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Skin Diseases Cheat Sheet by

Many gross skin stuff
dentistry     pathology

Defi­nit­ions:

Defi­nitions (cont.):

Skin Diagram:

Major Skin Cells:

1) Kerati­nocytes
2) Melano­cytes: anchor to basement membrane and pump out pigment for protection from sunlight damage
3) Langer­hans’ cells: antige­n-p­res­enting system

Normal Skin Structure and Functi­on:

Function: Barrier between the individual and the extrernal enviro­nment
Burn victims:
loss of barrier leading to loss of fluid and secondary bacterial infect­ions.
Ecze­ma/­Der­mat­itis:
damage to the skin resulting in inflam­mation and spongiosis with edema of the dermis. Hypers­ens­itive reaction to certain chemicals or drugs. Atopic eczema patients are predis­posed to allergic rhinitis and asthma.
Imme­rsi­on:
prolonged immersion in water may overwhelm the barrier (ie. occlusal dressing of burns or under surgical dressings) - can be an advantage in topical therapy.

Inci­dences of Skin Diseas­es:

Comm­on: acne, psoriasis, eczema, seborrheic warts and viral warts, actinic ratosis, basal cell carcinoma, squamous cell carcinoma.
Unco­mmon: pemphi­goid, pemphigus, melanoma and scabies.
Rare: xeroderma pigmen­tosum, mycosis fungoides.
Age, Sex, Anatomical Site, Rare, Exposure and Geogra­phy.

Diso­rders: Inflam­mat­ory­&H­ema­top­oietic cells

Poly­mor­pho­nuclear leucocytes (polym­orp­hs)– accumulate in the skin due to response to infections e.g Staphy­loc­occus aureus in impetigo.
Psor­ias­is: neutro­philic infiltrate with intra-­epi­thelial migration forming sterile abscesses. Others are Sweet’s disease and pyoderma gangre­nosum show a heavy dermal neutro­philic infiltrate – 2nd to chronic inflam­matory bowel disease.
Auto­immune condit­ions: e.g dermatitis herpet­iformis show neutro­philic infiltrate where as bullous pemphigoid shows an eosino­philic infilt­rate.
Lymp­hocytic infilt­rate: seen in most chronic inflam­matory skin diseases and comprises mostly T-lymp­hocytes (CD4/H­elper T-cells)
Ecze­ma: lympho­cytic infiltrate and spongiosis
Lupus erythe­matosus and lichen planus
Cuta­neous lympho­mas: primary (mycosis fungoides) or secondary ( peripheral T-cell lymphoma, anaplastic large cell lymphoma etc.)
Mycosis fungoi­des: T-cell lymphoma – Sézary syndrome
Hist­iocytic infilt­rat­es: seen in granul­omatous skin diseases e.g. bacterial (mycob­act­eria), fungal (candi­diasis) or protozoal infect­ions.
Systemic diseas­es: e.g. Sarcoi­dosis.
Primary granul­omatous skin diseas­es: granuloma annulare or necrob­iosis lipoidica.

Infe­cti­ons:

Clinical appearance depends on:
1. Site
 
2. Nature of organism
 
3. Nature of the body’s response to the infection.
Routes of transm­iss­ion: hemato­genous or penetr­ation of the skin barrier
 

Viral Infect­ions:

Viruses are obligate intrac­ellular organisms – metabolic basal cells.
Human Papilloma Virus (HPV): DNA virus with numerous subtypes.
Skin and oral mucosa causes squamous papill­omas, verrucae vulgaris, verruca plantaris, verruca plana, condyloma acuminatum (genital warts)
Moll­uscum contag­ios­um: DNA pox virus – umbili­cated self-l­imiting lesion in children.
Herpes virus: HVS1 and HPV2 (blist­ering vesicles), herpes zoster (chick­enpox) and shingles.
Human herpes virus 8 (HHV8): Kaposi’s sarcoma (HIV)

Bact­erial Infect­ions:

Impe­tigo: Staph.a­ureus in children but Strep. in elderly
Cell­uli­ltis: Strept­ococcus pyogenes
Tube­rcu­losis of the skin (lupus vulgar­is)­:­Myc­oba­cterium tuberc­ulosis or Mycoba­cterium bovis the cause of scrofu­lod­erma.
Leprosy (Hansen’s diseas­e): Mycoba­cterium leprae (lepro­matous and tuberc­uloid). Leprom­atous form fatal while tuberc­uloid form destroy tissue and nerves resulting in mutilated leonine facies and auto-a­mpu­tations of digits.

