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Thompson class fall 2015 > Exam 2: Week 6 (inflammation, etc.) > Flashcards

Exam 2: Week 6 (inflammation, etc.) Flashcards

1
Q

What commonly starts the inflammation process?

A
  • Sprains, strains, and contusions
  • Fractures
  • Foreign bodies (sutures)
  • Autoimmune diseases (RA)
  • Microbial agents (bacteria)
  • Chemical agents (acids, alkali)
  • Thermal agents (burns or frostbite)
  • Irradiation (UV or radiation)
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2
Q

Picture of inflammatory response

A
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3
Q

5 Factors affecting or contributing to cellular aging (for better or for worse)

A
  • Free radicals (for worse- for sure)
  • Telomere aging clock theory
  • Diet (can act as antioxidant)
  • Exercise (can act as antioxidant)
  • Hormones (can act as antioxidant)
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4
Q

What are aging cells less resistant to?

A

injury or disease

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5
Q

What can age-associated deterioration of cells lead to?

A

—tissue/organ deficiencies

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6
Q

What is the telomere aging clock theory?

A

—molecular clock that signals senescence, could be used as a malignancy marker

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7
Q

What determine’s the body’s reaction to injury at the cellular level? (3)

A

Amount, type, and severity of injury

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8
Q

Two different levels of severity for injury and how it can impact cells

A
  1. —Mild injury- alterations that are sublethal
  2. Moderate to severe injury- can be lethal
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9
Q

Ultimate goal for the healing process

A

regain 100% function through regeneration and restoration

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10
Q

True or False: All types tissue can regenerate

A

False

However, there is a growing body of research examining the potential for neuron, cardiac, muscle cells to regenerate

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11
Q

What is occuring with the tissue during the typical repairing process? (3)

A
  • —Connective tissue scarring (tissue is ok but not as good as the original)
  • Muscle fibrosis
  • Maintains integrity of the tissue but does NOT function as original cells and tissues
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12
Q

Mechanisms of Cell Injury

A
  1. Ischemia
  2. Infection
  3. Immune response (allergy, autoimmune disorder)
  4. Genetic (sickle cell anemia, diabetes)
  5. Nutritional factors (malnutrition)
  6. Physical factors (Brain injury, sunburn)
  7. Mechanical factors
  8. Chemical factors (chemical inside or outside of body, includes free radicals)
  9. Psychosocial factors (stress, anxiety)
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13
Q

Why would diabetes type I fall under immune category for mechanism of cell injury?

A

antigens produce T-lymphocytes to attack islet cells

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14
Q

Two pathologies Dr. Thompsn highlighted when discussing nutritional deficencies that result in damage to cells

A
  1. Kwashiorkor- protein deficient, causes swelling in belly
  2. Marasmus- protein/calorie deficient
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15
Q

What are free radicals?

Advantage and disadvantage

A
  • —Formed in body, by-product of metabolism
  • Caused by excess exercise, UV, pollutants, tobacco smoke, etc.

—Advantage: part of immune system

Disadvantage: in excess cause cell injury, ie heart disease, CVA, diabetes

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16
Q

What do antioxidents do and how do we acquire them?

A

—neutralize extra free radicals

—Acquired through vitamins, minerals, moderate exercise

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17
Q

How does cell react to a sublethal stimulus?

A
  • —Impaired cell function- increased ion content (Na+ and Ca+) leads to cell swelling due to fluid retention
  • Blebs form- plasma membrane seal off and detach

—If nucleus survives- cell can recover

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18
Q

List of adaptations to chronic sublethal stimulus (5)

A
  1. —Atrophy
  2. hypertrophy
  3. hyperplasia
  4. metaplasia
  5. dysplasia
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19
Q

What is hyperplasia?

A

the enlargement of an organ or tissue caused by an increase in the reproduction rate of its cells, often as an initial stage in the development of cancer.

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20
Q

What is metaplasia?

A

abnormal change in the nature of a tissue

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21
Q

What is dysplasia?

A

the enlargement of an organ or tissue by the _abnormal maturation o_f cells in a given tissue, as a developmental disorder or an early stage in the development of cancer.

