Dermatology Flashcards

1
Q

What is basal cell carcinoma?

A

A common neoplasm, related to exposure to sunlight-clinically presents as a pearly white papulo-nodule or firm plaque

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2
Q

What is the aetiology of basal cell carcinoma?

A

Repetitive and frequent sun exposure, as ultraviolet (UV) radiation induces DNA damage in keratinocytes

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3
Q

What is the epidemiology of basal cell carcinoma?

A

The most common malignancy of the skin in fair-skinned adults in the US, Australia, and Europe and its incidence is increasing
The incidence of BCC has been shown to increase markedly after the age of 40 years (incidence in younger people is steadily rising)

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4
Q

What are the presenting symptoms of basal cell carcinoma?

A

Pearly papules/plaques

Non-healing scabs

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5
Q

What are the signs of basal cell carcinoma on physical examination?

A

Plaques, nodules and tumours:

  • pearly appearance
  • rolled borders
  • small crusts, non-healing
  • associated Telangiectasis (tiny thread like blood vessels)
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6
Q

What are the appropriate investigations for basal cell carcinoma?

A

*Biopsy for dermatohistopathology:
(diagnosis of a cancer is histological)
-growth of nest(s) of varying size and shape
-either tightly associated with epidermis or follicular opening
-neoplasm composed of basophilic (blue) hyperchromatic cells
-stroma surrounding BCC is hypercellular, fibrous
-separation artefact between nests of neoplastic cells and the stroma (so-called stroma-epithelium split)

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7
Q

What is a burns injury?

A

A very common injury predominantly to skin and superficial tissues caused by heat from hot liquids, flame or contact with hot objects

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8
Q

How is the severity of burns injuries assessed?

A
  • Burn size (% of total body surface area)

- Depth ( first to fourth degree)

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9
Q

What symptoms and signs would be seen on physical examination for a burns injury?

A
Erythema
Dry/ wet and painful 
Dry and lacking of physical sensation (insensate) 
Cellulitis 
If face affected- clouded cornea
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10
Q

What are the risk factors for burn injuries?

A

Young children

Age > 60 years

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11
Q

What are the investigations for burn injuries?

A

FBC: Hb, Platelets, WCC, CRP, ESR
ABG: assessment of lungs/ inhalation injury
Wound biopsy and histology

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12
Q

What is candidiasis of the skin?

A

When Candida colonises on the skin causing an infection. Also known as cutaneous candidiasis

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13
Q

What is the aetiology of candidiasis of the skin?

A
  • Candida is a yeast-like fungus which is part of the normal commensal flora of the human gastrointestinal tract and the vagina
  • Candida albicans is the most common species and is responsible for over half of candidal skin infections
  • It is not part of the normal skin flora, but there may be transient colonization of fingers or body folds
  • Usually asymptomatic but where mucosal barriers are disrupted or if the host’s defences are lowered, it can cause infections
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14
Q

What is the epidemiology of candidiasis of the skin?

A

Candidiasis is common, being at extreme ages is a risk factor due to immature or weakened immunity

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15
Q

What are the risk factors for candidiasis of the skin?

A

More likely to occur where skin rubs on skin (such as between skin folds in an obese person) and where heat and moisture lead to maceration and inflammation
Other RF:
-Immunocompromised (HIV infection, chemotherapy, immunosuppressive drugs)
-General debility, for example from cancer or malnutrition
-Recent or concurrent use of drugs that promote candidal growth, particularly broad-spectrum antibiotics and inhaled or oral corticosteroids
-Diseases in which the barrier function of the skin is disturbed (such as psoriasis and seborrhoeic eczema).
-Endocrine disorders: Diabetes mellitus and Cushing’s syndrome
-**Iron deficiency anaemia — iron is the most common deficient essential micronutrient implicated in the colonization of Candida, as iron deficiency diminishes the fungistatic action of transferrin and other iron-dependant enzymes
-High-oestrogen contraceptive pill or pregnancy
-Poor hygiene

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16
Q

What are the presenting symptoms of candidiasis of the skin?

A

Rash-often causes redness and intense itching
Blisters and pustules may also occur
The rash is most likely to develop in the folds of the skin:
-armpits
-the groin
-between the fingers
-under the breasts
Candida can also cause infections in the nails, edges of the nails, and corners of the mouth

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17
Q

What are the signs of candidiasis of the skin on physical examination?

A

-Thin-walled pustules with a red base may be present
-Scales may accumulate, producing a white-yellow, curd-like substance over the infected area
In flexural areas (intertrigo), the skin fold is typically red and moist
-As the condition develops: a typical fringed, irregular edge and pustular or papular satellite lesions may be present
-If the web spaces of the toes or fingers are involved, marked maceration with a thick, horny layer is usually prominent

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18
Q

What are the appropriate investigations for candidiasis of the skin?

