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Second Year > Dermatology Pathology > Flashcards

Dermatology Pathology Flashcards

1
Q

What are some external causes of skin damage?

A

Temperature (frostbite, cold urticaria), UV, allergens, irritants, infection, trauma, meds (e.g. photosensitivity with some antibiotics, NSAIDs…)

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2
Q

What is dermatitis artefacta?

A

Sores caused by patient causing trauma to their own skin.

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3
Q

What are some internal causes of skin damage?

A

Systemic disease, genetics (e.g. eczema, psoriasis, neurofibromas), drugs (OTC can lead to macule formation), infection, autoimmune disease.

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4
Q

When describing skin lesions, what is considered small?

A

Less than 5mm.

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5
Q

What word is used to describe a small circumscribed area (i.e. flat rash with no change in texture, only colour)?

A

Macule

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6
Q

What word is used to describe a larger circumscribed area (i.e. flat rash with no change in texture, only colour)?

A

Patch

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7
Q

What word is used to describe a small raised area?

A

Papule

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8
Q

What word is used to describe a larger raised area?

A

Plaque

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9
Q

What word is used to describe a small fluid filled spot?

A

Vesicle

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10
Q

What word is used to describe a larger fluid filled spot?

A

Bulla

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11
Q

What word is used to describe a small pus filled spot?

A

Pustule

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12
Q

What word is used to describe a larger pus filled spot?

A

Abscess

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13
Q

What is an erosion?

A

Superficial loss of epidermis.

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14
Q

What is an ulcer?

A

Loss of epidermis and dermis (ulcers heal with scarring due to dermal loss).

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15
Q

What is urticaria?

A

Hives (wheels resulting from mast cell degranulation).

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16
Q

What are purpura?

A

Red or purple spots on the skin that do not blanch.

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17
Q

What is petechiae?

A

Small spots on the skin caused by minor bleeds of capillaries.

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18
Q

What is erythema?

A

Superficial reddening of the skin.

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19
Q

In which systemic conditions may you see skin signs?

A

Sarcoidosis
Vasculitis - purpuric rash
Malignancy - skin lesion/lymphoma/paraneoplastic phenomena
Autoimmune conditions

Erythema nodosum in pregnancy

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20
Q

What is eruptive xanthoma and when might you see it?

A

In hyperlipidaemia - loads of fat deposits in the skin.

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21
Q

How can you investigate dermatological diseases?

A

Bacterial dx suspected:
Charcoal swab
MC&S
If cellulitis have to do blood culture!

Viral dx suspected:
Viral swab for PCR (must go in viral medium)
Swab vesicle/bulla if it erupts
Can do throat swab if systemic illness

Fungal dx suspected:
Skin scrapping
Nail clipping
Hair sample
Fungal cultures

Can do punch biopsies of skin if need to do biopsy.

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22
Q

What is leukocystoclastic vasculitis?

A

Hypersensitivity vasculitis, in which there may be intradermal haemorrhage, seen as petechiae or purpura.

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23
Q

What is acanthosis nigrans and what it is associated with?

A

Flexular distribtution of hyperkeratosis, hyperpigmentation and papules. Gives velvety appearance.

Associated with insulin resistance, obesity and malignancy.

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24
Q

Name 4 viruses that can cause infection of the skin.

A

Human papilloma
Herpes simplex
Herpes Zoster
Molluscium contagiosum

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25
Q

Name 4 bacteria that can cause infection of the skin.

A

Staphylococcus aureus
Streptococcus
Corynebacterium
Ninutissimum

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26
Q

Name 3 yeast/fungi that can cause infection of the skin.

A

Candida alicans
Pityrosporum
True fungi

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27
Q

Name an ectoparasite that can cause a skin infection.

A

Scabies

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28
Q

Where can HSV infect?

A

Can be herpes labialis (primarily affecting the lips), genital or herpes whitlow (affecting fingers/thumb) or even corneal.

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29
Q

How is HSV spread?

A

Direct person to person contact. Vesicles are full of active virus.

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30
Q

What episode of HSV will be the worst?

A

1st will be the worst, longest and severe. Likely to be associated with lymphadenopathy and fever.

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31
Q

Why do you get recurrent HSV symptoms after the first episode?

A

If you leave it alone, symptoms resolve spontaneously (2-3wks), but virus migrates into dorsal root ganglia where it can reactive and travel back down the peripheral nerves (usually the ones it come up in the first place, hence why infection tends to be in same place).

I.e. it is latent.

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32
Q

What can trigger an episode of symptoms from the HSV?

A

Variety of triggers, e.g. immunosuppression with cold or stress etc.

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33
Q

What symptoms are associated with HSV?

A

Vesicles and pustules grouped closely together. Where skin is thin, will see multiple ulcers/erosions. All look roughly the same (monomorphic).

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34
Q

What 3 groups of people is it essential that avoid getting HSV?

A

Pregnant - has very damaging effects on unborn child (only if not already got it before pregnancy).

Immunosuppressed, as can go from trivial infections to life threatening.

Atopic eczema - can lead to widespread infection.

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35
Q

What group of people are more likely to get coldsores on their hands (whitlow Herpes)?

A

Healthcare workers.

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36
Q

How can you treat HSV infection?