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22
Q

True or False:

—Intracellular accumulations of lipids, proteins, carbohydrates, or pigment can cause cell injury

A

True

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23
Q

True or False: The tissue in the liver are unable to regenerate

A

False

Tissue in the liver can recover and regenerate from cell damage caused by issues such as excess storage of hepatocytes from alcohol abuse

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24
Q

4 types of irreversible cell injury

A
  1. —Dry gangrene- bacterial infection and ischemia
  2. Wet gangrene- liquefy tissue
  3. Gas gangrene- fermentation forms gas bubble
  4. —Calcification- atherosclerosis, TB (granulomas), calcific tendonitis, etc.
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25
Q

What is gangrene?

A

a condition that involves the death and decay of tissue, usually in the extremities due to loss of blood supply

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26
Q

Qualities of dry gangrene (4)

A
  1. no infection
  2. little tissue liquefaction
  3. In early stages- dull aching pain, extremely painful to palpate, cold, dry, and wrinkled
  4. In later stages skin gradually changes color: dark brown then dark purplish/blue then black
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27
Q

Qualities of wet gangrene (5)

A
  1. bacterial infection
  2. copious liquefaction
  3. offensive odor
  4. warm, red, and swollen
  5. usually develops rapidly due to blockage of venous and/or arterial blood flow.
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28
Q

Typical treatment for wet or dry gangrene

A

surgical debridement and amputation

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29
Q

Components of tissue healing (4)

A
  1. —Fibronectin
  2. Proteoglycans
  3. Elastin
  4. Collagen
30
Q

Why is fibronectin important?

A

—glycoprotein that provides tensile strength and acts as a glue for surrounding cells

31
Q

Why are Proteoglycans and Elastin important?

A

Proteins that support fibroblast proliferation

32
Q

Why is collagen important?

A

—fibrous protein that provides structural support and tensile strength of tissue

33
Q

List of factors affecting healing for (better or worse-11)

A
  1. —Growth factors (applied in creams such as hydrogel or quickderm)
  2. —Vascular supply
  3. Age
  4. Tissue health
  5. Underlying disease
  6. Psychological status
  7. Alcohol
  8. Smoking
  9. Nutrition
  10. Tissue type
  11. Medication

​………and the list goes on

34
Q

Phases of healing (4)

A
  1. —Hemostasis and degeneration- initiation phase
  2. Inflammation phase- prepares for healing
  3. Proliferation phase- rebuilds and strengthens damaged tissue
  4. Maturation phase- modifies tissue to mature form
35
Q

When does Hemostasis and Degeneration in the process of healing?

A

Immediately (during initial 24 hours)

36
Q

What more specifically is occuring duing Hemostasis?

A
  • —Stop the bleeding through coagulation casecade – platelets and growth factors proliferation
  • migration of epithelial cells, fibroblasts, and vascular endothelial cells
37
Q

What more specifically is occuring during the degeneration phase?

A
  • —Form hematoma
  • Necrosis of dead cells
  • —Starts the inflammatory response of fluid, neutrophils, macrophages
38
Q

3 Functions of inflammatory response

A
  1. —inactivate the injured tissue
  2. break down/remove dead cells
  3. —initiate healing
39
Q

What is occuring with the formation of the hematoma during the degeneration phase?

A
  • —Migration of fibroblast from margins of viable tissue into the defect area
  • —Secretion of proteins (fibronectin, proteoglycans, elastin, collagen)
  • —Proliferation and migration of epidermal cells seen, as the next phase begins
40
Q

5 cardinal signs of inflammation

A
  1. heat (calor)
  2. redness (rubor)
  3. swelling (tomor)
  4. pain (dolor
  5. loss of function (functio-laesa)
41
Q

When are the 5 cardinal signs expected to be most present in the inflammatory process?

A

During the acute phase

1-6 days

42
Q

Potential outcomes of acute inflammation

A
  • —Complete resolution and restoration of normal tissue structure
  • —Healing with scar formation
  • —Mild tissue damage
43
Q

What is hyperemia?

A

—increased blood flow (redness, erythema)

44
Q

What is the source of pain during the acute inflammatory process?

A

pressure

45
Q

What is happening with swelling during the acute inflammatory process?

A

—increased permeability of cells and vasodilatation (if blood, ecchymosis)

46
Q

What are topical antibiotcs best used for with injuries?

A

keeping wound moist

47
Q

What is chronic inflammation (4 bullet pts.)

A
  • —Progression of active inflammation
  • Tissue destructio
  • —Inflammation lasting 2 weeks or longer
  • Often related to an unsuccessful acute inflammatory response
48
Q

What may cause acute inflammation to change over to chronic inflammation?

