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NUR 612 Advanced Pathophysiology > Module 2.3 Inflammation, Tissue Repair and Wound Healing. > Flashcards

Module 2.3 Inflammation, Tissue Repair and Wound Healing. Flashcards

1
Q

Purpose of inflammation

A

Eliminate cause of injury

Generate new tissue

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2
Q

Acute Inflammation Summary

A
  1. Short duration
  2. Aim is removal of injuring agent and limiting tissue damage
  3. Infiltration of NEUTROPHILS
  4. Produces EXUDATE
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3
Q

Chronic Inflammation summary

A
  1. Lasts days to years.
  2. Infiltration of MACROPHAGES AND LYMPHOCYTES
  3. Proliferation of FIBROBLASTS - scarring
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4
Q

Types of chronic inflammation

A

Recurrent or progressive

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5
Q

How to differentiate between chronic and acute inflammation in a patient.

A

look at the WBC’s in the area. lymphocytes not seen in early stages, only in chronic.

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6
Q

Leukocytes of inflammation

A

Monocytes
Neutrophils
Basophils
Eosinophils

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7
Q

When an Eosinophil moves into the tissue it becomes a

A

Mast cell

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8
Q

When a Monocyte moves into the tissue it becomes a

A

Macrophage

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9
Q

Connective tissue cells of inflammation

A

Fibroblasts
Macrophages
Mast cells

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10
Q

Vascular phase of inflammation

A

Vasodilation (after very brief constriction).
causes Rubor and Calor
Increased vascular permeability > swelling (tumor)

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11
Q

Rubor

A

redness

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12
Q

Calor

A

Heat

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13
Q

Tumor (in inflammation)

A

swelling due to vascular permeability

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14
Q

Dolor

A

Pain

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15
Q

Functio Laesa

A

Loss of Function

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16
Q

5 Hallmark signs of inflammation

A
  1. Rubor
  2. Calor
  3. Tumor
  4. Dolor
  5. Functio Laesa
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17
Q

Immediate Transient response

A

Lasts 15-30 minutes.

Minor burns/bumps

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18
Q

Immediate Sustained response

A

May last several days.

Usually result of vascular injury

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19
Q

Delayed hemodynamic response

A

occurs 2-24 hours after exposure to radiation.

Sunburn, radiation therapy

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20
Q

Margination

A

Accumulation of leukocytes caused by cytokines (ie selections, integrins) which recruit WBC’s.

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21
Q

Adhesion

A

leukocytes slow down and role until they find site of high cytokine activity. (verify/read up on?)

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22
Q

Transmigration

A

Leukocytes extend foot and squeeze through vessel wall. into tissue spaces

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23
Q

What causes transmigration

A

Chemotactic factors

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24
Q

Why are chemokines important in early inflammation

A

They attract and direct leukocytes to needed areas

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25
Q

What immune cell secretes chemokines

A

macrophages

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26
Q

Stages of Phagocytosis

A

Recognition and adherence (detection of cells covered in opsin)
Engulfment (opsinization)
Intracellular killing

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27
Q

LISTEN TO 13 MINUTE MARK

A

LISTEN TO 13 MINUTE MARK

28
Q

Bacterial infections generally result in what WBC change?

A

Increased neutrophils

29
Q

Parasitic infections and allergies generally result in what WBC change?

A

Increased Basophils

30
Q

Effect of inflammation/infection on erythrocyte sedimentation rate

A

increased ESR

31
Q

Overwhelming infection may cause

A

Leukopenia - decreased WBC’s

32
Q

What cell releases histamines?