Fungal and Protozoa Infect­ions:

Fung­al:
Common ringworm (tinea) Tinea pedis (athletes foot) Candida, Blasto­myces and Norcardia
Prot­ozo­al:
Leishm­aniasis infections transm­itted by sandflies, organism infilt­rates the macrop­hages

Utic­aria:

Hives or wheals (reaction pattern), itching and swelling. Sudden marked increase in the permea­bility of the dermal blood vessels resulting in edema of the dermis – erythe­matous or edematous lesions.
Hist­olo­gy: shows marked infiltrate of eosino­phils and mast cells
Caus­es:­Plant and animal toxins, physical stimuli e.g. heat, cold or stress, various drugs (aspirin and antibi­otics)
Histamine is the mediator and increase in IgE.

Lupus erythe­matosus (SLE or LE)

-Autoi­mmune disease affecting connective tissue with antibodies directed against DNA.
-Multi­system disease involving almost any organ, most common is skin and kidneys.
-Epidermis and adnexa involved.
-Skin only: Discoid lupus – erythe­matous, scaly and older lesions show hyperp­igm­ent­ation.
-Often symmet­rical on the face with a butterfly rash over nose and cheeks, and on scalp it may cause scarring alopecia.
-Immun­ofl­uor­escence show IgG and IgM at the epidermal basement membrane – “lupus band test”

Psor­ias­is:

Geneti­cally determined – HLA haplotypes (HLA Cw6, B13 and B17).
Disease of epidermal prolif­eration and excess keratin produc­tion, driven by cytokines released from activated T-cells in the dermis
Silver­-grey scales of parake­ratosis on extensor surfaces such as knees and elbows.
First appearance may be at site of trauma e.g. surgical wound – “Koebner effect”.
Result in destru­ctive arthro­pathy (psoriatic arthritis)
Small bleeding points – Auspitz’s sign.
Hist­olo­gy: rete ridges becomes acanthotic with the dermal papillae covered by thin epidermis two or three layers thick.
Loss of the granular cell layer.
Erythe­matous lesions - caused by dilated vessels in upper dermis.
Numerous polymorphs that migrate from the vessels into the epidermis forming pustules (micro­-ab­sce­sses)- pustular psoriasis.
May also involves the sole of feet and palms of hands.
Trea­tme­nt: Coal tar, Methot­rexate and arsenic.
Current therapy: Retinoid (Vit A analog­ues).

Pann­icu­lit­is:

Inflam­mation of the subcut­aneous fat.
Most common type is Erythema nodosum which occurs as painful red nodules on the shins.
Follow a strept­ococcal infection or in associ­ation with inflam­matory bowel disease or tuberc­ulosis.

Lichen Planus:

- Charac­terized by destru­ction of kerati­noc­ytes, probably mediated by interf­ero­n-gamma and tumour necrosis factor from T-cell in the dermis.
- Affects the skin, most commonly the inner surface of the wrist.
- Appears as white lacy lesion – presents as itchy, polygonal, violaceous papules that may form blisters.
- May be caused by certain drugs or medica­tions.
- Mucosal surface white striae – Wickham’s striae.
- Histology shows a lympho­his­tio­cytic infiltrate in a band-like fashion at the dermo-­epi­dermal junction- classical lichenoid reaction pattern.
- Basal cell vacuolar degene­ration, apoptosis, kerati­nocyte necrosis.
- In contrast to psoriasis, LP show an increase in the granular cell layer.
- Rete ridges show “sawtooth” morpho­logy.
- Treatment: Steroids
 

Benign epidermal neoplasms & tumour­-li­ke:

Skin tags or fibro-­epi­thelial polyps: seen frequently in the elderly and common in the axilla. Due to friction rather than a true neoplasm.
Sebo­rrheic keratosis (basal cell papill­oma­s): common in the elderly, dark greasy looking nodules with an irregular surface. Rarely turn malignant. Stuck-on appear­ance.
Hist­olo­gy: Convoluted surface with keratin tunnels (horn cysts). The may become inflamed. Often remove for cosmetic purposes and to exclude melanoma.
Squamous papill­oma: Benign neoplasm of squamous epithe­lium, HPV induced lesion.
Cyst: Epidermal (infun­dib­ular) cyst and pilar (trich­ole­mmal) cyst are the most common.

