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UKMLA Prep > Dermatology > Flashcards

Dermatology Flashcards

MLA conditions and preperation

1
Q

Erythema multiforme

A

Hypersensitivity reaction that is most commonly triggered by infections.
It may be divided into minor and major forms.
Typically appears like target lesions on the skin.

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2
Q

Features of Erythema multiforme

A

-target lesions
-initially seen on the back of the hands / feet before spreading to the torso
-upper limbs are more commonly affected than the lower limbs
-pruritus is occasionally seen and is usually mild

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3
Q

Causes of erythema multiforme

A

-viruses: herpes simplex virus (the most common cause), Orf (Parapox virus)
-idiopathic
-bacteria: Mycoplasma, Streptococcus
-drugs: penicillin, sulphonamides, -carbamazepine, allopurinol, NSAIDs, oral -contraceptive pill, nevirapine
-connective tissue disease e.g. Systemic lupus -erythematosus
-sarcoidosis
-malignancy

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4
Q

Erythema multiforme major

A

The more severe form, erythema multiforme major is associated with mucosal involvement.

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5
Q

Who gets erythema multiforme commonly

A

most common in young adults (aged 20–40 years) with a modest predominance in males. There is no association with race.

HLA-DQB1*0301 allele associated with herpes

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6
Q

Medications which may trigger erythema multiforme (4)

A

Antibiotics (including erythromycin, nitrofurantoin, penicillins, sulfonamides, and tetracyclines)
Anti-epileptics
Non-steroidal anti-inflammatory drugs
Vaccinations (most common cause in infants).

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7
Q

Conditions associated with erythema multiforme

A

Inflammatory bowel disease
Hepatitis C
Leukaemia
Lymphoma
Solid organ cancer malignancy.

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8
Q

Clinical features of ertythema multiforme

A

fatigue,
malaise,
myalgia,
or fever.

These likely represent the course of precipitating illness rather than true prodrome.

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9
Q

Serious complications of erythema multiforme

A

Keratitis
Conjunctival scarring
Uveitis
Permanent visual impairment.

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10
Q

What tests should be carried out if erythema multiforme is suspected

A

Complete blood examination
Liver functions tests
ESR
Serological testing for infectious causes
Chest x-ray.

Skin biopsy with histopathology and direct immunofluorescence

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11
Q

Treatment of erythema multiforme

A
  • self limiting condition
  • cease medication which causes
  • prednisone for mucosal disease
  • antiviral therapy aciclovir
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12
Q

Erythema nodosum

A

inflammatory disorder affecting subcutaneous fat. It most commonly presents as bilateral tender red nodules on the anterior shins

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13
Q

Who gets erythema nodosum

A

Erythema nodosum can occur in all ethnicities, sexes, and ages, but is most common in women between the ages of 25 and 40

It is 3–6 times more common in women than in men except before puberty when the incidence is the same in both sexes

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14
Q

Infective causes of erythema nodosum? (6)

A
  • hypersensitivity reaction of unknown cause in 55%
    -usually associated with drugs, infection or malignancy

Throat infections (streptococcal disease or viral infection)
Primary tuberculosis (TB), a rare cause in New Zealand
Yersinia infection; this causes diarrhoea and abdominal pain
Chlamydia infection
Fungal infection: histoplasmosis, coccidioidomycosis
Parasitic infection: amoebiasis, giardiasis

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15
Q

Viral and bacteria diseases which are associated with erythema nodosum

A

-HSV
- viral hepatitis
-HIV
- campylobacter infection
- Salmonella infection

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16
Q

Drugs which cause erythema nodosum

A

Sulfonamide
Amoxicillin
Oral contraceptive
Non-steroidal anti-inflammatory drugs
Bromide
Salicylate
Iodide
Gold salt

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17
Q

Inflammatory diseases which cause erythema nodosum

A

Inflammatory bowel disease (ulcerative colitis or Crohn disease)
Sarcoidosis (11–-25%); X-ray shows bilateral hilar adenopathy in Löfgren syndrome
Malignancy
Lymphoma
Leukaemia
Behçet disease

—————————————————————

Pregnancy

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18
Q

Investigations for erythema nodosum

A

Complete blood count with differential, C-reactive protein levels (infectious and inflammatory causes)
Chest X-ray (tuberculosis and sarcoidosis)
Throat swab and anti-streptolysin O and streptodornase serology (streptococcal infection)
Viral serology (preferably two samples at four-week intervals)
Stool culture and evaluation for ova and parasites in patients with gastrointestinal symptoms
Mantoux test or QuantiFERON gold (tests for TB).
Deep incisional or excisional skin biopsy.

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19
Q

Septal Panniculitis

A

Various forms of scleroderma
Medium vessel vasculitis, for example, due to polyarteritis nodosa in which there are tender subcutaneous nodules associated with ulceration, necrosis, livedo racemosa, fever, joint pain, myalgia, and peripheral neuropathy
Necrobiosis lipoidica
Eosinophilic panniculitis
Rheumatoid nodule.

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20
Q

Treatment for erythema nodosum

A

Pain management may include extended rest, colchicine (1–2 mg/day), NSAIDs (non-steroidal anti-inflammatory drugs), and venous compression therapy [4].
Systemic corticosteroids (1 mg/kg daily until resolution of erythema nodosum) may be prescribed if infection, sepsis, and malignancy have been ruled out [9,11].
Oral potassium iodide as a supersaturated solution (400–900 mg/day) may be prescribed for one month if available

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21
Q

Guttate psoriasis

A

Distinct variant of psoriasis that is classically triggered by streptococcal infection (pharyngitis or perianal)

More common in Childern and adolescents

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22
Q

Features of guttate psoriasis

A

Tear drop papules on the trunk and limbs
gutta is Latin for drop

pink, scaly patches or plques of psoriasis
tends to be acute onset over days

Typically triggered by Streptococcal infection

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23
Q

What is the managment of guttate psoriasis

A

most cases resolve spontaneously within 2-3 months
there is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
topical agents as per psoriasis
UVB phototherapy
tonsillectomy may be necessary with recurrent episodes

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24
Q

Prodome (guttate vs Pityriasis rosea)

A

Many patients report recent respiratory tract infections but this is not common in questions

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25
Q

Appearance (Guttate vs Pityriasis rosea)

A

‘Tear drop’, scaly papules on the trunk and limbs

Herald patch followed 1-2 weeks later by multiple erythematous, slightly raised oval lesions with a fine scale confined to the outer aspects of the lesions.

May follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance

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26
Q

Treatment (Guttate vs Pityriasis rosea)

A

Most cases resolve spontaneously within 2-3 months
Topical agents as per psoriasis
UVB phototherapy
—————————————————————-

Self-limiting, resolves after around 6 weeks

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27
Q

Pityriasis rosea

A

Pityriasis rosea describes an acute, self-limiting rash which tends to affect young adults

characterised by a large circular or oval “herald patch”, usually found on the chest, abdomen, or back

Herald patch is followed some time later, typically two weeks or so, by the development of smaller scaly oval red patches, resembling a Christmas tree, distributed mainly on the chest and back.

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28
Q

What are the features of pityriasis rosea

A

In the majority of patients there is no prodrome, but a minority may give a history of a recent viral infection

herald patch (usually on trunk)

followed by erythematous, oval, scaly patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance

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29
Q

Managment of pitiyriasis rosea

A

self-limiting - usually disappears after 6-12 weeks

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30
Q

Common microbe in animal bites

A

polymicrobial
most common isolated organism is Pasteurella multocida.

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31
Q

Managment of animal bites

A

cleanse wound.
Puncture wounds should not be sutured closed unless cosmesis is at risk
current BNF recommendation is co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended

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32
Q

Microbes which are found in human bites

A

Common organisms include:
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella

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33
Q

Reccomended Tx for human and animal bites

A

Co-amoxiclav

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34
Q

other investigations/ tx after exposure to animal or human bites

A

HIV (6 weeks before sero-conversion, cosider pep)
Hepatitis C

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35
Q

Bed bugs

A

Cimex hemipteru.
Cimex lectulatius

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36
Q

Clinical features of bed bug bites

A

A small punctum (hole) may be seen at the site of the bite.
Some people develop cutaneous reactions with pruritus (itching) and (most commonly) 2–5 mm red bumps.
Purpura, petechiae, vesicles, urticaria, pustules, localised infection, and (rarely) anaphylaxis may also develop.
Hypersensitivity reactions may develop in some who become sensitised to bed bug saliva.
If bites are seen, they are often reported to be in a linear formation in groups of three, sometimes termed the ‘breakfast, lunch, and dinner’ pattern.
Bed bugs feed on exposed skin, therefore the limbs are a more common site for bites.

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37
Q

complications of bed bug bites

A

Localised infections including cellulitis, folliculitis, and infected eczema
Anaemia (a few reports of this secondary to chronic bed bug infestation)
Anaphylaxis
Psychological distress.

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38
Q

prophylaxis/ prevent future cases of bed bugs

A

Bed bug numbers may be controlled by hot-washing bed linen and using mattress covers.

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39
Q

managment of bed bug bites

A

A cool, damp cloth over areas of irritation can improve symptoms
Itchy lesions can be treated with topical steroids and/or oral antihistamines (hydrocortisone and ceterazie)
Secondary infection should be treated with antibiotics (Cephalexin, Doxycycline
Trimethoprim-sulfamethoxazole (co-trimoxazole)
Clindamycin)
Rare systemic anaphylactic reactions to bed bug bites may require intramuscular adrenaline.

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40
Q

Lyme disease microorganism

A

Borrelia burgdorferi

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41
Q

Early features of lyme disease in the first 30 days

A

erythema migrans
‘bulls-eye’ rash is typically at the site of the tick bite
typically develops 1-4 weeks after the initial bite but may present sooner
usually painless, more than 5 cm in diameter and slowlly increases in size
present in around 80% of patients.

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42
Q

Systemic features of lyme disease

A

headache
lethargy
fever
arthralgia

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43
Q

Later features of lyme disease

A

cardiovascular
heart block
peri/myocarditis
neurological
facial nerve palsy
radicular pain
meningitis

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44
Q

Investigations of Lyme disease

A

NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
erythema migrans is therefore an indication to start antibiotics
enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
if positive or equivocal then an immunoblot test for Lyme disease should be done

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45
Q

Erythema Migrans

A

typically a circular red area that sometimes clears in the middle, forming a bull’s-eye pattern.

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46
Q

Managment of tick bites

A

tick bites can be a relatively common presentation to GP practices, and can cause significant anxiety
if the tick is still present, the best way to remove it is using fine-tipped tweezers, grasping the tick as close to the skin as possible and pulling upwards firmly. The area should be washed following.
NICE guidance does not recommend routine antibiotic treatment to patients who’ve suffered a tick bite

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47
Q

fIrst aid response to
burns

A

airway, breathing, circulation
burns caused by heat: remove the person from the source. Within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes. Cover the burn using cling film, layered, rather than wrapped around a limb
electrical burns: switch off power supply, remove the person from the source
chemical burns: brush any powder off then irrigate with water. Attempts to neutralise the chemical are not recommended

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48
Q

Wallace Rule

A

Wallace’s Rule of Nines: head + neck = 9%, each arm = 9%, each anterior part of leg = 9%, each posterior part of leg = 9%, anterior chest = 9%, posterior chest = 9%, anterior abdomen = 9%, posterior abdomen = 9%

the palmar surface is roughly equivalent to 1% of total body surface area (TBSA). Not accurate for burns > 15% TBSA

Lund and Browder chart: the most accurate method

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49
Q

Superficial epidermal

A

-first degree
-Red and painful, dry, no blisters

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50
Q

Partial thickness (superficial dermal)

A
  • second degree burn
    -Pale pink, painful, blistered. Slow capillary refill
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51
Q

Partial thickness (deep dermal)

A
  • second degree burn
    Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
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52
Q

Full thickness burn

A
  • third degree burn
    -White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
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53
Q

when referral to secondary care needed for burns?

