MP321 week 5 Flashcards
functions of the skin (8)
- a physical barrier to noxious agents and the entry of pathogens
- an immunological barrier to the ingress of pathogenic organisms
- assists retention of heat and regulation of temperature
- retains moisture and maintains osmotic balance within the Body
- a sensory organ- touch, social contact
- excretion
- vitamin D production
- protection from UV in sunlight
epidermis
outer most layer waterproof codified outer layer of keratin proteins and lipids
dermis
supporting region of the skin just below the epidermis
dermis-blood and lymph vessels
nerves and hair roots (hair follicle with sebaceous gland and muscle in Demis)
sweat glands- apocrine and eccrine
eccrine gland
in the dermis layer
secrete directly onto skin surface
thermoregulation, salt excretion, antibacterials
apocrine gland
in the dermis layer
bud fatty secretions off into enclosed areas like hair follicles
especially found in axilla and public areas
layer of the epidermis
top nuclear squamous layer
granular layer
spindle layer
germinal layer- inner most
top nuclear squamous layer
Essentially dead as anuclear. Tough because of keratin, tightly joined. A tough waterproof barrier to the outside world and pathogens
Dead skin cells constantly shed off making dust, which is fed on by dust mites eat it and cause of allergy
granular layer
Where cells have vesicles containing keratin fibre. Gets its name from its granular appearance under a microscope. Keratin strengthens them making them tough
spindle layer
spindle layer cells form tight junctions anchored with adhesion proteins, cells glued into a sheet-like structure
differentiate and rise up further
this layer contains langerhans cells (APC or macrophages) specific to the skin
germinal layer
is where the stem cells replicate and constantly divide and renew
then they migrate upwards based on a potential difference of a very small charge
also melanocytes (which produce pigment)
the pilosebaceous unit
Look in more detail of an apocrine gland
The hair follicle bases is in the dermis layer with the hair poking through the epidermis and out
Hair follicles are housed in the pilosebaceous unit.
2. The arrector muscle. When the arrector muscle contracts it pulls the base to an upright position, making the hair stand up-goosebumps
3. The pilosebaceous unit produces sebum- a sticky substance secreted on surface skin.
It is antibacterial and has low pH. It contains proteins and waterproofing lipids
Can change lipid content to modulate sweat evaporation to control thermoregulation
If there is obstruction of sebum secretion it may become infected, causing acne and other skin conditions
meissner corpuscle
near the surface of the skin
responds to light pressure
pacinian corpuscle
deep in the skins layers
responds to deeper pressure
merkel cells
middle skin layer
respond to sustained light pressure
innervation of glabrous (non-hairy) skin
by fast conducting, low threshold mechanics-receptors (LTMRs) mediates sense of touch, vibration and pressure
specialised sensory nerves in the skin:
merkel cells
pacinian corpuscle
meissner corpuscle
examples of glabrous skin
non hairy
palms and soles of feet
rich in sensory nerves
examples of hairy skin
major part of body surface
back, scalp etc
microenvironment
different skin regions vary greatly in their appearance and in the amounts of moisture and oiliness they typically carry
temperature and pH also
wound healing stages (4)
- hemostasis
- inflammation
- proliferation
- remodelling
hemostasis in wound healing
- fibrin is released by platelets
- it is cross linked to make a plug to stop bleeding
- helps prevent infections taking hold
- langerhan cells patrol the local area and modulate response
- release of histamine via mast cells causes vasoconstriction
inflammation in wound healing
- chemotactic factors are released into the bloodstream
- monocytes move in by diapedesis
- more neutrophils are attracted
- mast cell activation
- a cycle of inflammation
- combats opportunistic infections
proliferation in wound healing
- helps to form a scab on top of the wound
- scab detached as skin grows underneath
- endothelial cells proliferation promotes angiogenesis
- fibroblast proliferation fills the underlying connective tissue and the skin
remodelling of the skin
- skin repairs itself at the surface
- wound edges come together to form a continuous barrier
- healing continues underneath
- myofibroblasts make pseudopods and migrate forward dragging cells behind them forward
- gradually this enables the ends to come together
- can take months to heal fully
factors directly affecting wound healing
Body site
Infection
Vascular supply
Oxygenation
Mechanical stress
Desiccation
Oedema
factors indirectly affecting wound healing
Age and nutrition, medication, alcoholism, drug abuse, hygiene
Diabetes
