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CSB520 - Disease processes > wk 3 - inflammation and repair > Flashcards

wk 3 - inflammation and repair Flashcards

1
Q

define hyperaemia

A

increase in blood to an area, first thing to happen after an injury. active process. the passive process is congestion.

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2
Q

define oedema and what is exudate

A

Excess fluid in interstitial fluid

exudate- rich in plasma proteins

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3
Q

define effusion

A

oedema in a body cavity.

Excess fluid in body cavities

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4
Q

define resolution

A

healing without scarring, restoration of structure and function

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5
Q

define organisation

A

healing by scarring

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6
Q

define ulcer

A

a lesion or sore on a body surface like the skin or mucous membrane. can be acute- if cause is removed/chronic- if not.

area of necrosis on the body surface

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7
Q

define abscess

A

a lesion not on the bodys surface so the body walls it off and develops an abscess when it cannot be sloughed off like an ulcer can

area of necrosis trapped in a tissue or organ

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8
Q

infections depend upon 3 factors

A
  1. the host and its susceptibility/ response
  2. site of infection
  3. virulence - ability of microbe to cause disease
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9
Q

what form of cell death causes an inflammatory response?

A

necrosis stimulates an acute inflammatory response

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10
Q

physical indicators of acute inflammation and their causes 5

A

heat- hyperaemia
red - hyperaemia
swelling- oedema
pain- stretch receptors and chemical mediators
loss of function- oedema and pain

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11
Q

what are the 3 features of acute inflammation?

A
  1. hyperaemia,
  2. oedmea
  3. neutrophils
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12
Q

what are the 3 possible outcomes of acute inflammation?

A
  1. resolution- healing without scarring
  2. organisation - healing by scarring (granulation tissue)
  3. chronic inflammation
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13
Q

what are the 3 main components of granulation tissue (immature scar tissue) and their role/purpose in repair?

A
  1. macrophages- remove dead neutrophils, clean up debris
  2. fibroblasts- secrete collagen
  3. angiogenesis- new vessels grow and provide oxygen and nutrients

macrophages and fibroblasts leave.
scar tissue is made up of collagen and decreases over time.

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14
Q

what are the consequences of healing through organisation?

A

replacing functional tissue with collagen that just fills in the gap.

loss of functional tissue

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15
Q

what is meant by sterile and non sterile sites in the human body?

A

sterile- microbes shouldn’t be present. no portals to the environment.

non-sterile: where theres microbes apart of our innate immunity.

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16
Q

what are the main differences between the innate and adaptive systems?

A

innate- fast, non specific, germline encoded

adaptive- slow, specific, memory

17
Q

what is the autoimmune response

A

when the immune system is targeting our self

18
Q

what is the hypersensitivity response

A

when the immune system is overreacting to something

19
Q

what is meant by immune-compromised and the patients at risk

A

immune system is impaired and not able to defend immunity to the standard level. makes patient susceptible to infection/disease

20
Q

what are the 3 outcomes of chronic inflammation

A
  1. unresolved acute - cause isn’t removed and body walls off area
  2. repeated acute
  3. special cases- no acute phase, straight to chronic.
21
Q

chronic inflammation looks like

A

-later onset
-longer duration
-lymphocytes and macrophages
-involves further injury and repeated attempts to repair
-only way to heal is through organisation (scarring)

22
Q

acute inflammation looks like

A

early onset
short duration
involves fluid exudation and neutrophils
may result in resolution or organisation

23
Q

3 main features of chronic inflammation

A
  1. continued injury/necrosis
  2. repeated attempts to repair
  3. lymphocytes- chronic inflammatory cell
24
Q

what types of cells does chronic inflammation involve 3

A

lymphocytes
macrophages
fibroblasts

25
Q

5 cardinal signs of acute inflammation and how are they related to vascular changes

A

red

heat due to hyperaemia

swelling due to hyperaemia and increased vascular permeability

pain due to stretching of tissue by oedmea and stimulation of pain fibres

loss of function due to oedema and pain

26
Q

what are the 3 microscopic features of acute inflammation and what are there roles

A
  1. hyperaemia
  2. oedmea
  3. recruitment of neutrophils

hyperaemia occurs, the increased permeability of vessels allows serum and proteins to enter affected tissue forming oedema (high protein=exudate). neutrophils are activated and attracted to the acutely inflammed tissue, they migrate through the vessel walls.

