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Year 4: Special Senses > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Describe how a patient with urticaria would present.

A

Itchy wheals

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2
Q

Describe the causes of urticaria.

A
  • Idiopathic
  • Food (e.g. nuts, sesame seeds, shellfish, dairy
    products)
- Drugs (e.g. penicillin, contrast media, non-steroidal anti-
inflammatory drugs (NSAIDs), morphine, angiotensin-converting 
enzyme inhibitors (ACE-i))
  • Insect bites
  • Contact (e.g. latex)
  • Viral or
    parasitic infections
  • Autoimmune
  • Hereditary
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3
Q

Describe how you would manage a patient with urticaria.

A
  • Antihistamines

- Corticosteroids is severe

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4
Q

Describe the potential complications of urticaria.

A

Normally uncomplicated

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5
Q

Describe the pathophysiology behind urticaria.

A

It is due to a local increase in permeability of capillaries and small venules.

A large number of inflammatory mediators (including prostaglandins, leukotrienes, and chemotactic factors) play a role but histamine derived from skin mast cells appears to be the major mediator.

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6
Q

Describe how a patient with angioedema would present.

A

Swelling of tongue and lips

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7
Q

Describe the causes of angioedema.

A
  • Idiopathic
  • Food (e.g. nuts, sesame seeds, shellfish, dairy
    products)
- Drugs (e.g. penicillin, contrast media, non-steroidal anti-
inflammatory drugs (NSAIDs), morphine, angiotensin-converting 
enzyme inhibitors (ACE-i))
  • Insect bites
  • Contact (e.g. latex)
  • Viral or
    parasitic infections
  • Autoimmune
  • Hereditary
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8
Q

Describe how you would manage a patient with angioedema.

A

Corticosteroids

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9
Q

Describe the pathophysiology behind angioedema.

A

Deeper swelling involving the dermis and subcutaneous tissues

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10
Q

Describe the potential complications of angioedema.

A
  • Asphyxia (unconsciousness)
  • Cardiac arrest
  • Death
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11
Q

Describe how a patient with anaphylaxis would present.

A
  • Bronchospasm
  • Facial and laryngeal oedema
  • Hypotension

(NOTE: can present initially
with urticaria and angioedema)

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12
Q

Describe the causes of anaphylaxis.

A
  • Idiopathic
  • Food (e.g. nuts, sesame seeds, shellfish, dairy
    products)
- Drugs (e.g. penicillin, contrast media, non-steroidal anti-
inflammatory drugs (NSAIDs), morphine, angiotensin-converting 
enzyme inhibitors (ACE-i))
  • Insect bites
  • Contact (e.g. latex)
  • Viral or
    parasitic infections
  • Autoimmune
  • Hereditary
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13
Q

Describe how you would manage a patient with anaphylaxis.

A
  • Adrenaline
  • Corticosteroids
  • Antihistamine
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14
Q

Describe the potential complications of anaphylaxis.

A
  • Asphyxia (unconsciousness)
  • Cardiac arrest
  • Death
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15
Q

Describe how a patient with erythema nodosum would present.

A
  • Discrete tender nodules which may become confluent

- The shins are the most common site

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16
Q

Describe the causes of erythema nodosum.

A
  • Group A beta-haemolytic streptococcus
  • Primary tuberculosis
  • Pregnancy
  • Malignancy
  • Sarcoidosis
  • Inflammatory bowel disease (IBD)
  • Chlamydia
  • Leprosy
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17
Q

Describe how you would manage a patient with erythema nodosum.

A
  • Reassurance and patient education
  • Lesions continue to appear for 1-2 weeks and leave bruise-like discolouration as they resolve
  • Lesions do not ulcerate and resolve without atrophy or scarring
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18
Q

Describe the pathophysiology behind erythema nodosum.

A

A hypersensitivity response to a variety of stimuli

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19
Q

Describe how a patient with erythema multiforme would present.

A

Mucosal involvement is absent or limited to only one mucosal surface

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20
Q

Describe the pathophysiology behind erythema multiforme.

A

Acute self- limiting inflammatory condition with herpes simplex virus being the main precipitating factor

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21
Q

Describe the causes of erythema multiforme.

A
  • Often unknown
  • Herpes simplex virus
  • Drugs
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22
Q

Describe how you would manage a patient with erythema multiforme.