A

Investigations are not usually necessary, but may be required to exclude a differential diagnosis or an underlying condition (such as diabetes or anaemia), especially in people with widespread or recurrent infection
Swabs are not routinely recommended. However, standard bacteriology swabs for microscopy and culture may be required if:
-Secondary bacterial infection is suspected
-The person is immunocompromised
-The diagnosis is uncertain

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19
Q

What is Cellulitis?

A

An acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue
Characterised by: erythema, oedema, warmth, and tenderness, and commonly occurs in an extremity

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20
Q

What is Cellulitis usually characterised by?

A
Erythema
Oedema
Warmth
Tenderness
Commonly occurs in an extremity
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21
Q

What is Erysipelas?

A

A distinct form of superficial cellulitis with notable lymphatic involvement and is raised, sharply demarcating it from uninvolved skin

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22
Q

What is the aetiology of Cellulitis?

A

Cellulitis develops when micro-organisms gain entry to the dermal and subcutaneous tissues via disruptions in the cutaneous barrier
The most common causative agents are:
-Beta-haemolytic streptococci
-Staphylococcus aureus

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23
Q

What is the epidemiology of Cellulitis?

A
Cellulitis is a common condition
Main risk factors are:
-skin break
-poor hygiene 
-poor vascularization of tissue (e.g. diabetes mellitus)
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24
Q

What are the presenting symptoms of Cellulitis?

A

There may be history of a cut, scratch or injury
Skin discomfort
Periorbital: Painful swollen red skin around eye
Orbital cellulitis: Painful or limited eye movements, visual impairment

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25
Q

What are the signs of Cellulitis on physical examination?

A
Lesion: 
-Erythema
-Oedema
-Warm tender indistinct margins
*Pyrexia may signify systemic spread
Exclude abscess: 
Test for fluid thrill or fluctuation- aspirate if pus suspected
Periorbital: 
-Swollen eyelids
-Conjunctival injection
Orbital cellulitis: 
-Proptosis (protrusion of the eyeball)
-Impaired acuity and eye movement
Test for relative afferent pupillary defect, visual acuity and colour vision
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26
Q

What are the appropriate investigations for Cellulitis?

A

Bloods: WCC, blood culture
Discharge: Culture and sensitivity
Aspiration: As it is often non-purulent, it is not usually necessary
CT/MRI scan: When orbital cellulitis is suspected (to assess the posterior spread of infection)

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27
Q

What is the management of Cellulitis?

A

Medical:
-Oral penicillins (e.g. flucloxacillin, benzylpenicillin, coamoxiclav)
-Tetracyclines are effective in most community acquired cases
-In the hospital- intravenous use may be necessary
Surgical:
-Orbital decompression may be necessary in orbital cellulitis(emergency)
Abscess: Abscesses can be aspirated, incised and drained or excised completely

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28
Q

What are the complications of Cellulitis?

A
Sloughing (shedding) of overlying skin
Localized tissue damage
In orbital cellulitis, there may be permanent vision loss and spread to brain
Abscess formation
Meningitis
Cavernous sinus thrombosis
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29
Q

What is the prognosis of Cellulitis?

A

Good with treatment

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30
Q

What is Eczema?

A

An inflammatory skin reaction to endogenous or exogenous agents characterised by dry, pruritic skin with a chronic relapsing course

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31
Q

What is the aetiology of Eczema?

A

Numerous varieties caused by a diversity of triggers

  1. Atopic: Impaired epidermal barrier function or immune function disorder
  2. Contact: Type IV delayed hypersensitivity to allergen (e.g. nickel, chromate, perfumes, latex and plants)
  3. Discoid
  4. Dyshidrotic
  5. Herpeticum
  6. Seborrhoeic: Pityrosporum yeast seems to have a central role
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32
Q

What is the epidemiology of Eczema?

A

Contact: Prevalence 4 %
Atopic: Onset is commonly in the first year of life, childhood incidence 10–20 %

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33
Q

What are the presenting symptoms of Eczema?

A

Itching (can be severe), heat, tenderness, redness, weeping, crusting
Enquire into occupational exposures or irritants used at home (e.g. bleach) and into family/personal history of atopy (e.g. asthma, hay fever, rhinitis)

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34
Q

What are the signs of Eczema on physical examination?

