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Year 2 > DERM > Flashcards

DERM Flashcards

1
Q

Functions of the skin

A 
1. Barrie rot infection 
2> thermoregulation 
3. Protection against trauma
4. Protection against UV
5. Vit D syntehsis
6. Regulate H20 loss
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2
Q

pH of the skin

A

5.5

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3
Q

Why is the skin pH 5.5

A

Allows proteases on the skin to do desquamination

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4
Q

What is the stratum corneum

A

Made of corner-desmosomes and desmosomes

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5
Q

What are cornel-desmosomes

A

Adhesion molecules that keep corneocytes together

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6
Q

Describe the layers of the skin

A
  1. Stratum lucidium
  2. Granulosum
  3. Spinous
  4. Basale
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7
Q

What nerve endings are found in the dermis

A

Meissner’s corpuscules - light touch

2. Pacinian corpuscle (vibration)

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8
Q

Role of keratinocytes

A

Produce keratin as a protective barrier

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9
Q

Role of Langerhans cells

A

Present antigens and activate T cells

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10
Q

Role of merkel cells

A

Specialised nerve endings for sensation

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11
Q

Common causes of itch with rash

A
  1. URTICARIA (hives)
  2. ATOPIC ECZMA
  3. Psoriasis
  4. Scabies
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12
Q

Common causes of itch with no rash

A
  1. Renal failure
  2. Jaundice
  3. Iron deficiency
  4. Lymphoma (hodgkin’s)
  5. Polycythaemia
  6. Pregnancy
  7. Drugs
  8. Diabetes
  9. Cholestasis
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13
Q

What is acne

A

Expansion and blockage of hair follicle and inflammation

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14
Q

Most common variant of acne

A

Acne Vulgaris

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15
Q

Pathophysiology of acne

A
  1. Hypercornfiictaion causes narrowing of hair follicle
  2. Increased sebum production
  3. Sebum is trapped which narrows follicle further
  4. Sebum stagnates at pit of follicle where there is no oxygen
  5. Anaerobic conditions allow propionibacterium acne to multiply
  6. P. acne breaks down triglycerides in sebum into free fatty acids = irritation, inflammation and attraction of neutrophils
  7. Pus formation as attract neutrophils come into the area
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16
Q

Whitehead vs blackhead

A

White - closed comedones

Black - open comedones

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17
Q

Clinical presentation of acne

A
  1. Whiteheads
  2. Blackheads
  3. Skin coloured papule (red spots)
  4. Inflammatory lesions when closed wall of comedones rupture
  5. Pustules (yellow spots)
  6. Nodules (large red bumps
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18
Q

Diagnosis of acne

A
  1. Skin swabs for culture

2. Hormonal test in females

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19
Q

Treatment of acne

A
  1. BENZOYL PEROXIDE
  2. CLINDAMYCIN GEL
  3. TAZAROTENE GEL (topical retinoid)
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20
Q

How does Benzoyl peroxide work

A

Increases skin turnover
Clears pores and reduces bacterial count
Causes dryness due to kertaolytic effect

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21
Q

How do topical retinoids work

A

Inhibit formation and reduce number of micromedones

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22
Q

Severe acne treatment

A
  1. ORAL DOXYCYCLINE
  2. ORAL MINOCYCLINE

HORMONE TREATMENT with ORAL CO-CYPRINDIOL (anti-androgen suppresses sebum productioN)

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23
Q

What is eczema/dermatitis

A

Breakdown of skin due to thinning of stratum corneum - increased risk of inflammation

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24
Q

What is endogenous eczema

A

Hypersensitivity caused (food allergies)

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25
Q

What is exogenous eczema

A

Contact dermatitis due to chemicals, sweat and abrasives

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26
Q

Pathophysiology of eczema

A
  1. Damaged filaggrin

2. CD4 lymphocytic activation = inflammation

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27
Q

Role of filaggrin

A

Skin barrier protein

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28
Q

Clinical presentation of eczema

A
  1. face and flexure surfaces of limbs
  2. Itchy, erythematous and scaly patches
  3. Dryness of skin
  4. Very acute lesions
    RECURRENT STAPHYLOCOCCUS AUREUS INFECTIONS
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29
Q

Diagnosis of eczema

A
  1. Atopic dermatitis:
    High serum IgE
    Itchy skin for 6 months
PULS:
History of involvement of skin creases
Asthma or hay fever
Dry skin history 
Childhood
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30
Q

Treatment of eczema

A
  1. Eductaion
  2. Avoid allergens
  3. Keep nails short
  4. E45 CREAM
  5. Topical corticosteroids
  6. Second line: Topical calcineurin inhibitors
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31
Q

How does E45 work (EMOLLIENT THERAPY)