A

-all deep dermal and full-thickness burns.
superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children
superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck

any inhalation injury (even small injury next to the nose)

any electrical or chemical burn injury
suspicion of non-accidental injury

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54
Q

1st management of burn

A

initial first aid

review referral criteria to ensure can be managed in primary care

superficial epidermal: symptomatic relief - analgesia, emollients etc

-superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24 hours

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55
Q

Burns which impact the airways

A

-smoke inhalation can result in airway oedema

-early intubation should be considered e.g. if deep burns to the face or neck, blisters or oedema of the oropharynx, stridor etc

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56
Q

IV fluids - when required in burns

A
  • children with burns greater than 10% of total body surface area.

-Adults with burns greater than 15% of total body surface area

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57
Q

Parkland formula

A

volume of fluid= total body surface area of the burn % x weight (Kg) x4.

half fluid needs to be given in the first 8 hours

also insert urinary catheter

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58
Q

Managment of complex burns

A

Complex burns, burns involving the hand perineum and face and burns >10% in adults and >5% in children should be transferred to a burns unit.

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59
Q

Circumferential burns

A

Circumferential burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue.

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60
Q

Escharotomies

A

Careful division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the torso),
relieve compartment syndrome and oedema (where a limb is involved)

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61
Q

Some causes of pruritis

A

hyper- and hypothyroidism
diabetes
pregnancy
‘senile’ pruritus
urticaria
skin disorders: eczema, scabies, psoriasis, pityriasis rose

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62
Q

Pruritis and liver- other symptoms

A

History of alcohol excess
Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
Evidence of decompensation: ascites, jaundice, encephalopathy

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63
Q

Pruritis and iron deficiency

A

Pallor
Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis

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64
Q

Prutitis and Polycythemia

A

Pruritus particularly after warm bath
‘Ruddy complexion’
Gout
Peptic ulcer disease

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65
Q

Chronic kidney disease and pruritis

A

Lethargy & pallor
Oedema & weight gain
Hypertension

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66
Q

Lymphoma and pruritis

A

Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue

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67
Q

Signs of pruritis

A

excoriations

Persistent scratching over a period of time may lead to:

Lichenification (thickened skin, lichen simplex)
Prurigo papules and nodules.

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68
Q

epidemiology of pruritis

A

Affects all people

The incidence of chronic pruritus increases with age, it is more common in women, and in those of Asian background.

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69
Q

localised rashes (scalp, back, hands, genitals, legs and feet)

A

Scalp: seborrhoeic dermatitis, head lice
Back: Grover disease
Hands: pompholyx, irritant and/or allergic contact dermatitis
Genitals: vulvovaginal Candida albicans infection, lichen sclerosus
Legs: venous eczema
Feet: tinea pedis

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70
Q

Neuropathic localised pain (face, hands, arm, back, geniral, dermatomal)

A

Face: trigeminal trophic syndrome
Hand: cheiralgia paraesthetica
Arm: brachioradial pruritus
Back: notalgia paraesthetica
Genital: pruritus vulvae, pruritus ani
Dermatomal: herpes zoster (shingles) during the recovery phase

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71
Q

Managment of pruritis

A

Wet dressings or tepid shower to cool the skin
Calamine lotion (contains phenol, which cools the skin): avoid on dry skin and limit use to a few days
Menthol/camphor lotion: gives a chilling sensation
Local anaesthetics, such as pramoxine (also called pramocaine), applied to small itchy spots such as insect bites
Regular use of emollients, especially if skin is dry
Mild topical corticosteroids for short periods
Topical calcineurin inhibitors are also used to reduce itch associated with inflammatory skin conditions
Topical doxepin, a tricyclic antidepressant and antihistamine, is an antipruritic used in eczema.

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72
Q

antidepressants and antipruritic action

A

Doxepin and amitriptyline are tricyclic antidepressants have antipruritic action and act on the central and peripheral nervous systems.
Tetracyclic antidepressants such as mirtazepine and selective serotonin reuptake inhibitors (paroxetine, sertraline, fluoxetine) may also help some patients with severe itch including when it is caused by cholestasis, T-cell lymphoma, malignancy or a neuropathic cutaneous dysaesthesia.

Anti-epileptic drugs such as sodium valproate, gabapentin and prega

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73
Q

Asprin and pruritis

A

Aspirin is sometimes effective if pruritus is mediated by kinins or prostaglandins and is noted to be effective in patients with pruritus due to polycythaemia vera. Note: aspirin may cause or aggravate itch in some patients.

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74
Q

Phototherapy

A

Ultraviolet B (UVB) phototherapy alone, or in conjunction with UVA, has been shown to be helpful for pruritus associated with chronic kidney disease, psoriasis, atopic eczema and cutaneous T-cell lymphoma.

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75
Q

Keloid scars

A
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76
Q

Pre-disposing factors of Keloid scars

A

ethnicity: more common in people with dark skin
occur more commonly in young adults, rare in the elderly
common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor surface of limbs, trunk

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77
Q

erythema migrans

A
  • Rash associated with Lyme disease
  • centre dark, one round outside is clear
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78
Q

Uticaria

A

Urticaria describes a local or generalised superficial swelling of the skin. The most common cause of urticaria is allergy although non-allergic causes are seen.