Pre-­mal­ignant lesions:

Actinic kerato­sis: In sun-ex­posed areas , show dermal solar elastosis, need to evaluate for kerati­nocyte intra-­epi­thelial neoplasia (KIN I-III)
Bowen’s disease: Squamous cell carcinoma in-situ.

Basal cell carcinoma (BCC):

Very common skin malign­ancy, most commonly on the face of elderly people.
Related to chronic sun exposure.
Locally very aggressive and destru­ctive, however metastasis are extremely rare.
Nodular or superf­icial BCC has a better prognosis while micro-­nodular and morphoeic are more aggressive and recurrence is high.
Associated with mutations in the Drosophila gene patched- PTCH1 (tumour suppressor gene)which is a member of the sonic hedge-hog pathway.
Clin­ica­lly: ulcerated irregular lesions – rodent ulcers with raised pearly borders and blood vessels visible on the border.
Hist­olo­gy:­cells look like normal basal epithelial cells, islands of basaloid cells with peripheral palisa­ding.
May develop from the basal cell layer or hair follicles.

Squamous cell carcinoma (SCC):

-Are common and usually caused by chronic UV exposure.
-Other: immuno­sup­pre­ssion, irradi­ation, chemical carcin­ogens, HPV infections and chronic infect­ions.
-More common in the elderly .
-Rarely SCC arises at the edge of a chronic skin ulcer (Majolin’s ulcer).
-Very aggressive and invasive however metast­asize late.
-Excision can be curative and SCC are more sensitive to radiation than BCC’s.

Kera­toa­can­tho­ma:

Rapidly growing, cup-shaped squamous epidermal lesion
Involves sun-ex­posed skin of elderly - face
Regresses sponta­neously if left untreated
Hist­olo­gy:
-Endop­hyt­ic-­end­ophytic squamous prolif­era­tion,
-Cup-s­haped lesion
-Crate­r-like center filled with laminated keratotic material
-Resembles a well differ­ent­iated squamous cell carcinoma

Mela­nocyte Derived Lesions:

> Melano­cytes are pigmented cells
> Found in basal layer of epidermis
> Melanin is synthe­sized by melano­somes
> Found on skin and mucosal surfaces – oral cavity, vagina, conjun­ctiva etc.

Types of Benign Lesions:

Lent­igos:
Increase in single melano­cytes in basal areas. Small, pigmented macule.
Naevi:
Increase in groups of melano­cytes. Melano­cytes form nests.
Frec­kle:
Increase in melanin production by normal melano­cytes which are taken up by adjacent kerati­noc­ytes. UV stimul­ation.

Naev­is:

Common in light-­skinned indivi­duals. Absent at birth and appear in early childhood. Increase in number through early adulthood. Found mainly on sun-ex­posed areas. Different stages
STAGE 1 - JUNCTI­ONAL:
At dermo-­epi­dermal junction –intra­epi­dermal nests. Tan or brown pin-point macules (1-2mm). Gradually enlarge. Increase in number of individual melano­cytes at dermo-­epi­dermal junction.
STAGE 2 – COMPOU­ND:
Nevus is elevated above skin surface. Childhood \ adoles­cen­ce.S­li­ghtly raised due to nests of melano­cytes
STAGE 3- INTRAD­ERM­AL:
Middle to old age. Nevus cells detach from dermo-­epi­dermal junction. Smaller, more mature and less metabo­lically active. Cannot divide. Two components Junctional and intrad­ermal. Pink due to lack loss of melanin
Hist­ology of Stage 2:
- Nests of melano­cytes at dermo-­epi­dermal junction and infilt­rating dermis
- Pigmented
- Dendrites lost
- Nuclei become round, incons­picious nucleoli
 

