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M2 Pathology > Wound healing and inflammation > Flashcards

Wound healing and inflammation Flashcards

1
Q

what is inflammation?

A
  • local physicological response to tissue injuries
  • it is a protective response that looks to destroy or wall of infective agents
  • closely related to the process of tissue repair
  • leads to accumulation of fluids and leucocytes in extravascular tissues
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2
Q

how can inflammation be harmful?

A
  • repair by fibrosis may lead to disfiguring scars
  • hypersensitivity may damage tissues
  • chronic inflammatory disease (Crohn’s disease, arthritis)
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3
Q

what are the two types of inflammation?

A
  • acute: initial rapid response, often short-lived

- chronic: subsequent, often long-lived response following the initial response

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4
Q

what are the causes of acute inflammation?

A
  • infections (eg. bacteria)
  • hypersensitivity (excessive immune response)
  • physical agents (eg. UV light, physical trauma)
  • irritants and corrosive chemicals (eg. acids)
  • foreign bodies (eg. sutures, dirt)
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5
Q

what are the physical characteristics of inflammation?

A
  • redness (due to dilation of blood vessels)
  • heat (due to increased blood flow)
  • swelling (due to increased fluid in extravascular tissues)
  • pain (due to stretched tissues)
  • loss of function (due to pain, severe inflammation may lead to immobilisation of the tissue)
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6
Q

what are the processes in acute inflammation?

A
  1. Vascular phase
    I. vasodilation
    II. increased permeability of blood vessels
  2. Exudative and cellular phase
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7
Q

how is the permeability of blood vessels increased?

A
  • by chemical mediators such as histamine and bradykinin
  • they are confined to postcapillary venules
  • the endothelial cells have contractile proteins which open the transient pores making the endothelial cells more permeable.
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8
Q

explain the exudative and cellular phase

A
  • during this phase, fluid and cells escape from the permeable venules
  • exudative fluid contains proteins important for the destruction
  • fibrinogen turns into fibrin upon contact w ECM
  • exudate is removed by the lymphatic vessel and replaced with new exudate
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9
Q

what is oedema

A
  • the net increase in extravascular fluid

- pharyngeal oedema can be life-threatening

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10
Q

how is the extent of oedema in tissues during acute inflammation limited?

A

lymphatic vessels dilate as they remove the oedema fluid

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11
Q

what are the cellular components of extracellular fluid?

A

neutrophils: to digest/kill/ degrade infective agents

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12
Q

state the stages of the way in which neutrophils reach the site of inflammation?

A
  1. migration
  2. adhesion
  3. transendothelial migration
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13
Q

explain the migration phase of neutrophils

A

normally blood cells flow in the centre of the lumen and the area adjacent to the blood vessel walls only contains plasma, but due to the decrease in intravascular fluid and increased viscosity of plasma cells, blood flow slower and neutrophils enter the plasmatic zone. this is known as migration which only occurs in venules.

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14
Q

explain the adhesion phase of neutrophils

A

there is increased contact between adhesive molecules of neutrophils and endothelial surface.

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15
Q

explain the transendothelial phase of neutrophils

A

once firm adhesion has been achieved, neutrophils insert pseudopodia into the endothelial junctions, then they cross through the basement membrane into the extracellular space.

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16
Q

how do neutrophils find the site of inflammation stimulus once in the ECS?

A
  • process called chemotaxis
  • chemotaxis compounds allow neutrophil to move along the increasing gradient of antigens to reach the site of inflammation
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17
Q

state some chemotaxis compounds

A
  • cytokines
  • products of bacteria
  • products produced by neutrophils it self
18
Q

state the process in which phagocytosis and killing of microorganism happens

A

1- recognition and attachment
2- engulfment
3- killing and degradation

19
Q

explain the recognition and attachment stage of phagocytosis

A
  • recognition of particles by leukocyte surface receptors
  • opsonization is the process in which the particle is coated to be targeted for phagocytosis
  • ## opsonin binds to the leukocyte receptors which greatly enhances phagocytosis
20
Q

explain the engulfment stage of phagocytosis

A
  • the cytoplasmic extensions of leukocytes flow around the particle, engulfing the particle in a phagosome.
  • phagosome membrane then fuses with the lysosome membrane, releasing lysosome content into phagolysosome.
21
Q

explain the killing and degradation stage of phagocytosis

A

occurs in 2 different mechanisms:

