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
which types of skin CA are most common?
How common is skin CA in canada? is this avoidable?
• 3 types are common: (first 2 account for about ~90%)
1) Basal cell carcinoma
2) Sqaumous cell carcinoma
3) Malignant melanoma
Skin CA
• Accounts for about a third of all CA diagnosed in Canada
• Largely avoidable
Et of skin CA?
“MUVAN”
• Excessive sun exposure (UV light)
• Skin damge is cumulative
• Nevus (pl: nevi) = moles - these are benign tumours, infrequently will become malignant
• Prevalnce of skin CA increases with age (culmulative damage); and is inversely proportional to the amount of melatonin content in the skin (darker the skin, more protective it is from UV rays)
What is the pre-CA lesion in skin CA called?
Why is this important for skin CA?
• Actinic keratosis = pre-CA lesion - is a bit like bad sun burn (appears similar)
o Actinic refers to radiation (solar)
o Keratosis = describes the lesion that forms
o Is good – tells us we can intervene and prevent the CA from happening
• Early detection + tx key – 95% cure rate
Basal Cell Carcinoma Origin? Fast or slow progression? Where does it appear? What does it look like? Does it invade + met? Tx?
*This of basil plant story
• Basal cell origin (in epidermis)
• Slow progression
• Appears on surfaces exposed to the sun (mostly head, face + neck)
• Dome-shaped/nodular lesion - canceraous lesions tend to change…is something to look for; not usually painful
• Local invasion + destruction
• Usually does not met
• Dx: biopsy – excision done – remove whole thing
• See fig 61-32
Which type of skin CA is most common?
basal cell carc
Squamous Cell Carcinoma Origin? Where does it present? Slow or fast? What do lesions look like? Infiltration/mets?
- Origin in epidermal keratinocytes
- Exposed areas
- Faster growing
- Poorly defined lesions
- Variable appearance
- May infiltrate local structures (adipose tissue,…?)
- Mets to local lymph nodes
- See fig 61-33 – the readneed areas in both pictures show the actinic keratinosis
What is the worst form of skin CA?
Malignant Melanoma
Malignant Melanoma
- origin
- progression
- where does it show?
- what are the main features?
• Melanocyte origin – produce pigment melanin
• Worst form
o Raid progression
o Mets
• Exposed + non exposed surfaces
• Main features = Lesion changes (occurs over months) - outlined in next card
• Mets to brain, bone, liver, lung
o Three of these are vital organs!
• Can be fatal (all, but particularly mal mel)
What sort of lesion changes are characteristic of malig mel?
” DICC PUB”
- may have been previously benign – these are suspicious changes not necessarily indicative of CA
• Doubling in size (3-8mnths)
• Color change
• Irregular border
• Pruritis
• Bleeding
• Crusting
• Ulceration
• Can be changes to existing lesion of changes in formation of new lesion
• These cahnges are not restricted to mal melanoma (can occur with other types as well)
• Fig 61-31 – see several colours in some of these lesions, is not uncommon
Tx of skin CA?
- Early detection usually, and dealt with successful
- Sx excision
- If advanced, follow sx with radiation or chemo
- Unless are mets, don’t usually require more than the incision
