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ESA 1 - Body Logistics > Session 5.4b - Lecture 2 - Dermatology > Flashcards

Session 5.4b - Lecture 2 - Dermatology Flashcards

Slides 14 -

1
Q

Fig. 14 (left)

Describe this rash.

A

A well-defined erythematous and scaly rash with a white silvery scale

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2
Q

Fig. 14 (left)

Give a differential diagnosis for this rash based on its appearance.

A

Psoriasis

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3
Q

What are typical places on the skin for psoriasis to present with?

A
  • Skull

- Backs of ears

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4
Q

Fig. 14 (middle)

Give a differential diagnosis for this patient and explain why.

A

Erythematous and scaly rash that presents at the back of the ears - this is typical of psoriasis.

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5
Q

Other than the skin, where else can psoriasis affect?

A
  • Joints (psoriatic arthritis)

- Nails

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6
Q

What are the typical changes in nail psoriasis?

A
  • Little pits in the nail: pitting
  • The nail plate can separate from the nail bed so it looks whiter: onycholysis
  • Yellow or brown areas that look like a drop of oil under the nail: discolouration
  • Nails can get really thickened: hyperkeratosis
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7
Q

What is onycholysis?

A

When the nail plate separates from the nail bed (appears whiter).

This is typical in psoriasis.

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8
Q

Fig. 14 (right)

What is this image showing?

A

Onycholysis (nail plate separation from the nail bed)

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9
Q

Fig. 14 (right)

Give a clinical condition this sign is typical of.

A

Sign - onycholysis

Condition - psoriasis

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10
Q

What does discolouration of the nails present as?

A

Yellow or brown areas that look like a drop of oil under the nail.

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11
Q

What is nail pitting?

A

Where little pits or dents present in the nail

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12
Q

What is it called when little pits present in the nail bed?

A

Nail pitting

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13
Q

What is it called when the nail plate separates from the nail bed?

A

Onycholysis

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14
Q

What is it called when yellow or brown areas appear under the nail?

A

Nail discolouration

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15
Q

What is hyperkeratosis?

A

When the nail (skin) gets really thickened

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16
Q

What is it called when you observe the nail being abnormally thicker?

A

Hyperkeratosis

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17
Q

Draw an image of how plaque psoriasis presents on a patient’s lower back.

A

See Fig. 14 (left)

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18
Q

Draw an image of how psoriasis presents in a typical location it is found.

A

See Fig. 14 (middle)

Backs of ears/scalp

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19
Q

Draw an image of someone’s nail who has nail psoriasis.

A

See Fig. 15 (right)

Show any of:

  • pitting
  • onycholysis
  • discolouration
  • hyperkeratosis
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20
Q

What is nail pitting a sign of?

A

It is very typical of psoriasis

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21
Q

What is onycholysis a sign of?

A
  • Infection (fungal nail infections)
  • Drugs
  • Trauma
  • Psoriasis/psoriatic arthritis
  • Hyperthyroidism
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22
Q

What can discolouration of the nails be a sign of?

A
  • Infection

- Psoriasis

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23
Q

What can hyperkeratosis of the nails be a sign of?

A
  • Psoriasis
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24
Q

Fig. 15 (left)

Describe the lesions in this image.

A

Fluid-filled blisters (vesicles)

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25
Q

Fig. 15 (left)

Give a differential diagnosis for this image and explain why.

A

Cold sore - typical fluid-filled blisters (vesicles) on mouth.

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26
Q

How do cold sores typically present?

A

Fluid-filled blisters (vesicles)

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27
Q

Draw an image of a patient presenting with a cold sore.

A

See Fig. 15 (left)

Fluid-filled blisters (vesicles)

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28
Q

What are fluid-filled blisters (vesicles) on the mouth typical of?

A

Cold sores (caused by HSV).

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29
Q

Fig. 15 (right)

Describe the lesions seen in this image (2 marks).

A

Larger fluid filled blisters (1) which are called bulla (1).

2 marks for statement of bulla alone

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30
Q

Fig. 15 (right)

What is this condition?

A

Bullous pemphigoid - fluid-filled bulla quite commonly seen in the elderly.