-pale, pink raised skin. Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
pruritic

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79
Q

what are the classifcations of uticaria

A

-Acute urticaria (< 6 weeks duration, and often gone within hours to days)

-Chronic urticaria (> 6 weeks duration, with daily or episodic weals)

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80
Q

acute causes of uticaria

A

Acute viral infection — upper respiratory infection, viral hepatitis, infectious mononucleosis, mycoplasma
Acute bacterial infection — dental abscess, sinusitis
Food allergy (IgE mediated)—usually milk, egg, peanut, shellfish
Drug allergy (IgE mediated drug-induced urticaria) — often an antibiotic
Drug-induced urticaria due to pseudoallergy — aspirin, nonselective nonsteroidal anti-inflammatory drugs, opiates, radiocontrast media; these cause urticaria without immune activation
Vaccination
Bee or wasp stings
Widespread reaction following localised contact urticaria — for example, latex

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81
Q

chronic uticaria causes ``

A

Chronic underlying infection, such as Helicobacter pylori (bowel parasites)
Chronic autoimmune diseases, such as systemic lupus erythematosus, thyroid disease, coeliac disease, vitiligo, and others.

Heat
Viral infection
Tight clothing
Drug pseudoallergy—aspirin, nonsteroidal anti-inflammatory drugs, opiates
Food pseudoallergy—salicylates, azo dye food colouring agents such as tartrazine (102), benzoate preservatives (210-220), and other food additives.
Inducible urticaria

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82
Q

Aquagenic urticaria

A

Hot or cold water
Fresh, salt, or chlorinated water

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83
Q

Vibratory urticaria

A

Jack hammer

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84
Q

Heat uricaria

A

Hot water bottle
Hot drink

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85
Q

Solar Uticaria

A

Sun exposure to non-habituated body sites
Often spare face, neck, hands
May involve long wavelength UV or visible light

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86
Q

Delayed pressure urticaria

A

Pressure on affected skin several hours earlier
Carrying heavy bag
Pressure from a seat belt
Standing on a ladder rung
Sitting on a horse

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87
Q

Contact urticaria

A

Eliciting substance absorbed through the skin or mucous membrane
Allergens (IgE-mediated): white flour, cosmetics, textiles, latex, saliva, meat, fish, vegetables
Pseudoallergens or irritants: stinging nettle, hairy caterpillar, medicines

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88
Q

Cholinergic urticaria

A

Sweat induced by exercise
Sweat induced by emotional upset
Hot shower

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89
Q

Cold urticaria

A

Cold air on exposed skin
Cold water
Ice block
Cryotherapy

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90
Q

Dermographism

A

Stroking or scratching the skin
Tight clothing
Towel drying after a hot shower

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91
Q

Managment of Utricaria

A

oral second-generation H1-antihistamine such as cetirizine or loratidine.

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92
Q

Onychomycosis

A

Fungal nail infection (onychomycosis) may involve any part of the nail, or the entire nail unit. Toenails are significantly more likely to become infected than fingernails

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93
Q

Severe Urticaria

A

A short course of an oral corticosteroid may required in addition to a non-sedating antihistamine

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94
Q

Toxic epidermal necrolysis

A

rare but important side effect of which to be aware of penicillins

life-threatening skin disorder that is most commonly seen secondary to a drug reaction

systemically unwell e.g. pyrexia, tachycardic
positive Nikolsky’s sign: the epidermis separates with mild lateral pressure

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95
Q

Drugs which induce TEN (6)

A

phenytoin
sulphonamides
allopurinol
penicillins
carbamazepine
NSAIDs

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96
Q

Managment of TENs

A

stop precipitating factor
supportive care
often in an intensive care unit
volume loss and electrolyte derangement are potential complications
intravenous immunoglobulin has been shown to be effective and is now commonly used first-line
other treatment options include: immunosuppressive agents (ciclosporin and cyclophosphamide), plasmapheresis

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97
Q

Chlorphenamine- sedating or non-sedating?

A

sedating

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98
Q

Loratadine- sedating or non-sedating?

A

non-sedating

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99
Q

ceterazine- sedating or non-sedating

A

non-sedating

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100
Q

What is this?

A

Erythema multiforme

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101
Q

What is this?

A

Erythema multiforme

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102
Q

What is this?

A

Erythema multiforme

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103
Q

What is this?

A

Erythema nodosum

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104
Q

What is this?

A

Erythema nodosum

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105
Q

What is this?

A

Erythema nodosum

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106
Q

what is this?

A

Guttate psoriasis

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107
Q

What is this?

A

Guttate psoriasis

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108
Q

What is this?

A

Pityriasis rosea

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109
Q

Acanthosis nigricans

A

Symmetrical, brown, velvety plaques
can be found
* neck
* axilla
* groin

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110
Q

Causes of Acanthosis nigricans

A

type 2 diabetes mellitus
gastrointestinal cancer
obesity
polycystic ovarian syndrome
acromegaly
Cushing’s disease
hypothyroidism
familial
Prader-Willi syndrome
drugs
combined oral contraceptive pill
nicotinic acid

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111
Q

Pathophysiology of acanthosis nigricans

A

insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)

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112
Q

What is this?

A

Acanthosis nigricans

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113
Q

What is this?

A

Acanthosis nigricans

114
Q

Features of Lichen Planus

A

* itchy, papular rash most common on the palms, soles, genitalia and flexor surfaces of arms
* rash often polygonal in shape,
* ‘white-lines’ pattern on the surface (Wickham’s striae)
* Koebner phenomenon may be seen (new skin lesions appearing at the site of trauma)
* oral involvement in around 50% of patients: typically a white-lace pattern on the buccal mucosa
* nails: thinning of nail plate, longitudinal ridging

115
Q

Drugs which cause Lichen planus (3)

A
  • gold
  • quinine
  • thiazides
116
Q

What is this?