  • oxygen-dependent: phagocytosis results in the product of oxygen reduction which causes the intracellular killing of micro-organism.
  • oxygen-independent: the action of substances in the leukocyte granules (eg. lysosome)
  • after killing of microorganism, acid hydrolase degrades the microorganism
  • leukocyte products are also released into the extravascular space.
22
Q

what white blood cells increase in number during bacterial, viral, parasitic and allergic infections?

A

bacterial: neutrophilia
viral: lymphocytics
parastite/allergic: eosinophilia

23
Q

state the different chemical mediators during acute inflammations

A
  • histamine
  • lysosome compound
  • serotonin
  • chemokines
  • leukotrienes
  • prostaglandins
24
Q

explain what plasma factor inflammation is

A

plasma contains 4 enzymatic cascade system which plays a role in aspects of acute inflammation

25
Q

what are the 4 enzymatic cascade systems of plasma factor information

A
  • compliment system
  • coagulation system
  • kinin system
  • fibrinolytic system
26
Q

what are the beneficial effects of acute inflammation?

A
  • enhanced immune response
  • dilution of toxins
  • entry of antibodies
  • fibrin formation
  • delivery of oxygen and nutrients
  • transport of drugs
27
Q

what the harmful effects of acute inflammation

A
  • swelling
  • inappropriate inflmmatory response
  • digestion of normal tissues
28
Q

what are the systemic effects of acute inflammation

A
  • fever
  • weight loss
  • haematological changes
  • reactive hyperplasia (increase in the number of organic tissues that results from cell proliferation)
29
Q

explain chronic inflammation

A
  • occurs in 2 different ways:
    developing from acute inflammation
    primarily chronic inflammation
30
Q

what are the factors favouring acute to chronic inflammation

A
  • indigestible material (glass/sutures)
  • deep-seated inflammations with inadequate drainage
  • recurrent episodes of acute inflammation and healing
31
Q

state the examples of primary chronic inflammation

A
  • resistant infective agents to phagocytosis
  • autoimmune disease
  • disease of unknown aetiology
32
Q

explain healing, repair and regeneration

A
  • cells are classified as labile (multiply throughout life), stable (multiply upon stimulation) and permanent (don’t multiply)
  • only labile and stable cells can be replaced if lost
  • healing is reinstitution with no or minimal residual side effects
33
Q

explain reinstitution

A

complete restoration of the tissue to normal

34
Q

what are the factors favouring reinstitution

A
  • minimal cell death or tissue damage
  • occurrence in an organ or tissue with regenerative abilities
  • rapid destruction of infective agents
  • rapid removal of exudate and debris by good local vascular drainage
35
Q

explain repair by connective tissue fibrosis

A

non-regenerated parenchymal cells replaced by connective tissues (granulation tissues) which in time produce scarring and fibrosis.

36
Q

what is organisation

A

tissue replacement by granulation tissues

37
Q

what are the factors favouring organisation

A
  • large amount of fibrin
  • substantial necrosis
  • exudate and debris cannot be removed
38
Q

explain the difference between first intention and second intention repair with scarring

A
  • first intention: surgical scar, close edges, minimal granulation tissue, minimal fibrosis
  • second intention: ulcerated surface, wide edges, prominent granulation tissue and fibrosis
39
Q

what are the local factors affecting wound healing?

A
  • infection
  • foreign body
  • size/location and type of wound
40
Q

what are the systemic factors affecting wound healing?

A
  • nutrient
  • hormone
  • metabolic state
  • circulation state
41
Q

what are the pathological aspects of wound repair

A
  • deficient scar formation
  • formation of contractures
  • excessive formation of repair components

M2 Pathology (2 decks)

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