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31
Q

What is bullous pemphigoid?

A

An autoimmune condition that causes itchy, red skin that presents with bulla. It commonly affects the elderly (> 60 y/o).

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32
Q

What age category does bullous pemphigoid primarily affect?

A

> 60 y/o (elderly)

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33
Q

Explain the pathophysiology of bullous pemphigoid.

A

It is an autoimmune disease, so the patients’ own body produces antibodies against their own skin - creating bulla as a result.

It is NOT contagious, an allergic reaction or affected by diet/lifestyle.

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34
Q

Draw an image showing how bullous pemphigoid typically presents.

A

See Fig. 15 (right)

Bulla in the elderly from autoimmune disease.

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35
Q

Fig. 16

Describe the lesion seen here.

A

Patient has developed redness (nodules) - this is inflammation deep on subcutaneous fat.

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36
Q

Fig. 16

Describe what would be felt on palpation?

A

Patient has developed redness, which is quite firm, and on palpation would feel quite deep (nodules) - this is inflammation deep on subcutaneous fat.

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37
Q

Fig. 16

What is the diagnosis?

A

Erythema nodosum

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38
Q

What is erythema nodosum?

A

Erythema nodosum is swollen fat under the skin causing red bumps and patches.

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39
Q

Erythema nodosum is a type of what group of diseases?

A

Panniculitis

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40
Q

What is panniculitis?

A

A broad term relating to inflammation of subcutaneous fat

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41
Q

What is the term used to described inflammation of subcutaneous fat?

A

Panniculitis

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42
Q

What causes erythema nodosum?

A

Erythema nodosum can be caused by lots of things but often the cause is not known. It is a reactive rash, and can be caused by infection, medication, sometimes even contraception, pregnancy.

Common causes include:

  • Crohn’s disease
  • ulcerative colitis
  • a bad reaction to some medicines
  • sarcoidosis
  • tuberculosis
  • pneumonia
  • streptococcal infection
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43
Q

List 7 causes of erythema nodosum.

A

Accept any from:

  • Crohn’s disease
  • ulcerative colitis
  • a bad reaction to some medicines
  • sarcoidosis
  • tuberculosis
  • pneumonia
  • streptococcal infection (NHS)
  • infection
  • medication
  • contraception
  • pregnancy (lecture)
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44
Q

How does erythema nodosum feel on palpation?

A

Firm and quite deep.

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45
Q

A patient presents with firm red nodules that are felt quite deep to the subcutaneous fat. They tell you they also have ulcerative colitis.

State a likely diagnosis.

A

Erythema nodosum

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46
Q

Draw how erythema nodosum would present on someone’s legs.

A

See Fig. 16

Red nodules from inflammation of the subcutaneous fat.

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47
Q

Fig. 17

Describe this mole.

A
  • Multicoloured mole (developed different colours)

- has a nodular component

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48
Q

Fig. 17

Give a likely diagnosis and explain why.

A

Suspicious of a cancerous mole - skin cancer - melanoma - due to the appearance of >2 colours in the mole.

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49
Q

When should you be suspicious of a mole being cancerous?

A

Always be suspicious if it has >2 colours.

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50
Q

A patient presents with a mole that is light brown, dark brown, black, blue and grey. What can this be indicative of?

A

The mole has more than 2 colours, so you must be suspicious of cancer.

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51
Q

What does it mean if we say the mole is nodular?

A

That the mole is quite deep, thus the patient has a poor prognosis.

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52
Q

At what age group does melanoma affect?

A

Melanoma can occur in young people - more than a quarter of skin cancer cases are diagnosed in people under 50, which is unusually early compared to most other types of cancer.

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53
Q

Draw the appearance of a cancerous skin mole (melanoma).

A

See Fig. 17

(Multicoloured, nodular component).

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54
Q

Fig. 18

Describe what you can see.

A

Hair loss (alopecia) that has no signs of inflammation (scaliness, itchy, weepy).

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55
Q

Fig. 18

Give a likely diagnosis for this patient and explain why.

A

Alopecia areata - hair loss that has no inflammatory component, thus not a suspected fungal infection.