A
  1. Returning to sports or activities too quickly (abusing the tissue that needs to heal)
  2. —High lipid and wax content of a microorganism- —ability to survive inside the macrophage
  3. —Toxins
  4. —Chemicals
  5. Particulate matter or physical irritants
49
Q

Want to see a picture of chronic inflammation?

A
50
Q

4 characteristics of chronic inflammation

A
  • —Dense infiltration of lymphocytes and macrophages
  • —Granuloma formation (usually in organs)
  • —Epithelioid cell formation
  • —Giant cell formation (seen in tendons and organs)
51
Q

What is the vascular response to the inflammatory process?

A
  • —Initial vasoconstriction- norepinephrine formed, mediated 5 to 10 minutes after injury. Shrinks up the small blood vessles
  • Vasodilation- histamine, Hageman factor, bradykinin, prostaglandins, and complement fractions formed and mediated 1 hour after injury
52
Q

Members of the clean up crew and their job duties during clot formation during vasoconstriction

A

while blood vessel linings adhere….

  • —Neutrophils migrate to injury area- Extravasation
  • —Leukocytes line vessel wall- margination
53
Q

Where do we typically see edema?

A

—in extravascular space and interstitial tissues

may see in granulation tissue

54
Q

—What is diapedesis as it relates to edema?

A

Leukocytes squeeze trough vessel wall

55
Q

How are leukocytes attracted to interstitial tissues?

A
  • —By chemotactic agents
  • Process called emigration
56
Q

What is effusion and what are four kinds of effusion we may encounter?

A

—Swelling contained in a cavity

  1. —Joint effusion
  2. Pleural effusion
  3. Ascites (in lungs)
  4. Peritoneal effusion

So effusion is basically edema in a cavity and the site of effsion determines its name

57
Q

4 kinds of edema/effusion and the stuff that makes it up

A

3 is least desirable with wound care

  1. —Transudate- dissolved electrolytes and H2O (not so bad because it provides lubrication
  2. Exudate- Plasma proteins, lipids, cellular debris (cloudy)
  3. Pus- neutrophils, digested tissue, fluid, bacteria
  4. Blood

Sometime #1 and #4 will go together

58
Q

4 components of vascular permiability

A
  1. Endothelial cell contraction- 15-30 minutes

—Opens spaces between cells

  1. Endothelial injury- altered substance release

—Contents of vessel spill into interstitium

  1. Leukocyte bind to injured area

—Release chemicals and enzymes creating injury

  1. Regenerating capillaries- angiogenesis

—In later stages of healing tight junctions yet to form

59
Q

Role of platelets in hemostatic response

A

bind to collagen, release fibrin

60
Q

Role of fibrin and fibronectin in hemostatic response

A

—limit fluid drainage and hemorrhaging

61
Q

What is hemarthrosis and what is a method of treatment?

A
  • bleeding into joint spaces. It is a common feature of Haemophilia.
  • joint aspiration
62
Q

Check out this flow chart of inflammation

A
63
Q

When does Proliferative Phase occur?

A

3-20 days

64
Q

What happens in Proliferative Phase

A
  • —Epithelial cells and connective tissue cover and strengthen injury site
  • Epithelialization
  • Collagen production
  • Wound contracture
  • Neovascularization
65
Q

2 intentions of wound healing

A
  1. —Primary intention- close approximation of tissues. If you have a wound, and it’s sutured together, not necessarily a really big scar
  2. Secondary intention- indirect union. Scar tissue forms from the inside the wound bed
66
Q

Componenets of Fibroplasia/Collagen Production

A
  • —Granulation tissue- newly healing tissue
  • Type III collagen initially- weak and thin (Many types of collagen- this is just the first kind to show up on the scene)
  • Glycosaminoglycan (GAG) and collagen form structure of scar
  • Type I collagen day 12- more mature and stronger
67
Q

Another picture of healing process with wound intention

A
68
Q

What happens during wound contraction?

A
  • —Pulls edges together
  • Myofibroblasts- smooth muscle cells
  • —Contractures- Wound contraction, adhesions, muscle shortening, tissue damage
  • Pressure/tension- red/swollen
69
Q

When does maturation phase occur?

A

9 days - up to 2 years

70
Q

How do you know if a scar is still healing and why do you care?

A
  • If it is red or pink
  • It can be influenced by remodeling

Thompson class fall 2015 (12 decks)

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