A

Mast Cells

33
Q

Role of histamines in inflammation

A

Vasodilation and increased permeability of venules

34
Q

What are the 2 arachidonic acid metabolites and where do they come from

A

Prostaglandins
Thromboxane
From cell membranes

35
Q

Effects of Prostaglandins

A

vasodilation
Bronchconstriction
potentiates Histamine (associated with anaphylaxis)
Uterine contractions during menstruation

36
Q

Effects of Thromboxane

A

Vasoconstriction
Bronchoconstriction
Promotes Platelet function

37
Q

Effects of Platelet Activation Factor

A

Activates Neutrophils
Attracts Eosinophils
Activates Platelets

38
Q

Plasma proteins as inflammatory mediators

A

Promotes blood clotting
Activates compliment system.
Vasoactive Peptides

39
Q

Bradykinin (vasoactive peptide)

A

increased vascular permeability

Dilation of blood vessels, contraction of smooth muscle

40
Q

Nitric Oxide as inflammatory mediator

A

Think free radicals!!
Platelet Aggregation
Causes increased tissue injury (can become never ending cycle)

41
Q

STUDY FIGURE 9.3

A

STUDY FIGURE 9.3

42
Q

Acute phase response of cell mediated response (TQ!)

A 
Fever
Anorexia
Hypotension
Tachycardia
Corticosteroid and ACTH released
43
Q

Serous Exudate

A

Watery
Low in protein content
Plasma entering the inflammatory site

44
Q

Hemorrhagic exudates

A

Severe tissue damage involving vessels or severe leakage of red cells from capilaries

45
Q

Membranous or Pseudomembranous exudates

A

Develop on mucous membrane surfaces.
Composed of necrotic cells enmeshed in fibro-purulent-exudate.
Seen in burns!

46
Q

Purulent or Suppurative Exudates

A

contain pus (WBC’s, proteins, tissue debris)

47
Q

Fibrinous Exudates

A

Large amount of fibrinogen

Form thick sticky meshwork

48
Q

READ INFO ON SLIDE 23! WILL BE ON TEST

A

READ INFO ON SLIDE 23! WILL BE ON TEST

49
Q

What is an abscess

A

A walled off inflamed area filled with purulent exudate.

50
Q

What are characteristics unique to chronic inflammation.

A

Granulomas
Infiltration with Macrophages and LYMPHOCYTES
proliferation of Fibroblasts

51
Q

What is chronic gramulomatous inflammation associated with

A

Foreign Bodies
Splinters, sutures, asbestos, silica

Microbes
TB, Syphilis, sarcoidosis, Deep fungal infections, brucellosis

52
Q

Parenchymal Tissue

A

Tissue containing the functional cells of the organ (hepatocytes, renal tubular cells)

53
Q

Stromal Tissue

A

Supporting tissue (Nerves, ECM, Blood Vessels, etc.)

54
Q

Labile Cells

A

Replaceable cells (skin, mucosa, GI tract)

55
Q

Stable Cells

A

Normally stop dividing when they reach maturity. May start again if damaged (partial liver removal)

56
Q

Example of stable cells

A

Parenchymal cells of liver and kidneys. smooth muscle cells, vascular endothelium.

57
Q

Permanent cells

A

Cannot undergo mitotic division.

Nerves, skeletal muscle, cardiac.

58
Q

Stages of wound healing

A

Inflammatory phase
Proliferative phase
Maturational (remodeling) phase

59
Q

inflammatory phase of healing

A

Injury
Blood clots and WBC’s migrate to site
Neutrophils arrive first, then macrophages.

60
Q

Proliferative phase

A

Fibroblasts are predominant cell.

Secrete reconstruction material (collagen, vascular growth factors for angiogenesis)

61
Q

Maturational or remodeling phase

A

~3 weeks post injury.

Scar formation

62
Q

Healing by primary intention

A

Small clean wound, well approximated, no tissue lost.

63
Q

Healing by secondary intention

A

great tissue loss, contamination, left open to heal.

Still minimal scarring if properly cared for

64
Q

What may delay wound healing

A 
DM
Corticosteroid use
Malnutrition
Impaired circulation/perfusion
Age
Infection
65
Q

Issues with healing in children

A

Electrolyte imbalances
Temp Instability
Immune insufficiency in very young kids
Nutritional needs (Short gut syndrome, DM)

NUR 612 Advanced Pathophysiology (21 decks)

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