A
  • Early recognition and call for help
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23
Q

Describe how a patient with Stevens-Johnson syndrome would present.

A

Mucocutaneous necrosis with at least two mucosal sites involved.

Skin involvement may be limited or extensive.

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24
Q

What can be seen on the histopathology of a patient with Stevens-Johnson syndrome?

A

Epithelial necrosis with few inflammatory cells

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25
Q

Describe the pathophysiology behind toxic epidermal necrosis.

A

Usually drug-induced

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26
Q

Describe how a patient with toxic epidermal necrosis would present.

A

Extensive skin and mucosal necrosis accompanied by systemic toxicity

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27
Q

What can be seen on the histopathology of a patient with toxic epidermal necrosis?

A

Full thickness epidermal necrosis with sub-epidermal detachment

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28
Q

What are the morality rates of Stevens-Johnson syndrome?

A

5-12%

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29
Q

What are the morality rates of toxic epidermal necrosis?

A

> 30%

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30
Q

Why do patients with Stevens-Johnson syndrome or toxic epidermal necrosis often die?

A
  • Sepsis
  • Electrolyte imbalance
  • Multi-system organ failure
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31
Q

What is the microbial cause of acute meningococcaemia?

A

Gram negative diplococcus - Neisseria meningitides

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32
Q

Describe how a patient with acute meningococcaemia would present.

A
  • Headache
  • Fever
  • Neck stiffness
  • Hypotension
  • Fever
  • Myalgia
  • Rash
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33
Q

Describe the characteristic rash of acute meningococcaemia.

A

Non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash

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34
Q

Describe how to manage a patient with acute meningococcaemia.

A
  • Antibiotics (e.g. benzylpenicillin)

- Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally within 14 days of exposure)

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35
Q

Name 4 complications of acute meningococcaemia.

A
  1. Septicaemic shock
  2. Disseminated intravascular coagulation
  3. Multi-organ failure
  4. Death
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36
Q

Describe the appearance of Erythroderma (‘red skin’).

A

Exfoliative dermatitis involving at least 90% of the skin surface

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37
Q

Name some causes of erythroderma (‘red skin’).

A
  • Previous skin disease (e.g. eczema, psoriasis)
  • Lymphoma
  • Drugs (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril)
  • Idiopathic
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38
Q

Describe how a patient with erythroderma (‘red skin’) would present.

A

Skin appears inflamed, oedematous and scaly and patients are systemically unwell with lymphadenopathy and malaise

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39
Q

Describe how a patient with erythroderma (‘red skin’) would be managed.

A
  • Treat the underlying cause
  • Emollients and wet-wraps to maintain skin moisture
  • Topical steroids may help to relieve inflammation
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40
Q

Name 5 complications of erythroderma (‘red skin’).

A
  1. Secondary infection
  2. Fluid loss and electrolyte imbalance
  3. Hypothermia
  4. High-output cardiac failure
  5. Capillary leak syndrome (most severe)
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41
Q

Describe how a patient with eczema herpeticum would present.

A
  • Extensive crusted papules, blisters and erosions

- Systemically unwell with fever and malaise

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42
Q

What microbe causes eczema herpeticum?

A

Herpes simplex virus

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43
Q

Describe how a patient with eczema herpeticum would be managed.

A
  • Antivirals (e.g. aciclovir)

- Antibiotics for bacterial secondary infection

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44
Q

Name 4 complications of eczema herpeticum.

A
  1. Herpes hepatitis
  2. Encephalitis
  3. Disseminated intravascular coagulation (DIC)
  4. Death
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45
Q

Describe the pathology necrotising fasciitis.

A

A rapidly spreading infection of the deep fascia with secondary tissue necrosis

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46
Q

Name the cause of necrotising fasciitis.

A

Group A haemolytic streptococcus

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47
Q

Name 3 risk factors of necrotising fasciitis.

A
  1. Abdo surgery
  2. Diabetes
  3. Malignancy
48
Q

Describe how a patient with necrotising fasciitis would present.

A
  • Severe pain
  • Erythematous, blistering and necrotic skin
  • Systemically unwell with fever and tachycardia
  • Presence of crepitus (subcutaneous emphysema)
  • X-ray may show soft tissue gas (absence should not exclude the diagnosis)
49
Q

Describe how a patient with necrotising fasciitis would be managed.

