Week 7 Quiz (Wound healing and alt. of Hematologic fx) Flashcards

1
Q

Resolution definition

A
  • injured tissue is replaced by cells of the same type

- restoration of the original structure and function

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2
Q

Repair definition

A
  • destroyed tissue is replaced by connective tissue (scar)

- fills in lesion and restores tensile strength but can not carry out physiologic functions of the destroyed tissue

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3
Q

when do resolution/repair occur?

A

they begin early during the inflammatory process

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4
Q

Regenerative capacity of different cell types

A
  • Labile cells
  • Quiescent cells
  • Permanent cells
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5
Q

Labile cells and examples

A
  • continuously dividing (proliferate thought life)

- skin, oral cavity, GI tract lining, urinary tract, bone marrow

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6
Q

Quiescent cells and examples

A
  • stable cells
  • usually demonstrate low level of replication, but stimulation can lead to rapid increases in division
  • bone, kidney, pancreas, fibroblasts, liver
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7
Q

Permanent cells and examples

A
  • nondividing cells
  • stopped dividing during prenatal life
  • nerve cells, cardiac m., skeletal m.
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8
Q

Skeletal muscle fiber repair

A
  • multinucleated, provide multiple copies of genes to speed up production of enzymes and structural proteins
  • myoblasts: embryonic cells which fuse to create the muscle fibers
  • satellite cells: assist with repair of damaged fibers = left-over myoblasts
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9
Q

Other factors which influence wound healing

A
  • site of the wound
  • mechanical factors
  • size of wound
  • infection (won’t heal until get rid of infection)
  • circulatory status (cartilage example)
  • nutritional and metabolic factors
  • age
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10
Q

Tension lines

A
  • most collagen and elastin fibers are in parallel bundles
  • their orientation depends on the stress placed on the skin during normal movement
  • clinical significance in surgery
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11
Q

Debridement

A
  • the first, absolutely essential step in wound healing is debridement
  • “clean-up” of particulate matter in the inflammatory exudate by phagocytosis
  • dissolution of fibrin clots by fibrinolytic enzymes
  • natural debridement occurs, but is slow (inflammation and phagocytosis)
  • surgical debridement speeds up healing
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12
Q

First intention healing

A
  • primary union
  • wounds with minimal tissue loss
  • example: sutured surgical wound
  • always preferred if possible
  • more likely to lead to resolution
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13
Q

Second intention healing

A
  • large, open defects and infected wounds
  • examples: degloving injuries, burns
  • formation of granulation tissue
  • more likely to lead to repair
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14
Q

Healing by second intention involves

A
  • formation of a healthy granulation bed (happy pink)
  • filling in the wound defect
  • covering or sealing the wound (epithelialization)
  • shrinking the wound (contraction)
  • wound maturation
  • remodeled (scars)
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15
Q

granulation tissue

A
  • has a soft, pink, granular appearance
  • represents a temporary scaffolding that changes over time
  • contains angioblasts and fibroblasts
  • angioblasts are cells that form new blood vessels
  • fibroblasts form collagen fibers for strong scar tissue
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16
Q

Repair involves and occurs in what two phases?

A
  • filling in the wound defect
  • epithelialization (covering or sealing the wound)
  • contraction (shrinking the wound)
  • reconstruction phase
  • maturation phase (think about us remodeling)
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17
Q

Epithelialization

A
  • epithelial cells from the surrounding healthy tissue migrate onto the granulation bed
  • use proteolytic enzymes to sever the connection between the clot and the wound surface and slide in between
  • make contact with similar cells from all sides of the wound and seal it (contact inhibition allows the cells to meet up and say they are done sealing)
  • epithelialization can be aided by keeping the wound moist
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18
Q

Phases of wound healing

A
  • inflammation
  • granulation tissue
  • wound contraction
  • collagen accumulation remodeling starts near the end of granulation tissue phase
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19
Q