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56
Q

Fig. 18

Explain why this is unlikely to be a fungal infection.

A

Although their is hair loss (alopecia), there are no signs of inflammation, such as scaling, weeping or itching (excoriations - scratch marks) - thus, it is unlikely to be a fungal infection.

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57
Q

What is alopecia areata?

A

Alopecia areata is an autoimmune condition, that causes non-scarring hair loss which can occur at any age.

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58
Q

A patient presents with patches of hair loss with no visible signs of inflammation. Give a likely diagnosis.

A

Alopecia areata

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59
Q

What is the pathophysiology behind alopecia areata?

A

It is an autoimmune condition, so their own body is trying to attack hair follicle

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60
Q

Why do the hairs come back again in the future for alopecia areata?

A

Although it is an autoimmune condition where the body attacks the hair follicles, it is not a complete destruction of them, so the hairs come back again in the future.

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61
Q

How can you differentiate between a fungal infection of the scalp and alopecia areata?

A

A fungal infection would be scaly, itchy and weepy, whereas alopecia areata

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62
Q

Draw how the patient’s scalp would look in alopecia areata.

A

See Fig. 18

Typically, it starts as one or more bald, smooth patches on the scalp, which are not inflamed or scaly. It usually causes small, coin-sized, round patches of baldness on the scalp.

It tends to affect the pigmented hair so there may be some white hairs left within the bald area in older people.

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63
Q

Fig. 19

Label the layers of the skin.

A
  • Epidermis
  • Basement membrane
  • Dermis
  • Subcutaneous tissue
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64
Q

Fig. 19

Label the layers of the skin. Caption the image

A
  • Epidermis
  • Basement membrane
  • Dermis
  • Subcutaneous tissue

Structure of the skin

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65
Q

Draw a cross section of the skin and label the layers.

A

See Fig. 19

  • Epidermis
  • Basement membrane
  • Dermis
  • Subcutaneous tissue

Structure of the skin

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66
Q

Fig. 20 (left)

This image shows normal skin histology. Label the layers and include a key.

A
  • stratum corneum
  • quiescent epidermis
  • blood vessels
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67
Q

Fig. 20 (right)

Describe this image.

A

Normal, elastic-looking skin.

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68
Q

Draw an image depicting the histology of normal skin.

A

See Fig. 20 (left)

  • stratum corneum
  • quiescent epidermis
  • blood vessels
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69
Q

Draw an image depicting what healthy skin looks like.

A

See Fig. 20 (right)

Normal, elastic-looking skin. No plaques. Single colour. Blood vessels may or may not be visible.

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70
Q

Fig. 20 (left)

What is this figure showing?

A

Epidermis, the outer layer of the skin

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71
Q

Fig. 20 (left)

Which cells are alive in the epidermis?

A

The quiescent epidermis

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72
Q

Fig. 20 (left)

Which cells are dead in the epidermis?

A

Stratum corneum

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73
Q

Which layer of cells are dead in the epidermis?

A

Stratum corneum

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74
Q

Fig. 20 (left)

What are the red dots interlaced between the quiescent epidermis?

A

Tiny little blood vessels

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75
Q

Fig. 21 (top left)

Label the skin histology.

A
  • stratum corneum
  • quiescent epidermis
  • blood vessels
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76
Q

Fig. 21 (bottom left)

Describe this image.

A

Normal, healthy skin.

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77
Q

Fig. 21 (right)

Give a diagnosis for this image.

A

Plaque psoriasis

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78
Q

Draw a picture of normal skin histology.

A

See Fig. 21 (top left)

  • stratum corneum
  • quiescent epidermis
  • blood vessels
    normal
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79
Q

Draw a picture of normal skin.

A

See Fig. 21 (bottom left)

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80
Q

Draw a picture of plaque psoriasis.

A

See Fig. 21 (right)

psoriasis

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81
Q

What happens to the epidermis in normal skin?

A

In normal skin, the epidermis has regenerated to normal pace, and the outermost layer of the epidermis, the stratum corneum, constantly shreds cells at a rate in keeping with the production of new skin cells, and that gives a healthy appearance.

