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Revision 24/25 > Dermatology COMPLETE > Flashcards

Dermatology COMPLETE Flashcards

REVIEWED ON 02/03/05 (81 cards)

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1
Q

Dermatitis can be classed as endogenous and exogenous. Give examples for each.

A

Endogenous:
Atopic
Seborrhoeic
Venous

Exogenous:
Contact allergic / irritant
Photosensitive

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2
Q

Yeast responsible for seborrhoeic dermatitis, and who is at highest risk of this?

A

Malassezia furfur / pitysporum ovale

Associated with HIV and Parkinson’s disease

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3
Q

Babies vs children vs adults distribution of eczema:

A

Babies:
Face
Scalp
Arms
Legs

Children:
Starting to get it in flexures

Adults:
Flexure sites
Hands
Neck

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4
Q

General measure for eczema include avoiding irritants, frequent emollients, bandages and soap substitutes. What is used for active areas, and what different strengths are they?

A

Topical steroids:

Hydrocortisone 0.5-2.5%

Eumovate (clobestasone butyrate 0.05%)

Betnovate (betamethasone 0.1%)

Dermovate (clobestasone propionate 0.05%)

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5
Q

What can be used long term topically as a steroid sparing agent in eczema?

A

Tacrolimus topical

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6
Q

3 types of oral therapy sometimes used in eczema and when?

A

Antibiotics - superimposed bacterial infection

Antivirals - superimposed viral infection e.g. HSV1

Antihistamines - for itch

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7
Q

What are specialist options used in severe, non-responsive cases of eczema?

A

Phototherapy - UVA and B, reduces number of t cells which mediates the inflammation.

Immunosuppressants e.g. ciclosporin

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8
Q

Exacerbating factors in psoriasis:

A

Trauma
Alcohol
Drugs inc BB, lithium, antimalarials, NSAIDs and ACEi
Withdrawal of systemic steroids

Strep infection for guttate psoriasis

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9
Q

What is going wrong in psoriasis?

A

Psoriasis is a t cell autoimmune disease with abnormal infiltration of T cells that release inflammatory cytokines.

Increased keratinocyte proliferation leads to scaling and crusting.

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10
Q

Types of psoriasis, in order of most to least common.

A

Plaque
Guttate
Pustular
Erythrodermic

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11
Q

What often triggers guttate psoriasis?

A

Streptococcal infection

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12
Q

What is the Auspitz sign?

A

Plaques flaking off and causing pinpoint bleeding

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13
Q

Give some nail changes in psoriasis.

A

Pitting
Ridging
Thickening
Onycholysis - coming off of the nail bed

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14
Q

What is Koebner’s phenomenon?

A

Development of psoriatic lesions in areas of skin trauma.

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15
Q

3 systemic diseases / conditions associated with psoriasis:

A

Psoriatic arthritis
Metabolic syndrome
IBD

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16
Q

First line for psoriasis management:

A

Potent steroids OD + Vitamin D analogue OD for 4 weeks. One evening, one night

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17
Q

Second line for psoriasis management:

A

Add BD vitamin D topical to the potent topical steroid,

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18
Q

Third line for psoriasis managment:

A

If third line not working after 8-12 weeks since starting treatment, add potent steroids BD, or coal tar.

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19
Q

Specialist input options for psoriasis management:

A

Narrow band UVB three times per week if that hasn’t worked

Psoralen + UVA light (photochemotherapy)

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20
Q

What is the action / benefit for each of the following topical therapies; emollient, steroid, salicylic acid, vitamin D analogue.

A

Emollient - stops skin from drying out

Steroid - reduces autoimmune response and therefore inflammation

Salicylic acid - breaks down hard thick dead skin

Vitamin D analogue - slows down keratinocyte proliferation

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21
Q

Bacteria associated with colonisation in acne?

A

Proprionibacterum acnes

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22
Q

Complication of long-term antibiotic use in acne (rare) and how to treat it?

A

Gram negative folliculitis

High dose trimethoprim

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23
Q

Why are oral anti-androgens sometimes used in females for acne?

