Skin Microbial Interactions and Wound Healing Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

When do skin microbial diseases arise?

A

Opportunity (e.g. wound)

Population imbalance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What prevents bacterial penetration to the dermis?

A

Keratinisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Within the dermis, where is the site of bacterial colonisation?

A

Sweat glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does gland secretions contain?

A

Slightly acidic sweat from the sebaceous glands

Anti-microbial peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which layer of bacterial penetration causes illness?

A

Hypodermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give an example of a disease associated with hypodermal bacterial entry

A

Necrotizing fasciitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes necrotizing fasciitis?

A

bacteria from soil enters the skin through through a deep wound and colonises in the hypodermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the immune defences in the epidermis?

A

Langerhan cells
Keratinocytes
CD8+ T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of keratinocytes in association with immune defence?

A
  • Possess Toll like receptors
  • Detect pathogen
  • Release cytokines to induce Langerhan’s and T cell movement to site of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the immune defences in the dermis?

A

Dermal dendritic cells
Macrophages
Innate lymphoid cells (ILC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the function of the innate lymphoid cells?

A

Orchestrate immune responses among T cells and can suppress attack of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three phases of wound healing?

A

1) Inflammatory phase
2) Proliferative phase
3) Remodeling phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens in the inflammatory phase?

A

Release of inflammatory cytokines to promote chemotaxis

Accumulation of pus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What promotes growth?

A

Mitogenic

Epithelial growth factor (EGF) - growth of fibroblasts and keratinocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do fibroblasts do in relation to the inflammatory phase?

A

Cause scaring through collagen and connective tissue deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do keratinocytes do in relation to the inflammatory phase?

A

Recreate the epidermal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of IL-6 in the inflammatory phase?

A

Induce fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the proliferative phase

A
  • Epithelization
  • Angiogenesis in the dermis
  • Fibroblast proliferation in the dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is epithelialisation?

A

Growth and division of epithelial cells from the stratum basale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is angiogenesis?

A

Production of new blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why is fibroblast proliferation important in the proliferative phase?

A

Deposit collagen into the dermis which provides a supportive matrix for epidermal keratinocyte growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do fibroblasts produce?

A

Dermal granulation tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does dermal granulation tissue consist of?

A
  • main signals are PDGF and EGF
  • collagen type III
  • Glycosaminoglycans
  • Fibronectin
  • Elastin fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What induces fibroblasts?

A

TGF-beta1

25
Q

What happens in the remodeling phase?

A
  • Scaring
  • Collagen reorganisation
  • Cross linking of collagen
26
Q

What causes scaring?

A

The conversion of type III collagen to type I

27
Q

Why is there cross linking of collagen?

A

Increase tensile strength

28
Q

What local effects affect wound healing?

A
Oedema 
Ischemia - perfusion of the wound 
Impaired healing 
Infection 
Foreign bodies
29
Q

where is beta-defensin secreted from?

A

All epithelial cells

- in the skin = keratinocytes and sebaceous duct cells

30
Q

What are defensins?

A

anti-microbial peptides

31
Q

what are defensins involved in?

A

Innate immune response mechanism

32
Q

How do defensins function?

A

Permeabilise bacteria outer wall causing lysis

33
Q

Give an example of a ‘good’ bacteria

A

Staphylococcus epidermidis

34
Q

Describe the function of staphylococcus epidermidis in terms of prevention of disease

A

has mechanisms for host immune invasion

resists harmful yeast and bacteria colonisation

35
Q

Give an example of a ‘bad’ bacteria

A

Staphylococcus aureus

36
Q

name a pathogen associated with staphylococcus aureus

A

MRSA

37
Q

how does the staphylococcus aureus function?

A

will colonise human skin, lung and gut.
opportunistic pathogen
causes boils and abscesses

38
Q

give 2 examples of what staphylococcus aureus secretes?

A

Coagulase (blood clots)

Lipase (degrades protective sebaceous oils)

39
Q

What is an infection caused by staphylococcus aureus

A

folliculitis

40
Q

How does the infection of follicultis arise?

A

Staphylococcus aureus invades down the shaft of the hair follicle
Causes inflammation and infection of the hair follicle and sebaceous gland.

41
Q

What is quorum sensing?

A

Homeostatic mechanism involving released peptide signals that keep bacterial populations stable

42
Q

what peptide signals do quorum sensing detect?

A

Autoinducer peptides

43
Q

What happens when there is a low concentration of s. epidermis?

A
Decrease the amount of inducer peptides 
Causes phosphorylation of the ArgC 
Activation of ArgA 
Growth and cell division 
Increase the concentration of s. epidermis
44
Q

What happens if you get a s. aureus infection?

A

Autoinducer peptides inhibit ArgC resulting in cell death

45
Q

Give an example of a fungal inhabitant of the epidermis

A

Malassezia - causes dandruff

46
Q

What is malassezia function

A

Secretion of phospholipase

Cleaves sebum lipids to inflammatory signals (e.g. arachidonic acid)

47
Q

how does malassezia alter skin epithelial function?

A

Synthesise anti-bacterial compounds from skin amino acids and peptides
Modifies keratinocyte sensitivity to UVA damage
Inhibits melanin production
Inhibits langerhans cell immune signalling

48
Q

Where is acne bacteria found?

A

dermal pores and hair follicles

49
Q

Where is the acne nutrient source from?

A

Sebum

Shed keratin

50
Q

where does the acne bacteria proliferate in?

A

The sebaceous gland

51
Q

how does the pustule head of acne form?

A

The proliferation in the sebaceous gland causes swelling of the lumen of the gland
this lumen filled with bacteria
the bacteria moves all the way up through the epidermsi

52
Q

how is sebum produced?

A

holocrine secretion

53
Q

What prevents acne?

A

Isotrentoin

54
Q

How does isotrentoin prevent acne?

A

inhibits sebaceous holocrine secretion

55
Q

Possible cause of acne

A

genetic condition involving failure of cell polarisation

56
Q

What does isotrentoin release?

A

13cis retinoic acid

57
Q

Two results of isotrentoin

A

Sebocyte secretion arrested

Sebocyte re-growth arrested

58
Q

How does sebocyte re-growth arresting cause reduced inflammation?

A

-> sebaceous gland lumen unblocked -> conditions less favourable for P. Acnes growth -> inflammation subsides