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504 - Tissue Bio > Lect 4 > Flashcards

Lect 4 Flashcards

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Biology 101 flashcards
1
Q

What is the largest organ in the body?

A

Skin - 16% of body weight

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2
Q

What are the layers of the skin?

A

Epidermis, dermis and hypodermis/subcutaneous layer/fat layer

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3
Q

What are some functions of the skin?

A

To act as a physical barrier against friction, protect against infection, prevention of excessive water loss, regulate temperature, sensation, antigen presentation and wound healing, synthesis of Vitamin D

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4
Q

What is the composition of the epidermis?

A

Aneural and avascular - nourished by the dermis and made up mostly of keratinocytes and melanocytes, DCs and merkel cells

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5
Q

What is the main function of the epidermis?

A

To protect from external environment including UV and chemicals, to insulate us and prevent loss of water and electrolytes and sense tough, pain and heat

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6
Q

What are the layers of the epidermis?

A

Stratum basale, stratum spinosum, stratum granulosum, stratum lucidum and stratum corneum

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7
Q

What is in the stratum basale layer of the epidermis? And where is it located?

A

Basal layer Located just above dermis – contains prolifering and non-prolifering keratinocytes, and melanocytes and merkel cells (sensory)

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8
Q

What is the stratum spinosum of the epidermis?And where is it located?

A

Spinuous layer located between stratum basale and stratum granulosum – contains kertainocytes through desmosomes that produce lipids to exocytose into granular layer, DCs present here

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9
Q

What is the stratum granulosum layer of the epidermis and where is it located?

A

Granular layer located between the stratum spinosum and the stratum lucidum – keratinocytes fill themselves with keratin protein - loss of nuclei and cytoplasm appears granular, lipids in keratinocytes are released into extracellular space through exocytosis to form lipid barrier

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10
Q

What is the stratum lucidum layer of the epidermis and where is it located?

A

Translucent layer only on palm and sole that contains 3-5 layers of dead keratinocytes – between stratum granulosum and stratum corneum

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11
Q

What is the stratum corneum layer of the epidermis and where is it located?

A

Cornified layer is located on very outside with 10-30 layers of cornocytes (fully differentiated dead cells) enveloped in water retaining keratin proteins and lipids

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12
Q

What are cornocytes?

A

Full differentiated dead keratinocytes

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13
Q

How long does it take to renew skin cells from basale to corneum?

A

~1 month

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14
Q

What is the dermis made up of?

A

A thick layer of fibrous and elatic connective tissue made up of collagen, elastin and gibrillin to give skin flexibility and strength made up of fibroblasts, macrophages and adipocytes

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15
Q

What is the main function of the dermis?

A

Nerve endings for sensation, sweat glands for thermoregulation, sebaceous glands to secret sebum to keep skin moist and blood vessel to regulate body temperature and provide nutrient

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16
Q

What are the other names for the subcutaneous layer?

A

Hypodermis, superficial fascia or fat layer

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17
Q

What is the hypodermis made up of?

A

A layer of fat that is contained in living fat cells held together by fibrous tissue – varies in thickness throughout body – consists primarily of loose connective tissue and lobules of fat and contains larger blood vessels and nerves than found in dermis, made up of fibroblasts, adipose cells and macrophages

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18
Q

What is the main functions of the hypodermis?

A

Serves to fasten skin to underlying surface, provide thermal insulation, absorb shocks from impact and used as energy source

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19
Q

Why are infants and elderly more susceptible to the cold?

A

They have less subcutaneous fat

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20
Q

What is the purpose of performing subcutaneous injections?

A

Highly vascularized so allows for greater absorption

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21
Q

What is a wound?

A

A disruption in the normal anatomic structure and function

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22
Q

What is acute vs chronic?

A

Acute - when wounds progress through orderly and timely healing process that restores anatomic continuity and function
Chronic - slow healing impairment lasting more than 3 months

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23
Q

What are the types of open wounds?

A

Abrasions, incisions, lacerations, puncture wounds

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24
Q

What is an abrasion?

A

When the epidermis is scraped off and wound is superficial

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25
Q

What is a laceration?

A

An irregular tear-like wound caused by blunt trauma

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26
Q

What are types of closed wounds?

A

Contusions and hematomas

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27
Q

What is a contusion?

A

AKA a bruise – blunt force trauma damaging tissue under skin

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28
Q

What is a hematoma?

A

Damage to a blood vessel that causes blood to collect under skin

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29
Q

What is the holy grail of types of wound healing?

A

Regenerative which is ideal healing (cosmetic healing) - leads to full restoration of structure and function

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30
Q

What is the next best thing to regenerative healing? ANd what is a tissue example?