A

Lichen Planus

117
Q

What is this?

A

Lichen Planus- buccal mucosa

118
Q

Managment of Lichen Planus

A
  • potent topical steroids are the mainstay of treatment
  • benzydamine mouthwash or spray (oral)
  • extensive lichen planus may require oral steroids or immunosuppression
119
Q

What are the features of Rosacea?

A
  • typically affects nose, cheeks and forehead
  • flushing is often first symptom
  • telangiectasia
  • later develops into persistent erythema with papules and pustules
  • rhinophyma
  • ocular involvement: blepharitis
  • sunlight may exacerbate symptoms
120
Q

What is this?

A

Rosacea

121
Q

What is this?

A

Rosacea

122
Q

What is this?

A

Rosacea

123
Q

simple managment of Rosacea

A
  • high factor sunscreen
  • camoflague creams
  • topical brimonidine gel may be considered for patients with predominant flushing but limited telangiectasia
    *
124
Q

Managment of mild-moderate papules or pustles

A

topical ivermectin is first-line
alternatives include: topical metronidazole or topical azelaic acid

125
Q

Moderate- to-severe papules or pustles

A

combination of topical ivermectin + oral doxycycline

126
Q

When referral for rosacea needed

A
  • symptoms have not improved with optimal management in primary care
  • laser therapy may be appropriate for patients with prominent telangiectasia
  • patients with a rhinophyma
127
Q

Seborrhoeic dermatitis

A

flammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia furfur

128
Q

Organism causes Seborrhoeic dermatitis?

A

Malassezia furfur

formerly known as Pityrosporum ovale

129
Q

What is this?

A

Seborrhoeic dermatitis

130
Q

What is this?

A

Seborrhoeic dermatitis

131
Q

conditions assoicated with Seborrhoeic dermatitis

A
  • HIV
  • Parkinson’s disease
132
Q

Managment of Seborrhoeic scalp disease

A
  • the first-line treatment is ketoconazole 2% shampoo
  • over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and **tar **(‘Neutrogena T/Gel’) may be used if ketoconazole is not appropriate or acceptable to the person
  • selenium sulphide and **topical corticosteroid **may also be useful
133
Q

Face and body managment of seborrhoeic dematitis

A
  • opical antifungals: e.g. ketoconazole
  • topical steroids: best used for short periods
  • difficult to treat - recurrences are common
134
Q

Seborrhoeic dermatitis in children managment

A
  • reassurance that it doesn’t affect the baby and usually resolves within a few weeks
  • massage a topical emollient onto the scalp to loosen scales, brush gently with a soft brush and wash off with shampoo.
  • if severe/persistent a topical imidazole cream may be tried
135
Q

Cradle cap

A
  • may develop in the first few weeks of life
  • erythematous rash with coarse yellow scales.
  • spontaneously may ressolve at 8 months
136
Q

What is this?

A

Fungal nail change

137
Q

Features of fungal nail changes

A
  • ‘unsightly’ nails are a common reason for presentation
  • thickened,
  • rough, opaque nails are the most common finding
138
Q

Risk factors for fungal nail infections

A

increasing age
diabetes mellitus
psoriasis
repeated nail trauma

139
Q

what are the causative agents for fungal nail infections?

A
  • dermatophytes (90% cases)
  • mainly Trichophyton rubrum
    yeasts (5-10% cases)
  • e.g. Candida
  • non-dermatophyte moulds
140
Q

ddx for fungal nail infections?

A
  • psoriasis
  • repeated trauma
  • lichen planus
  • yellow nail syndrome
141
Q

Investigations for fungal nail infections?

A
  • nail clippings +/- scrapings of the affected nail
  • microscopy and culture
  • should be done for all patients if antifungal treatment is being considered
  • the false-negative rate for cultures are around 30%, so repeat samples may need to be sent if the clinical suspicion is high
142
Q

Managment of fungal nail infections?

A
  • asymptomatic- no treatment needed
  • dermatophyte or Candida- amorolfine 5% nail lacquer; 6 months for fingernails and 9 - 12 months for toenails
  • more extensive dermaphyte- oral terbinafine
  • extensive candida- oral itraconazole is recommended first-line; ‘pulsed’ weekly therapy is recommended
143
Q

Nail pitting

A

psoriasis
alopecia areata

144
Q

Blue nails

A

Wilson’s disease

145
Q

Leuconychia

A

hypoalbuminaemia
less common: fungal disease, lymphoma

146
Q

Yellow nail syndrome

A

associated with congenital lymphoedema, pleural effusions, bronchiectasis and chronic sinus infections

147
Q

What is this?

A

Yellow nail syndrome **

148
Q

What is this?

A

Blue nail- wilsons disease

149
Q

What is this?

A

Nail pitting psoriasis

150
Q
A

Mild nail psoriasis

151
Q

Onycholysis

A

separation of the nail plate from the nail bed

152
Q

Causes on Onycholysis

A
  • idiopathic
  • trauma e.g. Excessive manicuring
  • infection: especially fungal
  • skin disease: psoriasis, dermatitis
  • impaired peripheral circulation e.g. Raynaud’s
  • systemic disease: hyper- and hypothyroidism
153
Q

What nail changes are seen in psoriasis?

A
  • pitting
  • onycholysis (separation of the nail from the nail bed)
  • subungual hyperkeratosis
  • loss of the nail
154
Q

Iron deficiency anaemia- features

A
  • Pallor
  • Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis
155
Q

Liver disease- features

A
  • History of alcohol excess
  • Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
  • Evidence of decompensation: ascites, jaundice, encephalopathy
156
Q

Polycythaemia

A
  • Pruritus particularly after warm bath
  • ‘Ruddy complexion’
  • Gout
  • Peptic ulcer disease
157
Q

Chronic kidney disease- features

A

Lethargy & pallor
Oedema & weight gain
Hypertension

158
Q

Lymphoma- features

A

Night sweats
Lymphadenopathy
Splenomegaly, hepatomegaly
Fatigue

159
Q

other potential causes of pruritis?