27
Q

examples of when the acute inflammatory process is life threatening

A

in the brain- odemea or a haemorrhage will cause an increase in intracanial pressure. Reduction in cerebrospinal fluid and decreased blood supply to the brain until the pressure leads to a herniation of the brain.

the lungs/throat- swelling within the walls which can close the airway lumen leading to breathing difficulties

the lungs- excessive iedema in the alveoli can impair gas exchange and place greater demands on the heart

28
Q

what type of oedema is in acute inflammation and how does it occur?

A

exudate, fluid high in proteins.

In acute inflammation the hyperaemia results in increased hydrostatic pressure which forces fluid
from the vessels into the tissue (transudate) but there is also increased vascular permeability which
allows plasma proteins to also enter the fluid hence why we get an exudate.

hyperaemia - increased hydrostatic pressure- increased vascular permeability - plasma proteins enter fluid - exudate

29
Q

what factors may prevent complete repair from occuring? (resolution)

A
  1. permanent tissues (brain, heart) because cant divide
    2.in labil/stable tissues, not possible when alot of tissue has been lost or there is overlying infection, poor immunity, poor nutrition or interuption of healing
30
Q

what happens to the heart in response to ischaemia

A

The infarcted tissue would stimulate the acute
inflammatory response so there would be hyperemia, oedema and the infiltration of the tissue by neutrophils. Because the heart is a permanent tissue, the formation of granulation tissue would
follow; macrophages will move into the necrotic tissue and continue to remove it along with the
increasingly apoptotic population of neutrophils. Fibroblasts would migrate into the area and
secrete collagen fibres to fill in the space once occupied by dead myocytes and new capillaries
would sprout into the area to provide growth factors, oxygen and nutrients for the granulation
tissue. Once the dead cells are removed and the tissue deficit filled with collagen, the
macrophages and fibroblasts migrate away and the new capillaries regress (die of by apoptosis).
As this is a case of organization as part of acute inflammation, the granulation tissue would
mature into a collagen scar which contracts over time pulling the edges of parenchymal tissue
together.

31
Q

positive and negatives of organisation

A

positive- allows repair, fills in tissue deficits for survival
negatives- loss of tissue function, scar tissue contracts over time pulling surrounding tissue with it which can distort the surrounding parenchyma

32
Q

what are the 3 main features of chronic inflammation

A
  1. Ongoing tissue injury and destruction
  2. Lymphocytes
  3. Repeated attempts at repair through the formation of granulation tissue and, when occurring in
    stable/labile tissues, proliferation of parenchymal cells.
33
Q

the link between inflammation and cancers

A

It is when cells are dividing & copying their DNA that they are most vulnerable to errors occurring.
If you make the cells divide more, during to inflammation then there is greater risk for mutation
and for that mutation to be passed onto daughter cells. In addition, to proliferation, during
inflammation there is often increased levels of oxidants & other mediators capable of damaging
DNA.

34
Q

following a myocardial infarction what type of inflammation and repair occurs

A

acute
organisation

35
Q

why does chronic inflammation increase the risk of carcinoma formation

A

When chronic inflammation
occurs in stable or labile tissues that contain epithelial
cells, surrounding epithelial cells will proliferate
(undergo hyperplasia) in a futile attempt to repair. This
increase in proliferation & the presence of free radicals
increases the chance of mutation. Note that it is not
the granulation tissue that causes cancer.

CSB520 - Disease processes (11 decks)

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