A

Aciclovir (topic if small area, or oral if more diffuse).

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37
Q

Is resistance an issue with HSV infection?

A

Not unless very severe.

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38
Q

What condition does infection with herpes zoster virus cause?

A

Chickenpox or shingles.

If you meet the virus for the first time you get chickenpox, but virus doesn’t go (resides in vestibular ganglion after symptom resolution) and it shouldn’t reactive but if it does - causes shingles (CANNOT have shingles if never had chickenpox).

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39
Q

What is chickenpox?

A

Widespread vesiculopustural episode and systemically unwell.

Once crusted and liquid dried up, no longer infectious.

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40
Q

What is shingles?

A

Lots of little vesicles grouped together in dermatomal distributions, can cross midline but not much. Preceded (4 days earlier) by pain and constitutional symptoms.

Can get post-herpetic neuralgia afterward - horrible burning pain after blistering gone.

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41
Q

In which group of people is it essential to avoid exposing to HZV?

A

Pregnant - very easily crosses placenta.

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42
Q

IF HZV in ophthalmicological region - what must you do?

A

Refer to ophthalmologist to test eye function.

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43
Q

What can HZV cause that HSV can’t?

A

Scaring.

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44
Q

How do you treat HZV infection?

A

Aciclovir, treat quickly.

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45
Q

What is scabies?

A

Infection cause by an ectoparasite. One of the itchiest things you can get.

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46
Q

How is scabies spread?

A

Human to human contact. Bugs usually on their hands and if you have close contact with someone for at least a minute can spread.

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47
Q

What are the symptoms of scabies? How does it manifest and how do you know it is scabies?

A

Might not know they have it for 5-6wks, after 6wks may see papules and vesicles in webbed parts of hands, after this become allergic to mite faeces –> allergic reaction, which is very very itchy (esp. at night). Must look for obvious burrows. Once you see the burrows you know it is scabies.

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48
Q

How do you treat scabies?

A

Treat patients and their contacts (even if asymptomatic). Permathin cream (liclear, which is made from a neurotoxin that fries the mite brains). Must put it everywhere apart from hair on head, leave for 12-18 hours and wash it off, then repeat 7 days later).

NB - itch can last for a few weeks after, can use topical steroids to reduce itch.

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49
Q

What are warts?

A

Outgrowths of skin caused by a type of human papilloma virus.

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50
Q

What is the peak incidence for warts?

A

12-16 years.

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51
Q

What are the different types of warts?

A

Common - usually symptomless, most regress within 2y.
Plantar - mostly in children and regress within 6mnths.
Genital - usually sexually transmitted
Others incl plane/filliform/mosaic

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52
Q

How are warts treated?

A

May be left as they are harmless.

Chemical paints, cryptotherapy (with liquid nitrogen), imiquimod (genital) and others.

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53
Q

What is the orf virus?

A

Mainly causes sores around mouths of sheep but can infect humans (mostly hands?). No treatment and can trigger erythema multiforme.

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54
Q

What does infection with molluscum contagiosum cause?

A

Pearly, elevated pink lesions.

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55
Q

What age does incidence of infection with molluscum contagiosum peak?

A

10y.

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56
Q

What is the treatment for infection with molluscum contagiosum?

A

None, cryptotherapy, expression and antiseptic.

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57
Q

What is impetigo? What is it caused by? What is its appearance?

A

Golden dry, flaky chunks, highly contagious. Can spread really easily through contact.
Usually staph/strep/both infection. Most commonly - staph aureus. Can get it anywhere, most commonly HN region.

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58
Q

How do you treat impetigo?

A

Rx - antibx to treat both (localised = topical, diffuse = oral).

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59
Q

What is a furuncle?

A

Abscess/infection in the hair follicle. Most commonly caused by by staph aureus.

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60
Q

How can you treat a furuncle?

A

Drain pus and give antibiotics.

Dip stick urine to check for diabetes if recurrent, as diabetics at higher risk of developing these.

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61
Q

What is ecthyma?

A

Crust and rim of erythema. Skin infection characterised by crust under which there are ulcers. Most commonly caused by staph aureus.

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62
Q

How do you treat ecthyma?

A

Oral antibiotics.

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63
Q

What is erysipelas? What symptoms are associated with erysipelas?

A

Streptococcus infection of skin. More superficial than cellulitis. Skin forms raised plateau of erythema and is very hot to touch. Systemically unwell and quite high mortality. May also have fever and rigours.

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64
Q

How do you treat erysipelas?

A

IV antibiotics. Cannot wait for oral stuff to kick in.

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65
Q

What is cellulitis? What symptoms are associated with it?

A

Swollen, red and hot. Patient will be sick (fever, rigours) if extensive cellulitis. Caused by a streptococcus infection in deeper layers of skin.

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66
Q

Where is cellulitis most common?

A

Lower limb, below the knee.

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67
Q

If very severe cellulitis what may occur?

A

Skin breaks down and ulcerates.

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68
Q

How might cellulitis happen?

A

Cracks in skin (e.g. from athletes foot), ulcers - any portal of entry allows for streptococcus to enter deeper layers of skin and spread.

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69
Q

How do you treat cellulitis?

A

Hospitalised, IV antibiotics for staph and strep.

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70
Q

What is the most common yeast infection?

