L14- Tissue Repair and Pathologic Calcification Flashcards Preview

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Flashcards in L14- Tissue Repair and Pathologic Calcification Deck (34):

define labile tissues, name some examples

-cells are continuously being lost and replaced by tissue stem cells
-possibly controlled by GFs (ex. CSF)
-Ex: intestinal epithelium (crypt cells), epidermis, hemopoietic cells


define stabile tissues, name some examples

-cells are in Go phase
-no stem cells
-if injured, cells have ability to replicate (Go --> G1)
-Ex: liver, kidney, pancreas, endothelial cells, fibroblasts, SM cells


define permanent tissues, name some examples

-cells are terminally differentiated, no ability to divide
-healing in organs => scar formation
-Ex: cardiac myocytes, brain (glial cell proliferation, no scar)


list the conditions where a tissue would heal with scar formation

-extensive injury (any tissue)
-injury to permanent tissue
-undrained pus (ex. abscess)
-foreign body
-some infectious agents


list the 4 steps of scar formation

1) maintenance of hemostasis- stops bleeding
2) inflammation- clears invaders
3) cellular proliferation- epithelial cells, endothelial cells, fibroblasts
4) tissue remodeling


The 3rd step of scar formation involves the proliferation of the following cells... (include function)

1) epithelial cells- to cover wound area
2) endothelial cells- angiogenesis (new BVs-- supplies nutrients for new cell formation)
3) fibroblasts- ECM formation (collagen III --> I)
-all contribute to granulation tissue


Gross appearance of granulation tissue: (1)

Microscopic appearance: (2)

1- pink, soft, granular appearance
2- fibroblasts, many thin-walled (new) and delicate capillaries, loose ECM (type III collagen) ----- mixed with inflammatory cells (macrophages mainly)


Angiogenesis occurs in response to (1), (2), (3); In (3), (4) is produced to enhance angiogenesis.

(NOTE- in adults)
1- tissue repair (following injury)
2- tumors
3- ischemia
4- VEGF (vascular endothelial growth factor)


list the 7 steps of angiogenesis

1) vasodilation (+ inc vascular permeability, NO mediated)
2) EPC recruitment to injury site (endothelial precursor cell)
3) capillary sprout formation (VEGF)
4) endothelial cell proliferation behind sprout
5) canalization => lumina formation
6) periendothelial cell recruitment
7) endothelial cell proliferation inhibition


Deposition of CT is also called (1). It starts with the (2) of fibroblasts at site of injury and then (3). Some fibroblasts will (4) in order to (5). (1) is followed by (6) and (7).

1- fibroplasia
2- migration and proliferation
3- deposition of ECM
4- differentiate into Myofibroblasts
5- close the wound
6- BV regression
7- scar contraction


(1) is the most important CK involved in fibroplasia as it is involved in the synthesis and deposition of (2); it is generated by (3) cells. (4) and (5) are CKs that are also involved in fibroplasia.

1- TGF-β (transforming GF)
2- CT tissue proteins
3- cells of granulation tissue (fibroblasts, endothelial and epithelial precursors) + M2 macrophages
4- PDGF (platelet derived GF)
5- FGF-2 (fibroblast GF)


how is tissue remodeling controlled

-Collagen + other ECM components are in a continuous state of synthesis and degradation (MMP enzyme)
-must be controlled to withstand mechanical stresses
(Type III collagen --> Type I collagen --> collagen cross-linking [simultaneous with collagen formation and degradation])


cutaneous wound healing can occur either through (1) or (2). (2) has the following steps: (3)

1- regeneration (1st intention)
2- scar formation (2nd intention)
3- hemostasis --> inflammatory phase --> proliferative phase --> remodeling phase


list the steps of the proliferative phase of scar formation in cutaneous wound healing

(3rd step of scar formation- the 2nd intention of skin healing)
-keratinocyte migration
-keratinocyte proliferation
-keratinocyte differentiation --> into stratified squamous epithelium
-reconstitution of basement membrane


In the remodeling phase of scar formation in cutaneous wound healing, the scar becomes stronger because of (1) and (2) after synthesis of (3) discontinues. The tensile strength of scar reaches up to (4)% of it original strength.