A
  • hyper- and hypothyroidism
  • diabetes
  • pregnancy
  • ‘senile’ pruritus
  • urticaria
  • skin disorders: eczema, scabies, psoriasis, pityriasis rosea
160
Q

Keloid scars

A

tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound

161
Q

Pre-disposing factors for keloid scars?

A
  • ethnicity: more common in people with dark skin
  • occur more commonly in young adults, rare in the elderly
162
Q

Sites where keloid scars are found?

A
  • Sternum
  • shoulder
  • neck
  • face
  • extensor surface of limbs
  • trunk
163
Q

Managment of Keloid scars?

A
  • early keloids-> intra-lesional steroids e.g.** triamcinolone**
  • excision (careful consideration needs to given to the potential to create further keloid scarring)
164
Q

Actinic keratoses

A
  • premalignant skin lesion that develops as a consequence of chronic sun exposure
  • AKA Actinic, or solar, keratoses (AK)
165
Q
A

Features of actinic Keratoses

166
Q

Features of AK

A
  • small, crusty or scaly, lesions
  • may be pink, red, brown or the same colour as the skin
  • typically on sun-exposed areas e.g. temples of head
  • multiple lesions may be present
167
Q

What is this?

A

Actinic keratoses

168
Q

Managment of Actinic Keratoses

A
  • Sun care (cover up, SPF)
  • fluorouracil cream- 2-3 weeks
  • milk AKs- topical diclofena
  • topical imiquimod: trials have shown good efficacy
  • cryotherapy
  • curettage and cautery

Fluorouracil can cause inflammation of the skin, may need to prescribe steroids with it

169
Q

Impetigo

A
  • skin infection caused by Staphylcoccus aureus or Streptococcus pyogenes
  • can be complication of eczema, scabies or insect bites
  • common in children, warm weather
170
Q

Where do Impetigo lesions normall occur?

A

face, flexures and limbs not covered by clothing.

171
Q

How does impetigo spread?

A
  • direct contact with discharges from the scabs of an infected person.
  • incubation 4-10 days
172
Q

Feaures of impetigo

A
  • honey-coloured scab
  • very contagious
173
Q

What is this?

A

Impetigo

174
Q

Managment of impetigo

A
  • well or high risk of complications- **hydrogen peroxide 1% cream **
  • topical antibiotic creams:
  • topical fusidic acid
  • topical mupirocin should be used if fusidic acid resistance is suspected
  • MRSA suspected- retapamulin
175
Q

Extensive disease (impetigo) managment

A

oral flucloxacillin
oral erythromycin if penicillin-allergic

176
Q

Impetigo and school exclusion

A
  • lesions must be crusted over and healed
    or
  • 48hr after AB tx
177
Q

Lipoma

A

common, benign tumour of adipocytes.

178
Q

Pathophysiology of Lipoma

A
  • they are generally found in subcutaneous tissues
  • rarely, they may also occur in deeper adipose tissues
  • malignant transformation to liposarcoma is very rare
179
Q

epidemiology of lipoma

A
  • lipomas are common, with an annual incidence of around 1 in 1,000
  • most commonly seen in middle-aged adults
180
Q

Features of Lipoma

A
  • smooth
  • mobile
  • painless
181
Q

Managment of lipoma

A
  • observe lump
  • remove if diagnosis not sure
182
Q

Liposarcoma

A
  • Size >5cm
  • Increasing size
  • Pain
  • Deep anatomical location
183
Q

Venous leg ulcers

A

Ulcers form due to capillary fibrin cuff or leucocyte sequestration

184
Q

Features of venous insufficiency

A
  • oedema
  • brown pigmentation
  • lipodermatosclerosis
  • eczema
185
Q

Managment of venous leg ulcers

A
  • 4 layer compression banding after exclusion of arterial disease or surgery
  • fail to heal after 12weeks or >10cm2- skin graft may be needed
186
Q

What is this?

A

venous leg ulcer

187
Q

Marjolin’s ulcer

A

Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb

188
Q

What is this?

A

Marjolin’s ulcer

189
Q

What is this?

A

Marjolin’s ulcer

190
Q

Arterial ulcer

A
  • Occur on the toes and heel
  • Typically have a ‘deep, punched-out’ appearance
  • Painful
  • There may be areas of gangrene
  • Cold with no palpable pulses
  • Low ABPI measurements
191
Q

Managment of Marjolin’s ulcers

A

Mohs surgery, wide local excision with 1 to 2 cm margins, and amputation proximal to the lesion.

192
Q

Arterial ulcer managment

A
  • Angioplasty
  • Endarterectomy
193
Q

What is this?

A

Arterial ulcer

194
Q

Neuropathic ulcers

A
  • Commonly over plantar surface of metatarsal head and plantar surface of hallux
  • The plantar neuropathic ulcer—> amputation in diabetic patients
  • Due to pressure
195
Q

Managment of Neuropathic ulcers

A

cushioned shoes to reduce callous formation

196
Q

What is this?

A

Neuropathic ulcer

197
Q

Pyoderma Gangrenosum

A
  • Associated with inflammatory bowel disease/RA
  • Can occur at stoma sites
  • Erythematous nodules or pustules which ulcerate
198
Q

what is this?