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82
Q

What is constantly shedding in normal skin?

A

The stratum corneum - outermost layer of epidermis.

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83
Q

Why do plaques grow in psoriasis?

A

In psoriasis, there is an increased turnover in the quiescent epidermis (from the basal layer upwards to the granular layer - these are making more skin cells), so the skin is growing faster and accumulates in the stratum corneum. That leads to hyperproliferation and thickening of the epidermis - there’s not enough time for all those cells to shred, so it gets really thickened, so there’s lots of scaling and cracking on the surface (plaques), and the blood vessels are enlarged/increased

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84
Q

What is the pathophysiology of psoriasis?

A

In normal skin, the epidermis has regenerated to normal pace, and the outermost layer of the epidermis, the stratum corneum, constantly shreds cells and that gives a healthy appearance.

But In psoriasis, there is an increased turnover in the quiescent epidermis (from the basal layer upwards to the granular layer - these are making more skin cells), so the skin is growing faster and accumulates in the stratum corneum. That leads to hyperproliferation and thickening of the epidermis - there’s not enough time for all those cells to shred, so it gets really thickened, so there’s lots of scaling and cracking on the surface, manifesting as plaques, and also the blood vessels are enlarged/increased

85
Q

What does an increased turnover of quiescent epidermis lead to?

A

Hyperproliferation and thickening of the epidermis (clinically - psoriasis).

86
Q

Why does hyperproliferation and thickening occur in psoriasis?

A

In the layers of the quiescent epidermis, the skin is growing faster than it can shed - so these cells accumulate at the top in the stratum corneum layer where the cells get really thick - so there’s lots of scaling and cracking on the surface of the skin.

87
Q

As well as the increased turnover of skin cells, what other physiological change occurs in psoriasis pathology?

A

Blood vessels are enlarged/increased

88
Q

What happens to the blood vessels in psoriasis?

A

They are enlarged/increased

89
Q

Fig. 22 (left)

Label the image.

A
  • Desquamating stratum corneum
  • Highly proliferative epidermis
  • Leucocyte infiltrates
  • Blood vessels
    psoriasis
90
Q

Fig. 22 (right)

Give a differential diagnosis for this image.

A

Plaque psoriasis

91
Q

Draw what the histology for psoriasis would look like.

A

See Fig. 22 (left)

  • Desquamating stratum corneum
  • Highly proliferative epidermis
  • Leucocyte infiltrates
  • Blood vessels
    psoriasis

desquamating stratum corneum (1)
thicker epidermis (1)
enlarged blood vessels (1)

92
Q

What does desquamating mean?

A

desquamate
verb

(of a layer of cells, e.g. of the skin) come off in scales or flakes.
“desquamated cells”

93
Q

Blood vessels are enlarged in psoriasis. Why is this clinically important?

A

Clinically, this gives you redness.

94
Q

Your consultant shows you a picture of an erythematous rash. Please describe what this would look like histologically.

A

Enlarged blood vessels

Redness = dilatation of the blood vessels

95
Q

How would dilatation of the blood vessels manifest clinically?

A

As redness

96
Q

Your consultant shows you a picture of an scaling/thickened rash. Please describe what this would look like histologically.

A

Thickening of the epidermis

If scaling/thick skin = then there would be thickening of the epidermis

97
Q

How would a thickened epidermis on histology manifest clinically?

A

As scaling/thickened skin.

98
Q

How can you correlate what you see clinically to histology in rashes?

A

Redness = dilatation of the blood vessels

Scaling/thick skin = thickening of the epidermis

99
Q

Why is inflammation easy to detect in dermatology?

A

The process of INFLAMMATION may readily

be observed in the skin

100
Q

The skin in psoriasis is inflamed.

True or false?

A

True

101
Q

What is good about diagnosing in the dermatology specialty?

A
  • Process of inflammation readily observed in skin
  • Don’t need invasive treatment to visualise things e.g. putting a tube inside the body
  • Can look at a patient and glean a lot of information
  • Interesting for visual people
102
Q

Describe the 3 major events which cause inflammation.

