cell injury, inflammation, and wound healing Flashcards

1
Q

what can result from cell injury?

A

outcome 1: reversible injury, cell recovery, and return to normal function
outcome 2: apoptosis (planned cell death), programmed removal- doesnt cause immune response
outcome 3: necrosis (not programmed, destructive, causes inflammation- because its explosive)-causes immune response

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2
Q

Example of Cellular Necrosis?

A

Gangrene

  • cell and tissue death
  • can spread
  • needs amputation
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3
Q

what can lead to necrosis?

A
cellular injury mechanism: 
1) free radicals
2) hypoxic injury 
3) reperfusion injury 
chemical injury to cells 
physical injury
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4
Q

What is a free radical?

A

also called a reactive oxygen species

  • an atom or group of atoms having an unpaired electron
  • causes “oxidative stress’ to the body
  • byproducts of normal metabolism
  • counteracted by antioxidants
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5
Q

what are some things that cause free radicals?

A
  • inflammation
  • metabolism
  • infection
  • stress
  • UV radiation
  • Pollution
  • ionizing radiation
  • charred bbq meat
  • ciggs
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6
Q

What is hypoxic injury?

A
  • decreased O2 to tissues
  • decreased or dysfunctional hemoglobin
  • decreased blood flow (ischemia)
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7
Q

what is hypoxia?

A

not enough 02 at the cell/tissue level

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8
Q

what is hypoxemia?

A

low levels of 02 in blood stream

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9
Q

what does “ischemia” mean?

A

decreased blood flow

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10
Q

what is an example of hypoxic injury?

A

cerebral palsy (CP)

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11
Q

what is cerebral palsy?

A

hypoxic injury to the brain before, during, or after birth, resulting in brain damage
- may have cognitive impairment

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12
Q

what is reperfusion injury?

A

where there has been ischemia (decreased blood flow)- the restoration of circulation actually causes inflammation and release of free radicals
ex, removal of blood clot causes damage
-there are mechanisms to reduce and prevent reprofusion injury

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13
Q

what chemicals can cause injury to cells?

A
drugs
lead, mercury
asbestos 
carbon monoxide
carbon tetrachloride 
air pollutants, insecticides, herbicides
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14
Q

what ways can physical force cause cell injury?

A

1) Mechanical force: ex. motor vehicle collision, gunshots, knife wounds…
2) extremes of temperature
3) electrical forces (goes through body, exists body through a body part. electrical injury causes more damage than visible)

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15
Q

what are some other mechanism that can cause cell injury?

A

1) changes in atmospheric pressure (ie, depression sickness- scuba divers), blast injuries, altitude sickness 2) Radiation injury (ionizing, non ionizing, UV)
3) environment (noise)

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16
Q

what Is the result of cell injury?

A
  • mitochondrial damage
    -less ATP production
    -Damage to cell membrane
    -NA-K pump fails
    -water enters into cell- swollen cell
    -Ribosome damage (protein misfolding)
    =DNA damage
    =leads to inflammation
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17
Q

what are some clues that hint towards cell damage that are noticeable? (systemic manifestations of cellular injury)

A
Fatigue 
Malaise 
Fever
Loss of appetite
Elevated plasma enzymes (such as LDH, CK, and troponin) 
triggers inflammatory response
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18
Q

How is it possible to determine systemic cellular injury through an elevated amount of LDH?

A

When there is cellular damage, Lactic dehydrogenase leaks out of cell and into capillaries, therefore, LDH can be measured which can determine cellular damage if LDH is in blood stream

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19
Q

is inflammation specific or non specific?

A

non specific- process is the same, regardless of trigger

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20
Q

what is inflammation activated by?

A

cellular injury or necrosis (cell death)

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21
Q

what are the goals and purpose of the inflammatory response?

A
  • Prevent infection and further damage
  • Contain bacteria
  • limits and controls the inflammatory process (those who have extreme inflammation are very ill)
  • prevents from spreading to health areas
  • initiates adaptive immune response
  • initiates healing
22
Q

what is the vascular response to inflammation?

A

when cell injury occurs, the blood vessels temporarily constrict, then dilate

  • with dilation comes increases vascular permeability, more fluid moves into tissues, blood becomes more viscous (thicc), and clotting occurs
  • capillaries become leaky so that WBC’s can go to damaged site
23
Q

what is the cellular response of the inflammatory response?

A

-white blood cells adhere to capillary, then squeeze through the capillary (emigration), Chemotaxis happens. signalling WBC’s to “come over”. Phagocytosis occurs, which is the ingestion of bacteria by phagocytes

24
Q

what is exudate?

A

pus, fluid, RBC’s, WBC’s, tissue debris, serous

25
Q

what two cellular components are primary in acute inflammation?

A

neutrophils, macrophages

26
Q

what are the five classic signs of inflammation?