A

Reduce sebum production

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24
Q

Most common and least dangerous malignant skin cancer:

A

BCC

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25
What is the most common type of BCC, and what kind of referral should be made if it is suspected?
Nodular - rolled, pearly edge. Routine referral, does not need to be urgent.
26
Pre-malignant lesions for SCC and treatment:
Actinic keratoses 'sun spots', flat macules Bowen's disease - more crusty, red lesions. Treat with flurouracil
27
Which cells are affected in SCC?
Epidermal keratinocytes
28
Risk factors for SCC:
UV exposure Type I/II skin Smoking Increasing age Burns or chronic inflammation e.g. Marjolin's ulcer Genetic Immunosuppression
29
In skin types V and VI, which is the most common skin cancer?
SCC
30
Melanoma is an invasive malignant tumour of the epidermal melanocyte. What are the 4 types?
Superficial spreading - legs. Spread horizontally first, then invasive. Nodular - trunk. Aggressive and metastasise early. Lentigo maligna - age spots turn malignant. Face . Acral - hands and feet, nail beds. Most common type in skin of colour.
31
What is the ABCDE assessment tool in dermatological examination? Which ones are the most likely to be suspicious in melanoma?
Asymmetry Border Colour variation Diameter >6mm? Evolution / growth Assymetry, colour variation, evolution.
32
What system is used to predict 5 year mortality from malignant melanoma?
Breslow thickness <0.75 95-100% 0.75-1.5 80-96% 1.5-4 60-75% >4 50%
33
TEN vs SJS in terms of body surface area? Management?
SJS <10% TEN >30% Both require admission to burn units. Ig FIRST LINE Supportive Mx, ICU? Fluids, ciclosporin, plasmapharesis SJS = mucocutaneous necrosis with ad least 2 mucosal sites involved. TEN includes systemic toxicity.
34
Type of reaction in SJS/TEN?
Type IV hypersensitivity reaction - delayed
35
SJS / TEN most commonly caused by drug reactions and have a flu like prodrome. Which drugs?
Drugs: Antibiotics especially beta lactams e.g. penicillins, cephalosporins. Allopurinol Carbamazepine and phenytoin Sulfasalazine All Antibiotics Can Present Severe !
36
What is Nikolsky's sign?
Mild lateral pressure causes separation of the epidermis.
37
Most common cause of erythema multiforme, and clinical features?
HSV1 Coin / target lesions, developing peripherally and spreading to torso. Self limiting in 4-6 weeks.
38
Erythema nodosum presents with:
Inflammation of subcutaneous fat. Painful red nodules, anterior shin.
39
Causes / risk factors for erythema nodosum:
Infection esp TB, chlamydia and strep throat Pregnancy Inflammatory e.g. IBD, sarcoidosis
40
3 cutaneous complications / manifestations of diabetes mellitus (type 2):
Leg ulcer Foot ulcer Acanthosis nigricans (insulin resistance)
41
Hyper vs hypothyroid cutaneous manifestations:
Hypothyroid - dry skin, loss of outer 1/3 of eyebrow, coarse rough skin Hyperthyroid - Grave's eye disease, pretibial myxoedema, nail changes, hyperhidrosis, facial flushing, diffuse alopecia
42
A patient with a leg ulcer described that it is more painful when lying down than when upright and walking. What type of ulcer is this likely to be, and what would it likely look like?
Arterial - gravity increases blood flow to the area and alleviates pain. Arterial - punched out, small lesion. ?Gangrene. Cold with no palpable pulses.
43
Where do arterial ulcers typically occur?
Toes and heel
44
Venous vs arterial ulcers:
https://zerotofinals.com/surgery/vascular/legulcers/
45
How do venous ulcers typically occur?
Secondary to venous insuffiency, superficial trauma and delayed healing. Accumulation of waste products
46
Management of arterial ulcers;
Urgent vascular referral Consideration of surgery to increase blood flow to area
47
Management of venous ulcers;
4 layer compression bandage Oral pentoxyphylline is a pripheral vasodilator improves healing rate MUST exclude arterial ulcer first though using ABPI Input from specialist nurses, tissue viability etc etc. Avoid NSAIDs
48
How is arterial disease excluded when assessing an ulcer?
ABPI
49
Rhinophyma is a late complication of which skin disorder?
Rosacea
50
Treatment of predominant erythema in rosacea;
Brimonidine gel - short term relief, lasts for about 6 hours. Alpha adrenergic agonist.
51
What kind of therapy may be appropriate for individuals with prominent telangiectasia in rosacea?
Laser therapy
52
