Dermatology - Lecture 9 Flashcards

1
Q

Name the skin layers and their cells

A

Epidermis- Keratinised stratified squamous epithelial cells, and contain keratinocytes, melanocytes, Merkel cells
Basal Membrane- thin adhesive layer
Dermis- strong flexible, contains NN, VV, AA and lymphatics

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2
Q

Types of primary skin lesions and examples

A
  • Macule (discoloured spot- Freckle) /Patch
  • Papule (sharp borders- Mole)/ plaque (large elevated surface= Psoriasis) / nodule (wart) or tumor (large lipoma) / wheal (localised area edema- Hive, insect bite)
  • Vesicle (elevation with fluid- blister, caused by herpes simplex)/ Bulla(large elevation with fluid- Large friction or burn blister)/ Pustule (vesicle or bulla filled with purulent fluid- acne, carbuncles)
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3
Q

Types of secondary skin lesions and examples

A
  • Scale (dandruff)
  • Crust (residue of impetigo)
  • Fissure (athletes foot)
  • Ulcer (pressure ulcer)
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4
Q

Dermatitis and types

A

inflammatory skin lesion

  • Infective -bacteria (impetigo or folliculitis) , viruses (herpes), Parasite (scabies)
  • Non-specific -eczematous dermatitis (Atopic dermatitis-hereditary or environmental, Contact Dermatitis- irritant or allergic, Gravitational Dermatitis- poor venous return in legs, Seborrhoeic dermatitis- irritant from yeast toxin on scalp & face)
  • Characteristic - Psoriatic, lichenoid
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5
Q

Acute Dermatitis

A

Immune response causes dilation and lymphocytic infiltrate= Red (erythema) & Itchy (pruritus) from inflame reaction to irritant (scratching leads to secondary trauma)
Spongiosis (fluid accum. between epidermal cells= vesicle formation)

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6
Q

Chronic Dermatitis

A

Chronic trauma to acute dermatitis
Thickened, cracked and scaly skin= Hyper keratinisation
Increased cells in Stratum spinosum-Epidermis (Acanthosis) = increased fibrosis in dermis
Constant picking of hyper-keratinised cells = localised thick, keratanised lesions “prurigo nodularis”- can lead to ulcer

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7
Q

Lichen Planus (Dermatitis)

A

Common inflame. D of skin
Characterised by shiny, flat topped, firm papules, purple in colour with fine white lines (wick hams striae)
Seen on front of wrists, lower back and ankles or on mucous membranes
Resolves after 18months
Damages basal layer of epidermis, scales form and lymphocytes infiltrate close to basal layer “Lichenoid pattern”

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8
Q

Psoriasis (Dermatitis)

A

Chronic intermittent D, 2% population, mild to severe
S+S: Raised (acanthosis) red plaques (oedematous & capillary dilation) covered by white scale (hyperkeratosis), and mostly symmetrical
Aet: poorly understood, partially genetic. linked to joint pain
Path: infiltrate mostly neutrophils

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9
Q

Bacterial Skin Infections

  • Impetigo (school sores)
  • Bacterial folliculitis
  • Erysipelas (streptococcal infect.)
  • Cellulitis
A

Impetigo- staphylococci, contagious, mostly with kids, large bullae, honey coloured crusted exudate, pruritus
Folliculitis- hair follicules, tiny pustules, boil formation
Erysipelas- streptococcal infection and spreads through lymph system, acute inflame deep dermis, common lower limbs or face, well defined border
Cellulitis-

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10
Q

Cellulitis

A

bacterial infection to skin
Or Periorbital Cellulitus (swollen eyes)-
Eit: streptococal or staphyloccocal bacteria entering cut to skin (bite, scratch) or Periorbital via sinuses or throat
S+S: sudden clearly defined area on skin red and tender.
Bright red, shiny, swollen, hot.
Can be accompanied by fever, chills, HA, nausea, swollen lymph nodes.
Risk factors: Problematic circulation, Diabetes, Pregnancy, Alcoholism, Obesity.
Tx: Antibiotic Tx immediately- norm 10days

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11
Q

Viral skin Infection

  • Herpes virus
  • Shingles (herpes zoster-varicella)
  • Human papillomavirus (warts)
A