A
  • Urgent referral for extensive surgical debridement

- Intravenous antibiotics

50
Q

What is Erysipelas?

A

Erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue

51
Q

What layer of the skin does cellulitis involve?

A

Deep subcutaneous tissue

52
Q

Name 2 microbial causes of erysipelas and cellulitis.

A
  1. Streptococcus pyogenes

2. Staphylococcus aureus

53
Q

Name some risk factors of erysipelas and cellulitis.

A
  • Immunosuppression
  • Wounds
  • Leg ulcers
  • Toe-web intertrigo
  • Minor skin injury
54
Q

Describe how a patient with erysipelas/ cellulitis would present.

A
  • Local signs of inflammation
  • May be associated with lymphangitis
  • Systemically unwell with fever, malaise or rigors (particularly with erysipelas)
55
Q

How is erysipelas distinguished from cellulitis?

A

Erysipelas is distinguished from cellulitis by a well-defined, red raised border

56
Q

Describe how a patient with erysipelas/ cellulitis would be managed.

A
  • Antibiotics (e.g. flucloxacillin or benzylpenicillin)

- Supportive care: rest, leg elevation, sterile dressings and analgesia

57
Q

Name 3 complications of erysipelas/ cellulitis.

A
  1. Local necrosis
  2. Abscess
  3. Septicaemia
58
Q

Describe how a patient with staphylococcal scalded skin syndrome would present.

A
  • Commonly seen in infancy and early childhood
  • Develops within a few hours to a few days, and may be worse over the face, neck, axillae or groins
  • A scald-like skin appearance is followed by large flaccid bulla
  • Perioral crusting is typical
  • Lesions are very painful
  • Recovery is usually within 5-7 days
59
Q

Describe the pathophysiology of staphylococcal scalded skin syndrome.

A

Production of a circulating epidermolytic toxin from phage group II, benzylpenicillin-resistant (coagulase positive) staphylococci

60
Q

Describe how a patient with staphylococcal scalded skin syndrome would be managed.

A
  • Antibiotics (e.g. a systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin)
  • Analgesia
61
Q

Describe the 3 main groups of superficial fungal infections.

A
  1. Dermatophytes (tinea/ringworm)
  2. Yeasts (e.g. candidiasis, malassezia),
  3. Moulds (e.g. aspergillus)
62
Q

Describe the presentation of tinea corporis.

A

Tinea infection of the trunk and limbs.

Itchy, circular or annular lesions with a clearly defined, raised and scaly edge is typical.

63
Q

Describe the presentation of tinea cruris.

A

Tinea infection of the groin and natal cleft. Very itchy.

64
Q

Describe the presentation of tinea pedis.

A

Athlete’s foot.

Moist scaling and fissuring in toe-webs, spreading to the sole and dorsal aspect of the foot.

65
Q

Describe the presentation of tinea capitis.

A

Scalp ringworm. Patches of broken hair, scaling and inflammation.

66
Q

Describe the presentation of tinea unguium.

A

Tinea infection of the nail. Yellow discolouration, thickened and crumbly nail.

67
Q

Describe the presentation of tinea manuum.

A

Tinea infection of the hand. Scaling and dryness in the palmar creases.

68
Q

Describe the presentation of tinea incognito.

A

Inappropriate treatment of tinea infection with topical or systemic corticosteroids. Ill-defined and less scaly lesions.

69
Q

Describe the presentation of candidiasis skin infection.

A

White plaques on mucosal areas, erythema with satellite lesions in flexures.

70
Q

Describe how to manage patients with fungal skin infections.

A
  • Establish the correct diagnosis by skin scrapings, hair or nail clippings (for dermatophytes); skin swabs (for yeasts)
  • General measures: treat known precipitating factors (e.g. underlying immunosuppressive condition, moist environment)
  • Topical antifungal agents (e.g. terbinafine cream)
  • Oral antifungal agents (e.g. itraconazole) for severe, widespread, or nail infections
  • Avoid the use of topical steroids
  • Correct predisposing factors where possible (e.g. moist environment, underlying immunosuppression)
71
Q

Describe the presentation of a patient with a BCC.

A
  • Nodular basal cell carcinoma is a small, skin-coloured papule or nodule with surface telangiectasia, and a pearly rolled edge; the lesion may have a necrotic or ulcerated centre (rodent ulcer)
  • Most common over the head and neck
72
Q

Name 6 morphological types of BCCs.

