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Clinical Medicine > Injury, Inflammation, and Repair > Flashcards

Injury, Inflammation, and Repair Flashcards

1
Q

what is inflammation?

A
  • a wound that swells up, turns red and hurts

~ generally speaking ~ its the bodies immune system response to a stimulus
- ex. wound or splinter

  • happens when immune system is fighting against something that may be harmful
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2
Q

uncontrolled inflammation

A

is potentially damaging

  • regulation is critical

ex. irritable bowl disease -> critical of digestive tract

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2
Q

does inflammation facilitate tissue repair?

A

yes

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2
Q

controlled inflammation

A

critical in protecting the body from harmful invaders

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3
Q

inflammation provoked response to tissue injury

A
  • chemical agents
  • cold
  • heat
  • trauma
  • invasion of microbes
  • cancerous cells
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3
Q

inflammation: reparative

A

includes and supports tissue repair

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4
Q

when is inflammation potentially harmful?

A

when it leads to chronic conditions such as arthritis and chronic obstructive bowel disease

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4
Q

inflammation: protective

A

destroys and contains the injurious agent

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4
Q

inflammation desirable response

A

controlled and proportional

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4
Q

inflammation undesirable response

A

chronic and harmful

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5
Q

what distinguishes acute and chronic inflammation?

A
  • onset
  • duration
  • type of infiltrating inflammatory cells
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6
Q

acute inflammation causative agent

A
  • pathogens
  • irritants
  • damage
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7
Q

acute inflammation major cells

A
  • neutrophils
  • basophils
  • eosinophils
  • monocytes
  • macrophages
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8
Q

acute inflammation onset

A

immediate

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9
Q

acute inflammation duration

A

few days

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10
Q

acute inflammation outcomes

A
  • resolution
  • abscess formation
  • chronic inflammation (if longer than 2 weeks)
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11
Q

chronic inflammation causative agent

A
  • persistent acute inflammation due to non-degradable pathogens
  • persistent foreign bodies or autoimmune reactions
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12
Q

chronic inflammation major cells

A
  • monocytes
  • macrophages
  • lymphocytes
  • plasma cells
  • fibroblasts
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13
Q

chronic inflammation onset

A

delayed

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14
Q

chronic inflammation duration

A

up to many months or years

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15
Q

chronic inflammation outcomes

A
  • tissue destruction
  • fibrosis
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16
Q

cardinal signs of acute inflammation

A
  • heat
  • swelling
  • redness
  • pain
  • loss of function
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17
Q

inflammation physiology

A

1) foreign agent enters the body
2) local vasodilation and increased vascular permeability
3) accumulation of WBC in blood vessels
4) WBC exit the blood vessels
5) drawn to an area of foreign agent/injury = chemotaxis

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18
Q

the two components of inflammation physiology

A
  • vascular
  • cellular
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19
Q

vascular components of inflammation physiology

A
  • vasoconstriction
  • vasodilation
  • increased permeability
20
Q

vasoconstriction

A

release of vasoconstrictor substances
- few seconds of blanching
- usually happens with blood trauma

21
Q

vasodilation

A

smooth muscle relaxes called active hyperemia
- what causes redness

22
Q

increased permeability

A

vascular leakage -> edema
- increased seperation of cells

23
Q

cellular component of inflammation physiology

A

leukocyte accumulation and infiltration

24
Q

vasodilation: active hyperemia

A
  • due to arteriolar dilation
  • sympathetic stimulation
  • affected tissue is redder than normal because of engorgement with oxygen blood

~ accounts for redness, swelling, and warmth

25
Q

transudate leakage

A
  • low cell/protein
  • result of high hydrostatic pressure and low osmotic pressure
  • clear fluid
26
Q

exudate leakage

A
  • cell/protein rich
  • result of increased vascular permeability
  • cloudy fluid

~ supplies antibodies and complement protein to affected areas to contribute to swelling -> causes pain and decreased mobility

27
Q

vascular permeability mediators

A
  • histamines
  • bradykinins
  • leukotrienes
28
Q

histamines, bradykinins and leukotrienes all cause what response?