A 
The process of INFLAMMATION results from
three major events:
– Vasodilation (causing rubor and calor)
– Increased microvascular permeability resulting
in production of a protein-rich exudate
(causing tumor)
– Influx of leukocytes
103
Q

What does vasodilatation cause in inflammation?

A

Redness and warmth (rubor and calor)

104
Q

Why does the skin feel warm in inflammation?

A

Due to vasodilatation

105
Q

Why does the skin look red in inflammation?

A

Due to vasodilation

106
Q

What happens to the blood vessels in inflammation?

A

– Vasodilation (causing rubor and calor)

107
Q

What happens to the permeability of the blood vessels in inflammation?

A

– Increased microvascular permeability resulting
in production of a protein-rich exudate
(causing tumor)

108
Q

What is there influx of in inflammation?

A

– Influx of leukocytes (inflammatory cells)

109
Q

What does increased permeability in inflammation cause?

A

Loss of things like proteins within the exudate comes out of the blood vessels and skin (production of protein-rich exudate)

110
Q

Why do you get a protein-rich exudate in inflammation?

A

Due to increased microvascular permeability causing loss of things like protein within the exudate to come out

111
Q

How does increased microvascular permeability of inflammation manifest clinically?

A

As a swollen (tumor) area - due to production of a protein-rich exudate.

112
Q

Why is the skin swollen in inflammation?

A

There is increased microvascular permeability which results in production of a protein-rich exudate (loss of fluid with proteins in).

113
Q

What are leukocytes?

A

Inflammatory cells

114
Q

Name the inflammatory cells that influx into the inflamed area during inflammation.

A

Leukocytes

115
Q

What are the signs of inflammation?

A

4 Cardinal signs described by Celsus in 1st century AD:

  1. Rubor (redness)
  2. Tumor (swelling)
  3. Calor (warmth)
  4. Dolor (pain - symptom not a sign!)

5th sign added by Galen in 2nd century AD:
5. Functio laesa (loss of function)

6th sign added by dermatologists in the 20th century:
6. Pruritus (itchy)

116
Q

What does an inflamed area of skin look like?

A

Inflamed area of skin = inflammation

So signs of inflammation

  1. Rubor
  2. Tumor
  3. Calor
  4. Dolor
  5. Functio laesa
  6. Pruritus
117
Q

What are the 6 signs of inflammation?

A
  1. Rubor
  2. Tumor
  3. Calor
  4. Dolor
  5. Functio laesa
  6. Pruritus
118
Q

What are the four cardinal ‘signs’ of inflammation described by Celsus in first century AD?

A
  • Rubor
  • Tumor
  • Calor
  • Dolor (symptom not a sign!)
119
Q

Rubor, tumor, calor and dolor indicate what?

A

The four cardinal ‘signs’ of inflammation described by Celsus in first century AD.

120
Q

Define rubor

A

Redness

121
Q

What is the medical term for redness (Latin) as a sign in inflammation?

A

Rubor

122
Q

Define tumor

A

Swelling

123
Q

What is the medical term for swelling (Latin) as a sign in inflammation?

A

Tumor

124
Q

Define calor

A

Warmth

125
Q

What is the medical term (Latin) for warmth as a sign in inflammation?

A

Calor

126
Q

Define dolor

A

Pain

127
Q

What is the medical term (Latin) for pain as a sign in inflammation?

A

Dolor

Note: not a sign, a symptom!

128
Q

Which of the 4 cardinal signs of inflammation is actually a symptom?

A

Dolor - pain.

129
Q

Why is dolor different to the other 3 cardinal signs of inflammation?

A

It is actually a symptom, not a sign!

Dolor = pain

130
Q

What is the fifth sign of inflammation added by Galen in second century AD?

A

Functio laesa (loss of function)

131
Q

What does functio laesa represent?

A

The fifth sign of inflammation added by Galen in second century AD?

132
Q

What does functio laesa mean?

A

Loss of function

133
Q

What is the Latin for loss of function?

A

Functio laesa

134
Q

Fig. 27

Give a differential diagnosis for this patient.

A

Toxic epidermal necrolysis (TEN)

Other DDx can include SJS

135
Q

Draw an image of what a patient with toxic epidermal necrolysis would look like?