A

Candida albicans.

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71
Q

Where is it common for obese people to get candida albican infections?

A

If they don’t wash properly, can get under breasts, as it likes sweaty, moist areas.

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72
Q

What is the appearance of a candida albican infection?

A

Brick red erythema and satellite pustules (filled with yellow pus).

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73
Q

Who else may be at risk of a candida albican infection?

A

Hairdressers, bar staff etc. who have their hands wet.

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74
Q

What is paronchyia?

A

Inflammation of the nail fold, can be acute or chronic.

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75
Q

What is the commonest cause of chronic paronchyia?

A

Candida albicans, which has penetrated into nail fold, will see yellow pus discharge.

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76
Q

What is the commonest cause of acute paronchyia?

A

Staph aureus.

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77
Q

How do you treat canidida albicans infection?

A

Clotrimazole for local treatment (canisten) or if difficult place, may need anti-candidial drugs.

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78
Q

What is tinea pedis?

A

Athlete’s foot - lots of white, lacerated skin and flakey bits of skin. Really common.

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79
Q

What causes tinea pedis/corpis/cruris/barbre etc.?

A

Dermatophytes (fungal infection of the skin).

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80
Q

How do you treat tinea pedis?

A

Clotrimazole or tolnaftate

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81
Q

What is tinea corpis? How do you investigate it?

A

Fungal infection of the body. Aka. ring worm. Will see enlarging rings and flakey bits at the edge. Dermapack to microbiology if unsure of diagnosis (scrapping from ends as healthiest fungus there).

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82
Q

What is tinea cruris?

A

Fungal infection of the crotch area.

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83
Q

What is tinea cognito?

A

Fungal infection of the skin masked by topic corticosteroid use. Do not use steroids on fungal infections as it will spread.

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84
Q

What is tinea barbre and how is treated directly from other tineas?

A

Fungal infection of hair follicles. Deeper and won’t respond to topical treatment alone, must use oral and topical treatment.

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85
Q

What is kerion?

A

Fungal infection of scalp. More common in children 9as they produce less sebum). Leads to very swollen, sore scalp.

Can send hair to microbiology.

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86
Q

How is kerion treated?

A

Drainage and antibiotics (oral and topical).

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87
Q

What is a carbuncle?

A

Collection of boils that develop under the skin.

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88
Q

What infections of the skin are related to staph aureus?

A

Boils, carbuncles, styes, folliculitis, impetigo, ecthyma, ezcema flare ups.

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89
Q

What infections of the skin are related to streptococci?

A

Impetigo, ecthyma, erysipelas, cellulitis, eczema flare-ups (necrotising fascitis, guttate psoriasis).

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90
Q

What infections of the skin are related to corynebacterium. miniutissimum?

A

Erythrassma, pitted keratolyis.

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91
Q

What infections of the skin are related to Candida?

A

Thrush (oral, vaginal), balantitis, angular stomatitis, intertrigo, nappy rash, chronic paronychia.

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92
Q

What infections of the skin are related to true fungi?

A

Tinea pedis/cruris/corpis/faceii/barbae, onychomycosis.

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93
Q

What would result if the skin failed to be a barrier to infection?

A

Sepsis

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94
Q

What would result if the skin failed to regulate temperature?

A

Hypo and hyperthermia

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95
Q

What would result if the skin failed to play its role in vitamin D synthesis?

A

Renal failure

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96
Q

What is erythroderma?

A

A descriptive term - any inflammatory skin disease affecting <90% of the total skin surface.

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97
Q

What can cause erythroderma?

A

Psoriasis, eczema, drugs, cutaneous lymphoma, hereditary disorders.

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98
Q

How do you treat erythroderma?

A

ITU/burns unit. Remove offending drugs, fluids and nutrition (avoid albumin excess), temperature regulation, emollient to protect skin (liquid paraffin and soft white paraffin mix (protection and moisturise), oral and eye care (e.g. eye drops), anticipate and treat infection. Treat symptoms (e.g. itch) and underlying cause.

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99
Q

Give an example of a mild drug reaction.

A

Morbilliform exanthema (macularpapular rash).

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100
Q

Given examples of severe drug reactions.

A

Erythroderma, Steven Johnson Syndrome/Toxic epidermal necrolysis, DRESS

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101
Q

What is SJS/TEN?

A

Two conditions thought to be part of same spectrum. SJS less severe (less skin involvement).

Secondary to drugs (e.g. antibiotics, anticonvulsants, allopurinol, NSAIDs).

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102
Q

What are the clinical features of SJS?

A

Fever, malaise, arthralgia, rash (maculopapular target lesions, blisters, erosions covering <10% skin surface), mouth ulceration (greyish white membrane, haemorrhagic crusting) ulceration of other mucous membranes (eyes, genitalia).

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103
Q

What are the clinical features of TEN?

A

Prodromal febrile illness, ulceration of mucus membranes, rash (macular, purpuric or blistering and becomes confluent). Sloughing off of large areas of dermis. High mortality.

Nikolsy’s sign - rub the skin, and it leads to exfoliation of the outer layer.

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104
Q

What are the long term complications of TEN/SJS?

A

Pigmentary skin changes, scarring, eye disease and blindness, nail and hair loss, joint contractures.