A

Acute:
-Poorly demarcated erythematous oedematous dry scaling patches
-Atopic: Particularly affects face and flexures (inside elbow and knee)
-Papules, vesicles with exudation and crusting, excoriation marks
Chronic:
-Thickened epidermis
-Skin lichenification
-Fissures
-Change in pigmentation
Seborrhoeic: Yellow greasy scales on erythematous plaques, particularly in the nasolabial folds, eyebrows, scalp and presternal area

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35
Q

What are the appropriate investigations for Eczema?

A

Primarily clinical
Contact:
-Skin patch testing: Disc containing postulated allergen is diluted and applied to back for 48 h
-Positive if allergen induces a red raised lesion
Atopic:
-Laboratory testing, including IgE levels, are not used routinely and are not currently recommended
-Swab for infected lesions (bacteria, fungi and viruses)

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36
Q

What are Epidermoid and pilar cysts (sebaceous cysts)?

A

Benign small bumps beneath the skin
They can appear anywhere on the skin, but are most common on the face, neck and trunk
Two of the most common types of cysts

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37
Q

What is the aetiology of Epidermoid and pilar cysts?

A

Most form when cells from the epidermis move deeper into the skin and multiply rather than slough off
Sometimes the cysts form due to irritation or injury of the skin or the most superficial portion of a hair follicle.

The epidermal cells form the walls of the cyst and then secrete the protein keratin into the interior
The keratin is the thick, yellow substance that sometimes drains from the cyst
This abnormal growth of cells may be due to a damaged hair follicle or oil gland in your skin

Cysts that form around hair follicles are Pilar cysts

*These cysts used to be called sebaceous cysts but this term is no longer correct, as the origin of these cysts is not from the sebaceous glands in the skin, as was once thought

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38
Q

What is the epidemiology of Epidermoid and pilar cysts?

A

Epidermoid cysts: most common in young and middle-aged adults (develop on the face, neck, chest, upper back)
Pilar cysts: most common in middle-aged women and develop most commonly on the scalp

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39
Q

What are the presenting symptoms of Epidermoid and pilar cysts?

A

A small, round bump under the skin, usually on the face, neck or trunk
A tiny blackhead plugging the central opening of the cyst
A thick, yellow material that sometimes drains from the cyst
Redness, swelling and tenderness in the area, if inflamed or infected

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40
Q

What are the appropriate investigations for Epidermoid and pilar cysts?

A

The diagnosis of an epidermoid or pilar cyst is usually clinical
However, if suspicious the tissue can be excised and submitted for histology

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41
Q

What is Erythema multiforme?

A

An acute hypersensitivity reaction ( inflammatory condition) of the skin and mucous membranes, which is often self-limiting but often relapsing

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42
Q

What is the pathology of Erythema multiforme?

A

Degeneration of basal epidermal cells and development of vesicles between the cells and the underlying basement membrane
Lymphocytic infiltrate is seen around the blood vessels and at the dermal – epidermal junction
Immune complex deposition is variable and non-specific
Precipitating factor is only identified in only 50 % of cases

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43
Q

What is the aetiology of Erythema multiforme?

A
Drugs: Sulphonamides, penicillin, phenytoin, barbiturates
Infection:
-Viral: HSV, EBV, coxsackie, adenovirus
-Bacterial: Mycoplasma pneumoniae, Chlamydiae 
-Fungal: Histoplasmosis
Inflammatory: 
-Rheumatoid arthritis
-SLE
-Sarcoidosis
-Ulcerative colitis
-Systemic vasculitis
Malignancy: 
-Lymphomas
-Leukaemia
-Myeloma
Radiotherapy
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44
Q

What is the epidemiology of Erythema multiforme?

A

Any age group, but most commonly children and young adults

M:F: 2:1

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45
Q

What are the presenting symptoms of Erythema multiforme?

A

Non-specific prodromal symptoms of upper respiratory tract infection
Sudden appearance of itching/burning/painful skin lesions which may fade, leaving behind pigmentation
Recurrent disease

46
Q

What are the signs of Erythema multiforme on physical examination?

A

Classic lesions with 3 zones (red rim, clearance zone, and central blister or erosion) on the distal extremities
-target (‘bull’s eye’) lesions with a rim of erythema surrounding a paler area
-often symmetrical
-distributed over the arms and legs including the palms,
soles and the extensor surfaces

47
Q

What is Stevens–Johnson syndrome?

A

A severe form of Erythema multiforme with bullous lesions and necrotic ulcers, characterised by:

  • Affecting >2 mucous membranes: Conjunctiva, cornea, lips (haemorrhagic crusts), mouth, genitalia
  • Systemic symptoms: Sore throat, cough, fever, headache, myalgia, arthralgia, diarrhoea and vomiting
  • Shock: Hypotension, tachycardia
48
Q

What are the appropriate investigations for Erythema multiforme?