A

See Fig. 27

Very red and inflamed

136
Q

How can the functions of the skin be ascertained?

A

By having looking at a pt with a v severe skin condition (e.g. TEN) - think about what can go wrong, how do you manage this pt and then you can think of the functions of the skin.

137
Q

Give 4 facts about toxic epidermal necrolysis (TEN).

A
  • Severe muco-cutaneous drug reaction
  • Full thickness epidermal damage
  • Skin separated to leave raw, oozing dermis
  • Life threatening, high mortality
138
Q
  • Severe muco-cutaneous drug reaction
  • Full thickness epidermal damage
  • Skin separated to leave raw, oozing dermis
  • Life threatening, high mortality

Name the syndrome that is defined by these characteristics.

A

Toxic epidermal necrolysis (TEN).

139
Q

Fig. 28

Name the condition and give some facts.

A

Toxic epidermal necrolysis (TEN)

  • Severe muco-cutaneous drug reaction
  • Full thickness epidermal damage
  • Skin separated to leave raw, oozing dermis
  • Life threatening, high mortality
140
Q

Draw what a patient with TEN would look like, and label with some characteristics of the disease.

A

See Fig. 28

Toxic epidermal necrolysis (TEN)
• Severe muco-cutaneous drug reaction
• Full thickness epidermal damage
• Skin separated to leave raw, oozing dermis
• Life threatening, high mortality
141
Q

What is toxic epidermal necrolysis?

A

A very severe rash that leaves full thickness epidermal damage, caused by drug reaction.

142
Q

What is TEN often caused by?

A

Mostly a drug reaction, i.e. the patient has been given a medication

143
Q

What is a mucocutaneous drug reaction?

A

Drugs that affect the mucocutaneous junctions.

144
Q

What are mucocutaneous junctions?

A

A region of the body in which mucosa transitions to skin.

In humans, mucocutaneous junctions are found at the lips, nostrils, conjunctivae, urethra, vagina (in females), foreskin (in males), and anus.

At a mucocutaneous junction, epithelium transitions to epidermis, lamina propria transitions to dermis, and smooth muscle transitions to skeletal muscle.

145
Q

TEN causes a severe muco-cutaneous drug reaction.

With that in mind, what areas of the body does it affect?

A

They start with a rash that can affect the skin, then the mucosa, the eyes, cracked lips etc. to then cause full thickness epidermal damage

146
Q

TEN causes a severe muco-cutaneous drug reaction.

What does this result in?

A

Full thickness epidermal damage.

147
Q

A patient with TEN has experienced full thickness epidermal damage. What does this mean for the patient?

A

The whole outer layer of skin (epidermis) has died - so all the functions of the skin (which you need to know) are lost.

148
Q

How does full thickness epidermal damage (such as in TEN) present?

A

Skin separated to leave raw, oozing dermis.

149
Q

Skin separated to leave a raw, oozing dermis indicates what?

A

Full thickness epidermal damage (such as in TEN).

150
Q

How do you manage a patient with TEN?

A

You need to know the function of the skin - as inflammation causes loss of function. Thus, you then manage the patient accordingly to the functions lost.

151
Q

What is the prognosis for a patient with TEN?

A

Life threatening, high mortality.

152
Q

What are the basic functions of the skin? Need to know

A
  • Barrier from external insults - infection, physical, chemical
  • Physiological - electrolyte and fluid balance
  • Temperature regulation
  • Sensation
  • Immunological
  • Vitamin D synthesis
  • Psychosocial/cosmetic
153
Q

Why are patients with TEN at risk of infection?

A

TEN is a severe rash that has arisen from inflammation. The fifth cardinal sign of inflammation is loss of function, therefore they have lost function of the skin.

One of the main functions of the skin is a barrier to protection from external insults, including infection, as well as physical and chemical. Thus, the patient who has TEN has loss of function of skin and therefore loss of protection from infection.

154
Q

What are patients with TEN at risk of developing?

A

Infection, due to loss of function of the skin.

155
Q

What balances are lost from the patient in TEN?

A

Electrolyte and fluid balance bc they can’t keep all their water

156
Q

Patients with TEN are unable to retain all their water. What does this mean physiologically?