A

Pyoderma gangernosum

199
Q

5ps of Pyoderma gangerosum

A

Painful, Progressive, Purple, Pretibial, Pathergy

200
Q

Managment of Pyoderma gangerosum

A
  • cyclosporine.
  • Other options include mycophenolate (Cellcept), immunoglobulins, dapsone, infliximab (Remicade) and tacrolimus (Protopic
201
Q

Predisposition to leg ulcers

A
  • malnourishment
  • incontinence: urinary and faecal
  • lack of mobility
  • pain (leads to a reduction in mobility)
202
Q

scale used for pressure sores

A

waterlow score

203
Q

Grade 1 of pressure ulcers

A

Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin

204
Q

Grade 2 pressure ulcers

A

Partial thickness skin loss involving epidermis or dermis, or both. The
ulcer is superficial and presents clinically as an abrasion or blister

205
Q

Grade 3 pressure ulcers

A

Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.

206
Q

Grade 4 pressure ulcers

A

Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss

207
Q

Managment of pressure ulcers

A
  • Hydrocolloid dressings and hydrogel
  • discourage soap use
  • swab wounds
  • consider referral to tissue viability nurse
  • surgical debidement
208
Q

Venous ulcer location

A

typically above the medial malleolus

209
Q

Investigations for venous ulceration

A
  • ankle-brachial pressure index (ABPI)
  • normal- 0.9-1.2
  • below or above could be arterial disease
210
Q

Managment of venous ulceration

A
  • compression bandages (4 layers)
  • oral pentoifylline (peripheral vasodilator)
211
Q

Atrophic vaginitis

A
  • vaginal dryness in post-menopausal women
212
Q

AV presentation

A
  • vaginal dryness
  • dyspareunia
  • occasional spotting.
  • On examination, the vagina may appear pale and dry.
213
Q

Causes of Pruritus vulvae

A
  • Irritant contact dermatitis (e.g. latex condoms, lubricants): most common cause
  • atopic dermatitis
  • seborrhoeic dermatitis
  • lichen planus
  • lichen sclerosus
  • psoriasis: seen in around a third of patients with psoriasis
214
Q

Managment of women with Pruritis vulvae

A
  • women should take showers rather than baths
  • clean vulval area with emoilent
  • clean only once a day
  • topical steroids
  • Seborrhoeic dermatitis- use steroid-antifungal
215
Q

What is acne?

A

disease of the pilosebaceous unit.

216
Q

What lesions are seen in acne?

A
  • white heads
  • black heads
  • papules
  • pustules
  • nodules
  • cysts
  • ice-pick scars
  • hypertrophic scars
217
Q
A
218
Q

Drugs associated with acne?

A
  • steroids
  • lithium
  • Phenytoin and carbamazepine
  • Isoniazid
  • Cyclosporine
  • Halogens
219
Q

Acne fulminan

A

Very severe acne associated with systemic upset (e.g. fever).
Hospital admission is often required and the condition usually responds to oral steroids

220
Q

classification of mild acne

A

open and closed comedones with or without sparse inflammatory lesion

221
Q

moderate acne classification

A

widespread non-inflammatory lesions and numerous papules and pustules

222
Q

Severe acne classification

A

xtensive inflammatory lesions, which may include nodules, pitting, and scarring

223
Q

mild to moderate acne managment

A
  • 1st line: 12-week course of topical combination therapy
  • fixed combination of topical adapalene with topical benzoyl peroxide
  • fixed combination of topical tretinoin with topical clindamycin
  • xed combination of** topical benzoyl peroxide with topical clindamycin**

monotherapy topical benzoyl peroxide if options are contraindicated or the person wishes to avoid using a topical retinoid or an antibiotic

224
Q

When to avoid tetracyclines?

A
  • pregancy
  • under 12
  • use erythromycin instead
225
Q

minocycline

A

Not appropriate due to pigmentation

226
Q

Gram-negative folliculitis

A

high-dose oral trimethoprim

227
Q

Dianette

A
  • anti-androgen properties.
  • However, it has an increased risk of venous thromboembolism compared to other COCPs,
228
Q

Reducing antibiotic resistance

A
  • monotherapy with a topical antibiotic
  • monotherapy with an oral antibiotic
  • a combination of a topical antibiotic and an oral antibiotic
229
Q

acne

when to refer to derm?

A
  • patients with nodulo-cystic acne
  • conglobate acne:
230
Q
A

Acne conglobate
*Extensive inflammatory papules, suppurative nodules (that may coalesce to form sinuses)
* cysts on the trunk
* most common in men

231
Q

acne

when to consider referral to derm

A
  • mild to moderate acne has not responded to two completed courses of treatment
  • moderate to severe acne has not responded to previous treatment that includes an oral antibiotic
  • acne with scarring
  • acne with persistent pigmentary changes
  • acne is causing or contributing to persistent psychological distress or a mental health disorder
232
Q

main types of skin cancer

How many types of skin cancer are there?

A

three

233
Q

Main types of skin cancer

A
  • Basal cell carcinoma (BCC)
  • squamous cell carcinoma (SCC)
  • melanoma
234
Q

What is this?

A

BCC

235
Q

What is this?

A

BCC

236
Q

Features of BCC

A
  • sun-exposed sites, especially the head and neck account for the majority of lesions
  • initially a pearly, flesh-coloured papule with telangiectasia
  • may later ulcerate leaving a central ‘crater
  • Metastases are extremely rare
237
Q

What is BCC

A
  • Basal Cell Carcinoma (BCC) is the most common type of skin cancer
  • originating from the basal cells of the epidermis.
238
Q

Risk factors for BCC

A
  • Sun exposure
  • Fair skin
  • history of sunburns
  • genetic predisposition
239
Q

Description of BCC

A

BCC often presents as a pearly or waxy bump, a flat, flesh-colored
brown scar-like lesion, or a pinkish patch of skin. It may bleed easily or develop a crust.