Herpes- blistering lesions, after infection virus persist in dorsal root ganglion in latent state, no cure. Herpes simplex I (non genital), II (genital), III (chicken pox/shingles)
Shingles- from dormant virus in DRG from chic pox, affects skin of corresponding dermatome creating vesicles, burning pain & tingling. P still present after rash gone.
Human Pap- 50 types benign epithelial tumour. genital W increase risk of cancer

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12
Q

Fungal skin Infections

  • Trichophyton
  • Microsporum
  • Epidermophyton
  • ring worm or tinea
A

40 species fungi, spores live up to yr on skin, reffered to as ‘ringworm’ or ‘tine’
Normally superficial infection. subcutaneous rare
Fungal hyphae or yeast resides in Keratin layer= little inflame response
sometimes infect hair follicle and will increase inflame response

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13
Q

Dermatological pathologies

A
Dermatitis
Acute vs. Chronic
Lichenoid Planus and Psoriasis 
Infection
Viral 
Herpes Zoster, Shingles and Human Papillomavirus (HPV)
Fungal
Bacterial
Impetigo and Cellulitis
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14
Q

Basal Cell Carcinomas

  • Character
  • 3 x types
A

-Develop from keratinocytes in basal layer
-linked to UV exposure
-local invasion but rare metast.
-lesions erode deep into tissue ‘rodent ulcer’
Nodular
Morphoeic
Superficial

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15
Q

Nodular BCC

A
  • most common, in over 50s mostly, on forehead & face
  • Firm, raised nodule, may centrally ulcerate and sink
  • Shiny, pearly raised spot
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16
Q

Morphoeic BCC

A

-less common BCC (hard to detect clinically)
-Flat thickened yellowish or whitish plaque, looks like pale scar
-may be sunken or firm, with focal ulceration
-Aggressive growth & significant tissue destruction
Contrast to Nodular= Edges are indistinct & tumour may extend to dermis & beyond the visible palpable borders

17
Q

Superficial Basal Cell Carcinoma

A
  • Flat, red plaque with irregular edges
  • slightly dry, scaly & often eroded n crusted
  • commonly on face but occur on trunk n limbs
  • sometimes raised areas within tumour= nodular BCC arising within lesion
  • grow broadly, generally not penetrating deeply into underlying dermis
  • can be confused psoriasis, dermatitis, tinea
18
Q

Squamous cell carcinoma

-2X types

A

-tumours of outer epidermis
-metastasise more commonly than BCC
-often form within precursor lesion (Actinic Keratoses- hard, scaly, red growth caused by sun exposure, benign)
Intraepidermal SCC
Invasive SCC

19
Q

SCC

  • Intraepidermal
  • Invasive
A

Intraepidermal: ‘Bowens Disease’, slowly enlarging plaque, usually some scaling n crusting
Invasive: Hardened nodule, thick keratotic scale, can erode or ulcerate, can express horny material from lesion

20
Q

Melanoma characteristics

A

NZ 2nd highest rate in world
4% of all skin cancers & 74% all skin canc. deaths
Develop from Melanocytes in groups Naevi or Moles
Can often metastasise

21
Q

-4x types Melanoma

A

Lentigo Malignant Mel: 4-10%, slow growth, flat Naevi, sun exposed areas, biphasic long radial growth before invasion
Superficial Spreading Mel: 70%, Naevis with raised edge, odd colour/outline radius, ulcerate & bleeds, prevalent in intermittent sun exposure & those who burn easily. biphasic
Nodular Mel: 15-30%, raised dome shape, black/blue, mono phasic W no rad growth phase
Acral Lentiginous Malignant Mel: 2-8%, occur on plams, soles of feet, nail beds an mucous membranes, appearance similar to lentigo

22
Q

2x stages of Melanoma growth

A

Radial Growth- remains in epiderm, no metastatic potential

Vertical growth- Invades dermis, can metastasise through lymph or vacs

23
Q

Melanoma Appearance warning signs

ABCDE

A
Asymmetry
Border
Colour
Diameter
Evolution
24
Q

Melanoma Risk Factors

A

Phenotype- fair skin, blue eyes, red hair
Generic Risk Factor: F.H. cancer
Presence of Naevi: atypical naevi, many naevi, large congenital naevi
Immunosuppression: other diseases or medication

25
Q

What is a port-wine stain and a Haemangioma?

A

Port-wine stain: at birth, flat purple-redish area on face, slow growing malformation of capillaries, rarely regresses
Haemangioma: common babies, located on trunk, buttock, face, from dark pink tumour. Benign vacs tumour & regresses 5-7yrs age