Reconstructive phase

A
  • wound is initially sealed off by a blood clot containing fibrin and trapped cells
  • debridement by macrophages and neutrophils (or by a surgeon)
  • chemical mediators of inflammation are secreted by macrophages and promote growth and activity of angioblasts, and fibroblasts
  • granulation tissue forms in 2-5 days
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20
Q

Angiogenesis

A
  • capillary buds sprout out of vascular endothelial cells on wound margins
  • new endothelial cells migrate into the scaffolding and organize into vessels
  • allows influx of blood with oxygen, nutrients, and more phagocytic cells and chemical mediators
  • also called neovascularization
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21
Q

Fibrosis (Fibroplasia)

A
  • fibroblasts enter the area and proliferate
  • they deposit fibrous structural proteins
  • fibroblasts produce collagen which gradually develops more strength (scar tissue made of collagen and there are several types of collagen)
  • collagen not inside of cells
  • original collagen that is laid down is later replaced by better collagen that is more parallel to tension lines
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22
Q

wound contraction

A
  • myofibroblasts have features of both fibroblasts and smooth muscle cells
  • the myofibroblasts establish connections with neighboring cells
  • they anchor themselves to the wound bed and exert pull on neighboring cells
  • contraction alone may move the wound edge by 0.5mm per day (just like a muscle)
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23
Q

Maturation phase of healing (scar remodeling)

A
  • continuation of collagen deposition, tissue repair, and wound contraction
  • scar tissue is remodeled and gains its maximum strength
  • collagen fibers are initially almost random, but now become highly organized
  • “immature” type III collagen is replaced by stronger type I collagen
  • this process often continues for months
24
Q

Wound healing order

A
  1. Induction of acute inflammatory response by the initial injury
  2. Debridement
  3. Formation of a healthy granulation bed
  4. Angiogenesis and fibroplasia
  5. Epithelialization
  6. Wound contraction
  7. remodeling of tissue elements to restore function and to increase wound strength
25
Q

glucocorticoids

A
  • aka steroids
  • strong anti-inflammatory drugs
  • slows the migration of phagocytic cells to the site of injury
  • cause phagocytic cells already in the area to become less active
  • mast cells exposed to steroids are less likely to release histamine and other chemicals that promote inflammation
  • good: decrease excess inflammation
  • bad: suppress immune system & affect normal adrenal gland function
  • NSAID’s (these drugs don’t affect the immune system)
26
Q

hematocrit

A

% of whole blood that is made up of RBC’s

27
Q

anemia

A

-conditions in which there is a decrease in the quality or quantity of hemoglobin and/or RBCs (decreased hematocrit)

28
Q

causes of anemia

A
  • defective RBC’s or defective hemoglobin (sickle cell, CO)
  • blood loss (trauma, neoplasms, ulcers)
  • increased RBC destruction (= hemolysis) which is autoimmune or blood parasites
29
Q

Polycythemia vera

A

conditions in which there are excessive RBC numbers or volume (dehydration ism most common cause of increased hematocrit)

30
Q

Clinical manifestations of anemia

A
  • acute vs chronic
  • decrease of RBC’s or hemoglobin function -> hypoxia
  • signs are:
  • energy level: fatigue
  • skin/mucus membrane color: pale or jaundice
  • respiratory rate: increased rate and depth
  • CNS: dizziness, lethargy
31
Q

compensation for anemia occurs by

A
  • cardiovascular system (increased heart rate, capillary dilation)
  • respiratory system (increased rate & depth)
  • renal system (decreased blood flow to kidney triggers renin-angiotensin system)
  • hematologic system (bone marrow stimulation: erythropoietin)
32
Q

classification of anemias by bone marrow activity

A
  • regenerative vs non-regenerative
  • reticulocyte count = # immature RBC’s in blood
  • regenerative: bone marrow working hard to fix problem
  • hemolytic blood disorders, or blood loss
  • non-regenerative: bone marrow is the problem
  • decreased erythropoiesis
33
Q

