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PATH > Unit 5: > Flashcards

Unit 5: Flashcards

1
Q

what is resolution

A

the “return to normal” following uncomplicated acute inflammation

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2
Q

what is regeneration

A

the replacement of lost or necrotic parenchymal cells by new cells of the same tupe

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3
Q

what happened is tissue damage is extensive in acute inflammation

A

there will be some degree of regeneration, scarring, or a combination of the 2

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4
Q

what happens following tissue injury in chromic inflammation

A
  • resolution may not occur due to much more tissue injury
  • with loss of parenchymal cells, regeneration and/or scarring will take place
  • necrotic cells and inflammatory debris will be removed
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5
Q

what does the extent of regeneration depend on

A
  • the ability of that cell type to divide
  • the number of surviving cells
  • if there is connective tissue “framework” for normal tissue structure
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6
Q

regenerative capacity of labile cells

A
  • these cells divide actively throughout life
  • have a short intermitotic phase
  • injury to these cells is rapidly followed by regeneration
  • occurs from basal germinative layers of epithelial cells
  • occurs from bone marrow stem cells of bone marrow
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7
Q

regenerative capacity of stable cells

A
  • long-lived cells that have a low rate of division
  • in the intermitotic phase for years but can divide if needed
  • examples = cells of liver, kidney, and pancreas, fibroblasts, endothelial cells
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8
Q

regenerative capacity of permanent cells

A
  • cells which cannot divide after fetal life
  • examples = cells of nervous system and cardiac muscle
  • injury can only heal by scarring (functional cells replaced)
  • extensive injury leads to functional defects
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9
Q

what are cyclins

A

the primary motivators of cell replication - determine the rate of proliferation
- interact with CDKs to control entry and progression of cells in the cell cycle

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10
Q

what can modify the rate of cyclin activity

A

1, external growth factors
- interact with cell surface or nuclear surface antigens to indirectly up regulate cyclin activity
- e.g. growth factors and interleukins
2. Inhibitory signals
- normally regulate cell proliferation in healthy cells
- monitor cells for abnormalities and, have effects such as impaired proliferation and induction of apoptosis

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11
Q

the net rate of cell proliferation is dependent on…

A
  • the ability to replicate
  • the balance between proliferative and inhibitory signals (cyclin activity)
  • the balance between the rate of cell proliferation and cell loss secondary to apoptosis
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12
Q

what is healing dependent on

A
  1. the regenerative capacity of different cell populations
  2. the type of lesion
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13
Q

what are rotaviruses

A

disease that commonly causes villus atrophy and diarrhea
- have high morbidity but low mortality

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14
Q

why does diarrhea occur in rotaviruses

A
  • the mature villous enterocytes are needed to absorb nutrients and water from food in the GI tract
  • nutrients that are nor absorbed produce an osmotic effect that draws fluid from body into faces
  • the intestinal tract is healed via regeneration as crypt cells and normal framework are preserved
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15
Q

morphologic alterations of celiac disease

A
  1. villus atrophy
  2. increased number of IELs
  3. epithelial proliferation and crypt elongation
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16
Q

examples of when injury to a liable population doesn’t end well

A
  • canine parvovirus: pathogen targets fast-dividing crypt stem cells
  • ischemia: pathogen causes sever nonspecific injury to intestinal mucosa
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17
Q

how does intestine injury heal

A

intestine injury to crypt cells - heal by regenerating new cells and restore crypt structures
intestine injury to villus atrophy lesions - heal by reestablishing villi structure to improve nutrient absorption

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18
Q

what happens is a dog ingests antifreeze

A
  • ethylene glycol is rapidly absorbed by the GI tract
  • some is metabolized in the liver to a variety of toxic metabolites (including glycolic acid)
  • renal tubular (kidney) damage is caused by production of calcium oxalate crystals
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19
Q

5 factors for management of ethylene glycol toxicity

A
  1. increasing renal blood flow
  2. inhibiting metabolism of ethylene glycol
  3. enhancing the excretion of ethylene glycol
  4. managing the acidosis
  5. give time to allow possible regeneration of tubular epithelium
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20
Q

healing of stable cells in the kidney depending on severity of injury:

A

mild injury - renal tubular epithelial cells will regenerate and normal function will return
moderate injury - repair occurs slowly with regeneration and scarring
severe injury - regeneration of tubular epithelial cells cannot occur, will die from kidney failure

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21
Q

renal tubular cells vs hepatocytes proliferation rate

A

renal tubular cells = proliferate slow, chronic healing phase
hepatocytes = proliferate rapidly, insult will not enter chronic healing phase

22
Q

what is scarring

A

the result of healing by fibrosis - replacement of normal tissue by dense collagenous connective tissue after injury