A

Bloods:

  • FBC: abnormal white cell count
  • Electrolytes: may be elevated if reduced fluid intake/dehydrated
  • HSV serology: may be positive
  • Investigations for cause: PCR, CXR (Mycoplasma pneumonia)
49
Q

What is Erythema nodosum?

A

Panniculitis (inflammation of the subcutaneous fat tissue) presenting as red or violet subcutaneous nodules

50
Q

What is the aetiology of Erythema nodosum?

A

Delayed hypersensitivity reaction to antigens associated with various infectious agents, drugs, and other diseases:
Infection: Bacterial (Streptococcus, TB, Yersinia, rickettsia, Chlamydia, leprosy), viral (EBV), fungal (histoplasmosis, blastomycosis, coccidioidomycosis), protozoal (toxoplasmosis)
Systemic disease: Sarcoidosis, IBD, Behcet’s disease Malignancy: Leukaemia, Hodgkin’s disease
Drugs: Sulphonamides, penicillin, OCP
Pregnancy
25 % of cases have no underlying cause identified

51
Q

What is the epidemiology of Erythema nodosum?

A

Usually affects young adults F:M is 3: 1

52
Q

What are the presenting symptoms of Erythema nodosum?

A

Tender red or violet nodules develop bilaterally on the shins and occasionally on the thighs and forearms
Fatigue, fever, anorexia, weight loss and arthralgia are often also present

53
Q

What are the signs of Erythema nodosum on physical examination?

A

Crops of red or violet dome-shaped nodules usually present on both shins (occasionally involving thighs or forearms) which are tender to palpation
Low-grade pyrexia
Joints may be tender and painful on movement
Sarcoidosis: uveitis, red eyes, retinal nodules

54
Q

What are the appropriate investigations for Erythema nodosum?

A

Bloods:
-FBC: high WCC, leukocytosis
-anti-streptolysin O titre: elevated in streptococcal infection, ideally checked at first visit, and repeated 2 to 4 weeks later
-Serum ACE (raised in sarcoidosis)
Throat swab and culture
Purified protein derivative skin testing: positive in tuberculosis
CXR:
-Bilateral hilar adenopathy indicates sarcoidosis
-Unilateral hilar adenopathy indicates tuberculosis, histoplasmosis, coccidioidomycosis, and brucellosis

55
Q

What is Herpes Simplex Virus?

A

Disease resulting from HSV1 or HSV2 infection

56
Q

What is the aetiology of Herpes Simplex Virus?

A

HSV is an alpha-herpes virus with double-stranded deoxyribonucleic acid (dsDNA)
Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse)

57
Q

What is the epidemiology of Herpes Simplex Virus?

A

90% adults seropositive for HSV1 by 30 years
35% adults >60 years seropositive for HSV2
Over 1/3 world population has recurrent HSV infections
Most common cause of encephalitis

58
Q

What are the presenting symptoms of Herpes Simplex Virus?

A

HSV1:
Primary infection often asymptomatic
Usual symptoms:
-Pharyngitis;
-Gingivostomatis, may make eating very painful
-Herpetic whitlow, inoculation of virus into a finger

Recurrent infection/reactivation (herpes labialis/‘cold sore’):

  • Prodrome (6 h) peri-oral tingling and burning
  • Vesicles appear (48 h duration), ulcerate and crust over -Complete healing 8–10 days

HSV2:
Very painful blisters and rash in genital, perigenital and anal area
Dysuria
Fever and malaise

59
Q

What are the signs of Herpes Simplex Virus on physical examination?

A

HSV1:
Primary infection:
-Tender cervical lymphadenopathy
-Erythematous, oedematous pharynx
-Oral ulcers filled with yellow slough (gingivostomatitis)
-Digital blisters/pustules (herpetic whitlow)

Herpes labialis: Perioral vesicles/ulcers/crusting

HSV2:

  • Maculopapular rash
  • Vesicles and ulcers (external genitalia, anal margin, upper thighs)
  • Inguinal lymphadenopathy
  • Pyrexia
60
Q

What are the appropriate investigations for Herpes Simplex Virus?

A

Usually a clinical diagnosis

Vesicle fluid: Electron microscopy, PCR, direct immunofluorescence, growth of virus in tissue culture

61
Q

What is a Lipoma?

A

Low-growing, benign, mesenchymal tumours that form well-circumscribed, lobulated lesions composed of adipocytes

62
Q

What is the aetiology of Lipomas?

A

The aetiology for most lipomas is idiopathic
However, they may also appear on a hereditary basis in patients with familial multiple lipomatosis or in patients with Gardner’s syndrome (subtype of familial adenomatous polyposis (FAP))

63
Q

What is the epidemiology of Lipomas?