Normal reticulocyte count in %

A

<1%

34
Q

Classification of anemias by cell size and color

A
  • macrocytic-normochromic anemias (result from abnormal DNA synthesis and die prematurely, larger than normal)
  • Microcytic-hypochromic anemias (disorders of iron metabolism, disorders of porphyrin, heme, or globin synthesis, smaller than normal)
  • Normocytic-normochromic anemias (relatively normal size and color, but insufficient number)
35
Q

macrocytic-normochromic anemias

A
  • pernicious anemia

- folate deficiency

36
Q

pernicious anemia

A
  • can’t take oral supplement
  • cause by malabsorption of vitamin B12
  • lack of gastric intrinsic factor which is needed for vitamin B12 absorption
37
Q

folate deficiency anemia

A
  • lack of folic acid which is essential for RNA and DNA synthesis in the RBC
  • humans are totally dependent on dietary intake of folate
38
Q

Microcytic-hypochromic anemias

A
  • iron deficiency anemia
  • lack of iron can also result in gastritis, irritability, headache, numbness, etc.
  • 26mg iron needed daily for new RBCs (dietary requirement is 1-2 mg/day)
39
Q

iron deficiency anemia

A
  • women- pregnancy and menorrhagia
  • ulcers, ulcerative colitis, cancer, etc
  • medications that cause GI bleeding (NSAIDs)
  • insufficient dietary intake of iron
  • children < 2 yrs of age
40
Q

Normocytic-normochromic anemias

A
  • aplastic anemia
  • posthemorrhagic anemia
  • hemolytic anemia
  • anemia of chronic inflammation
41
Q

aplastic anemia

A

infiltrative bone marrow disorders

42
Q

posthemorrhagic anemia

A

sudden blood loss with N iron stores

43
Q

hemolytic anemia

A

auto immune, drugs, toxins, blood parasites

44
Q

anemia of chronic inflammation

A

AIDS, SLE, malignancies, renal failure

45
Q

Sickle cell disease

A
  • homozygous
  • production of abnormal hemoglobin S due to an inherited autosomal recessive disorder
  • RBC become stretched into an elongated “sickle” shape
  • the abnormally shaped RBC’s are very prone to hemolysis
  • high incidence of sickle cell trait in Afro-americans and east africans which may provide protection against malaria
46
Q

Quantitative disorders of leukocyte function

A
  • WBCs
  • absolute # or relative number (%)
  • decreased bone marrow activity
  • premature destruction or WBC’s in circulation
47
Q

Qualitative disorders of leukocyte function

A

altered function of WBC’s in inflammation or immune processes

48
Q

Actual Quantitative WBC disorders

A
  • leukocytosis

- leukopenia

49
Q

leukocytosis

A
  • increased number WBC
  • can be a normal protective response
  • can also be caused by pathologic conditions
50
Q

leukopenia

A
  • decreased # of WBC

- never a normal response, never beneficial

51
Q

Neutrophil disorders

A
  • neutrophilia
  • neutropenia
  • agranulocytosis
52
Q

neutrophilia

A

=increased number

  • seen in early phases of infection (esp. bacterial), inflammation or tissue necrosis
  • “left shift”= premature release of somewhat immature neutrophils into the circulation (bands - protective mech.)
  • physiologic: stress
  • with hemorrhage or hemolysis
  • some drugs, metabolic disorders, and neoplasms
53
Q

neutropenia

A
  • decreased number
  • severe prolonged infections
  • abnormal distribution and sequestration (collect in one spot)
  • decreased bone marrow production
  • chemo (doesn’t allow bone marrow to produce), aplastic anemia, radiation
  • neupogen: recombinant DNA engineered: stim. bone marrow production (G-CSF) (granulocytes = G)
  • increased destruction
  • splenomegaly, immune reactions
54
Q

agranulocytosis

A

-drastically low neutrophils, eosinophils, and basophils (all 3 granulocytes)

55
Q

Eosinophil disorders

A
  • eosinophilia

- eosinopenia

56
Q

eosinophilia

A
  • increased number
  • allergic disorders
  • dermatologic disorders
  • parasite infestation
  • some malignancies
  • some drugs
57
Q

eosinopenia

A
  • decreased number
  • stress responses
  • Cushing’s syndrome (glucocorticoids)