What ocular involvement can occur in rosacea?
Blepharitis - inflammation of eyelid margins. Grittiness and discomfort , ?swollen eyelids, ?sticky. Often due otto mebonium gland dysfunction.
53
Mild to moderate papules / pustules in rosacea - management?
Topical ivermectin
54
Severe rosacea combination therapy:
Oral doxycycline and topical ivermectin
55
Bullous pemphigoid vs pemphigus vulgaris:
Bullous pemphigoid - classically SPARING of the mucous membranes
56
What are the antibodies directed against in the autoimmune disease pemphigus vulgaris?
Desmoglein 3 - cadherin epithelial cell adhesion molecule
57
What are the antibodies directed against in the autoimmune disease bullous pemphigoid?
Hemidesmosomal proteins BP180 and BP230
58
What type of hypersensitivity reaction occurs in pemphigus vulgaris and bullous pemphigoid?
Type II - cell mediated, IgG and M
59
Give an example of a sedating antihistamine.
Chlorphenamine
60
The most common cause of urticaria is allergy. Give some drugs that commonly cause urticaria.
I'm itching to play the P(i)ANO Penicillins Aspirin NSAIDs Opiates
61
You can get acute and chronic urticaria, usually caused by allergy and autoimmune respectively. What is the pathophysiology of urticaria presentation?
Urticaria is due to the release of histamine from mast cells. Associated with angioedema and flushing.
62
Chronic urticaria is an autoimmune conditions where autoantibodies target mast cells and trigger them to release histamine and other chemicals. Give 3 sub-categories it can be divided into:
Chronic Idiopathic Chronic Inducible Autoimmune - related to autoimmune conditions e.g. SLE.
63
Chronic inducible urticaria describes episodes of chronic urticaria that can be triggered by e.g. -
Sunlight Temp change Exercise Strong emotions Hot or cold weather Pressure (dermatographism)
64
What is the antihistamine of choice for chronic urticaria?
Fexofenadine
65
Most common cellulitis organism?
Strep pyogenes
66
Investigations in cellulitis?
CLINICAL DIAGNOSIS Bloods and blood cultures only needed if patient is being admitted and septicaemia is suspected.
67
Which classification is used to grade cellulitis?
ERON classification I No systemic features or uncontrolled comorbidities II Systemically unwell, OR systemically well with a comorbidity that could complicate the cellulitis e.g. PAD, obesity. III Significant systemic upset IV Sepsis or severe life threatening infection e.g. nec fasc
68
What constitutes 'significant systemic upset' as per the Eron classification of cellulitis (Class III)?
Acute confusion Deranged obs e.g. tachypnoea, tachycardia, hypotension Unstable comorbidities Limb threatening infection due to vascular compromise
69
Who should be admitted for IV antibiotics with cellulitis?
Eron class III/IV Severe or rapidly deteriorating <1 year or very frail Immunocompromised Significant lymphoedema Facial or periorbital Class II may avoid inpatient care if there are facilities in the community to give IV abx and monitor
70
First, second and pregnancy treatment for Eron class I cellulitis:
1. Oral flucloxacillin 2. Oral clarithromycin Erythromycin in pregnancy
71
Type I Nec fasc is caused by:
Mixed anaerobe and aerobes, usually post-surgery in diabetics.
72
Type 2 nec fasc is caused by:
Usually strep pyogenes
73
The most common pre-existing medical condition in nec fasc is diabetes. Which drug further increases this risk?
SGT2i
74
Most commonly affected site in nec fasc
Perineum Fournier's
75
What is pyoderma gangrenosum?
Rare, non-infectious inflammatory disorder. Neutrophilic infiltration into the affected tissue.
76
Where is pyoderma gangrenosum typically found?
Lower leg Often at the site of minor injury
77
Most common / defining features of pyoderma gangrenosum:
Painful blisters Purple edge Deep necrotic ulcer late stage ?Fever, myalgia
78
Treatment for pyoderma gangrenosum:
Oral steroids
79
Causes / associations of pyoderma gangrenosum:
50% idiopathic IBD 10-15% RA, SLE Lymphoma, myeloid leukaemia, myeloproliferative disorders PBC GPA
80
Alopecia areata is presumed to be an autoimmune condition. What is the pattern of hair loss, and prognosis?
Localised, well demarcated patches of hair loss. Small broken exclamation mark hairs at the edges. 50% regrow by 1 year, and 80-90% eventually.
81
Potential treatments for alopecia areata:
Topical steroids Topical minoxidil Phototherapy Dithranol

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