A

Partial regeneration – liver is an example that can regenerate up to 70% of itself without eschar

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31
Q

What do most wounds heal by?

A

Acute healing - acceptable healing - associated with eschar - gives so thickened epidermis, contraction, eschar and fibrosis and loss of hair follicles

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32
Q

What are two dangerous types of healing? and what are some examples?

A

Excessive where there is too much fibrotic tissue and chronic where it is stuck in inflammation – excessive examples are keloid and contracture can lead to loss of function with outgrowth of scar tissue, diabetic foot ulcer or pressure ulcer are examples of chronic

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33
Q

What is the type of healing that is stuck in the inflammatory phase?

A

Chronic

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34
Q

What is eschar?

A

Disorganized extracellular matrix, mainly collagen

35
Q

What are the 4 stages of acute healing?

A

Hemostasis, inflammation, proliferation, and remodeling

36
Q

Is the inflammatory response larger in regenerative healing or scar–associated healing?

A

Scar associated

37
Q

Which cytokines are upgredulated in skin over mucosa?

A

TNFalpha, IL1alpha and beta, TGFalpha and beta

38
Q

Which cytokine can enhance regenerative healing?

A

IL-1

39
Q

What happens in hemostasis of acute healing and when?

A

Limiting blood loss – constriction of vessels - There is a temporary seal placed over wound, provisional matrix is laid down for cellular migration and platelets respond by releasing chemokines and growth factors to attract leukocytes and stick to blood vessels to form platelet plug, bibrin clot – immediately after injury, up to a few hours

40
Q

What is the main function of the inflammation phase of acute healing?

A

Destroy invading pathogens and jumpstart healing through inflammatory cytokines and growth factors - early and late phases

41
Q

What happens in the early inflammatory phase of acute healing? and when?

A

Lasts 1-2 days after injury - activation of complement to control infection and to draw neutrophils by C5a - platelets release chemokines and growth factors, neutrophils combat invading pathogens

42
Q

What are PMNs?

A

Neutrophils

43
Q

What happens in the late inflammatory phase of acute healing and when?

A

Begins 24-48 hours after injury and lasts about a week - monocytes attracted to wound by chemoattractants from early inflammatory stage - monocytes mature into macrophages and destroy invading pathogens, release cytokines to recruit fibroblasts, keratinocytes and endothelial cells to help with repair, promote angiogenesis, release proteolytic enzymes like collagenase, initiate inflammatory resolution by clearing apoptotic cells

44
Q

What are M1 type macrophages?

A

Killers that produce nitric oxide form arginine

45
Q

What are M2 type macrophages?

A

Involved in repair and healing and produce ornithine from arginine – lousy in fending off pathogens

46
Q

What happens in the proliferative phase of acute healing and when?

A

About 3 days after injury and lasts for 2-3 weeks - fibroblasts migrate to wound in response to chemoattractants and produce ECM – provisional matrix is replaced by granualation tissue – angiogenesis continues and epithelial cells close wound (re-epithelization)

47
Q

What happens in the remodeling phase of acute healing and when?

A

Begins 2-3 weeks after injury and lasts for year or more – most enodthelial cells, monocytes and fibroblasts exit wound or under apoptosis and matrix matures as type I collagen is layed down to give increased wound strength – tissue never regains properties of uninjured skin

48
Q

What cell type has an unknown function in wound healing?

A

Lymphocytes

49
Q

What cell types are important in inflammation stages?

A

Neutrophils and marophages

50
Q

What cell types are important in proliferation?

A

Fibroblasts

51
Q

What recognizes the inflammatory response?

A

PRRSs Pattern recognition receptors

52
Q

What is the function of clot formation?

A

To prevent blood loss, establish provisional matrix and jumpstart inflammation

53
Q

What are the steps in clot formation?

A

Platelet adhesion - interaction with Von Willebrand Factor and exposed cartilage
Platelet activation - plateletes change shape after binding to collagen and release signaling molecules like Thromboxane A2 and chemokines
Platelet aggregation - deformed platelets stick together and form plug like chewing gum “temporary seal”
Coagulation - fibrin strands keep platelet plug together in meshwork that can withstand blood flow

54
Q

What does Thromboxane A2 do?

A

Recruits more plateles

55
Q

What is the intrinsic pathway of coagulation?

A

Platelet aggregation leads to Factor XII –> Factor XI —–> Factor IX) –> Factor X –> Prothrombin –> Thrombin –> fibrin crosslinking

56
Q

What is the extrinsic pathway of coagulation?

A

Tissue damage leads to Factor VII –> Factor X –> prothrombin –> Thrombin –> fibrin crosslinking

57
Q

What is the common factor in the intrinsic and extrinsic pathway of coagulation and what class of enzymes are the factors?

