Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology > Unit 1 - Chapter 5 - Inflammation and Healing > Flashcards

Unit 1 - Chapter 5 - Inflammation and Healing Flashcards

1
Q

what is the bodies first line of defense (list 4)

A

nonspecific
mechanical barrier
unbroken skin and mucous membranes
secretions - tears/gastric juices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the bodies second line of defense (list 3)

A

nonspecific
phagocytosis
inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the bodies third line of defense (list 2)

A

specific defense
production of specific antibodies or cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

expand on normal capillary exchange

A

not all capillaries in a particular capillary bed are open
- depends on the metabolic needs of the cells or need of removal of wastes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the movement of fluid, electrolytes, oxygen and nutrients on arterial end based on?

A

net hydrostatic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what will venous end-osmotic pressure facilitate?

A

movement of fluid, carbon dioxide and other wastes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

expand on the physiology of inflammation

A
  • a normal protective defense mechanism
  • disorders have the ending “itis”
  • signs and symptoms serve as a warning sign
  • not the same as an infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the causes of inflammation

A
  • direct physical damage
  • caustic chemicals
  • ischemia or infraction
  • allergic reactions
  • extreme hot or cold
  • foreign bodies
  • infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the steps of inflammation

A

 Release of bradykinin from injured cells
 Activation of pain receptors by bradykinin
 Mast cells and basophils release histamine.
 Capillary dilation (bradykinin and histamine)
 Increased blood flow and capillary permeability
 Bacteria may enter the tissue.
 Neutrophil and monocytes come to injury site.
 Neutrophils phagocytize bacteria.
 Macrophages leave bloodstream for phagocytosis of
microbes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

expand on acute inflammation

A

 Process of inflammation is the same, regardless
of cause.
 Timing varies with specific cause.
 Chemical mediators affect blood vessels and
nerves in the damaged area:
- Vasodilation
- Hyperemia
- Increase in capillary permeability
- Chemotaxis to attract cells of the immune
system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the source and major action of histamine

A
  • source is mast cell granules
  • action is immediate vasodilation and increased capillary permeability to form exudate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the source and major action of chemotactic factors

A
  • source is mast cell granules
  • major action to attract neutrophils to site
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the source and major action of platelet-activitating factor

A
  • source is cell membranes of platelets
  • action if activate neutrophils and platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the source and major action of cytokines

A
  • source is t lymphocytes and macrophagues
  • action is increase plasma proteins, erythocyte sedimentation rate and induce fever, chemotaxis and leukocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the source and major action of leukotrienes

A
  • source is synthesis from arachidonic acid in mast cells
  • action is later response; vasodilation and increased capillary permearbility chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the source and major action of prostaglandins

A
  • source is synthesis from arachidonic acid in mast cells
  • action is vasodilation, increased capillary permeability, pain, fever, potentiate histamine effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the source and major action of kinins (bradykinin)

A
  • source is activitation of plasma protein
  • action is vasodikation and increased capillary permeability, pain, chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the source and major action of the complement system

A
  • source is activation of plasma protein cascade
  • action if vasodilation and increased capillary permeability, chemotaxis, increased histamine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the 4 local effects of inflammation

A
  • redness and warmth
  • swelling (edema)
  • pain
  • loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is redness and warmth caused by

A

increased blood flow to damaged area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is swelling caused by

A

shift of protein and fluis into the interstitial space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is pain caused by

A

increased pressure of fluid on nerves; release of chemical mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what causes loss of function

A

when cells lack nutrients, edema may interfere with movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what does exudate refer to

A

collection of interstitial fluid formed in the inflamed area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

expand on serous exudate

A

watery, consists primarily of fluid, some proteins and white blood cells

26
Q

expand on fibrinous exudate

A

thick, sticky, high cell and fibrin content

27
Q

expand on purulent exudate

A

thick, yellow/green, contains more leukocytes, cell debris and microorganisms

28
Q

expand on hemorrhagic exudate

A

present when blood vessels are damages

29
Q

what are the systemic effects of inflammation

A
  • mild dever
  • malaise (feeling unwell)
  • fatigue
  • headache
  • anorexia
30
Q

what are the 8 steps in the course of a fever

A

1 - release of pyrogens in circulation
2 - resent hypothalamic control
3 - body responses that increase body temperature
4 - body reaches new high temperature
5 - treatment to remove purogens
6 - reset hypothalamus to normal
7 - body responses that increases heat liss
8 - body returns to normal temperature

31
Q

what does leukocytosis change in the blood with inflammation

A

increased numbers of white blood cells, especially neutrophils

32
Q

what does different counts change in the blood with inflammation

A

proportion of each tupe of white blood cell alteres, depending on the cause

33
Q

what does plasma proteins change in the blood with inflammation

A

increaed fibrinogen and prothrombin

34
Q

what does c-reactive protein change in the blood with inflammation

A

a protein not normally in the blood, but appears with acute inflammation and necrosis withing 24-48 hours