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105
Q

How do you treat TEN/SJS?

A

Stop culprit drug. Supportive - high dose steroids, IV Ig, anti-TNFalpha, cyclosporin.

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106
Q

What can be used to assess mortality in TEN/SJS?

A

SCORTEN (graded 1-5 and considers age, malignancy, HR, initial epidermal detachment, serum urea, serum glucose, serum bicarbonate).

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107
Q

What is DRESS?

A

Drug reaction with eosinophilia and systemic symptoms.

Adverse drug reaction occurring 2-8wks after drug exposure.

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108
Q

What are the signs of DRESS?

A

Eosinophilia with derranged LFTs, lymphadenopathy and other organ involvement.

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109
Q

What are the symptoms of dress?

A

Fever, widespread rash.

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110
Q

How do you treat DRESS?

A

Stop causative drug, symptomatic and supportive, systemic steroids +/- immunosuppression or immunoglobulins.

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111
Q

What is erythema multiforme?

A

Hypersensitivity reaction usually triggered by infection (most commonly HSV and then mycoplasma pneumonia).

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112
Q

What are the symptoms of erythema multiforme?

A

Abrupt onset of up to 100s of lesions over 24h (distal to proximal), palms and soles, mucosal surfaces (=EM major - more serious), evolves over 72h (pink macule become elevated and may blister in centre –> target lesions).

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113
Q

How do you treat erythema multiforme?

A

Self-limiting, resolves over 2wks (can take up to 6wks).

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114
Q

What is pemphigus?

A

Skin disorders that cause blistering of the skin, commonly affecting the mucous membranes of the mouth.

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115
Q

What causes pemphigus?

A

Autoimmune disease where antibodies are targeted at desmosomes.

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116
Q

What are the signs/symptoms of pemphigus?

A

Nikolskys sign may be positive. Easily rupturing flaccid blisters on skin (may appear as ulcer/erosion). Common sites - face, axillae, groins (may also affect mouth, nose, eyes, genitalia).

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117
Q

What is pemphigoid?

A

Autoimmune disease where antibodies are direct at the demo-epidermal junction. So intact dermis forms the roof of the blister - these blisters are therefore normally intact.

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118
Q

How could you image these blisters in pemphigoid and pemphigus?

A

Immunofluorescence and histopathology.

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119
Q

What are the main differences between pemphigoid and pemphigus?

A

Pemphigoid more common and seen in elderly patients, blisters in tact and tense, patients well even fi extensive.

Pemphigus - uncommon, middle aged, blisters very fragile, mucous membranes usually affected, patients unwell if extensive.

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120
Q

How do you treat pemphigoid?

A

Topical steroids (systemic if diffuse).

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121
Q

How do you treat pemphigus?

A

Systemic steroids, dress erosions, supportive.

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122
Q

What is eczema herpeticum?

A

Disseminated herpes virus infection on background of poorly controlled eczema.

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123
Q

What is the appearance and symptoms of eczema herpeticum?

A

Monomorphic blisters and pouched out erosions, generally not itchy. Fever, lathery, lymphadenopathy.

124
Q

How do you treat eczema herpeticum?

A

Aciclovir, mild topical steroid to treat eczema. If periocular –> refer to ophthalmologist.

If adults consider underlying immunocompromise.

125
Q

What is a staphylococcal scalded skin syndrome? What are the symptoms?

A

Staph infection that leads to diffuse erythematous skin rash with tenderness (flexural). Blistering and desquamousation follows (staphylococcus produces toxins that target Desmoglein 1). Fever and irritability also common.

126
Q

Who are SSSS seen in?

A

Children, immunocomp adults.

127
Q

How do you treat SSSS?

A

Admission, IV antibiotics, supportive care.

Generally resolves within 5-7 days.

128
Q

What is urticaria?

A

Central swelling surrounded by erythema and dermal oedema. Itches, burns (histamine release into dermis). Tends to have fleeting nature (<14h).

129
Q

What is angiooedema?

A

Deeper swelling of skin or mucous membranes.

130
Q

What are the two types of urticaria?

A

Acute <6wks

Chronic >6wks

131
Q

What are the causes of acute urticaria?

A

Idiopathic, infection (viral), drugs/food (IgE mediated).

132
Q

How do you treat acute urticaria?

A

Oral antihistamines, oral steroids. Avoid opiates and NSAIDs as they exacerbate.

133
Q

What can cause chronic urticaria?

A

Idiopathic/autoimmune, physical (press, cold, light trauma), vasculitic (inflammation of blood vessels in skin, more associated with burning sensation).

134
Q

How is chronic urticaria managed?

A

Chronic spontaneous urticaria can use omalizumab. Little role for oral steroids.

135
Q

What is psoriasis?

A

Chronic immune mediated disease where patients develop sharply demarcated erythematous plaque with micaceous scale

136
Q

In which age groups is psoriasis most common?

A

20-30y, 50-60y

137
Q

What is the aetiology of psoriasis?

A

Polygenic predisposition (FH, HLA-Cw6, psoriasis susceptibility regions (PSORS1-9)

Environmental triggers (infection, drugs, trauma, sunlight)

138
Q

What is acne vulgaris?

A

A disease of the pilo-sebaceous unit

139
Q

Where does acne vulgaris affect most on the body?

