Integumentary disorders Flashcards
How does ahmed differentiate between the integument and the skin?
• Integument + skin are not the same! When deal with skin, often dealing with subcutaneous (or did he say cutaneous?) layer. THe cutaneous + subcutaneous layers together form the integument
What is the cause of cellulitis?
How does it get in?
- Strep pyogenes or Staph aureus
- Bact infection of deeper dermis + subcut layer → deeper part of integument affected
- Entry via compromised skin (eg: wounds) problematic when integument is compromised as permits entry; will enter often through the feet (such as in those with athlete’s foot)
Strep pyogenes
aerobic, opportunistic, quite common is causing strep throat (lots of O2 here) + infections of skin
o Have low numbers of this in upper resp tract as normal flora
Staph aureus
o Normal in outer layers of skin - If gets into deeper layers of skin, causes problem
o Also normal in some individual’s nasal passages in small numbers
Patho of cellulitis?
• Usually affects legs, then hands, then pinna → erythema, warmth, edema, fever, pain
- Bacteria spread through tissue spacesMoves through to subcut layer – which is comprised of a lot of “vacant” space where bacteria can move through and affect other areas of body (widening spread)
- Can affect lymphatic system – moves into this system while infiltrating skin layers
Who is more susceptible to cellulitis infection?
elderly, immunocompromised, compromised skin
Tx of cellulitis?
What is a major concern in this illness?
Risk of not treating?
- Mild: oral abx
- Severe: IV Abx (7-14d)
- recurrence
is very pressing problem in these pt’s!
• If not treated, run into very serious problems: lymphangitis (inflm of lymph vessels), bacteremia/septicemia, gangrene
What is PSORIASIS
- Chronic inflm disorder
* Variable course - therefore hard to deal with
How does progression of cells through epidermis occur?
• Epidermis comprised of several layers, lower is basal layer with basal cells, which replicated + progress into upper layers of epidemis, die + form outermost layer
o Takes about 1 month from replication to when appear on surface + die
o Several stages in maturation process (says can look this up…do we have to?)
o If do this process rapidly, you’ll make a mess of it! Cells haven’t undergone proper development; instead of shedding, will stack + form of scaley surface on skin
Et of psoriasis?
- Largely idiopathic → but what’s know about it is:
- Genetic component (~30%)
- Autoimmunity involved (HLA + MHC genes!)
Patho of psoriasis?
What is this condition exacerbated by?
- Not sequential
- T cells altered (d/t genetics) + mount altered T cell immune response
- Skin trauma seen as possibly what triggers this response → T cells activated → mediators → these cause accelerated epidermal (not epithelial!) cell cycle → Abn growth of keratinocytes + blood vessels
- Influx of inflm cells →attract more inflm cells → inflm damage = even more skin damage beyond the original trauma
- Inc epidermal cell turnover (not completed in 3-4 days instead of 30!)
- Cells stack instead of shedding → scaly patches
- Exacerbated by stress, trauma, infection, drugs – person will go into remission (skin symptoms dissapear) + then recur worse then they were before
Keratinocytes?
these cells produce protein keratin, found in hair and nails
A keratinocyte is the predominant cell type in the epidermis, the outermost layer of the skin, constituting 90% of the cells found there
Manifestations of psoriasis?
- Psoriatic patches - Most commonly on elbow, knees, scalp, sacral region
- Dystrophy + pitting of the nails – appear broken (problem with production of keratin) → will see this in later stages when individual has had for a while
- Psoriatic arthritis (distal joints)?? – damage to joints, resulting in swelling + deformity (this is not septic arthritis like STI) – not everyone gets this
Tx of psoriasis?
• No cure
• Topical vit D
• Topical steroids
• Topical retinoids
• As disease progresses becomes more severe..these no longer adequate so move into systemic management
o Methotrexate, cyclosporine (toxic drug, is immunosuppressant) – have similar action, would be using one or other
o Phototherapy – controlled exposure to UV rays (very damaging to skin) – UVB rays (not A) used here to suppress the division of the cells
o May also use Topical application of tar
o Biologic agents (eg: TNF) - brings about apoptosis
Benefits of vit D for psoriasis?
Steroids?
Retinoids?
is suggested that modulates keratinocytes + regulates T cells – likely won’t work on its own
addressing inflm that occurs
– are anti-inflm + bring keratinocytes under control
