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NURS 2003 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What is sublethal injury?

A

Alters function without causing cell destruction. Injury potentially reversible if harmful stimulus is removed.

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2
Q

What is a lethal injury?

A

Irreversible process that causes cell death.

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3
Q

What is hypertrophy?

A

An expansion in the size of cells, which results in increased tissue mass without cell division.

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4
Q

What is physical hypertrophy?

A

Results from increased workload on an organ or tissue that is not caused by disease.

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5
Q

What is hyperplasia?

A

A multiplication of cells as a result of increased cellular division.

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6
Q

What is atrophy?

A

A decrease in the size of a tissue or organ as a result of a reduction in the number or size of individual cells.

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7
Q

What is metaplasia?

A

The transformation of one cell type into another in response to a change in physiological condition or an external irritant.

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8
Q

What is dysplasia?

A

Abnormal differentiation of dividing cells that results in changes in their size, shape, and appearance.

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9
Q

What is anaplasia?

A

Cell differentiation to a more immature or embryonic form.

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10
Q

What is apoptosis?

A

Programmed cell death.

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11
Q

What is necrosis?

A

Tissue death that results from traumatic injury, infection or exposure.

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12
Q

What is gangrene?

A

Can result from degenerative changes that occur with certain chronic diseases, such as atherosclerosis or diabetes.

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13
Q

What is wet gangrene?

A

Occurs as the result of sudden rapid elimination of blood flow, seen in severe burn or traumatic crush injury.

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14
Q

What is the inflammatory response?

A

A biological response to cell injury caused by pathogens, irritants, chronic health conditions.

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15
Q

What is selectins?

A

Cell surgace carbohydrate binding proteins that mediate cell adhesion, involved in leukocyte extraversion during the immune response.

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16
Q

What are integrins?

A

cell receptors that mediate attachment between endothelial cells and surrounding tissues, also involved in leukocyte extraversion during the immune response.

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17
Q

What is regeneration?

A

The replacement of lost cells and tissues with cells of the same type.

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18
Q

What is repair?

A

Healing as a result of lost cells being replaced by connective tissue

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19
Q

What are fibroblasts?

A

Immature connective tissue cells that migrate into the healing site and secrete collagen.

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20
Q

What are adhesions?

A

Bands of scar tissue that form between or around organs.

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21
Q

What is dishence?

A

The separation and distribution of previously joined wound edges.

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22
Q

What is evisceration?

A

occurs when wound edges separate to the extent that intestines protrude through the wound.

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23
Q

What are fistulas?

A

Abnormal passage that forms between organs or a hollow organ and the skin.

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24
Q

What is a hypertrophic scar?

A

Inappropriately large, red, raised, and hard scar.

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25
Q

What is a keloid?

A

a protrusion of scar tissue that extends beyond the wound edges and may form tumour like masses of scar tissue.

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26
Q

What is a pressure sore?

A

Localized injury to the skin or underlying soft tissue, usually a boney prominence or related medical or other devices as a result of pressure or pressure in combination with shear, friction, or both.

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27
Q

What is shearing force?

A

Pressure exerted on the skin when it adheres to the bed and the underlying skin layers slide in the direction of body movement, friction and excessive moisture.

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28
Q

What is pathological hypertrophy?

A

result of disease. Ex. enlargement/ thickening of heart ventricle from chronic hypertension.

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29
Q

What is compensatory hypertrophy?

A

result from increased workload caused by reduced function. Ie. when a kidney is removed, remaining kidney enlarges due to increased workload.

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30
Q

What is physical hyperplasia?

A

adaptive response to normal body changes. Ex. cells during pregnancy.

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31
Q

What is pathological hyperplasia?

A

result of disease. Eg. endometrial hyperplasia caused by excess estrogen.

32
Q

What is compensatory hyperplasia?

A

process whereby cells of certain organs regenerate. Ie. the liver.

33
Q

What is metaplasia?

A

Transformation of one cell type in the response to a change in physiological conditions.

34
Q

What are the adaptive processes?

A

Hypertrophy, hyperplasia, atrophy, metaplasia.

35
Q

What are maladaptive processes?

A

Dysplasia, anaplasia.