A

Face
Chest
Back

140
Q

What is the medical term that describes a blocked follicle?

A

Comedo(nes)

141
Q

What is the pathogenesis of acne vulgaris?

A

Androgen stimulate sebaceous follicles to over produce sebum so follicles become blocked

Hyperkeratinization of epithelium –> accumulation and follicle blocking

Propionibacterium acnes replicates within follicle –> releases lipase –> sebum converted to FFA –> release of cytokines and infalmmation

142
Q

What is a closed comedo?

A

White head

143
Q

What is an open comedo?

A

Blackhead

144
Q

When is the peak onset of acne vulgaris?

A

15-18y

145
Q

What is the dose of isotretonin use to treat acne vulgaris?

A

1mg/kg/day for 16 weeks

146
Q

Who can prescribe isotretinoin?

A

Skin specialists only

147
Q

What is isotretinoin?

A

A retinoid

148
Q

What is the most effective treatment for stubborn/severe acne?

A

Isotretinoin

149
Q

What are the drawbacks with isotretinoin?

A 
Very teratogenic 
Many SEs (dry skin, hair loss, mood swings/depression/suicide, abnormal LFTs, hypertriglyceridaemia)
150
Q

What are the different types of acne vulgaris?

A

Mild - occasional comodones, papules and pustules

Moderate - multiple pustules, nodules on trunk

Severe - cystic, large nodules, persistent trunk involvement, scarring

151
Q

What medications can cause acne vulgaris?

A

Lithium
Glucocorticoids
Anabolic steroids

152
Q

What conditions can cause acne?

A

PCOS
Hormonal imbalance
Infection
Stress

153
Q

What topical treatments can be used for acne vulgaris?

A

Retinoids
Benzoyl peroxide
Antibiotics (clindamycin, tetracycline, erythromycin)

154
Q

What systemic treatments can be used for acne vulgaris?

A

Antibiotics: tetracyclines, erythromycin
Anti-androgens, e.g. COCP/dianette
Isotretinoin
Light based treatments

155
Q

What is eczema?

A

A common INFLAMMATORY skin condition

156
Q

Where does eczema tend to affect?

A

FLEXURAL surfaces

157
Q

What age group is most affected by eczema?

A

Babies/children

60% clears by adulthood

158
Q

Define atopic eczema

A

An itchy skin condition in the last 12 months, + 3 of:

  • Onset before 2y
  • Hx flexural involvement
  • Hx of generally dry skin
  • Hx of another atopic dx (asthma/hayfever) or hx in first degree relative if <4y
159
Q

What is the pathogenesis of eczema?

A

Epidermal barrier dysfunction due to genetic + environmental factors

160
Q

What is the key role implicated in eczema?

A

Filaggrin gene

161
Q

What atopic diseases are associated with eczema?

A

Atopic eczema, asthma, hayfever, food allergy

162
Q

What is the atopic triad?

A

Asthma
Hayfever
Eczema

163
Q

What are the histological findings in eczema?

A

Spongiosis (intracellular oedema) within the dermis
Acanthosis
Inflammation (superficial perivascular lymphohistiocytic infiltrate)

164
Q

What is acanthosis?

A

Thickening of the epidermis

165
Q

What are causes for acute flares of eczema?

A

Viral illness
Period of poor health
Environmental triggers (cold, heat, allergens, e.g. HDM, cat/dog dander)
Food allergies

166
Q

What are the clinical features of eczema?

A

Itch, redness, scaling, papules, vesicles

167
Q

What chronic changes can you get in eczema?

A

Lichenification
Plaques
Fissuring

168
Q

What is lichenification?

A

Thick, leathery patches of skin

169
Q

What are the main two classes of eczema?

A

Exogenous - external

Endogenous - internal

170
Q

What are the ‘external’ eczemas?

A

Contact dermatitis - irritant, allergic
Lichen simplex
Photoallergic/photoaggrevated

171
Q

What are the ‘internal’ eczemas?

A 
Atopic 
Discoid
Venous 
Seborrhoeic dermatitis
Pomphloyx
Juvenile plantar dermatitis
172
Q

What type of hypersensitivity reaction is allergic contact dermatitis?

A 
Type 4 (delayed) 
Can take 48-27h to develop reaction
173
Q

What is the pathophysiology of allergic contact dermatitis?

A

APC take allergen to LNs and present o naïve T cells
Clonal expansion of these T cells + T cells released into bloodstream

When T cells next encounter hapten –> mast cell degranulation, vasodilation + neutrophils are recruited

174
Q

What is irritant contact dermatitis?

A

Skin is injured by friction (e.g. microtrauma, cumulative) and environmental factors (cold, over exposure to water, acids, alkalis, detergents + solvents)

175
Q

What occupations are at risk of irritant contact dermatitis?

A

Hairdressers
NHS staff
Cleaners

176
Q

What is nappy rash?

A

Irritant contact dermatitis possibly from wipes

177
Q

How is patch testing done?

A

Potential allergens applied, removed after 3 days, re-assess after another 3 days

178
Q

Who do you see seborrheic dermatitis in?

A

Infants (<6m usually)

179
Q

Where does seborrheic dermatitis tend to affcet?