A
  1. Nodular (most common)
  2. Superficial (plaque-like)
  3. Cystic
  4. Morphoeic (sclerosing),
  5. Keratotic
  6. Pigmented
73
Q

Name some risk factors for BCCs.

A
  • UV exposure
  • History of frequent or severe sunburn in childhood
  • Skin type I (always burns, never tans)
  • Increasing age
  • Male sex
  • Immunosuppression
  • Previous history of skin cancer
  • Genetic predisposition
74
Q

Describe the management of BCCs.

A
  • Surgical excision: treatment of choice as it allows histological examination of the tumour and margins
  • Cryotherapy
  • Curettage and cautery
  • Topical photodynamic therapy
  • Topical treatment (e.g. imiquimod cream)
75
Q

Describe the pathology of BCCs.

A

A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals, only rarely metastasises.

76
Q

Describe the pathology of SCCs.

A

A locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has the potential to metastasise

77
Q

Name some risk factors for SCCs.

A
  • UV exposure
  • Pre-malignant skin conditions (e.g. actinic keratoses)
  • Chronic inflammation (e.g. leg ulcers, wound scars)
  • Immunosuppression
  • Genetic predisposition
78
Q

Describe the presentation of a patient with a SCC.

A

Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate

79
Q

Describe the management of SCCs.

A
  • Surgical excision

- Radiotherapy (for large, non-resectable tumours)

80
Q

Describe the pathology of a malignant melanoma.

A

An invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise

81
Q

Name some risk factors for malignant melanomas.

A
  • Excessive UV exposure
  • Skin type I (always burns, never tans)
  • History of multiple moles or atypical moles
  • Family history
  • Previous history of melanoma
82
Q

Describe the presentation of a patient with malignant melanoma.

A 
Asymmetrical	shape
Border	irregularity	 
Colour	irregularity*	 
Diameter	>	6mm	 
Evolution	of	lesion	(e.g.	change	in	size	and/or	shape)*	 
Symptoms	(e.g.	bleeding,	itching)
83
Q

Name 4 types of malignant melanoma.

A
  1. Superficial spreading melanoma
  2. Nodular melanoma
  3. Lentigo maligna melanoma
  4. Acral lentiginous melanoma
84
Q

Describe the common site, demographics and causes of the subtype nodular melanoma.

A
  • Common on the trunk
  • Young and middle-aged adults
  • Related to intermittent high-intensity UV exposure
85
Q

Describe the common site, demographics and causes of the subtype lentigo maligna melanoma.

A
  • Common on the face
  • Elderly population
  • Related to long-term cumulative UV exposure
86
Q

Describe the common site, demographics and causes of the subtype acral lentiginous melanoma.

A
  • Common on the palms, soles and nail beds
  • Elderly population
  • No clear relation with UV exposure
87
Q

Describe the common site, demographics and causes of the subtype superficial spreading melanoma.

A
  • Common on the lower limbs
  • Young and middle-aged adults
  • Related to intermittent high-intensity UV exposure
88
Q

What is the current staging system for melanoma in the UK?

A

2009 American Joint Committee of Cancer Staging System (AJCC)

89
Q

Describe the management of malignant melanoma.

A
  • Surgical excision is the definitive treatment (often a second surgery, wide local excision is needed after the initial excision biopsy).
  • Radiotherapy may sometimes be useful
  • Chemotherapy is used for metastatic disease
90
Q

Describe the presentation of a patient with atopic eczema.

A
  • Commonly present as itchy, erythematous dry scaly patches
  • More common on the face and extensor aspects of limbs in infants, and the flexor aspects in children and adults
  • Acute lesions are erythematous, vesicular and weepy (exudative)
  • Chronic scratching/rubbing can lead to excoriations and lichenification
91
Q

Describe the pathophysiology of atopic eczema.

A

A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin)

92
Q

Name 5 exacerbating factors involved with atopic eczema.

A
  1. Infections
  2. Allergens (e.g. chemicals, food, dust, pet fur),
  3. Sweating
  4. Heat
  5. Severe stress
93
Q

Describe the potential nail changes in a patient with atopic eczema.

A

Pitting/ ridging

94
Q

Describe the management of atopic eczema.