36
Q

What are causes of lethal cell injury?

A

Heat, cold, radiation, electrothermal injury, mechanical trauma, chemical injury, viruses, bacteria, antigen, autoimmune response.

37
Q

What is the mononuclear phagocyte system?

A

Monocytes and macrophages, considered fixed or free,. Functions include recognition and phagocytosis of foreign materials, immune response and removal of old damaged cells.

38
Q

What do the arterioles do in the vascular response to inflammation?

A

Arterioles undergo transient vasoconstriction, which is stimulated by the SNS.

39
Q

What does firbin-platelet clot release?

A

Histamine.

40
Q

What does the release of histamine cause?

A

Hyperemia, which results in increased filration pressure, causing endothelial cell retraction, and increases capillary permeability.

41
Q

When is fibrin formed?

A

When fibrinogen leaves the blood.

42
Q

What does fibrin do?

A

Fibrin strengthens the blood clot formed by platelets.

43
Q

What does the clot in the healing process do?

A

Traps bacteria, prevents spread, releases growth factors, begins healing process.

44
Q

What does nitric oxide do?

A

Used to inhibit vascular smooth muscle contraction and growth, platelet aggregation and leukocyte adhesion to endothelium. Released by phagocytes.

45
Q

What do cytokines do?

A

released by macrophages, cause endothelial cells to express cellular adhesion molecules selectins and integrins.

46
Q

What do neutrophils do?

A

first WBCs to arrive at injury site (6-12 hrs after injury). They phagocytize bacteria, foreign material and damaged cells. Dead neutrophils form pus. To keep up, bone marrow produces more neutrophils, thus resulting in an elevated WBC.

47
Q

What do monocytes do?

A

arrive to the site 3-7 hrs after injury, transform to macrophages upon entering the cell. Assist phagocytes in clearing debris. Cleans area before healing begins. Can form into giant cell, turning into a granuloma, which can cause chronic inflammation.

48
Q

What do lymphocytes do?

A

arrive later at site. Assist with humoral and cell-mediated immunity.

49
Q

What do eosinophils do?

A

eosinophils released in large quantities during allergic reaction. Release chemicals to control effects of histamines and serotonin. Also involved in phagocytosis of allergen-antibody complex. Eosinophils contain chemicals that can destroy parasites cell surfaces.

50
Q

What do basophils do?

A

carry histamine and heparin in granules, which are released during inflammation.

51
Q

What is histamine?

A

stored in granules of basophils, mast cells, platelets. Causes vasodilation and increased vascular permeability by stimulating contraction of endothelial cells and creating widened gaps between cells.

52
Q

what does serotonin do?

A

stored in granules of basophils, mast cells, platelets. Causes vasodilation and increased vascular permeability by stimulating contraction of endothelial cells and creating widened gaps between cells.

53
Q

What does kinins do?

A

produced from precursor factor kininogen as a result of activation of Hageman factor of clotting system. Causes smooth muscle contratction and dialation, stimulates pain.

54
Q

What do complement components do?

A

Anaphylatoxic agents generated from complement pathway activation. Stimulate histamine release, stimulate chemotaxis.

55
Q

What do fibropeptides do?

A

produced from activation of the clotting system. Increase vascular permeability; stimulate chemotaxis for neutrophils and monocytes.

56
Q

What do prostaglandins and leukotrines do?

A

produced from arachidonic acid. Prostaglandins E1 and E2 cause vasodilation; leukotriene B4 stimulates chemotaxis.

57
Q

What do cytokines do?

A

secreted by WBCs and other cells. Act as messengers between cell types, instruct cells to alter their proliferation differentiation, secretion or activity.

58
Q

What is the complement system?

A

an enzymatic cascade consisting of pathways to mediate inflammation and destroy invading pathogens. Major functions include advanced phagocytosis, chemotaxis, cellular lysis.

59
Q

What are anaphylotoxins in the complement system?

A

C3a, C4a and C5a, bind to receptors on mast cells and basophils, triggering histamine release.

60
Q

What are the clinical manifestatons of inflammation?

A

redness, swelling, heat and pain. Systematic manifestations include leukocytosis w/ shift to left, malaise, nausea, fever, high pulse and rr.