240
Q

Managment of BCC

A
  • Surgical excision is the primary treatment
  • Mohs micrographic surgery
  • Cryotherapy,
  • imiquimod or 5-fluorouracil.
241
Q

Mohs micrographic surgery

A

visible tumor and a thin layer of tissue around it is removed.

242
Q

Prognosis of BCC

A
  • Excellent prognosis with early detection and appropriate treatment.
  • Recurrence is possible, emphasizing the importance of regular follow-ups.
243
Q

Squamous Cell Carcinoma (SCC)

A

Common skin cancer originating from squamous cells of epidermis.

244
Q

Risk factors for skin cancer

A
  • Sun exposure
  • fair skin
  • history of sunburns
  • immunosuppression.
245
Q

Appearance of SCC

A
  • Reddish, scaly patch, wart-like growth, ulceration.
  • Typically found in sun exposed areas#
  • growth is faster than BCC
246
Q

Managment of SCC

A

Surgical excision, Mohs surgery, radiation therapy, topical medications.

247
Q

Melanoma

A

Aggressive skin cancer from melanocytes.

248
Q

Risk factors for melanoma?

A
  • Sun exposure
  • family history
  • fair skin
  • multiple moles
  • blistering sunburns.
249
Q

Appearance of melanoma

A
  • Irregularly shaped mole, asymmetrical, border irregularity, color variation, diameter >6mm.
  • can occur in non-sun exposed skin
  • Extremly rapid growth
250
Q

Managment of melanoma

A

Surgical excision, lymph node biopsy, immunotherapy, targeted therapy.

251
Q

Metastasize of melanoma

common locations which it spreads to

A
  • regional lymph nodes
  • skin
  • liver
  • lungs
  • brain
  • bone
252
Q

What is this?

A

squamous cell carcinoma

253
Q
A
254
Q

What is this?

A

melanoma

255
Q

What is this?

A

Bowen’s disease

256
Q

Bowen’s disease

A

A type of squamous cell carcinoma in situ, also known as squamous cell carcinoma in situ (SCCIS).

257
Q

Risk factors for Bowen’s disease

A
  • Sun exposure
  • fair skin
  • immunosuppression
  • human papillomavirus (HPV) infection
258
Q

Apperance of Bowen’s disease

A
  • Red, scaly patch or plaque, well-defined borders, often mistaken for eczema or psoriasis.
  • Any sun-exposed area, commonly found on the legs, arms, face, and neck.
  • slow growing, doesn’t invade deeper tissues or metastasize
259
Q

Managment of Bowen’s disease

A
  • Surgical excision
  • cryotherapy,
  • topical medications 5-fluorouracil, imiquimod
260
Q

Melanoma vs Bowen’s disease

A
  • B has well defined borders compared to M
  • B on skin exposed skin, M anywhere
  • B slow growth, M quick
  • B no invasion into dermis
261
Q

cellulitis

A

Bacterial infection of the skin and underlying tissues.

262
Q

Risk factors for cellulitis

A
  • Skin wounds or breaks
  • compromised immune system
  • obesity
  • diabetes.
263
Q

Symptoms of Cellulitis

A
  • Red (well-defined margins)
  • swollen
  • warm
  • tender skin
  • fever+ chills
  • fatigue
264
Q

What is the classification used for cellulitis

A

Eron classification

265
Q

class and features of cellulitis

A
266
Q

cellulitis and when to use IV antibiotics

A

Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.

267
Q

Class I cellulitis managment

A
  • oral antibiotics
  • oral flucloxacillin as first-line treatment for mild/moderate cellulitis
  • oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin
268
Q

Cellulitis III and IV managment

A
  • admit
  • NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
269
Q

Cellulitis class II managment

A
  • NICE recommend: ‘
  • Admission may not be necessary if the facilities and expertise are available in the community
  • give intravenous antibiotics and monitor the person
  • check local guidelines
270
Q

Complications of cellulitis

A

Abscess formation, lymphangitis, sepsis

271
Q

Eczema herpeticum

A

severe primary infection of the skin by herpes simplex virus 1 or 2.

272
Q

Epidemiology and presentation of eczema herpeticium

A
  • commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash.
  • monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1-3 mm in diameter are typically seen.
273
Q

pityriasis versicolor treatment

A

Ketoconazole shampoo

274
Q

Pityriasis versicolor predisposing factors

A

occurs in healthy individuals
immunosuppression
malnutrition
Cushing’s

275
Q

Managment of Pityriasis versicolor,

A

topical antifungal. NICE Clinical Knowledge Summaries advise ketoconazole shampoo as this is more cost effective for large areas
if failure to respond to topical treatment then consider alternative diagnoses (e.g. send scrapings to confirm the diagnosis) + oral itraconazole

276
Q

Pityriasis versicolor features

A

most commonly affects trunk
patches may be hypopigmented, pink or brown (hence versicolor). May be more noticeable following a suntan
scale is common
mild pruritus

277
Q

Anti-tissue transglutaminase antibody.

A

Dermatitis herpetiformis
associated with coeliac disease, and it often presents as a pruritic, blistering rash on extensor surfaces such as the elbows, knees, and buttocks.

278
Q

Anti-mitochondrial antibody

A

associated with primary biliary cholangitis (PBC), a chronic liver disease characterised by destruction of intrahepatic bile ducts.

279
Q

Anti-nuclear antibody (ANA)

A

systemic lupus erythematosus (SLE) or Sjogren’s syndrome. Although these conditions can present with skin manifestations like rashes, they do not typically present with the characteristic vesicular rash seen in dermatitis herpetiformis.

280
Q

, Anti-Jo-1 antibody

A

polymyositis and dermatomyositis

281
Q

Anti-tissue transglutaminase antibody

A

haracteristic presentation of dermatitis herpetiformis

282
Q
A

UKMLA Prep (38 decks)

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