A

Factor X – and they are serine proteases

58
Q

How do tissues prevent excessive coagulation?

A

Coagulation inhibitors such as anti-thrombin III and fibrinolysis by enzymes that degrade fibrin like plasmin

59
Q

What makes up the response mechanism of a neutrophil?

A

3 waves with 4 receptors to recognize damage or bacterial product

60
Q

How do neutrophils kill pathogens?

A

Directly using degradative enzymes and by ROS inside phagolysosomes – Indirectly by antimicrobial peptides

61
Q

What are AMPs?

A

Antimicrobial peptides - used indirectly to kill pathogens by neutrophils – they are natural antibiotics that come in cationic (primary), anionic, and neutral forms and work by pore formation

62
Q

How are inflammatory cells drawn into injured tissues during inflammatory phase?

A

PAMPs, MAMPs, or DAMPs are recognized by PPRs or TLRs leading to cytokine and chemokine production - complement C5 isactivated and growth factors serve as chemoattractants

63
Q

Are PRRs membrane bound?

A

Can be membrane associated like TLRs or soluble like NODs

64
Q

What is the general structure of a TLR?

A

Extracellular portion contains a leucine rich repeat LRR

Cytoplasmic regions have TIR domain needed for signaling ~200AA

65
Q

What family do TLRs belong to?

A

IL-1Rs

66
Q

What is the TLR signal transduction response?

A

TLR receptor binds to PAMPs, CD14 and LBR leading to activation of cascade which can give proinflammatory cytokine response from NFkB or Type I interferons from IRF3

67
Q

Besides the PRR what else must be activated in order to get inflammatory response?

A

Inflammasome

68
Q

What are the two inflammasome pathways?

A

Canonical which activates caspase 1 and non-canonical that activates caspase 11 to directly interact with LPS in mice

69
Q

What releases growth factors and what do they signal to?

A

Injured cells, platelets, macrophages all signal for growth factors that recruit endothelial cells to produce wound healing by angiogenesis and epithelialization

70
Q

What are MMPs?

A

Matrix metalloproteinases that are inc dependent and are enzymes that come to degrade debris and remove provision matrix to allow for growth of ECM for cells to be able to move on

71
Q

What is the proccess of re-epithelization?

A

Closure of the wound borders when monocytes, platelets and keratinocytes produce EGF and TGF-alpha that induce cell migration to move into denuded area and cover wound surface

72
Q

What is the pyramid growth pathway of getting bacteria into a wound?

A

Contamination, colonization, infection both local and invasive and septicemia

73
Q

What do pathogenic bacteria have that allows them to colonize easier and what do they produce to protect themselves?

A

Virulence factors and form biofilm

74
Q

What is a common in vitro assay to study wound healing?

A

Scratch assay across cells using pipette tip to see if cells come back together, advantage is that it is simple, affordable and convenient but disadvantages is that it lacks complexity and physiological relevance

75
Q

What is a common ex vivo assay to study wound healing?

A

Using cartilage explant – advantage of being simple and convenient and more physiologically relevant, but disadvantage is that it still lacks complexity and tissues are harder to come by

76
Q

What is a common in vivo model of wound healing?

A

Drosophila embryos, mice and porcine – more expensive and time consuming but more physiologically relevant

77
Q

What is debridement?

A

Removal of hyperkeratotic epidermis (callus) or necrotic dermal tissue, foreign debris and bacterial element from wound

78
Q

How can wounds be treated?

A

Wound dressing, pressure off loading, revascularization by surgery, management of injection by antibiotics, and adjunctive treatments including growth factors, skin substitutes, electrical stimulation, etc.

79
Q

What is the shared common characteristic of all chronic wounds?

A

An abnormal wound environment with persistent and un-resolving inflammation

80
Q

Why do chronic wounds not heal?

A

Deficient growth factors, unresponsive or senescent cells, bacterial interference and inflammatory environment

81
Q

What are biological markers for chronic wounds?

A

Excessive infiltration by neutrophils - bacterial environment and excessive ROS - increased protease activity - MMP activity elevated

82
Q

What is a model of diabetic mice?

A

STZ for T1D and db/db for T2D – mimic ulcer conditions – T2D ulcer size remained the same over controls – diabetic skin harbors more bacteria on tissue

83
Q

Why can’t diabetic wounds control infection?

A

Phagocytic leukocytes are impaired (neutrophils and monocytes) and antimicrobial peptides (AMPs) are reduced – delayed inflammatory response at which point bacteria have already entered and formed biofilm – leading to greater infection by pathogens, allowing colonization and exacerbation of wounds and inhibition of cartilage deposition

504 - Tissue Bio (8 decks)

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