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BDS1 Pathology > Accute Inflammation > Flashcards

Accute Inflammation Flashcards

1
Q

What is acute inflammation the driving force of?

A

The innate Immune response

  • The response of living tissue to infection/damage
  • Acute inflammation is the initial and essential process for innate immunity
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2
Q

How quickly does acute inflammation develop and how long does it last?

A

Develops quickly (mins-hours) and lasts a few hors to days

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3
Q

What are the 3 main interlinked processes of acute inflammation?

A
  • Vascular dilation (change in blood vessel calibre)
  • Increased vascular permeability - allows for cells and molecules to support inflammatory response
  • Neutrophil activation and migration
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4
Q

What are the 4 main causes of acute inflammation?

A

Microbial infection
- Inflammation can be induced by microorganisms

Physical agents

  • Physical trauma
  • UV or other ionising radiation
  • Heat (burns) or cold (frostbite)

Irritant and corrosive chemicals

  • Acids and alkalis
  • oxidising agents
  • Infective agents may release specific chemical irritants which lead directly to inflammation

Tissue necrosis
- Lack of oxygen or nutrients due to inadequate blood flow (infarction)

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5
Q

What are the cardinal signs of acute inflammation according to Celsus?

A

Rubor (redness) - due to dilation of small blood vessel in damaged areas

Calor (heat) - due to increased blood flow (hyperaemia)

Tumor (swelling) - due to accumulation of fluid in extra vascular space (oedema)

Dolor (pain) - Stretching/distortion of tissue due to oedema. Chemical mediators bradykinin, prostaglandins induce pain

Loss of function - related to chronic inflammation

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6
Q

What are the vascular responses of acute inflammation?

A
  • Small blood vessels adjacent to site of damage become dilated with increased blood flow
  • Endothelial cells swell and partially retract - opening up of gaps between them
  • Exudation - the vessels become ‘leaky’ and allow passage of water, salts and some proteins (blood flow slows)
  • Endothelial cells activated to promote immune cells passage to damage tissues (mainly neutrophils and monocytes/macrophages)
  • The endothelial cells can change what they express on their surfaces to change what they are attracting - so they can attract immune cells
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7
Q

What is the process involved in bacterial induced acute inflammation (gingivitis)?

A
  • Bacteria trigger macrophages to release cytokines and chemokines
  • Vasodilation and increased vascular permeability causes redness, heat and swelling and allows the passage of fluid and cells
  • Inflammatory cells migrate into tissues, releasing inflammatory mediators that cause pain (cells and fluid aim to resolve inflammation)
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8
Q

What happens to capillaries in response to acute inflammation?

A
  • Dilation of capillaries which increases the blood flow

- This is done by the opening of sphincters so a lot more blood is flowing to the area

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9
Q

What does oedema mean?

A

Excess of fluid

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10
Q

What does the inflammatory exudate provide to the affected tissue?

A

Fluids and salts

  • Dilute toxins in tissues
  • Allows diffusion of mediators across membranes

Glucose and oxygen
- Supports macrophages

Complement proteins and antibodies
- Opsonins for invading microorganisms - support phagocytosis

Fibrin (long insoluble filamentous protein)

  • Polymerised via coagulation cascade
  • Provides scaffold entrapping microbes and assist immune cell migration to area
  • Important in blood clots
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11
Q

What are the chemical mediators of acute inflammation?

A
  • Histamine
  • Bradykinin
  • Leukotrienes
  • Serotonin
  • Prostaglandins
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12
Q

What are the protein mediators of acute inflammation?

A
  • Cytokines

- Chemokines

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13
Q

How is histamine formed?

A

Product of the breakdown of AA histidine

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14
Q

Where is histamine stored?

A

In granules of immune cells such as mast cells

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15
Q

How is degranulation of histidine to release histamine stimulated?

A
  • Stimulated by C3a, C5a - complement

- Also caused by antigens

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16
Q

What are the roles of histamine?

A
  • Role as neurotransmitter - itching (acts upon nerve fibres)
  • Causes vascular dilation
  • Multiple functions in immune response
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17
Q

What are prostaglandins the product of?

A

Fatty acid metabolism

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18
Q

What is the most abundant prostaglandin?

A

Prostaglandin E2 (PGE2)

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19
Q

What are the roles of prostaglandins in acute inflammation?

A
  • Causes vascular dilation
  • Regulate cytokine production from cells
  • Regulate chemokine production - attracts immune cells
  • Act on nerve fibres (neurotransmitter) - pain
  • Involved in tissue remodelling
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20
Q

What are prostaglandins regulated by?

A

The enzyme Cyclo-oxygenase II (COX II)

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21
Q

What targets COX II enzyme?

A

NSAIDS (non steroidal anti inflammatory drugs)

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22
Q

What are plasma factor systems?