A

Approximately 1% of the general population has a lipoma

Although they can occur at any age, they are most common between 40 and 60 years of age

64
Q

What are the presenting symptoms and signs of a Lipoma?

A

Cutaneous mass:

  • Diameter <5cm
  • Soft: doughy in texture, similar to the consistency of subcutaneous fat
  • Mobile
  • Superficial
  • Painless (some can cause some discomfort if they undergo abrasion from clothing)
65
Q

What are the appropriate investigations for Lipomas?

A

MRI:
-Modality of choice for extremity and head and neck lesions
-If a lesion is more than 3 cm and seems deep to the superficial fascia, imaging should be considered
-Typically discrete, encapsulated, homogeneous mass
CT scan:
-For truncal lesions more than 3 cm in diameter
-Typically discrete, encapsulated, homogeneous mass
Ultrasound:
-considered in the setting of clinically suspect superficial subcutaneous lipoma
Biopsy:
-any extremity or truncal soft-tissue mass that is symptomatic or enlarging, larger than 3 cm, or new and persisting beyond 4 weeks - CORE BIOPSY
-well-circumscribed, lobulated, mesenchymal tumours composed of adipocytes and demarcated from surrounding fat by a thin, fibrous capsule
-Incisional if core biopsy is inconclusive
-Excisional biopsy is recommended for cutaneous or subcutaneous tumours more than 3 cm in size

66
Q

What is a Melanoma?

A

A malignant tumour arising from melanocytes, the pigment-forming cells of the skin
It is the leading cause of death from skin disease

67
Q

What is the aetiology of Melanomas?

A

DNA damage in melanocytes caused by ultraviolet radiation results in neoplastic transformation
50 % arise in pre-existing naevi, 50 % in previously normal skin

68
Q

What are the four histopathological types of Melanoma?

A
  1. Superficial spreading (70 %): Typically arises in a pre-existing naevus, expands in radial fashion before vertical growth phase
  2. Nodular (15 %): Arises de novo, aggressive, no radial growth phase
  3. Lentigo maligna (10 %): More common in elderly with sun damage, large flat lesions, follow an indolent growth course. Usually on the face
  4. Acral lentiginous (5 %): Arise on palms, soles and subungual areas. Most common type in non-white populations
69
Q

What is the epidemiology of Melanomas?

A

Steadily increasing incidence, 17 per 100,000 diagnosed in the United Kingdom
Among the most common forms of cancer, and causes of cancer-related death, in young adults
Either gender and any ethnic group may be affected, although men and fair-skinned people are more likely to develop melanoma

70
Q

What are the presenting symptoms of Melanomas?

A

A melanocytic (pigmented) lesion that is changing with regard to size, shape, or colour
Naevi: visible clusters of cells in the skin (large amounts, atypical)
Redness
Bleeding
Crusting
Ulceration

71
Q

What are the signs of Melanomas on physical examination?

A
ABCD criteria for examining moles: 
A Asymmetry
B Border irregularity/bleeding
C Colour variation
D Diameter > 6 mm
E Elevation
72
Q

What are the appropriate investigations for Melanomas?

A

Dermatoscopy: melanocytic lesion with abnormal appearance concerning for melanoma
Skin biopsy: abnormal melanocytic proliferation in the epidermis and/or dermis typical of melanoma (excisional)
Others:
-Sentinel lymph node biopsy (SLNB): presence or absence of metastatic disease, (if primary and < 1 mm depth)
-Serum LDH: used to classify metastatic disease
-Imaging: CXR, CT chest/abdominal, PET, CT/MRI of brain: may show metastases
-BRAF mutational analysis: may show mutation in the BRAF gene/protein

73
Q

What is Molluscum contagiosum?

A

A common childhood skin infection with multiple small translucent vesicle- like papules that have a central punctum
Caused by the molluscum contagiosum virus, a ubiquitous poxvirus that escapes immune destruction for months to years

74
Q

What is the aetiology of Molluscum contagiosum?

A

The lesions are caused by the molluscum contagiosum virus (MCV), of which there are three types:

  • MCV 1 and 1v are seen in children as the result of child-to-child contact or fomites (any inanimate object that, when contaminated with or exposed to infectious agents, can transfer disease to a new host)
  • MCV 2 is a sexually transmitted virus noted in the groin in adults and generalised in immunocompromised people
  • MCV 3 is a rare subtype in any age group
75
Q

What is the epidemiology of Molluscum contagiosum?

