.g. after a burn.

47
Q

How does serous exudate differ from transudate and plasma?

A

Doesn’t contain fibrinogen like plasma

Contains plasma proteins (transudate doesn’t)

48
Q

Describe fibrinous exudate

A

Significant deposition of fibrin e.g. blood clot without the RBC’s. When fibrinous exudates occur in the viscera it means that serosal surfaces no longer slide smoothly over each other.

49
Q

What is hereditary angio-oedema?

A

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 (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues). They also experience recurrent abdominal pain which is due to intestinal oedema. Family history of sudden death (laryngeal involvement)

50
Q

What is alpha 1-antitrypsin deficiency?

A

Autosomal recessive disorder with varying levels of severity 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 within the lung act unchecked and destroy normal parenchymal tissue. Liver disease also occurs as the hepatocytes produce and abnormal version of the protein which is incorrectly folded. It polymerises and cannot be exported from the endoplasmic reticulum. This causes hepatocyte damage and eventually cirrhosis.

51
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 many chronic infections in the first year of life. Numerous granulomas and abscesses affecting the skin, lymph nodes, and sometimes the lung, liver, and bones occur, however, they are ineffective at eliminating the infectious agents.

52
Q

Describe the key characteristics of acute inflammation

A

Rapid, stereotyped, response of living tissue to any injury. Changes controlled by short lived chemical mediators.

Pathological Processes (13 decks)

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