A

Areas rich in sebaceous glands - scalp, face, upper trunk

180
Q

What causes seborrheic eczema?

A

Malassezia yeast

181
Q

What do the lesions look like in seborrheic eczema?

A

Red, sharply marginated lesions covered with greasy looking scales

182
Q

What is a common precursor to adult seborrheic eczema?

A

Dandruff

183
Q

How is seborrheic eczema treated?

A

Ketoconazole

184
Q

If an adult has very severe seborrheic eczema what must you consider?

A

HIV testing

185
Q

What does discoid eczema look like?

A

Circular plaques of eczema

186
Q

Where does discoid eczema develop?

A

Can develop at sites of trauma/irritation

187
Q

What is pompholyx/vesicular eczema?

A

Affects palms + soles
V. itchy
Sudden onset crops of vesicles
Desquamation

188
Q

What is asteatotic eczema?

A

Very dry, cracked, scaly skin

Tends to be on shins

189
Q

What can cause asteatotic eczema?

A

Hot climate

Excessive washing/soaps

190
Q

Where does venous eczema tend to be?

A

On ankle and lower leg

191
Q

What causes venous eczema?

A

Increased venous pressure –> oedema

192
Q

What can help with venous eczema?

A

Resolution of oedema - e.g. compression stockings

193
Q

What is eczema herpeticum?

A

Disseminated HSV infection

194
Q

What does eczema herpeticum present like?

A

Fever
Unwell
Itchy clusters of blisters + erosions
Swollen LNs

195
Q

What strains of HSV can cause eczema herpeticum?

A

HSV 1 and 2

196
Q

How do you manage eczema herpeticum?

A

Admission
Antivirals
Consider secondary bacterial infection

197
Q

How do you treat eczema?

A 
Pt education
Avoid causative/exacerbating factors
Emollients (moisturisers)
Soap substitutes
Intermittent topical steroids
Antihistamines/antimicrobials
Calcineurin inhibitors
198
Q

What types of emollients are there?

A

Ointments - greasy, but effective
Creams
Lotions - most watery

199
Q

Give two examples of calcineurin inhibitors

A

Topical Pimecrolimus and Tacrolimus`

200
Q

What other treatments may be used for severe eczema?

A

UV light

Immunosupression - e.g. azathioprine, ciclosporin, mycophenolate mofetil, methotrexate

201
Q

What two regulatory bodies can approve medicines for use in the uk?

A

MHRA - medicines and healthcare products regulatory agency

EMA - European medicines agency

202
Q

What are the three types of medicines used without a license?

A

Unlicensed
Off label
Specials

203
Q

What does unlicensed mean?

A

Not approved for use in the Uk

204
Q

What does off label mean?

A

A licensed medication that is being used for an unlicensed indication

205
Q

What are common causes of prescription errors?

A

Lack of knowledge
Mistake writing/generating prescription
Poor communication
No local/national guidelines

206
Q

Define pharmacology

A

Branch of medicine concerned with uses, effects and modes of actions of drugs

207
Q

Define pharmacokinetics

A

Effect of body on the drug

208
Q

Define pharmacodynamics

A

Effect of the drug on the body

209
Q

What are the four components of pharmacokinetics

A

Absorption
Distribution
Metabolism
Elimination

210
Q

In which kinds of diseases may the metabolism of a drug be distributed?

A

Liver disease

211
Q

In which kinds of diseases may the elimination of a drug be distributed?

A

Renal disease

212
Q

What things must you think about about the pharmacodynamics of a drug?

A

Individual variation in response

Age of pt, pregnancy risk, DDIs, pharmacogenetics

213
Q

What are factors that make it more likely patients will adhere to prescribed medication?

A 
Female
Married
Employed
Not paying for prescription 
Increasing age
214
Q

What are factors that make it less likely patients will adhere to prescribed medication?

A 
Psychiatric co-morbs
Slower acting agents
Multiple applications per day 
Lack of pt education 
Cosmetic acceptability of treatments
Unintentional non-adherence
215
Q

What is a topical therapy?

A

Medication applied to the skin

216
Q

What are the two components of a topical agent?

A

Vehicle + active drug

217
Q

What is the vehicle in a topical agent?

A

Pharmacologically inert, physically + chemically stable substance that carries the active drug

218
Q

What factors affect the absorption of a topical agent?

A 
Concentrate
Vehicle
Chemical properties of the drug
Thickness/hydration of stratum corneum
Temperature
Skin site
Occlusion
219
Q

Give examples of vehicles for topical agents

A 
Solution 
Cream 
Lotion
Gel
Tape
Paste
Shampoo
Paint
220
Q

Give e.g.s of topical drugs

A 
Corticosteroids
Antibiotics
Antivirals
Vitamin analogues
Chemotherapy
Parasiticidals 
Coal tar 
Anti-inflammatories
221
Q

What are the actions of topical steroids?

A

Anti-inflammatory + immunosuppressive:

  • Regulate pro-inflammatory cytokines
  • Supress fibroblast, endothelial + leukocyte function
  • Vasoconstriction
  • Inhibit vascular permeability
222
Q

How many g does a finger tip unit equate to?

A

0.5g

223
Q

What area of skin should a finger tip unit treat?

A

Double the size of one hand

224
Q

What are side effects of topical steroids?