Blue Naevis:

- Occurs in deep dermis
- Bluish tinge
- Any area of skin
- Less than 5mm in diameter
- Solitary
- Malignant transf­orm­ation is rare

MALI­GNANT LESIONS: Melanoma

- Common skin cancer
- Can arise from any melano­cyte, composed of malignant melano­cytes.
- Usually pigmented but may be unpigm­ented.
- Etiology associated with fair skin and sunburn
- Asymme­trical (ABCDE)
- Irregular borders
- Varying colours: blue, black-­brown, ulcerated
- >6mm
- Evolution
- Prognosis depends on thickness of lesion and presence of surface ulceration – Breslow thickness
- > 1 mm depth indicates signif­icant risk for metastasis
- Cure rate for completely excised non-ul­cerated melanomas below 1mm is 100%
Main Varian­ts:
1. Lentigo maligna melano­ma: - sun damaged skin of the elderly, develops from a pre-ex­isting in situ lesion termed a lentigo maligna (Hutch­inson’s melanotic freckle).

2. Acral lentig­inous melano­ma: – palms and soles, most common type in Non-Ca­uca­sians.

3. Superf­icial spreading melano­ma:- most common type in people from European descent

4, Nodular melano­ma: -retain no features to identify a pre-ex­isting in situ lesion

Vesi­cul­o-B­ullous Condit­ions:

Fluid –filled cavities
Within the skin
Caused by the separation of two layers of tissue and leakage of plasma into the space
Bullae: > 5mm
Vesicles: < 5mm

DISTINCT MECHANISMS OF BLISTER FORMAT­ION:

Direct destru­ction of bonds between epithelium e.g. pemphigus
Cells forced apart by edematous fluid e.g. eczema
Cellular destru­ction leaving gaps e.g. herpes infection
Basement membrane or its attach­ments to epidermis or dermis altered e.g. bullous pemphigoid

Pemp­hig­us:

BONDS BETWEEN EPITHELIUM IS BROKEN
Common in middle­-aged to elderly
Mortality rate of approx­imately 40%
Autoan­tib­odies directed against desmosomes
Bridges lysed and epidermis falls apart
- Blister formed containing epithelial cells within cavity (acant­hol­ysis)

- Various forms:
Pemphigus vulgaris
Pemphigus foliaceus
Pemphigus vegetans

- Skin very fragile
- Firm pressure on normal­-lo­oking skin will cause blister formation (Nikol­sky’s sign)

Bullous Pemphigoid (BP):

More common than pemphigus
Usually over 60 years of age
Self-l­imiting
Associated with periods of pruritis
Blister forms at dermo-­epi­dermal junction
Etio­logy:
> Circul­ating antibodies against lamina lucida of the BM.
> Linear deposition of antibodies along basement membrane (IgG)
> Causes antige­n-a­ntibody complexes and release of complement factors as well as degran­ulation of mast cells
> Blisters are more persistent

DERM­ATITIS HERPET­IFO­RME:

- Charac­terized by small, itchy blisters
- On extensor surfaces of knees and elbows
- Young adults
- May be associated with Coeliac disease
- Pruritic lesions
- Bullous forms at dermo-­epi­dermal junction
- Immu­nof­luo­res­cen­ce: Granular deposits of IgA
- Therapy: Response to dapsone

Bullous and Acanth­olytic Dermat­osis:

Intr­a-e­pid­erm­al/­Sup­rabasal Cleft:
1. Pemphigus Vulgaris: IgG (inter­cel­lular) 2.Pemp­higus Foliaceus: IgG (subco­rneal) 3. Pemphigus Erythe­matous: IgG
Sub-­epi­dermal Cleft:
1. Bullous Pemphi­goid: linear IgG and C3 at basement membrane. 2. Dermatitis Herpet­ifo­rmis: granular IgA papillary dermis. 3. bullous Systemic Lupus Erythe­mat­osu­s:IgG, IgA and C3.

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