A

The condition most commonly affects children, with an overall prevalence in children estimated to be between 5% and 12%
Adults may also be infected via sexual transmission
There is no sex or ethnic trend in the incidence of molluscum

76
Q

What are the presenting symptoms and signs of Molluscum contagiosum?

A

Pearly papules with central dells (depression)
Surround erythema
Pruritus

77
Q

What are the appropriate investigations for Molluscum contagiosum?

A

Curettage biopsy: Rarely required but may be used to confirm diagnosis
-Haematoxylin and eosin staining: provides a definitive diagnosis, Henderson-Patterson bodies
Tzanck stain: difficult to interpret, purple ovoid keratinocytes
Important to test for HIV in adults

78
Q

What are Pressure Sores?

A

Also known as pressure ulcers
Localised injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure or of pressure in combination with shear
*most commonly occur over bony prominences but can develop on any part of the body, including mucosal surfaces

79
Q

What is the aetiology of Pressure Sores?

A

Rraditionally been thought to develop through the interplay of 4 main factors:
-Pressure
-Shear
-Friction
-Moisture
Pressure is clearly the most important factor and both the duration and intensity of pressure are important
Irreversible tissue damage may occur as a result of relatively short exposures to high levels of pressure or longer exposure to lower levels of pressure
While it is generally recommended that patients be repositioned every 2 hours, it is likely that in some situations, considerably less time is required for tissue damage to occur

80
Q

What is the epidemiology of Pressure Sores?

A

General acute care ranged from 2.8% to 9.0%
In long-term care, the incidence rates ranged from 3.6% to over 50%, and in home care from 4.5% to 6.3%
Most pressure ulcers, regardless of setting, were located on the sacrum or coccyx and heels

81
Q

What are the presenting symptoms and signs of Pressure Sores?

A

Localised skin changes on areas subjected to pressure:
Non-blanching erythema or purple localised area of discolored intact skin
-May be painful, firm, mushy, boggy, or warmer or cooler than adjacent tissue
Shallow open wonder tissue areas (ulcer): A blister or a shiny or dry shallow ulcer involving partial loss of dermis
Full-thickness wound with/without major tissue involvement (exposed bone, tendon, or muscle)- where there is exposed bone, osteomyelitis should be considered
Localised tenderness and warmth around the area: suggestive of infection
Increased exudate and/or foul odour: indicates infection

82
Q

What are the appropriate investigations for Pressure Sores?

A

Usually clinical diagnosis
Others:
-Wound swab: positive culture in infection
-ESR: Suggests osteomyelitis (>100 mm/hour)
-WCC: >15.0 x 10^9/L suggests osteomyelitis
-Serum glucose to exclude diabetes
-Deep tissue biopsy: definitive method for diagnosing infection but not always practical in a clinical setting
MRI: appropriate whenever bony involvement is possible

83
Q

What is Psoriasis?

A

A chronic inflammatory skin disease characterised by erythematous, circumscribed scaly papules, and plaques

84
Q

What is the aetiology of Psoriasis?

A

Unknown
Genetic, environmental factors and drugs (e.g. may be triggered by streptococcal infections, antimalarial agents, b-blockers, lithium)

85
Q

What is the epidemiology of Psoriasis?

A

Affects 1–2 % of the population
Peak age of onset 􏰀 20 years

86
Q

What are the associations of Psoriasis?

A

Guttate psoriasis: Streptococci sore throat
Palmoplantar pustulosis: Smoking, middle-aged women, autoimmune thyroid disease, SAPHO (synovitis, acne, palmoplantar pustulosis, hyperostosis seen on radiographs, osteitis – chronic recurrent multifocal inflammation of bones, e.g. sternoclavicular, sacroiliac joint)
Generalised pustular: Hypoparathyroidism.

87
Q

What are the presenting symptoms of Psoriasis?

A

Skin lesions on elbows, knees, extensor surfaces of limbs, scalp, and, less commonly, nails, ears, and umbilical region
Itching or occasionally tender skin.
Pinpoint bleeding with removing scales (Auspitz phenomenon)
Skin lesions may develop at the site of trauma/scars (Koebner phenomenon)

88
Q

What are the signs of Psoriasis on physical examination?