A

They have an imbalanced electrolyte and fluid composition.

157
Q

Why are patients with TEN warm?

A
  • Calor; cardinal sign of inflammation

- Loss of function of skin - so cannot temperature regulate - thus stay warm

158
Q

Fig. 29

Label what functions this patient would have lost.

A

Basic functions of the skin

  • Barrier from external insults - infection, physical, chemical
  • Physiological - electrolyte and fluid balance
  • Temperature regulation
  • Sensation
  • Immunological
  • Vitamin D synthesis
  • Psychosocial/cosmetic
159
Q

Draw what a patient with toxic epidermal necrolysis syndrome would look like and label the functions lost.

A

See Fig. 29

Basic functions
• Barrier from external insults - infection, physical, chemical
• Physiological - electrolyte and fluid balance
• Temperature regulation
• Sensation
• Immunological
• Vitamin D synthesis
• Psychosocial/cosmetic
160
Q

What is the sixth ‘sign’ of inflammation added by dermatologists in the twentieth century?

A

Pruritus

161
Q

Is pruritus a sign of inflammation?

A

Sixth ‘sign’ of inflammation added by dermatologists in the twentieth century.

162
Q

Define pruritus.

A

Itchy skin

163
Q

What is the medical term for itchy skin?

A

Pruritus

164
Q

What is lichenification?

A

Thickening of skin, increased skin marking

165
Q

What is the term used in dermatology to denote thickening of the skin, increased skin markings?

A

Lichenification

166
Q

What does lichenification indicate?

A

And this is what I was referring to, so you could tell, if you have a look at these pts, their skin has been affected by different flares of eczema on and off many times, and then their skin gets a little bit thickened, and we call that lichenification

167
Q

How does the skin appear when it has been affected by many flares of eczema?

A

Thickened - lichenification

168
Q

Where does lichenification often occur?

A

It is quite flexural, it occurs in flexors

169
Q

Give 3 examples of flexural surfaces that eczema is common in

A
  • neck
  • antecubital fossa
  • popliteal fossa
170
Q

What do the anterior portion of the neck, antecubital fossa and popliteal fossa have in common?

A

They are flexural surfaceso f the skin (thus, eczema is common here)

171
Q

Lichenification can cause what?

A

Skin fissures

172
Q

What are skin fissures?

A

Little cracks

173
Q

What are little cracks in the skin called?

A

Skin fissures

174
Q

What is the significance of skin fissures in dermatology conditions?

A

They can get infected

175
Q

What can get infected in dermatological conditions such as eczema?

A

Skin fissures

176
Q

Fig. 31 (top left)

Describe this image.

A

Lichenification - thickening of skin, increased skin markings.

Caused by many recurring flares of eczema. Common in flexural joints (e.g. antecubital fossa, popliteal fossa, anterior neck). This can create fissures, which can sometimes get infected.

177
Q

Fig. 31 (top right)

Describe this image.

A

Lichenification - thickening of skin, increased skin markings.

Caused by many recurring flares of eczema. Common in flexural joints (e.g. antecubital fossa, popliteal fossa, anterior neck). This can create fissures, which can sometimes get infected.

178
Q

Fig. 31 (bottom left)

Describe this image.

A

Lichenification - thickening of skin, increased skin markings.

Caused by many recurring flares of eczema. Common in flexural joints (e.g. antecubital fossa, popliteal fossa, anterior neck). This can create fissures, which can sometimes get infected.

179
Q

Fig. 31 (bottom middle)

Describe this image.

A

Lichenification - thickening of skin, increased skin markings.

Caused by many recurring flares of eczema. Common in flexural joints (e.g. antecubital fossa, popliteal fossa, anterior neck). This can create fissures, which can sometimes get infected.

180
Q

Fig. 31 (bottom right)

Describe this image.

A

Lichenification - thickening of skin, increased skin markings.

Caused by many recurring flares of eczema. Common in flexural joints (e.g. antecubital fossa, popliteal fossa, anterior neck). This can create fissures, which can sometimes get infected.