A
  • Proteolytic cascades

- Stepwise activation involving formation of enzyme complexes and protein cleavage

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23
Q

What are the 4 plasma factors enzymatic cascades?

A
  • Complement
  • The kinin system
  • Coagulation
  • Fibrinolytic system
24
Q

Are all 4 of the plasma factor enzymatic cascade systems interlinked?

A

Yes, the Hageman factor is important as it is the driver for most of these cascades

25
Q

What does the Kinin system require for activation?

A

Activation of Hageman factor (XII –> XIIA) which occurs in response to damage on exposed surfaces

26
Q

What does XIIA convert prekallikrein into in the Kinin system?

A

Kallikrein

27
Q

What does Kallikrein convert high-molecular-weight kininogen into in the Kinin system?

A

Bradykinin

28
Q

What are the roles of bradykinin in acute inflammation?

A
  • Important role in activating complement
  • Increased vascular permeability
  • Stimulates nerves - pain
  • Induce expression of cytokines and chemokines
  • Induce production of chemical mediators of inflammation
29
Q

What does coagulation mean?

A

Formation of a blood clot

30
Q

What are the names of the 3 pathways in the coagulation system?

A
  • Common
  • Extrinsic
  • Intrinsic
  • Intrinsic and extrinsic both diverge from the common pathway
31
Q

What is the intrinsic pathway of the coagulation system?

A
  • Activated when blood comes into contact with sub-endothelial connective tissues (outside blood vessel)
32
Q

What is the extrinsic pathway of the coagulation system?

A
  • Damaged blood vessel means Human Factor VII (FVII) leaves vessel and encounters Tissue factor on surrounding tissue which activates the extrinsic pathway
33
Q

What is the common pathway of the coagulation system?

A

Production of thrombin which in turn produces fibrin (building block of clot)

34
Q

What glycoprotein is the building block of a clot?

A

Fibrin

35
Q

What is fibrinolysis?

A

The enzymatic breakdown of the fibrin in blood clots

- Without the ability to break down clots we would clot to death

36
Q

What is the molecule that breaks down blood clots?

A

Plasmin

37
Q

In health what 2 processes are balanced in the relation to blood clotting?

A

Coagulation and fibrinolysis

38
Q

What does the fibrinolytic system result in the activation of?

A

Plasmin

39
Q

What are the roles of the fibrinolytic system?

A
  • Activates compliment (plasmin cleaves C3)

- Indirect role as fibrin breakdown products (split products) promote vascular permeability

40
Q

What does congenital mean?

A

Born with it

41
Q

What are the 3 congenital coagulation disorders?

A
  • Von Willebrand Disease
  • Haemophilia A
  • Haemophilia B
42
Q

What is meant by a congenital coagulation disorder?

A

Deficiency or lack of specific clotting factor

43
Q

What Clotting factor is a person lacking if they have Von Willebrand disease?

A

Deficiency in Von Willebrand factor (protein which binds factor VIII and stabilises - lack of VWF leads to low levels of factor VIII)
- This is not a life threatening disease but need to be careful if need any potential surgery as can bleed very heavily

44
Q

What clotting factor is a person lacking if they have Haemophilia A?

A

Deficiency in factor VIII

45
Q

What clotting factor is a person lacking if they have Haemophilia B?

A

Deficiency in factor IX

46
Q

What drugs cause acquired coagulation disorders?

A
  • Warfarin - anti-coagulant - inhibits numerous coagulation factors
  • Heparin - anti-coagulant - potentiates antithrombin
47
Q

What does sequelae mean?

A

The outcome

48
Q

What does the outcome of the pathways of coagulation depend upon?

A
  • Tissues involved
  • Amount of tissue destruction
  • Nature of the injurious agent (what is causing it?)
49
Q

What is suppuration?

A

The formation of pus (abscess)

50
Q

What is pyogenic bacteria?

A

Puss forming bacteria

51
Q

What is suppuration caused by?

A

Neutrophil infiltration which function to eliminate bacteria

52
Q

What is pus?

A

Bacteria with dead and dying neutrophils

53
Q

How is the spread of bacteria reduced by the process of pus formation?

A
  • Once pus accumulates it is surrounded by a pyogenic membrane - the body will try to wall off with membrane - abscess
  • Bacteria within an abscess relatively inaccessible also prevents spread
54
Q

What are the 3 types of dental abscess?

A
  • Gingival
  • Periodontal
  • Periapical
55
Q

What is the definition of resolution in reference to acute inflammation?

A

The complete restoration of tissues after an episode of acute inflammation

56
Q

What does resolution of acute inflammation require?

A
  • Minimal cell death and tissue damage
  • Occurrence in tissues with regenerative capacity
  • Rapid elimination of causative agent
  • Rapid removal of fluid and debris by vascular/lymphatic drainage

BDS1 Pathology (14 decks)

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