Autoimmune diseases
Venous stasis
Predisposition to keloids (prominent scar tissue)
Some genetic skin diseases
Immunocompromised state (AIDS, cancer)
Obesity, immobility, vasculitis, neuropathy,
tanning
- UV light exposure induces double stranded breaks in DNA in keratinocytes
- causes activation of a protein called p53(which is a tumour suppressor gene)
- transcription of proopiomelaocortin (POMC)
- POMC is cleaved into 2 species- B-endorphin acts as a local analgesic and A-melanocyte stimulating hormone (MSH) causes melanocytes to produce a pigment
- melanosomes transfer pigment to keratinocytes
- melanin absorbs UV light before it can reach DNA and damage it
melanomas
Superficial spreading melanoma
Amelanotic melanoma
Nodular melanoma
Acral lentiginous melanoma
Uveal melanoma
skin microenvironment and the human microbiota
- about 1 million bacteria per cm^2 of skin
- thus healthy skin is home to many bacteria, viruses and fungi
- together they make up a microbial bio community called the microbiota
the skin microbiota
Microbiota composition varies by area
Skin folds can affect microbiota
Oily skin can also influence this
Fungi tend to colonise creases and folds between the toes
Bacteria are found all over but particular species have their own favoured niches Staphylococcus tends to favour enclosed/creases
Damage to the skin – Infections:
Possible contributions of the microbiota
Skin microbiota can cause skin infections
Genetic predisposition
can make skin more vulnerable
increased sensitivity to particular microbes
Change in microbial density/composition
more bacteria present mean it is easier to penetrate the skin
Metabolic diseases can alter the nutrients on the skin and the vascular supply
Change in the type of microbes?
Contextual pathogens
In a wound, normal microbes can become pathogenic
Drug treatments
Antibiotic or topical steroids can change growth conditions
Overgrowth or harmful bacteria?
vesicles
fluid filled blisters the size of a pin head
bullae
fluid filled blister like eruptions around 1 cm in diameter
acne vulgaris
Common in adolescence but can occur at any time
As a result of oily skin and the colonisation of blocked pilosebaceous unit
Causes: blockage of the pilosebaceous unit can allow infection (propionium bacterium acnes) and formation of pustules.
Signs and symptoms: If the infection is severe and the hair follicle ruptures, scarring can ensue.
Treatment: Depending on the severity, a variety of preparations are available. Topical benzoyl peroxide is one treatment, and tetracycline might be considered if symptoms are severe.
impetigo
Bacterial infection in the skin: Commonly affects face or extremities following injury. Bullae and or vesicles can form. Very contagious.
Causative factors: Usually caused by S. aureus or S. pyogenes. Commonly affects face or extremities in children following injury.
Signs and symptoms: Non-bullous type has pinhead pustules on red skin which erupt to give a yellow-brown crust after skin injury. (About 70% of cases)
Bullous type has larger blisters which release clear yellow liquid to leave a golden yellow crust (usually S. aureus on intact skin)
The golden crust is a key distinguishing symptom
Treatment: For most patients, topical treatment with bacitracin or mupirocin, although resistance in some areas. Also perhaps some care in playgroups etc. to avoid crowded conditions where it could spread.
ecthyma
Causative factors: Often progresses from untreated impetigo (causing a deeper infection). Seen in homeless folk with poor hygiene, or soldiers in the tropics, especially if an affected area has been enclosed (as in footwear). Also occurs in immunocompromised individuals.
Although commonly associated with S. pyogenes and S. aureus, other bacterial species can also be associated with ecthyma.
Signs and symptoms: The infection penetrates to deeper layers of the skin causing the appearance of painful ulcers
Treatment: Warm compresses and antibiotics e.g. dicloxacillin
Treatment is difficult and can take a long time
folliculitis
Causes: Infection of hair follicles by S. aureus usually. Often affects beard, armpits, back of the neck,
Signs and symptoms: Red pustules (furuncles) form and eventually rupture in a few days.
Treatment: Should be self-limiting and resolve naturally. Topical clindamycin and erythromycin on affected areas if necessary and anti-bacterial soap. Larger abscesses (carbuncles) may need to be surgically drained.
erysipelas and cellulitis
Erysipelas (superficial infection) and cellulitis (deeper into the skin):
Causes: Involves lymphatic vessels. Erysipelas is often caused by S. pyogenes and cellulitis by S. aureus. Can travel through lymph to become a serious systemic condition (therefore than be life threatening)
Signs and symptoms: painful, warm, red swelling which forms a well defined plaque.