1- excessive collagen synthesis
2- structural modifications of collagen fibers (cross-linking, inc fiber size)
3- collagen
4- 80%


healing by first intention (of cutaneous wound) occurs with injury that only involves...

epithelial layer- main repair mechanism is epithelial regeneration

ex- clean surgical incisions, edges have been approximated by sutures (minimizes area of granulation and therefore area of scar formation)


healing by first or second intention is also called....

healing by primary or secondary union


healing by second intention (of cutaneous wound) differs from first intention healing by the following characteristics...

-larger clot --> more granulation tissue
-wider wound gap (healing involves contraction to approximate the edges)
-more inflammation b/c more necrotic tissue and possible bacterial contamination


list the local factors that can slow wound healing

-infection (=> persistent inflammation)
-poor blood supply
-excessive movement
-presence of foreign material


list the systemic factors that can slow wound healing

-nutritional status
-drugs (i.e. steroids inhibit fibrous tissue formation)
-co-morbidities (i.e. DM, cancer)


extensive scar formation (wound healing) results in...

-keloid formation**
-hypertrophic scar**


deficient wound healing results in.....

1- chronic ulcer: healing locked in inflammatory phase
2- weak wound, therefore edges separate (called scar dehiscence)


list the phases of bone fracture healing

-hematoma formation (+ granulation tissue)
-immobilization by callus formation (cartilage --> bony)
-repair of the fracture gap


list some complications that can arise in bone fracture healing

-delayed union (delayed ossification after fibrous union)
-mal-union (healing with angulation)


fracture sites are usually (1), so infections only occurs is (2) or (3) happens

1- sterile
2- communication with skin (open fracture)
3- insertion of device for fixation


list the local factors that influence bone fracture healing

-excessive mobility
-interposition of muscles


list the systemic factors that influence bone fracture healing

nutrition of specific substances: i.e. VitC deficiency (necessary for collagen formation)


Pathologic calcification is when Ca salts deposit in tissues that aren't (1) or (2). Ca2+ can accumulates in the (3) of dying cells. Ca salts appear as (4) in H&E stains.

1- bones
2- teeth
3- mitochondria (membrane damage)
4- deeply basophilic (purple), irregular, granular


list the two types of pathologic calcification



Dystrophic calcification is characterized by Ca-salt deposition in (1) and with (elevated/normal/low) serum Ca. This occurs because the accumulation of (3) in (1) tissue binds with (4), which reacts with Ca ions to create (5). Examples include the following: (6).

1- necrotic or degenerated tissue (expected whenever cell injury/death occurs)
2- normal serum Ca (elevated in metastatic)
3- denatured proteins
4- phosphate ions
5- Ca-PO4 precipitate
6- deformed valves, atherosclerotic coronary arteries, breast tissue after trauma, healing granulomas, necrotic cancer cells


Metastatic calcification is characterized by Ca-salt deposition in (1) and with (elevated/normal/low) serum Ca. (2) can occur due to (3) or (4). Common areas of deposition include: (5).

1- apparent normal tissue
2- elevated (hypercalcemia- normal in dystrophic)
3- excess bone metabolism => inc Ca
4- excess Ca absorption in the gut
5- gastric mucosa, skin, kidneys, + everywhere


list some causes of metastatic calcification

(Note- same as the causes of hypercalcemia)
-renal failure
-vitD intoxication
-tumors: via PTH secretion OR metastasis to bone
-milk alkali syndrome
-prolonged immobilization


in scar formation, type (1) collagen is converted to type (2) collagen which will then undergo extensive (3)

1- type III (scaffolding), granulation tissue
2- type I, scar formation
3- cross-linking
Note- new BVs undergo regression


compare keloid with hypertrophic scar

-Both are excessive collagen deposition --> raised scar
-Keloid: beyond wound margins --> malignant potential
-Hypertrophic Scar: within wound margin --> no malignant potential