A

Typically erythematous, circumscribed scaly papules and plaques on elbows, knees, extensor surfaces of limbs, scalp
Others:
-Discoid/nummular psoriasis: Symmetrical well-demarcated erythematous plaques with silvery scales over extensor surface (knee, elbows, scalp, sacrum)
-Flexural psoriasis: Less scaly plaques in axilla, groins, perianal and genital skin
-Guttate: Small (􏰀1 cm) drop-like lesions over trunk, limbs.
-Palmoplantar: Erythematous plaques with pustules on palms and soles
-Generalized pustular psoriasis: Pustules distributed over limbs and torso
-Nail: Pitting, onycholysis (lifting off of the nail-plate from the nail-bed), subungual hyper-keratosis, ‘salmon patch’ on the nail
-Joints: Seronegative arthritis with six possible presentations:
1. monoarthritis
2. distal asymmetrical oligoarthritis (distal interphalangeal joints)
3. dactylitis (interphalangeal arthritis and flexor tenosynovitis)
4. rheumatoid arthritis-like (symmetrical polyarthritis)
5. arthritis mutilans (telescoping of the digits)
6. ankylosing spondylitis

89
Q

What are the appropriate investigations for Psoriasis?

A

*Clinical diagnosis
Skin biopsy: when diagnosis is in doubt
-intra-epidermal spongiform pustules
-Munro neutrophilic microabscess within the stratum corneum
Others:
-Guttate psoriasis: Anti-streptolysin-O titre, throat swab
-Flexural lesions: Skin swabs (exclude candidiasis)
-Nail: Analyse nail clippings to exclude onychomycosis (fungal infection)
-Joint involvement: Rheumatoid factor (negative), radiographs (distal interphalangeal joints)

90
Q

What is squamous cell carcinoma of the skin?

A

The proliferation of atypical, transformed epidermal keratinocytes in the skin with malignant behaviour

91
Q

What is the aetiology of squamous cell carcinoma of the skin?

A

The incidence of non-melanoma skin tumours varies dramatically on:

  • Skin phototype or constitutive pigmentation
  • Cumulative sun exposure (geographic latitude)
  • Solar UV exposure (MAIN RF)
  • Ionising radiation
  • Burns
  • Hereditary skin conditions
  • Environmental toxins such as arsenic and tar
  • Human papillomavirus
  • Some immunocompromised states
92
Q

What is the epidemiology of squamous cell carcinoma of the skin?

A

Second most common cutaneous malignancy (20% of skin cancers)
Often occurring in middle-aged and elderly light-skinned individuals
Annual incidence is about 1/4,000
Male > female (2/3:1)

93
Q

What are the presenting symptoms of squamous cell carcinoma of the skin?

A

Skin lesion:

  • Ulcerated
  • Recurrent bleeding or non-healing
  • Growing
  • Marjolin ulcer presents in an area of previously traumatised, chronically inflamed or scarred skin
94
Q

What are the signs of squamous cell carcinoma of the skin on physical examination?

A
Variable appearance: 
-Ulcerated 
-Hyperkeratotic 
-Crusted or scaly 
-Non-healing lesion 
*often on sun-exposed areas 
Palpate for local lymphadenopathy- metastatic disease
95
Q

What are the appropriate investigations for squamous cell carcinoma of the skin?

A

Skin biopsy: Confirms malignancy (full thickness keratinocyte atypia) and distinguishes it from other skin lesions
Fine-needle aspiration or lymph node biopsy: Only necessary if suspicion of metastasis
Staging: CT and/or MRI, PET scanning: lymphadenopathy and/or visceral nodules
Bloods: normal unless metastasis

96
Q

What are the differences between Basal Cell Carcinoma and Squamous Cell Carcinoma?

A

SCC are fast growing, penetrate deeper

BCC are slow growing, rarely metastasise

97
Q

What is Urticaria?

A

A skin condition characterised by erythematous, blanching, oedematous, non-painful, pruritic lesions that typically resolve within 24 hours and leave no residual markings

98
Q

What is the aetiology of Acute Urticaria?

A

Many cases of acute urticaria are allergic in nature and caused by an IgE-mediated reaction
The most common agents involved are drugs (e.g., penicillins, sulfonamides, muscle relaxants, diuretics, NSAIDs) and foods (e.g., milk, eggs, peanuts, tree nuts, finfish, shellfish). Insect bites can also lead to acute urticaria
Non-IgE-mediated mechanisms can also be responsible and these cases tend to involve certain drugs (e.g. NSAIDs, opioids, vancomycin), radiocontrast dye, or acute viral infections (especially in children)

99
Q

What is the aetiology of Chronic Urticaria?

A

Approximately 40% of cases are thought to be autoimmune in nature, while many cases are idiopathic
individuals with acute or chronic urticaria experience spontaneous and unpredictable lesions

100
Q

What is the epidemiology of Urticaria?

A

The life-time prevalence for acute urticaria is approximately 20%.
While the majority of these cases are acute and self-limiting events, roughly 30% of people will go on to experience prolonged symptoms
Acute urticaria is more common in children and adolescents than in adults, while chronic urticaria more typically affects adults
In chronic urticaria, women are affected more often than men

101
Q

What are the presenting symptoms/signs of Urticaria?

