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Patho I > Powerpoint-Chap3 > Flashcards

Powerpoint-Chap3 Flashcards

1
Q

What happens in wound healing

A 
angiogenesis
acute inflammation
fibrobast and parenchymal regeneration
ECM proteins
scar formation
remodeling of parenchymal elements
remodeling CT
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2
Q

What layer is critical for regeneration and restoration of tissue

A

the ECM

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3
Q

What parts of our body can completely regenerate

A

epidermis, GI tract, epithelium and the RBCs

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4
Q

does the liver truly regenerate

A

no, compensatory hyperplasia

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5
Q

what is the term resolution when talking about wound healing

A

complete restoration to original function

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6
Q

What are labile cells

A

continuously dividing cells from M to G1 to S to G2 to M

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7
Q

what are types of labile cells

A

epidermis, mucosal epithelium, GI epithelium and stel cells

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8
Q

what are stable cells

A

low level replication

Go to G1 to S to G2 to M

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9
Q

what are types of stable cells

A

hepatocytes, renal tubular epithelium, pancreatic acini

stem cells

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10
Q

what is the proliferative potential of permanent cells

A

almost never divide, stuck in Go

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11
Q

what are examples of permanent cells

A

CNS neurons, cardiac and skeletal myocytes

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12
Q

What is a totipotent stem cell

A

very early embryonic

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13
Q

what is a pluripotent stem cell

A

in embryo- embryonic stem cell

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14
Q

what is a multipotent stem cell

A

in fetus and adult

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15
Q

what is a progenitor or lineage committed stem cell

A

closer to final destination

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16
Q

what is an induced pluripotent stem cell

A

embed nucleus of differentiated cell into cytoplasm of oocyte

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17
Q

What stem cell can make the placenta and fetal membranes

A

the totipotent

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18
Q

What is transdifferentiation

A

non stem cell transforms into different cell type

already differentiated stem cell creates cells outside already established differentiation path

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19
Q

what is transduction

A

genes from a host cell (bacterium) are incorporated into genome of bacterial virus (bacteriophage) and then carried to another host

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20
Q

what are the stem cells in skel m

A

satellite cells

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21
Q

what are the stem cells of GI tract

A

crypt cells

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22
Q

what are the stem cells in liver

A

oval cells

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23
Q

what layer are the stem cells of epidermis in

A

the basement membrane

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24
Q

where are the corneal stem cells

A

limbus

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25
Q

what factors influence regeneration

A

cell-cell interaction, conditioned medium, contact inhibition
Growth Factors
ECM

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26
Q

what are the 2 major components of the ECM

A

laminin and fibronectin

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27
Q

what are the parts of laminin

A

epithelia and fibroblasts

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28
Q

what are the parts of fibronectin

A

epithelia and fibroblasts

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29
Q

What are the 3 ways in which cells communicate

A

paracrine, autocrine, and endocrine

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30
Q

describe paracrine signaling

A

short term, local effects

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31
Q

what is autocrine signaling

A

cells tell themselves to do things

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32
Q

What is the role of platelet derived growth factor

A

activates fibroblasts, sm m, monocytes

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33
Q

what is the role of fibroplast growth factor

A

mitogenic fo rmost msesnchymal cells and induces endothelial cells to release proteolytic enzyme
important in scar formation

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34
Q

what is the role of epidermal growth factor

A

mitogenic for epithelial cells, fibroblasts, glial cells and SMC

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35
Q

what is the role of transforming growth factor

A

alpha is the same as epidermal growth factor

beta acts as a growth stimulator OR inhibitor

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36
Q

what is the role of VEGF

A

angiogenesis

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37
Q

what are the roles of IL 1 and TNF

A

induce fibroblast proliferation and collagen synthesis

TNF can also stimulate angiogenesis

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38
Q

What factor has a role in cachexia

A

TNF

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39
Q

What are the main growth factors for monocyte chemotaxis

A

FGF and TGF beta

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40
Q

what is keratinocyte growth factor

A

from fibroblasts and stimulates keratinocyte migration, proliferation and differentiation

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41
Q

What type of things stimulate G protein coupled receptors

A

odorants, light R

proteins, lipids, amines etc

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42
Q

What are the components of the ECM

A

collagen, elastin, proteoglycans, adhesive glycoproteins, integrins

43
Q

what is the baseline structure for physical stress

A

elastin

44
Q

what is the function of proteoglycans in ECM

A

help regulate ECM structure and permeability
modulate cell growth and differentiation
maintain cell morphology

45
Q

what is the function of adhesive glycoproteins

A

induce fibronectin, laminin and vitreonectin

link ECM components to cells via cell surface integrins

46
Q

what is the role of integrins in ECM

A

cell surface R that mediate adhesion of cells to ECM

47
Q

What collagen makes up the basememnt membrane

A

collagen IV

48
Q

what type of collagen makes up cartilage

A

type II

49
Q

what collagen is involved in repair

A

collagen III

50
Q

what connects hyularonidase to cell surface

A

CD44

51
Q

what does granulation tissue look like on slide

A

soft, pink and granular
many fibroblasts
alot of new thin-walled capillaries

52
Q

what is a granuloma

A

chronic inflammatory response (macrophages, multinucleate giant cells)

53
Q

what do fibroblasts make

A

collagen
first type III then I
resulting in fibrosis with CT

54
Q

what is a 1st intention or 2nd intention wound

A

1st can be closed because not too wide- can be approximated

2nd- leaves much larger scar, have to leave open, sometimes b/c size or infection already there and needs to drain