181
Q

Draw an image of symmetrical lichenification on the antecubital fossa.

A

See Fig. 31 (top left)

182
Q

Draw an image of asymmetrical lichenification on the antecubital fossa.

A

See Fig. 31 (top right)

183
Q

Draw an image of symmetrical lichenification on the popliteal fossa.

A

See Fig. 31 (bottom left)

184
Q

Draw an image of erythematous lichenification on the antecubital fossa. Include excoriations.

A

See Fig. 31 (bottom middle)

185
Q

Draw an image of lichenification on the antecubital fossa in a patient with darker skin.

A

See Fig. 31 (bottom right)

186
Q

Fig. 32 (top left)

Describe this image.

A
  • Lichenified atopic eczema
  • Increased skin markings
  • Usually in flexural areas
  • Shows post-inflammatory hyperpigmentation
187
Q

Fig. 32 (bottom left)

Describe this image.

A
  • Lichenified atopic eczema
  • Increased skin markings
  • Usually in flexural areas
  • Shows post-inflammatory hyperpigmentation
188
Q

Fig. 32 (bottom middle)

Describe this image.

A
  • Lichenified atopic eczema
  • Increased skin markings
  • Usually in flexural areas
  • Shows post-inflammatory hyperpigmentation
189
Q

Fig. 32 (right)

Describe this image.

A
  • Lichenified atopic eczema
  • Increased skin markings
  • Usually in flexural areas
  • Shows post-inflammatory hyperpigmentation
190
Q

Draw an image of lichenified atopic eczema with hyperpigmentation on a patients’ anterior forearm.

A

See Fig. 32 (top left)

191
Q

Draw an image of lichenified atopic eczema with hyperpigmentation on a patients’ popliteal fossa.

A

See Fig. 32 (bottom left)

192
Q

Draw an image of lichenified atopic eczema on a patients’ ankle joint.

A

See Fig. 32 (bottom middle)

193
Q

Draw an image of lichenified atopic eczema with post-inflammatory hyperpigmentation on a patients’ leg and foot.

A

See Fig. 32 (right)

194
Q

What is post-inflammatory hyperpigmentation?

A

Post-eczema flares, as the skin is inflamed, as it heals it leaves darker pigmentation, sometimes with areas of paler skin dotted throughout.

195
Q

When does post-inflammatory hyperpigmentation occur?

A

Post-eczema flares

196
Q

What is the term used to describe darker pigmentation of the skin after eczema flares, which sometimes contain lighter patches of skin?

A

Post-inflammatory hyperpigmentation

197
Q

What is a common misconception of what causes post-inflammatory hyperpigmentation?

A

Steroids

198
Q

Why is a problem that some patients believe steroids cause post-inflammatory hyperpigmentation?

A

Some patients, particularly some parents, believe the steroids have caused it, and are therefore then reluctant to use them so the patient is left with persistent eczema which is hard to treat/manage.

199
Q

What is an appropriate treatment for very active eczema?

A

Steroids

200
Q

Should you provide steroids for very active eczema?

A

Yes, they are very appropriate and useful

201
Q

Do you need to worry about thinning of the skin with topic steroid use for eczema?

A

It is a consideration, however, patients with severe eczema - it is much more common for them to develop lichenification due to lack of use of steroids than skin atrophy with overuse of steroids

202
Q

Why are parents reluctant to give their children steroids for eczema use?

A

They believe it thins the skin

203
Q

What is a complication of not using enough topical steroids to manage eczema?

A

Lichenification

204
Q

What is a complication of overusing steroids?

A

Skin atrophy - however, it is much more likely a patient will develop lichenification with severe eczema than skin atrophy from overuse.

205
Q

Is lichenification reversible?

A

Severe lichenification and post-inflammatory hyperpigmentation is basically irreversible, although eczema is not a scarring condition

206
Q

Is eczema a scarring condition?

A

No, although severe lichenification and post-inflammatory hyperpigmentation is basically irreversible,

207
Q

What causes severe lichenification?

A

Multiple flare ups of eczema that is not managed correctly.

208
Q

What % of GP consultations are skin related?

A

20%

ESA 1 - Body Logistics (18 decks)

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