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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

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2
Q

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

A

nonspecific
phagocytosis
inflammation

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3
Q

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

A

specific defense
production of specific antibodies or cell mediated immunity

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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

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5
Q

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

A

net hydrostatic pressure

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6
Q

what will venous end-osmotic pressure facilitate?

A

movement of fluid, carbon dioxide and other wastes

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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
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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
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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.

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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

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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
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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
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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
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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
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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
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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
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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
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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
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19
Q

what are the 4 local effects of inflammation

A
  • redness and warmth
  • swelling (edema)
  • pain
  • loss of function
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20
Q

what is redness and warmth caused by

A

increased blood flow to damaged area

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21
Q

what is swelling caused by

A

shift of protein and fluis into the interstitial space

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22
Q

what is pain caused by

A

increased pressure of fluid on nerves; release of chemical mediators

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23
Q

what causes loss of function

A

when cells lack nutrients, edema may interfere with movement

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24
Q

what does exudate refer to

A

collection of interstitial fluid formed in the inflamed area

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25
expand on serous exudate
watery, consists primarily of fluid, some proteins and white blood cells
26
expand on fibrinous exudate
thick, sticky, high cell and fibrin content
27
expand on purulent exudate
thick, yellow/green, contains more leukocytes, cell debris and microorganisms
28
expand on hemorrhagic exudate
present when blood vessels are damages
29
what are the systemic effects of inflammation
- mild dever - malaise (feeling unwell) - fatigue - headache - anorexia
30
what are the 8 steps in the course of a fever
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
what does leukocytosis change in the blood with inflammation
increased numbers of white blood cells, especially neutrophils
32
what does different counts change in the blood with inflammation
proportion of each tupe of white blood cell alteres, depending on the cause
33
what does plasma proteins change in the blood with inflammation
increaed fibrinogen and prothrombin
34
what does c-reactive protein change in the blood with inflammation
a protein not normally in the blood, but appears with acute inflammation and necrosis withing 24-48 hours
35
what does increased ESR change in the blood with inflammation
elevated plasma proteins increase the rate at which red blood cells settle in a sample
36
what does cell enzymes changes in the blood with inflammation
released from necrotic cells and enter tissue fluids and blood, may indicate the site of inflammation
37
what are diagnostic tests used for
- leukocytosis - erthrocyte sedimentation rate - differntial count - circulating plasma proteins - cell enzymes - necrosis
38
what are potential complications of infection
 Microorganisms can more easily penetrate edematous tissues.  Some microbes resist phagocytosis.  The inflammatory exudate also provides an excellent medium for microorganisms.
39
what are potential complications of skeletal muscle spasm
 May be initiated by inflammation  Protective response to pain
40
expand on chronic inflammation
 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
what are potential complications of chronic inflammation
 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
what are 4 drugs used to treat inflammation
 Acetylsalicylic acid (ASA) -----Aspirin  Acetaminophen----Tylenol  Nonsteroidal antiinflammatory drugs (NSAIDs)------- Ibuprofen  Glucocorticoids----- Corticosteroids
43
what are the antiinflammatory effects of glucocorticoids
 Decreased capillary permeability  Enhanced effectiveness of epinephrine and norepinephrine  Reduced number of leukocytes and mast cells  Reduces immune response
44
what are the adverse efects of glucocorticoids
 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
expand on the the abbrevation of the "RICE" therapy for injuries
rest ice compression elevation
46
what are the 3 types of healing
resolution regeneration replacement
47
expand on resolution type of healing
minimal tissue damage
48
expand on regeneration type of healing
damages tissue replaces with cells that are functional
49
expand on replacement type of healing
functional tissue replaces by scar tissue loss of function
50
expand on the loss of function when it comes to scar formation
 Result of loss of normal cells and specialized structures * Hair follicles * Nerves * Receptors
51
expand on contractures and obstructions when it comes to scar formation
 Scar tissue is nonelastic.  Can restrict range of movement
52
expand on adhesions when it comes to scar formation
bands of scar tissue joining two surfaces that are normally seperated
53
expand on hypertropic scar tissue when it comes to scar formation
 Overgrowth of fibrous tissue * Leads to hard ridges of scar tissue or keloid formation
54
expand on ulceration when it comes to scar formation
 Blood supply may be impaired around scar. * Results in further tissue breakdown and ulceration at future time
55
what can burns be caused by
- thermal (flames, hot fluids) - chemicals - radiation - electricity - light - friction
56
expand on superficial partial-thickness (first degree burns)
 Involve epidermis and part of dermis  Little, if any, blister formation
57
expand on deep partial-thickness (second degree) burns
 Epidermis and part of dermis  Blister formation
58
expand on full thickness (third and fourth degree) burns
 Destruction of all skin layers and often underlying tissues
59
what are the effects of a burn injurt
 Both local and systemic  Dehydration and edema  Shock  Respiratory problems  Pain  Infection  Hypermetabolism during healing period after burn
60
expand on the healing of burns
 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 (11 decks)

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