A

Erythematous oedematous lesions that may be distributed on any part of the body
Typically pruritic, although occasionally patients may report a painful or burning sensation
Generally resolve within 24h
Swelling of the face, tongue or lips (up to 40% of cases of urticaria have associated angio-oedema)
*Urticarial lesions blanch when palpated:
Non-blanching lesions should raise suspicion for vasculitis

102
Q

What are the appropriate investigations for Urticaria?

A

Mainly for chronic urticaria
Bloods:
-FBC: may provide evidence of occult infection, anaemia, or findings suggestive of chronic illness
-Metabolic profile: May provide evidence of chronic illness, such as hepatitis or nephritis
-ESR and CRP: non-specific elevation
-anti-Ig E antibodies: reassures both the patient and the physician that there are no exogenous factors causing the condition
-Antithyroid/antinuclear antibodies: exclude thyroid/rheumatic causes of chronic illness

Skin biopsy: may show urticarial vasculitis in setting of atypical urticarial lesions

103
Q

What is Varicella Zoster?

A

Primary infection is called varicella (chickenpox)

Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles)

104
Q

What is the aetiology of Varicella Zoster?

A

VZV is an herpes ds-DNA virus

Highly contagious, transmission is by aerosol inhalation or direct contact with the vesicular secretions

105
Q

What is the epidemiology of Varicella Zoster?

A

Chickenpox peak incidence occurs at 4–10 years
Shingles peak incidence occurs at >50 years
About 90% of adults are VZV IgG positive (previously infected)

106
Q

What are the presenting symptoms of Varicella Zoster?

A

*Incubation period 14–21 days
Chickenpox:
-Prodromal malaise
-Mild pyrexia
-Sudden appearance of intensely itchy spreading rash affecting the face and trunk more than the extremities, the oropharynx, conjunctivae and genitourinary tract
-As vesicles weep and crust over, new vesicles appear
-Contagious from 48 h before the rash and until all the vesicles have crusted over (within 7–10 days)

Shingles:
-May occur after a period of stress
-Tingling/hyperaesthesia in a dermatomal distribution, followed by painful skin lesions
Recovery in 10–14 days

107
Q

What are the signs of Varicella Zoster on physical examination?

A

Chickenpox (disseminated varicella):
-Macular papular rash evolving into crops of vesicles with areas of weeping (exudate) and crusting (vesicles, macules, papules and crusts may all be present at one time)
-Skin excoriation (from scratching)
-Mild pyrexia
Shingles:
-Vesicular macular papular rash, in a dermatomal distribution
-Skin excoriation

108
Q

What are the appropriate investigations for Varicella Zoster?

A

*Clinical diagnosis: typical vesicular rash at different stages, with pruritus, fever, malaise

Others:
-Vesicle fluid: Electron microscopy, direct immunofluorescence, cell culture, viral PCR (all
rarely necessary)
-Chickenpox: Consider HIV testing especially in adults with prior history of varicella infection

109
Q

What is the management for Varicella Zoster?

A

Chickenpox (primary infection):

  • Children: Treat symptoms (calamine lotion, analgesia, antihistamines)
  • Adults: Consider acyclovir if within 24 h of rash onset especially if elderly, smoker, immunocompromised or pregnant (especially second or third trimester)

Shingles (reactivation):

  • Aciclovir, valaciclovir or famciclovir if within 72 h of appearance of the rash if elderly, immunocompromised or ophthalmic involvement.
  • Low-dose amitriptyline may benefit those with moderate/severe discomfort
  • Simple analgesia (paracetamol)

Prevention:

  • VZIG(immunoglobulin blood product that is offered to individuals at high risk of severe chickenpox) may be indicated in the immunosuppressed and in pregnant women exposed to varicella zoster
  • Chickenpox vaccine is licensed in the United Kingdom, but no guidelines available for appropriate use
110
Q

What are the complications of Varicella Zoster?

A

Chickenpox:

  • Secondary infection e.g. Pneumonia, encephalitis, cerebellar syndrome, congenital varicella syndrome
  • Scarring

Shingles:

  • Postherpetic neuralgia
  • Zoster opthalmicus (rash involves opthalmic division of trigeminal nerve)
  • Ramsay Hunt’s syndrome (bilateral facial weakness)
  • Sacral zoster may lead to urinary retention
  • Motor zoster (muscle weakness of myotome at similar level as involved dermatome)
111
Q

What is the prognosis of Varicella Zoster?

A

Depends on the complications

Worse in pregnancy, the elderly and immunocompromised