A

and early, brief (30min) immediate response in the from of reversible endothelial cell contraction

29
Q

cytokine mediators

A

reversible endothelial cell junction retraction

~ 4-6 hours post injury/infection, lasting 24 hours or more

30
Q

sever injuries may cause ____ making them ______?

A

may cause immediate direct endothelial cell damage making them leaky until they are repaired

31
Q

leukocytes may adhere to and damage the endothelium through?

A

activation and release of toxic radicals and proteolytic enzymes making the vessel leaky

32
Q

transcytosis

A
  • brings proteins and molecules across endothelium
  • some vesicles may fuse to create temporary channels
33
Q

vascular permeability mechanisms that cause leakiness

A
  • mediators
  • cytokine mediators
  • severe injures
  • leukocytes that adhere and damage the endothelium
  • mediators that increase transcytosis
34
Q

diapedesis

A

leukocytes leave the vasculature and enter the interstitium through:

1) margination and rolling
2) adhesion
3) chemotaxis
4) activation
5) transmigration

35
Q

what are leukocytes free to participate in?

A
  • degranulation
  • phagocytosis
  • leukocyte/cytokine -> protection and repair (controlled)
  • leukocyte/ cytokine -> ; ‘storm’ induced tissue injury (uncontrolled/chronic)
36
Q

degranulation

A

cellular process that releases
- neutrophils
- basophils
- eosinophils
- mast cells
- cytotoxic cells
- natural killer cells

~ main purpose is to destroy pathogens (innate immune system)

37
Q

stages of acute inflammation

A

1) vasoconstriction (<60)
2) vasodilation
3) increased vascular permeability
4) diapedesis

38
Q

MOA for vasodilation

A

1) cellular release of mediators
- histamine
- prostacyclin
- nitric oxide
2) relaxation of blood vessel walls

39
Q

why does vasodilation occur?

A

due to increased hydrostatic pressure ( pressure inside the vessel pushing out) that causes a decrease of blood flow rate

40
Q

MOA for increased vascular permeability

A

occurs through the release of histamine and leukotrienes (mediators)

41
Q

why is there an increased vascular permeability

A

to allow fluid and protein to move to the interstitial tissue

  • results in edema or increased fluid in the interstitial tissue
42
Q

endothelial contraction

A
  • immediate response
  • initiated via cell mediators: histamine and leukotrienes
  • time: immediate up to 30 min
43
Q

endothelial cell retraction

A
  • delayed response
  • initiated via cell mediators: cytokines
  • time: 4-6 hour delayed response (long lasting)
44
Q

direct endothelial injury

A
  • immediate sustained response
  • time: immediate

(physical mechanism) ex. major incision on leg

45
Q

activation of macrophages by pathogens causes a release of?

A

cytokines

46
Q

the release of cytokines from the activation of macrophages causes?

A

endothelial cells of local blood vessels to secrete adhesion moleculrs

47
Q

what are leukocytes attracted to during acute stages of inflammation?

A

the presence of cytokines and adhesion molecules

48
Q

what happens during rolling and rolling adhesion

A
  • circulating leukocytes bind to adhesion molecules with moderate affinity causing leukocytes to slow done and begin rolling along the inner surface of blood vessel walls
49
Q

firm and tight adhesion

A

release of chemokine by macrophages to transition from moderate affinity to high affinity (bonding to endothelial cells)

50
Q

transmigration

A

cytoskeleton reorganization in conjunction with leukocyte pseudopod extensions -> leukocytes pass through gaps in endothelial cells

51
Q

how do blood vessels escape during acute stages of inflammation?

A

diapedesis

52
Q

how doe leukocytes migrate during acute inflammation?

A

chemotactic gradient to injury or infection

53
Q

acute infalmmation

A
  • rapid onset
  • lasts minute to days
  • exudation of fluid and protein from vessels
  • emigration of WBCs
54
Q

purpose of acute inflammation

A

quick attack on foreign agents and initiate the repair process

55
Q

cardinal sign of acute inflammation

A
  • rubor
  • heat
  • edema
  • pain
  • tumor
  • loss of function
56
Q

what causes acute inflammation?

A
  • infection
  • trauma
  • physical and chemical agents
  • necrosis
  • foreign bodies
  • immune reaction

Clinical Medicine (5 decks)

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