A
  1. Traps moisture in skin to increase hydration and acts as barrier to water loss

Natural moisturising factor in corneocytes is depleted in eczema

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32
Q

How often is E45 applied

A

Every 4hours / 3 - 4 times a day

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33
Q

What topical corticosteroids are given as first line treatment for eczema

A
  1. CLOBETASOL PROPIONATE
  2. FLUCINONIDE
  3. CLOBETASOL BUTYRATE
  4. HYDROCORTISONE
    used for inflamed skin
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34
Q

What topical calcineurin inhibitors are given

A

PIMECROLIMUS or TACROLIMUS ointment

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35
Q

How do topical calcineurin inhibitors work

A
  1. Inhibit IL 2 which reduces inflammation and do not cause skin atrophy
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36
Q

3rd line treatment for eczema

A
  1. CICLOSPORIN
  2. AZOTHIOPRINE
  3. ORAL PREDNISOLONE
  4. FLUCLOXACILLIN
  5. PHOTOTHERAPY with UV A
  6. CHLORPHENAMINE
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37
Q

What is psoriasis

A

Hyper proliferation of keratinocytes + inflammatory cell infiltration

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38
Q

What aged people are effected by psoriasis

A

ADULTS

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39
Q

What environmental triggers cause psoriasis

A
  1. Infection by group A strep
  2. Lithium
  3. UV
  4. Alcohol
  5. Stress
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40
Q

Pathophysiology of psoriasis

A
  1. T cell activation = up regulation of INF gamma, IL1,2,8

2. Increased uncontrolled proliferation of keratinocytes

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41
Q

Clinical presentation of psoriasis

A
  1. Pitting and onycholysis (separation of finger nail from nail bed)
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42
Q

Clinical presentation of chronic plaque psoriasis

A
  1. Disc shaped salmon-pink-silvery plaques on exterior surfaces of elbows and knees
  2. Plaques on hair margin
  3. Thickened epidermis
  4. New plaques at skin trauma sites
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43
Q

How is chronic plaque psoriasis treated

A
  1. E45
  2. CALCIPQOTRIOL CREAM (topical vit D analogues)
  3. HYDROCORTISONE CREAM (topical corticosteroids)
  4. TAZAROTENE GEL (topical retinoid)
  5. UV B
  6. COAL TAR
  7. DITHRANOL CREAM (anti-mitotic)
  • ——SEVERE——-
    1. UV A
    2. DMARD (METHOTREXATE and FOLIC ACID)
    3. CICLOSPORIN
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44
Q

Clinical presentation of flexural psoriasis

A
  1. Red, glazed non-scaly plaques

2. Confined to flexures (groin, natal cleft and sub-mammary areas)

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45
Q

How is flexural psoriasis treated

A
  1. HYDROCORTSIONE - causes atrophy

2nd line: CALCIPQOTRIOL CREAM (irritating so don’t use for face)

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46
Q

Clinical presentation of Guttate psoriasis

A
  1. Trunk, upper arms and legs
  2. Small circular and oval plaques afterr 2 weeks of strep sore throat
  3. CHILDREN
47
Q

treatment of GUTTATE PSORIASIS

A
  1. HYDROCORTISONE or CLOBETASOL UTYRATE
  2. UV B
  3. Coal tar
48
Q

Clinical presentation of Palmoplantar psoriasis

A
  1. Thickening of palms and soles
49
Q

Treatment of palmoplantar psoriasis

A
  1. Emollients
  2. SALICYLIC ACID
  3. FLUCINONIDE
  4. UV A
  5. ORAL ACITRETIN (anti-proliferative)
  6. Anti-TNF biologics (IV INFLIXIMAB or IV ADALIMUMAB)
50
Q

Define venous skin ulcers

A

Loss of skin below knee on leg or foot that takes 2 weeks to heal

51
Q

What causes venous skin ulcers

A

Sustained venous hypertension in superficial veins

52
Q

What causes sustained venous hypertension

A
  1. Incompetent valves in deep veins
  2. Previous DVT
  3. Atherosclerosis
  4. Vasculitis (RA and SLE)
53
Q

Risk factors for venous skin ulcers

54
Q

Pathophysiology of venous skin ulcers

A
  1. Increased pressure causes extravasation of fibrinogen through capillary walls giving his ego perivascular fibrin deposition = poor oxygenation of surrounding skin
55
Q

Clinical presentation of venous skin ulcers

A
  1. Sloping and gradual edges
  2. Large, irregular ulcer
  3. Minimal pain
  4. Oedema of lower leg
  5. Venous eczema
  6. Brown pigmentation from haemosiderin
  7. Varicose veins
  8. Pulses present
  9. Warm skin
56
Q