A 
Thinning/atrophy
Striae
Bruising 
Hirsutism
Telangiectasia
Acne/rosacea/perioral dermatitis
Glaucoma 
Systemic absorption
Cataracts
225
Q

What systemic treatments may be used in dermatology?

A

Retinoids
Traditional immunosupressants
Biolgoics

226
Q

What vitamin are retinoids analogues of?

A

Vitamin A

227
Q

What are the actions of retinoids?

A

Normalise keratinocyte function

Anti-inflammatory and anti-cancer effects

228
Q

What is a serious complication of retinoid use?

A

Teratogenicity

229
Q

What are side effects of retinoids?

A

Chelitis (dry lips), xerosis (dry skin)
Increased serum transaminases and triglycerides
Rarely psychiatric, eye, bone side effects

230
Q

What immunosupressants may be used to treat dermatological diseases?

A 
Oral steroids
Azathioprine
Ciclosporin
Methotrexate
Mycophenolate mofetil
231
Q

What are the adverse effects of immunosupressants?

A

Risk of malignancy + infection

232
Q

What blood tests are needed for patients on methotrexate?

A

LFTs, FBC

233
Q

What blood tests are required for those on ciclosporin?

A

Renal function tests

234
Q

What blood tests are required for those on azathioprine?

A

FBC

235
Q

What are biologics?

A

Genetically engineered proteins derived from human genes that inhibit specific components of the immune system

236
Q

What does the suffix ‘-cept’ indicate?

A

A biologic that is genetically engineered fusion protein

237
Q

What does the suffix ‘-mab’ indicate?

A

Biologic that is a monoclonal antibody

238
Q

With relation to biologics - what does the infix ‘zu’ indicate?

A

Humanised

239
Q

With relation to biologics - what does the infix ‘ix’ indicate?

A

Chimeric

240
Q

With relation to biologics - what does the infix ‘u’ indicate?

A

Fully human

241
Q

With relation to biologics - what does the infix ‘li/l’ indicate?

A

Immunomodulator

242
Q

What are the adverse effects of biologics?

A

Risk of infection - may reactive TB, cause serious infection
Risk of malignancy
TNF inhibitors have risk of demyelination

243
Q

What should people on biologics avoid?

A

Live vaccines

244
Q

What resources can you use to get reliable information about a drug?

A 
SPC (summary of product characteristics)
SMC
BNF
BAD guidelines
Local formulary
245
Q

What is Curth’s postulates?

A

Criteria that can help distinguish between a skin sign and a malignancy occurring together being a chance occurrence or an associated event

246
Q

What are Curth’s postulates?

A 
Concurrent onset
Parallel course
Uniform site or type of neoplasm 
Statistical association 
Genetic linkage
247
Q

What are the features of carcinoid syndrome?

A 
Episodic flushing (lasting mins-hours) 
Facial telangiectasia
248
Q

What is carcinoid syndrome associated with?

A

GI carcinoid ONLY if there are liver mets

Bronchial or ovarian cancers (can occur without liver mets)

249
Q

What are the features of paraneoplastic pemphigus?

A

Erosive stomatitis, rash

250
Q

What is paraneoplastic pemphigus associated with?

A

Non-hodgkins, Castlemans disease (produces the autoantibody)

251
Q

What is erythema gyratum repens?

A

Concentric erythematous lesions

Assoc. with various malignancies

252
Q

What is acquired hypertrichosis lanuginosa?

A

Acute onset of lanugo hairs on face and body

253
Q

What is acquired hypertrichosis lanuginose associated with?

A

Colorectal cancer > lung > breast (usually advanced)

254
Q

What are the features of Leser-Trelat syndrome?

A

Eruptive seborrheic keratoses

255
Q

What is Leser-Trelat syndrome associated with?

A

GI adenocarcinomas

256
Q

What are the features of Bazex syndrome?

A

Hyperkeratosis of extremities

Looks like psoriasis

257
Q

What is Bazex syndrome associated with?

A

SCC - bronchial, oropharyngeal, GI

Gastric, colon, biliary, adenocarcinomas

258
Q

What is ectopic ACTH syndrome?

A

Tumour production of ACTH leads to generalised hyperpigmentation

259
Q

Why does xs ACTH lead to hyperpigmentation?

A

ACTH –> inc. MSH –> release of melanin from melanocytes

260
Q

What is Paget’s disease?

A

Eczematous plaque at nipple/areola

extends into underlying ductal adenocarcinoma

261
Q

What skin conditions are strongly associated with cancer in all/most cases?

A 
Carcinoid syndrome
Paraneoplastic pemphigus
Erythema Gyratum Repens 
Acquired hypertrichosis
Leser Trelat
Bazex syndrome
Ectopic ACTH 
Pagets disease
262
Q

What two conditions are strongly associated with malignancy?

A

Acanthosis nigricans

Dermatomyositis

263
Q

What kind of cancer does acanthosis nigrians most commonly precede?

A

Gastric adenocarcinoma

264
Q

What are red flags for acanthosis nigricans?

A 
Older patient
Rapid onset
Other skin signs
Involves lips
Wt loss
265
Q

What are the features of dermatomyositis?