55
Q

What are the steps of angiogenesis

A

proteolytic degradation of BM
migration of endothelial cells
proliferation of endothelial cells
maturation

56
Q

What cells begin angiogenesis

A

endothelial precursor cells from the bone marrow and preexisting vessels

57
Q

What agents can induce angiogenesis besides VEGF

A

hypoxia, TGFbeta, PDGF, TGF alpha

58
Q

Which is the VEGF receptor for lymphatic endothelial cells

A

VEGFR-3

59
Q

How do the tip cells talk to the cells behind them

A

there is negative feedback through notch signaling to say stop replicating so the blood vessels growth in one direction

60
Q

What is the role of DLL4 in angiogenesis

A

dec sprouting, dec EC proliferation

inc vessel size and organization

61
Q

what does VEGF drive

A

increase sprouting, EC proliferation and survival, decrease vascular organization

62
Q

What is the role of granulation tissue in wound healing

A

anti-infection and protecting the wound surface
filling incision and wound
replacing necrotic tissue, effusion and other foreign body
vessels provide conduit for nutrients and cells

63
Q

What are the characteristics of scar tissue

A

pale avascular tissue

collagen, fragments of elastic tissue, ECM and inactive fibroblasts

64
Q

What are the advantages of scar tissue

A

resilient permanent patch

tensile strength, integrity and strength for tissue after healing

65
Q

what are the actions of macrophages

A 
debridement, removal injured tissue
antimicrobial
chemotaxis
fibroblasts
angiogenesis
deposition of ECM
66
Q

what factors from macrophages are released for matrix synthesis

A

TGF, EGF, PDGF, cytokines:TNF IL1 and IFNgamma

67
Q

What is primary union of skin

A

healing by first intention

surgical incision with sutures, surgical glue

68
Q

when do cells mirgrate into healing by first intention

A

24 hours

69
Q

when does regeneration start in healing by first intention

A

3 days

70
Q

when is the scar present in wounds by first intention

A

7-10 days

71
Q

how long can it take for a scar to mature in a wound by first intention

A

1 month-2 years

72
Q

what is involved in early scarring

A

capillaries bridge wound, lymph vessels near, macrophages scavenge, collagen type I, apoptosis
cross-linking of collagen (pink to white transition)

73
Q

inflammation of wound peaks on what time scale

A

about a day

74
Q

when is majority of matrix deposition taking place on wound healing time scale

A

about 3 days

3-10

75
Q

what cells are proliferating through skin healing

A

epithelial and fibroblasts

76
Q

what seals the wound by second intention

A

fibrin

77
Q

What stimulates collagen synthesis in scarring

A

TNF IL1 IL4 IL13

from macrophages

78
Q

what is the role of metalloproteinases

A

break down the collagen

79
Q

what are conditions that interrupt healing process

A 
vit deficiency
glucocorticoids
immune status
infection
DM
80
Q

what is wound dehiscence

A

separation of layers of surgical wound

sutures break

81
Q

what are healing abnormalities

A

contractures
cicatrization
pyogenic granuloma

82
Q

What are keloids

A

excessive scar formation

83
Q

what the most common cause of wound contracture

A

burns

84
Q

what is the difference between hypertrophic scar and keloid

A

if scar is confined to area that is wounded- hypertrophic scar

85
Q

what goes up in liver obstruction

A

all the liver enzymes. In addition- specifically bilirubin

86
Q

widened chest and decreased tissue in lung is clinical key to what

A

emphysema

87
Q

in heaptic necrosis what will a liver profile show

A

increased liver enzymes

88
Q

Increased TLC and RV

decreased FEV1 is indicative of what

A

emphysema

89
Q

why is a liver nodular if Px has hepatitis

A

normal architecture destroyed, hepatocytes regenerating forming nodules

90
Q

What is a PAS stain used for? what color is it

A

to see fibrosis, glycogen
with diastase- to digest away glycogen
dark red

91
Q

how do we stain for alpha 1 antitrypsin

A

using immunohistochemistry to make Ab for antigen. Then Ab to Ab that has brown chromogen

92
Q

which type of genotype causes worst version of alpha1 antitrypsin deficiency

A

ZZ homozygous

93
Q

If you have a null alleles for a1 antitrypsin would the immunohistochem work

A

no because wouldn’t have any of it

94
Q

where do abnormally folded proteins build up in cells, and what is the net result

A

in the ER.

causing ER stress- signaling cytochrome C– apoptosis

95
Q

what results from the ER trying to degrade misfolded proteins

A

oval cytoplasmic globular inclusions

hepatocellular degeneration, giant cell formation, cholestasis, cholangitis, cirrhosis

96
Q

When ER releases contents what ion is important

A

Ca because that is activating all the phospholipases and everything starts degrading

97
Q

what cell is mainly responsible for the scarring in hepatitis

A

macrophages

98
Q

The development of regenerative nodules in liver can lead to what

A

DNA damage and neoplasia

99
Q

What is scarring of liver called

A

cirrhosis

100
Q

why does a1antitrypsin lead to emphysema

A

walls of alveoli destroyed because of increased secretion of elastase.
missing SA so causing hypoxia. also have fibrosis

101
Q

how does a1antitrypsin deficiency cause fat necrosis

A

elastase break down skin and fat

102
Q

What are Tx methods for a1antitrypsin deficiency

A

IV alpha1 antitrypsin and NSAIDs

103
Q

with alpha1 antitrypsin deficiency and a FEV1 below 20% predicted what is the 2 year mortality

A

40%

104
Q

With liver cirrhosis and alpha1 antitrypsin deficiency what is mean survival

A

2 years

Patho I (6 decks)

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