Diagnosis of venous skin ulcers

A
  1. Ankle brachial pressure index is normal

2. Doppler ultraosund

57
Q

Treatment of venous skin ulcers

A
  1. High compression 4 layered bandage
  2. Leg elevation to reduce hypertension
  3. Antibiotics
  4. IBUPROFEN
  5. Support stockings for life
58
Q

What are arterial ulcers

A

Present as punched-out, painful higher up the leg or on the feet

59
Q

Risk factors for arterial ulcers

A
  1. Atherosclerosis
  2. Smoking
  3. Hypercholesterolaemia
  4. Diabetes Mellitus
60
Q

Clinical Presentation of arterial ulcers

A
  1. Punch-out ulcers higher up on the leg or on feet
  2. Pain is worse when elevated
  3. Leg is cold and pale
  4. Ulcer is small and sharply defined with necrotic base
  5. Shiny pale skin and loss of hair
  6. Absent peripheral pulses
  7. Arterial bruits (murmurs caused by turbulent blood flow
  8. NO OEDEMA
61
Q

Diagnostics of arterial ulcers

A
  1. Doppler Ultrasound

2. ABPI

62
Q

Treatment of arterial ulcers

A
  1. Cover and clean ulcer
  2. Analgesia (IBUPROFEN)
  3. Vascular reconstruction
  4. NEVER USE COMPRESSION BANDING
63
Q

What is a neuropathic ulcer

A

Seen over pressures of the feet which are painful

DIABETES and LEPROSY

64
Q

Clinical presentation of neuropathic ulcer

A

Warm skin and normal peripheral pulses

65
Q

Treatment of neuropathic ulcer

A
  1. Keep ulcer clean and remove pressure or trauma from affected areas
  2. Correctly fitting shoes and specialist podiatrist help for diabetics
66
Q

What is a vasculitic ulcer

A
  1. Blood vessels causing endothelial damage
67
Q

How is cutaenosu vasculitis diagnosed

A

SKINBIOPDY

68
Q

What is Leucocytoclastic vasculitis

A
  1. Appears on the lower legs as symmetrical palpable purport
69
Q

What causes lecuocytoclastic vasculitis

A
  1. Drugs
  2. Infection
  3. Inflammatory disease
  4. Malignant disease
70
Q

Clinical presentation of leucocytoclastic vasculitis

A
  1. Haemorrhagic papules
  2. Pustules
  3. Nodules
  4. Plaques
  5. NON BLANCHING PURPURIC LEISIONS
  6. Pyrexua and arthralgia
71
Q

Treatment of leucocytoclastic vasculitis

A
  1. Analgesia
  2. Support stocking s
  3. DAPSONE or PREDNISOLONE
72
Q

What kind of cancer is skin cancer

A

SQUAMOUS CELL CARCINOMA of the keratinocytes

73
Q

Why is SCC more aggressive than BCC

A

Metastases to the lymph nodes

74
Q

What is Bowen’s disease

A

SCC confined to the epidermis

75
Q

Risk factors of SCC

A
  1. UV

2. Chronic inflammation

76
Q

Clinical presentation of SCC

A
  1. Sun-exposed sites
  2. Lesions are keratotic that may ulcerate
  3. Grow very rapidly
  4. Ulcerates lesions on lower lip or ear ar more aggressive
    5
77
Q

Treatment of SCC

A
  1. Surgical excision with margin of 5mm

2. Raiodtherapy

78
Q

Where are Basalc ell carcinomas found

A

Elderly on head and neck

79
Q

What is a rodent ucler

A

Ulceration of basal cell carcinoma

80
Q

What is basal cell carcinoma

A

Tumour of basal keratinocytes

81
Q

Risk factors of BCC

A
  1. UV
  2. Skin type I
  3. Ageing
82
Q

What is skin Type I

A

Skin that burns and doesn’t tan

83
Q

Clinical presentation of BCC

A
  1. Border of ulcerated lesion raised with pearly appearance
  2. Slowly enlarging, shiny nodule on head and neck area which bleeds following minor trauma and does not heal
  3. Slowly causes local tissue destruction if not treated
84
Q

How is BCC treated

A
  1. Surgically excised to ensure clear and adequate tumour margins
  2. Cryotherapy + Photodynamic therapy
  3. Radiotherapy for those who don’t tolerate surgery
85
Q

What is malignant melanoma

A
  1. Malignant tumour of melanocytes
86
Q

Age effected by malignant melanoma

A

Younger patients

87
Q

Risk factors for malignant melanoma

A
  1. UV exposure
  2. Red hair
  3. High density freckles
  4. Skin type I
  5. Atypical moles
  6. Multiple melanocytic nave
  7. Sun sensitivity
  8. Immunosuppression
  9. Family History
  10. Pale Skin
88
Q