A

redness, heat, pain, loss of function, swelling

27
Q

what are some systemic manifestations of acute inflammation?

A
fever 
leukocytosis (increased number of WBC's)
fatigue, anorexia
lymphadenitis (enlarged lymph nodes)
elevated "markers": Erythrocyte sedimentation rate (ESR) nd C-reactive protein
28
Q

What is ESR? What is it used for? what it do?

A

Erythrocyte sedimentation rate
Its how fast do RBC’s separate to the bottom, leaving plasma on top?
- if the sink fast, means inflammation

29
Q

what is chronic inflammation? When is it considered chronic?

A
  • inflammation lasting 2 weeks or longer
  • persistence of an “irritant” ie, infection, antigen, foreign body
  • or due to an unsuccessful acute inflammatory response
  • long term, self perpetuation, often debilitating
30
Q

how is chronic inflammation different than acute inflammation?

A

The phagocytic cells are different; neutrophils (what engulf and destroy bacteria) die, and lymphocytes are activated

  • immune / inflammatory substances can further injure cells
  • fibroblasts and scar tissue formation-> leads to loss of function
31
Q

what is chronic inflammation a MAJOR risk factor for?

A

many cancers, coronary artery disease, and other chronic diseases

32
Q

what is arthritis?

A

inflammation, scar tissue that has formed over a joint

33
Q

what are systemic manifestations of chronic inflammation?

A
Same as acute (leukocytosis and increased antibody production) elevated markers, fever, fatigue, anorexia 
PLUS 
hyperplasia (increase in size) of spleen or lymph nodes 
anemia 
pain
activity intolerance 
depression, insomnia 
weight loss (prolonged anorexia)
34
Q

what are the three phases of healing?

A

1) inflammation
2) proliferation of new tissue formation
3) remodelling and maturation phase

35
Q

what is the inflammation phase?

A
  • the first stage of wound healing
  • neutrophils and macrophages clean up injured area
  • blood clot acts as a scaffold for new tissue
36
Q

what is proliferation and new tissue formation phase?

A
  • building of new tissue
  • fibroblasts secrete collagen, growth factors -new
  • epithelial cells and granulation tissue
  • fragile stage- if interrupted, can be delayed
37
Q

what is the remodeling and maturation phase?

A
  • scar tissue formation

- scar remodeling (mature scar- can take up to two years) -continuous synthesis and breakdown of collagen

38
Q

what is cutaneous wound healing?

A

healing depending on extent of tissue loss, by primary, secondary, and tertiary intention

39
Q

what is primary intention?

A

wounds that heal under conditions of minimal tissue loss

ie, simple wound, edges are very close together ex, paper cut

40
Q

what is secondary intention?

A

wounds that require a great deal more tissue replacement (some tissue loss) ex, pressure ulcer

41
Q

what is tertiary intention?

A

require more connective tissue (scar tissue) than wounds that heal by secondary intention. An example of a wound healing by tertiary intention is an abdominal wound that is initially left open to allow for drainage but is later closed

42
Q

what are some factors that affect healing and tissue repair?

A
  • Age (elderly have slow healing process
  • blood supply/ temp (cold areas dont heal as fast- blood flow related)
  • moisture - not too hot, not too cold
  • nutrition
  • tension on tissue (obesity affects immune response)
  • drugs and stress hormones (higher levels of cholesterol = slower healing)
  • chronic disease
43
Q

what are some examples of dysfunctional wound healing?

A
  • adhesions- (an abnormal union of membranous surfaces due to inflammation or injury ex, scare tissues adheres to something its not supposed to)
  • strictures (An abnormal narrowing of a body passage, especially a tube or a canal.)
  • contractures (a condition of shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints.)
  • infection
  • excess scar tissue formation (keloids)
  • dehiscence (surgical complication in which a wound ruptures along a surgical incision), evisceration
44
Q

what is a monocyte

A

A large blood cell produced in the bone marrow; migrates via the bloodstream to the site of cellular injury where it matures into a macrophage

45
Q

what is a macrophage

A

Large cell involved in the later phagocytosis of foreign particles and the secretion of substances that promote wound healing

46
Q

what is a neutrophil

A

The predominant phagocytic cell in the early inflammatory response whose primary role is the removal of bacteria from wounds

47
Q

what is an eosinophil

A

Lysosome-containing granulocyte which dissolves the surface of membrane parasites

48
Q

what is a mast cell

A

Histamine-containing cell which is the most important activator of the inflammatory response

49
Q

what is a platelet

A

A cell that helps to stop bleeding at the injury site

50
Q

what is the correct order of phases of inflammation and tissue repair?

A

1) cellular injury
2) vasoconstriction
3) vasodilation and increased capillary permeability
4) phagocytosis and debridement
5) proliferation of epithelial cells and collagen cells
6) remodeling