61
Q

What causes general symptoms of malaise?

A

Interleukin-1, interleukin-6 and tumour necrosis factor.

62
Q

What are the benefits of fever?

A

killing microorganisms, increased phagocytosis via neutrophils, increased proliferation of T cells, and enhances interferon

63
Q

Explain the process of fever.

A

Fever-release of cytokines initiates metabolic changes in temp-regulating center of hypothalamus. PGE2 has direct effect on fever. Hypothalamus activates ANS to stimulate shivers, and decrease sweating. Adrenaline released to increase metabolic rate. Body basically picks a new temperature to regulate to, hence why someone can feel cold, but is burning hot. Cytokines and fever trigger bodies defence mechanisms.

64
Q

What is acute inflammation?

A

healing occurs in 2-3 weeks, no residual damage. Neutrophils dominant.

65
Q

What is subacute inflammation?

A

same as acute, but lasts longer.

66
Q

What is chronic inflammation?

A

Weeks to years. Persistant injury to tissue. Lymphocytes and macrophages predominant. Ie, RA, TB. May alter immune response.

67
Q

What are the phases of primary intention?

A

inflammatory, granulation, maturation phase and scar contraction.

68
Q

What is the inflammation phase?

A

3-5 days. Incision is aligned and sutured.

69
Q

What is the granulation phase?

A

5 days to 3 weeks. Includes proliferating fibroblasts, proliferating capillary sprouts, various types of WBCs. Wound is pink and vascular.

70
Q

What is maturation and scar contraction?

A

Overlaps with granulation phase. 7 days post injury. The scaring process.

71
Q

What is secondary intention?

A

Wounds that are not well approximated. Ie. Chronic wounds. Debriding may need to take place. Essentially the same as primary intention. Healing takes place outside in, bottom up.

72
Q

What is teritary intention?

A

delayed primary intention. Occurs when wound is intentionally left open (ie. animal bite). Results in larger scar.

73
Q

What are complications of wound healing?

A
  • Adhesions
  • Contractures
  • Dehiscence - 3 potential causes, infection, granulation tissue, obseity.
  • Excess granulation
  • Fistula formation
  • Infection
  • Hemorrhage
  • Formation of hypertrophic scars and keloids.
74
Q

What are some factors that delay healing?

A
  • Vit C deficiency- delays formation of collagen fibres and capillary development.
  • Protein deficiency- decreases supply of amino acids for tissue repair.
  • Zinc deficiency- impairs epithelization.
  • Inadequate blood supply- decreases supply of nutrients to injured area, removal of debris, inhibits inflammatory response.
  • Smoking- nicotine is vasoconstrictor and stops blood flow in areas.
  • Corticosteroid drugs- impair phagocytosis by WBCs, inhibit fibroblast proliferation and function, depress formation of granulation tissue, inhibit wound contraction.
  • Infection- increase inflammatory response and tissue destruction
  • Anemia- reduces supply of oxygen
  • Age- slows collagen, synthesis of fibroblasts, impairs circulation, alters phagocytosis and immune response.
  • Obesity- decreases supply in fatty tissues.
  • Diabetes- decreases collagen synthesis, impairs phagocytosis due to hyperglycemia.
  • Poor general health
  • Mechanical friction on wound
  • Cold Temperature
  • Excessive moisture
75
Q

What are the stages of fever?

A
  • Prodrome: non-specific complaints, headache, fatigue, malaise.
  • Chill: cutaneous vasoconstriction, pale skin, feeling chilled, generalized shivering,
  • Flushing: overall warming, flushing of the skin, person feels warm
  • Defervescence: sweating, causes body temp to lower.
76
Q

What is a tool you can use to assess wounds?

A

Measure height, width, depth

Exudate

Appearance of wound bed (red, yellow, black, mixed)

Suffering, pain, quality and intensity

Undermining

Reevaluate

Edge

77
Q

What are factors that enhance wound healing?

A
  • Good diet, low fat, high fluid intake
  • Add carbs, vit A and C, Zinc, watch for vit B deficiency
  • Clean wound
  • No friction
  • Good moisture
  • Regular blood glucose

NURS 2003 (12 decks)

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