A

Inflammatory myopathy + rash -

  • Periorbital heliotrope rash
  • Gottron papules
  • Shawl sign
  • Photosensitive poikiloderma
  • Scalp erythema
266
Q

What are Gottron papules?

A

Red maculo-papular lesions over knuckles usually

267
Q

What conditions may be associated with an underlying malignancy?

A 
Bullous pemphgoid
Sweets Syndrome
Pyoderma gangrenosum
Acquired ichthyosis
Acquired angioedema
Primary systemic amyloid
Cryoglobulinaemia
268
Q

What cancers are associated with Peutz-Jeghers?

A

Melanosis, colon hamaratomas, colon ca

269
Q

What cancers are associated with Muir-Torre?

A

Sebaceous tumours, keratocanathomas, GI, breast, GU

270
Q

What are the features of neurofibromatosis?

A

Café au lait spots, axillary freckling, neurofibromas, nerve sheath tumours, carcinoid syndrome, phaeochromocytoma

271
Q

What are the features of xeroderma pigmentosum?

A

Inability to repair sun damage
Sarcoma
Leukaemia
GI and lung cancers

272
Q

What skin signs do you see in IBD?

A

Erythema nodosum

Pyoderma gangrenosum

273
Q

What is the pathophysiology of alopecia?

A

T lymphocyte + cytokine mediated rejection of hair

274
Q

What are the three types of alopecia?

A

Totalis - total scalp loss of hair
Universalis - total hair loss of entire body
Areta - patchy loss of hair on scalp

275
Q

What causes vitiligo?

A

Destruction of melanocytes via autoimmune process

276
Q

What is the most common type of non-melanoma skin cancer?

A

BCCs

277
Q

What are risk factors for non-melanoma skn cancers?

A 
UV radiation 
Photochemotherapy 
Chemical carcinogens
Ionising radiation 
HPV
Familial cancer syndromes
Immunosupression
278
Q

Describe the appearance of a BCC

A

Pearly rolled edge
Telangiectasia
Central ulceration
Arborising vessels on dermoscopy

279
Q

Give e.g.s of types of BCC

A

Pigmented

Morphoeic

280
Q

How do you treat BCC?

A

Excision is gold standard

Curettage in some cases

281
Q

How do you excise a BCC?

A

Ellipse (with rim of unaffected skin)

282
Q

What drug can be used for locally advanced BCC that is not suitable for radio or surgery or metastatic BCC?

A

Vismodegib

283
Q

How does vismodegib work?

A

Selectively inhibits abnormal signalling in the Hedgehog pathway

284
Q

What are SEs of vismodegib?

A

Hair loss, wt loss, altered taste

Muscle spasms, nausea, fatigue

285
Q

What cells are SCCs derived from?

A

Keratinising squamous cells

286
Q

Where do SCCs tend to occur?

A

Sun exposed sites

287
Q

How do SCCs appear?

A

Tender, scaly/crusted or fleshy growths

Can ulcerate

288
Q

Of SCC and BCC which are faster growing and more aggressive?

A

SCC

289
Q

How is SCC treated?

A

Excision +/- radio

290
Q

What SCCs are considered high risk and should be followed up post-treatment?

A 
Immunosupressed pt
>20mm diameter
>4mm depth 
Ear, nose, lip, eyelid
Perineural invasion 
Poorly differentiated
291
Q

What is keratocanthoma?

A

Variation of SCC
Erupts from hair follicles in sun damaged skin
Rapidly growing

292
Q

How are keratocanthomas managed?

A

May resolve itself after a few months

Surgical excision

293
Q

What are risk factors for melanoma?

A

UV radiation
Genetic susceptibility - fair skin, red hair, blue eyes, tendency to burn easily
Familial melanoma + melanoma susceptibility genes

294
Q

What is the ABCDE rule for identifying lesions that may be melanoma?

A 
Asymmetry 
Border
Colour
Diameter
Evolution
295
Q

What is the 7 point checklist for identifying melanoma?

A

MAJOR FEATURES:
Change in size
Change in shape
Change in colour

MINOR FEATURES
Diameter >5mm
Inflammation
Oozing or bleeding
Mild itch/altered sensation
296
Q

What apparatus is used to look up close at lesions on the skin?

A

Dermoscope

297
Q

Name the types of melanoma

A 
Superficial spreading malignant melanoma
Lentigo maligna melanoma
Nodular melanoma 
Acral lentiginous melanoma
Subungal melanoma 
Ocular melanoma
298
Q

How do you treat melanoma?

A

Urgent surgical excision

299
Q

What is Breslow thickness?

A

Description of how deep a melanoma has invaded

300
Q

What kind of excision should be done for a melanoma?

A

Wide local excision

+ sentinel LN biopsy

301
Q

What other treatments may be used for melanoma besides surgery?

A

Chemotherapy

Immunotherapy

302
Q

What drugs can be used to treat melanoma?

A

Ipilimumab
Pembrolizumab
Vemurafenib and dabrafenib

303
Q

How does Ipilimumab work?

A

Inhibits CTLA-4 molecule

304
Q

How does Pembrolizumab work?

A

Targets PD-1 receptor on tumour cell

305
Q

How does Vemurafenib and dabrafenib work?

A

Blocks B-RAF protein (only useful in B-RAF mutation)

Second Year (9 decks)

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