23
Q

how is scarring different from regeneration

A
  • scarring results in local loss of norma tissue parenchymal cells
24
Q

what are the 2 situations scarring occurs in

A
  1. when regeneration is not possible - injured cells are permanent cells or widespread necrosis has happened
  2. when acute inflammation is not resolved - ongoing tissue necrosis from chronic inflammation
25
Q

5 steps in scar development

A
  1. inflammation and debridement
  2. granulation tissue formation
  3. angiogenesis
  4. collagenization
  5. maturation
26
Q

step 1 or scar development: inflammation and debridement

A
  • hemostatic plug forms at site of injury, allows scaffold for neutrophils to migrate to
  • neutrophils release lysosomal enzymes to liquify debris
  • macrophages debride the area
27
Q

what is debridement

A
  • the cleanup of debris which allows scar formation to occur
28
Q

step 2 of scar formation: granulation tissue formation

A
  • fills the injured area until more mature scar tissue can develop
  • granulation tissue consists of proliferating fibroblasts, newly formed capillaries and some inflammatory cells - highly vascular connective tissue
29
Q

step 3 of scar formation: angiogenesis

A
  • the formation of new blood vessels occurs, mainly by sprouting of new vessels
  • newly formed vessels join up with other vessels to form a new vascular bed
30
Q

step 4 of scar formation: collagenization

A
  • collagen is synthesized by fibroblasts and laid down in the area
  • collagen is the insoluble fibrillary protein which gives the tensile strength of scar tissue
31
Q

step 5 of scar formation: maturation

A
  • granulation tissue is gradually replaced by mature connective tissue
  • content of collagen increases and granulation decreases
  • scar becomes stronger as type I collagen changes to type III and there is increased cross-linking
  • contraction of scar occurs at it matures, decreasing its size
32
Q

what causes contraction of scars in early and later phases

A

early contraction = actomyosin filaments
later contraction = increased collagen

33
Q

what is granulation tissue

A
  • new connective tissue and capillaries that form on the surfaces of a wound during the healing process
  • delays the rate of healing as it prevents epithelium from bridging over the wound
34
Q

how does granulation tissue form

A
  • synthesized by endothelial cells, fibroblasts and macrophages
  • fibronectin also has an important role in its formation
  • chemotactic fibroblasts “organize” endothelial cells Inyo are capillaries
35
Q

composition of normal skin

A
  • comprised of dermis and epidermis layers
  • more superficial epidermis is made of squamous epithelium
  • keratinized layers are continuously being lost and replaced by cells moving up from the basal layer
  • deeper dermis consists of supportive collagen, blood vessels and the adnexa
36
Q

what is the adnexa comprised of

A

hair follicles, sebaceous glands, apocrine glands, sweat glands

37
Q

skin cells are ___ cells

A

liable

38
Q

what is an abrasion

A
  • a scrape, mildest skin injury
  • epidermal cells of the skin are removed
  • basal layers or epidermal cells are not affected, so regeneration occurs from below the abrasion
39
Q

what is laceration

A
  • the result of tearing of tissues, especially over boney surfaces
  • affects the dermis and epidermis
  • minimal loss of basal epidermal cells
40
Q

what is an incision

A
  • a cut of the tissue
  • both epidermis and dermis are affected
  • minimal loss of basal epidermal cells
41
Q

what is a contusion

A
  • a bruise produced by blunt trauma
  • blood vessel damage and hemorrhage into tissue
42
Q

what is avulsion

A
  • the tearing away of a part of skin due to severe trauma
43
Q

what do crush injuries, burns and larger lacerations have in common

A

all cause extensive loss of epidermis

44
Q

what is a puncture wound

A
  • a “stab”, penetration of an object into the skin
  • penetrating wounds cause deep injury to tissues
  • perforating wounds have both entry and exit wounds
45
Q

what is a scab

A

clotted blood and some inflammatory cells that act as a bandage to protect the wound from infectious agents

46
Q

how are scabs resolve

A
  • in small wounds the epidermal cells rapidly grow under the scab to re-establish integrity
  • the scab will separate when the new epidermis retires and starts shedding keratinized layers
47
Q

healing by first intention

A
  • wound edges are brought close together
  • occurs quick and scarring is minimized
  • if sutures are left in too long there is risk of bound infection and scarring increases
48
Q

healing by second intension

A
  • slower than first intension, defect is larger
  • granulation tissue is more prominent than in first intension
  • may result in keloid formation - consists of abnormal nodular masses of collagen
49
Q

factors that influence extent and effectiveness of wound healing

A

nutritional factors: Vit C, protein or zinc deficiency = defective collagen synthesis
drugs: corticosteroids = delayed wound healing
foreign material: necrotic tissue and clots = delay rate of healing
blood supply: if compromised = delayed healing
age: advanced age = less effective wound healing

50
Q
A

PATH (11 decks)

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