35
Q

what does increased ESR change in the blood with inflammation

A

elevated plasma proteins increase the rate at which red blood cells settle in a sample

36
Q

what does cell enzymes changes in the blood with inflammation

A

released from necrotic cells and enter tissue fluids and blood, may indicate the site of inflammation

37
Q

what are diagnostic tests used for

A
  • leukocytosis
  • erthrocyte sedimentation rate
  • differntial count
  • circulating plasma proteins
  • cell enzymes
  • necrosis
38
Q

what are potential complications of infection

A

 Microorganisms can more easily penetrate
edematous tissues.
 Some microbes resist phagocytosis.
 The inflammatory exudate also provides an excellent
medium for microorganisms.

39
Q

what are potential complications of skeletal muscle spasm

A

 May be initiated by inflammation
 Protective response to pain

40
Q

expand on chronic inflammation

A

 Follows acute episode of inflammation
 Less swelling and exudate
 Presence of more lymphocytes,
macrophages, and fibroblasts
 Continued tissue destruction
 More fibrous scar tissue
 Granuloma may develop around foreign
object.

41
Q

what are potential complications of chronic inflammation

A

 Deep ulcers may result from severe or
prolonged inflammation.
 Caused by cell necrosis and lack of cell regeneration
that causes erosion of the tissue
* Can lead to complications such as perforation of viscera.
* Extensive scar tissue formation

42
Q

what are 4 drugs used to treat inflammation

A

 Acetylsalicylic acid (ASA) —–Aspirin
 Acetaminophen—-Tylenol
 Nonsteroidal antiinflammatory drugs (NSAIDs)——- Ibuprofen
 Glucocorticoids—– Corticosteroids

43
Q

what are the antiinflammatory effects of glucocorticoids

A

 Decreased capillary permeability
 Enhanced effectiveness of epinephrine and
norepinephrine
 Reduced number of leukocytes and mast
cells
 Reduces immune response

44
Q

what are the adverse efects of glucocorticoids

A

 Atrophy of lymphoid tissue; reduced
hemopoiesis (Increased risk of infection)
 Catabolic effects (Increased tissue breakdown; decreased protein synthesis)
 Delayed healing
 Delayed growth in children
 Retention of sodium and water
 Increased gluconeogenesis

45
Q

expand on the the abbrevation of the “RICE” therapy for injuries

A

rest
ice
compression
elevation

46
Q

what are the 3 types of healing

A

resolution
regeneration
replacement

47
Q

expand on resolution type of healing

A

minimal tissue damage

48
Q

expand on regeneration type of healing

A

damages tissue replaces with cells that are functional

49
Q

expand on replacement type of healing

A

functional tissue replaces by scar tissue
loss of function

50
Q

expand on the loss of function when it comes to scar formation

A

 Result of loss of normal cells and specialized
structures
* Hair follicles
* Nerves
* Receptors

51
Q

expand on contractures and obstructions when it comes to scar formation

A

 Scar tissue is nonelastic.
 Can restrict range of movement

52
Q

expand on adhesions when it comes to scar formation

A

bands of scar tissue joining two surfaces that are normally seperated

53
Q

expand on hypertropic scar tissue when it comes to scar formation

A

 Overgrowth of fibrous tissue
* Leads to hard ridges of scar tissue or keloid
formation

54
Q

expand on ulceration when it comes to scar formation

A

 Blood supply may be impaired around scar.
* Results in further tissue breakdown and ulceration at future time

55
Q

what can burns be caused by

A
  • thermal (flames, hot fluids)
  • chemicals
  • radiation
  • electricity
  • light
  • friction
56
Q

expand on superficial partial-thickness (first degree burns)

A

 Involve epidermis and part of dermis
 Little, if any, blister formation

57
Q

expand on deep partial-thickness (second degree) burns

A

 Epidermis and part of dermis
 Blister formation

58
Q

expand on full thickness (third and fourth degree) burns

A

 Destruction of all skin layers and often underlying tissues

59
Q

what are the effects of a burn injurt

A

 Both local and systemic
 Dehydration and edema
 Shock
 Respiratory problems
 Pain
 Infection
 Hypermetabolism during healing period after
burn

60
Q

expand on the healing of burns

A

 Hypermetabolism occurs during healing period.
 Immediate covering of a clean wound is needed
to prevent infection.
 Healing is a prolonged process.
 Scar tissue develops, even with skin grafting.
 Physiotherapy and occupational therapy may be
necessary.
 Surgery may be necessary to release restrictive
scar tissue.

Pathophysiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions