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Beatey > tissue repair > Flashcards

tissue repair Flashcards

1
Q

2 ways of restoration of tissue architecture and function after an injury:

A
  1. Regeneration
    Proliferation of residual (uninjured) cells
    Maturation of tissue stem cells
    Returns to normal state
  2. Repair
    When injured tissues incapable of complete restitution, or supporting structures severely damaged
    Laying down connective fibrous tissue
    May result in scar formation
    Although the fibrous scar is not normal, it provides enough structural stability that the injured tissue is usually able to function
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2
Q

Regeneration is:

A

Replacement of damaged tissue with native tissue
1. Labile tissues

Continuously dividing cells
Small intestine or epithelium
Stable tissues

  1. Quiescent cells (G0), but can re-enter cell cycle to regenerate cells when necessary
    slower, but still regenerating
    paechymal cells of solid organs: liver!!! regeneration, kidney, etc
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3
Q

permanant:

A

Permanent tissues
Lack regenerative potential
Repair replaces damaged tissue with fibrous scar
skeletal heart brain

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4
Q

Inflammation:

A

Macrophages play central role in repair

VEG-F promotes angiogenesis

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5
Q

Angiogenesis:

A

New blood vessel development from existing vessels

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6
Q

Formation of granulation tissue

A

Migration and proliferation of fibroblasts, blood vessels and deposition of loose connective tissue (3-5 days)

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7
Q

Deposition of connective tissue

A

Deposition of ECM proteins produced by fibroblasts

Processes orchestrated by locally produced cytokines and growth factors (PDGF, FGF-2, and TGF-β)

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8
Q

Remodeling of connective tissue

A

Myofibroblasts contract scar
dependent on metal ions (zinc) for activity
need Zinc for metalloproteinases to work: otherwise results in weak connective tissue

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9
Q

Repair by Scar: Mechanism

A
  1. Injury induces inflammation, which clears dead cells and microbes (if any)
  2. Formation of vascularized granulation tissue
    Fibroblasts deposit collagen III
    Capillaries provide nutrients
    Myofibroblasts to help contract wound
  3. Scar deposition of extracellular matrix
    Collagenase replaces collagen III with collagen I
    Requires zinc as a co-factor

Type I collagen has high tensile strength and is present in skin, bone, tendons, and most organs

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10
Q

TEST: What is the co-factor for scar deposition of extracellular matrix?

A
  1. Scar deposition of extracellular matrix
    Collagenase replaces collagen III with collagen I
    Requires zinc as a co-factor
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11
Q

Healing by First Intention

A
  1. Inflammation
  2. Proliferation of epithelial and other cells
  3. Maturation of the connective tissue scar
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12
Q

Healing by Second Intention

big ulcer

A
  1. larger Inflammatory reaction more intense
  2. Development of abundant granulation tissue: big ulcer
  3. Accumulation of ECM and formation of a large scar
  4. Wound contraction by the action of myofibroblasts
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13
Q

Fibrosis =

A

=excessive deposition of collagen in internal organs

Heart: fibrosis compromises function

Pathologic process induced by persistent injurious stimuli such as chronic infections and immunologic reactions
Typically associated with loss of tissue
May be responsible for substantial organ dysfunction and even organ failure

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14
Q

most common cause of delayed healing?

A

infection

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15
Q

other causes of delayed healing?

A

foreign body/local, suture

systemic: nutrition: lack of zinc

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16
Q

excessive deposition of collagen in internal organs
Pathologic process induced by persistent injurious stimuli such as chronic infections and immunologic reactions
Typically associated with loss of tissue
May be responsible for substantial organ dysfunction and even organ failure

A

Dehiscence = rupture of wounds

Ulceration = inadequate vascularization

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17
Q

Excessive formation of the components of the repair process

A

Accumulation of excessive amounts of collagen
Hypertrophic scar = excessive collagen confined to wound → localized raised scar

Keloid = scar tissue grows beyond original wound boundary and does not regress
Characterized by collagen type III
Genetic pre-disposition – more common in African Americans
Classically affects earlobes, face, upper extremities

Exuberant granulation tissue
AKA “Proud Flesh”
Protrudes above the level of the surrounding skin and blocks reepithelialization
Must be removed surgical excision to permit restoration of the continuity of the epithelium

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18
Q

2 types of fluid accumulation

A

transudate: few cells, due to increased pressure
exudate: many cells, due to leaky blood vessels, etc

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19
Q

for transudate in lung

A

left side heart build up, congestive heart failure

20
Q

for exudate to build up in lung?

A

infection

21
Q

2 types of fluid accumulations in the lungs:

A

transudate (left side congestive heart failure) exudate infection 2 pulmonary edema

22
Q

effusions happen in:

A

plueral effusion, pericardiacal effusion

23
Q

most important protein in blood regulation of osmotic pressure

A

albumin

24
Q

lack albumin:

A

edema

25
Q

three most important organs associated with edema?

A

heart, liver, kidneys (albumin, sodium)

26
Q

dependent edema?

A

pitting edema in leg

27
Q

ascites:

A

cirrhosis of liver

28
Q

elephantiasis

A

lymphatic liariasis due to w. bancrofti

29
Q

2 types of increased blood flow:

A

hyperemia (active process, more oxygenated blood)

congestion (passive process, impaired outflow from tissue affected region is cyanotic)

30
Q

wherever you have _____ you have ______

A

congestion, edema

31
Q

nutmeg liver is caused by:

A

right side heart failure, backs up into inferior vena cava and cause edema in liver

32
Q

left side of heart failing causes:

A

pulmonary chronic passive congestion: lung edema

33
Q

4 types of hemorrhages:

A

(filling body cavity): hemothorax, hemopericardium, etc

Ecchymoses (bruise) >1-2 cm
Trauma (degradation of hemoglobin: color changes)

Purpura >3 mm hemorrhages
Vasculitides, thrombocytopenias, platelet/clotting coag defects, infections

Petechiae 1-2 Massivemm hemorrhages
skin, mucous membranes, serosal surfaces

34
Q

endothelial cells roll in hemostasis?

A

turn blood on and off

35
Q

sequence of hemostasis:

A

Vasoconstriction: slow down blood
Localized secretion of endothelin (potent vasoconstrictor)

Primary hemostasis
Platelets adhere and become activated
Exposure of highly thrombogenic extracellular matrix

Secondary hemostasis: make fibrin from fibrogen
Activation of coagulation cascade
Exposure of tissue factor, procoagulant factor

  1. Thrombus
    Polymerized fibrin forms solid, permanent plug
    Counter-regulatory process, e.g. t-PA, set in motion t
36
Q

Thrombosis:

A

Inappropriate activation of normal hemostasis

Formation of blood clot (thrombus) in normal vasculature

37
Q

thrombosis is described with:

A

virchow triad

38
Q

top of virchow triad is:

A

endothelial injury, bc artherosclerosis, slowest blood flow in legs, etc

39
Q

important site of thrombosis hyper lamina flow?

A

bifurcation: Turbulence: arterial thrombosis

Disruption of laminar flow

40
Q

patients that ____ are _____

A

smoke hypercoagule

41
Q

arterial thrombosis:

A

Lines of Zahn
Alternating pale layers of platelets with dark layers of trapped RBCs
Imply thrombosis at site of blood flow, i.e. antemortem

42
Q

what steps happen with thrombus?

A

Propagation (obstruction)

  1. Embolization
    Thrombi may dislodge and travel to other sites in vasculature
  2. Dissolution
    Thrombi may be removed by fibrinolytic activity
  3. Organization and recanalization
    Thrombi induce inflammation, fibrosis, and re-endothelialization, ultimately re-establish vascular flow
43
Q

Embolization

A

Detached intravascular solid, liquid, or gas carried by blood to distant site from point of origin
Dislodged thrombi represent 99% of all emboli
I.e. thromboembolism
downstream eschemic necrosis

44
Q

pulmonary thromboembolism originates in:

A

lower leg (usually multiple)

45
Q

systemic thromboembolism originates:

A

heart: can go anywhere

46
Q

Paradoxical Embolism

A

Embolus passes through an intraventricular defect to gain access to systemic circulation

Beatey (4 decks)

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