Treatment: Erysipelas: penicillin; cellulitis: dicloxacillin
Necrotizing Fasciitis
Even deeper infection
Pathophysiology: Infection of subcutaneous tissue which can occur after surgery or trauma. Can be caused S. pyogenes alone but often involves a mixture of bacteria.
Signs and symptoms: Starts with warm red skin but lesion rapidly expands vertically and horizontally. The tissue becomes, dark, pustular then necrotic with gangrene.
Treatment: Fatal without prompt treatment. Surgical intervention is required along with parenteral antibiotics such as gentamycin and clindamycin
rapid expansion of the lesion
dermatophytoses
fungal infection
Trychophyton rubrum is most common infectious fungus, and most fungal infections involve the genera Trichophyton, Microsporum and Epidermophyton
Forms of tinea (fungal skin infections):
Tinea pedis (athletes foot)
Tinea cruris (jock itch),
Tinea capitis (can cause cradle cap in babies)
Tinea corporis (also called ringworm)
Tinea unguium (onychomycosis) infection of nails
Topical treatment: with terbinafine, clotrimazole or econazole
Tinea versicolor
Pathophysiology: Caused by the widespread yeast Malassezia furfur, more common in hot climates
Signs and symptoms: Results in lightened pigmentation of the skin in upper body and limbs. This can have psychological impact
Treatment: selenium sulfide shampoo or topical antifungal agents
Candidiasis
Caused by the yeast Candida albicans part of the normal microbiota
Associated with immunosuppression
Can be associated with poor oral hygiene and dentures
Signs and symptoms: Inflammed and itchy membranes in moist mucous tissues such as mouth, vagina, armpits etc.
Treatment: topical antifungals, plus possibility of systemic antifungals such as ketoconazole, fluconazole
herpes simplex 1
viral infection
Pathophysiology: 85% of population have antibodies to
HSV type 1. Virus resides in dorsal ganglia, until reactivated.
Signs and symptoms: Self limiting eruption around mucous membranes of mouth
Treatment: Acyclovir is favoured treatment
Herpes: Varicella zoster (chicken pox) and shingles:
viral infection
Pathophysiology: during chicken pox, the virus travels to sensory ganglia where it remains for life
Signs and symptoms: Pain and paresthesia in an affected dermatome
Treatment: Usually resolves with rest and analgesics, but acyclovir can be used, especially if virus is disseminated
warts
caused by human papilloma virus (HPV)
Warts are benign skin tumors caused by infection with the human papilloma virus (HPV)
Have dark necrotized blood vessels (dark specks) at the heart of the wart.
There are many strains of HPV. It is a very common virus, and most strains are benign.
Common (plane) wart (verruca vulgaris) affects the hands and face and knees and can spread.
Plantar wart- (verruca plantaris) grows into the skin of the foot and can cause pain.
Warts will often resolve spontaneously, but can be removed by some form of chemical, cryo or surgical ablation.
Some strains of genital warts can increase the risk of cervical cancer, but there is now a vaccine against this- Gardasil
Molluscum contaginosum:
Pathophysiology: Caused by the pox virus.
Transmitted by direct skin contact.
Signs and symptoms: Hyperplasia
Raised pink, pus filled lesions with a central depression.
Treatment: Often resolves spontaneously, but can linger in immunocompromised individuals. Children treated conservatively, but broadly similar treatment options as for warts with addition of curettage and cantharidin.
main causes of resistance in TB
Poor compliance
Inadequate treatment and diagnosis (“tools”)
Poor health care infrastructure
Lack of education and knowledge
Global location causes severe logistical issues
TB spread
inhalation of droplets
Why the resurgence of TB?
Complex chemotherapy used to treat the disease causes low compliance - old drugs!
Drug resistant strains have emerged (M/X/C DR-TB)
Strong epidemiological co-existence between HIV and TB as patients who are immuno-compromised easily catch TB (host defences can not fight bacteria in body)
Bacterial persistence in TB
After treatment a small percentage of bacteria may remain in a dormant state in macrophage
Complex mechanism between host and pathogen
These can become reactivated many years later
Patients shows no symptoms – carriers
2 - 23% lifetime risk of reactivation to secondary TB
Increased by 10% if immuno-suppressed (HIV or immuno-suppressants)
treatment of TB
2 phases- initial and continuation