Clinical Presentation of Malignant Melanoma

A
  1. Men - Back
  2. Women - Lower legs
  3. Very dark colour, black
  4. ABCDE:
    A - Asymmetrical shape
    B - Border irregularity
    C - Colour Irregularity
    D - Diameter > 6
    E - Elevation/Evolution (change of lesion)
  5. Itching
  6. Inflammation, crusting or bleeding
89
Q

Types of melanomas

A
  1. Superficial Spreading
  2. Lentigo maligna (on face)
  3. Acral (restricted to palms and soles
90
Q

Differential diagnosis of melanomas

A
  1. Benign pigmented naevus
  2. Seborrhoeic wart
  3. Pyogenic granuloma
91
Q

How is Malignant Melanoma treated

A
  1. Surgical excision in early stages

2. Removal of regional lymph nodes, isolated limb perfusion, radiotherapy, immunotherapy and chemotherapy

92
Q

Metastases of malignant melanoma

A
  1. Lung, Liver, CNS
93
Q

Prognosis of Malignant Melanoma

A
  1. Thin lesions (<1mm) have best prognosis
  2. If over 60 then lower 5 year survival
  3. Generally there is a female advantage in prognosis
  4. Ulceration
  5. Poor prognosis if present on trunk vs limbs
94
Q

What is cellulitis

A
  1. Bacterial Infection of the deep sub-cutaneous tissues
95
Q

Where is cellulitis commonly seen

A

Lower extremities

96
Q

What causes cellulitis

A
  1. STREPTOCOCCUS PYOGENES (Group A beta-haemolytic)

2. Staph Aureus

97
Q

Risk factors for cellulitis

A
  1. Lymphedema
  2. Leg Ulcer
  3. Immunosuppression
  4. Traumatic wounds
  5. Athletes for
  6. Leg Oedema
  7. Obesity
98
Q

Clinical Presentation of cellulitis

A
  1. Local inflammation (spreads to proximal body)
  2. Hot erythema in affected area
  3. Poorly demarcated margins, swelling, warmth and tenderness
  4. Blister if oedema is present
  5. FEVER
99
Q

Diagnosis of cellulitis

A
  1. Clinical
  2. Skin Swabs negative
  3. Serological testing for streptococcal infection (antistreptolysin O titre)
100
Q

How is cellulitis treated

A
  1. ORAL PHENOXYMETHYLPENICILLIN or ERYTHROMYCIN if allergic to penicillin
  2. IV for 3-5 days of antibiotics if infection is widespread
  3. PHENOCYMETHYPENICILLIN ORALLY twice a day for prophylaxis
101
Q

What is Necrotising Fasciitis

A
  1. Deep-seated infection of the subcutaneous tissue causing fulminant and spreading destruction of fascia and fat which spares the skin initially
102
Q

What is type I necrotising fasciitis

A
  1. Caused by a mixture of aerobic and anaerobic bacteria following abdo surgery or in diabetics
103
Q

What is type II necrotising fasciitis

A
  1. Caused by group A beta-haemolytic streptococci
104
Q

Risk factors for type II necrotising fasciitis

A
  1. Abdo surgery

2. Immunosuppression

105
Q

Clinical presentation of type II necrotising fasciitis

A
  1. Severe pain out of proportion to the skin findings at initial site of infection
  2. Infection rapidly spreads along tissue planes causing erythema and pain + crepitus
  3. Patients with fever, toxicity and pain that is out of proportion to skin findings - necrotising fasciitis should be suspected
  4. Multi-organ failure is common and mortality is high
106
Q

Diagnostics of necrotising fasciitis

A
  1. Soft tissue gas seen on X-ray
  2. Raised CRP
  3. Raised WCC
    4
107
Q

Treatment of necrotising fasciitis

A
  1. IV BENZYLPENICILLIN and IV CLINDAMYCIN
  2. IV METRONIDAZOLE for widespread IV antibiotics if unknown cause
  3. Surgical debridement or amputation
108
Q

Adverse effects of corticosteroids

A
  1. Skin thinning, telangiectasia and contact dermatitis
  2. Perioral dermatitis and acne on the face
  3. Withdrawal
109
Q

Adverse effects of Emollients

A

Greasiness of skin and exacerbates acne on face

110
Q

Name two kertolytics

A

ALLANTOIN and SALICYLIC ACID

111
Q

Role of keratolytics

A

Softens skin and causes cells of epidermis to shed more rapidly, opening clogged pores

112
Q

Adverse effects of keratolytics

A

Hypersensitivity and chemical burns

2. Sun protection needed

113
Q

When should retinoids be avoided

A

SEVERE TERATOGEN

Year 2 (155 decks)

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