A
  • General measures - avoid known exacerbating agents, frequent emollients +/- bandages and bath oil/soap substitute
  • Topical therapies – topical steroids for flare-ups; topical immunomodulators (e.g. tacrolimus, pimecrolimus) can be used as steroid-sparing agents
  • Oral therapies - antihistamines for symptomatic relief, antibiotics (e.g. flucloxacillin) for secondary bacterial infections, and antivirals (e.g. aciclovir) for secondary herpes infection
  • Phototherapy and immunosuppressants (e.g. oral prednisolone, azathioprine, ciclosporin) for severe non- responsive cases
95
Q

Name 2 complications of atopic eczema.

A
  1. Secondary bacterial infection (crusted weepy lesions)
  2. Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum
96
Q

Describe the pathophysiology of acne vulgaris.

A

An inflammatory disease of the pilosebaceous follicle

97
Q

Describe the presentation of a patient with acne vulgaris.

A
  • Non-inflammatory lesions (mild acne)
  • Open and closed comedones (blackheads and whiteheads)
  • Inflammatory lesions (moderate and severe acne) papules, pustules, nodules, and cysts
  • Commonly affects the face, chest and upper back
98
Q

Describe the management of acne vulgaris.

A
  • Topical therapies (for mild acne)- benzoyl peroxide and topical antibiotics (antimicrobial properties), and topical retinoids (comedolytic and anti-inflammatory properties)
  • Oral therapies (for moderate to severe acne)- oral antibiotics, and anti-androgens (in females)
  • Oral retinoids (for severe acne)
99
Q

Describe the complications of acne vulgaris.

A
  • Post-inflammatory hyperpigmentation
  • Scarring
  • Deformity
  • Psychological and social effects
100
Q

Describe the pathophysiology of psoriasis.

A

Hyperproliferation of keratinocytes and inflammatory cell infiltration

101
Q

Describe the presentation of a patient with psoriasis.

A
  • Well-demarcated erythematous scaly plaques
  • Lesions can sometimes be itchy, burning or painful
  • Common on the extensor surfaces of the body and over scalp
  • Auspitz sign (scratch and gentle removal of scales cause capillary bleeding)
102
Q

Describe the management of psoriasis.

A
  • General measures: avoid known precipitating factors, emollients to reduce scales
  • Topical therapies (for localised and mild psoriasis): vitamin D analogues, topical corticosteroids, coal tar preparations, dithranol, topical retinoids, keratolytics and scalp preparations
  • Phototherapy (for extensive disease): phototherapy i.e. UVB and photochemotherapy i.e. psoralen+UVA
  • Oral therapies (for extensive and severe psoriasis, or psoriasis with systemic involvement): methotrexate, retinoids, ciclosporin, mycophenolate mofetil, fumaric acid esters, and biological agents (e.g. etanercept, adalimumab, ustekinumab)
103
Q

Describe the complications of psoriasis.

A
  • Erythroderma

- Psychological and social effects

104
Q

Name 6 types of psoriasis.

A
  1. Chronic plaque
  2. Guttate (raindrop lesions)
  3. Seborrhoeic (naso-labial and retro-auricular)
  4. Flexural (body folds)
  5. Pustular (palmar-plantar)

6 Erythrodermic (total body redness)

105
Q

Name 5 potential precipitating factors in a patient with psoriasis.

A
  1. Trauma
  2. Infection
  3. Drugs
  4. Stress
  5. Alcohol
106
Q

Name 2 associated pathological changes that some patients with psoriasis experience.

A
  1. 50% have associated nail changes (e.g. pitting, onycholysis)
  2. 5-8% suffer from associated psoriatic arthropathy
107
Q

Name 7 common causes of blisters.

A
  1. Impetigo
  2. Insect bites
  3. Herpes simplex infection
  4. Herpes zoster infection
  5. Acute contact dermatitis
  6. Pompholyx (vesicular eczema of the hands and feet)
  7. Burns
108
Q

What is bullous pemphigoid?

A

A blistering skin disorder which usually affects the elderly

109
Q

Describe the pathophysiology of bullous pemphigoid.

A

Autoantibodies against antigens between the epidermis and dermis causing a sub-epidermal split in the skin

110
Q

Describe the presentation of a patient with bullous pemphigoid.

A
  • Tense, fluid-filled blisters on an erythematous base
  • Lesions are often itchy
  • May be preceded by a non-specific itchy rash
  • Usually affects the trunk and limbs (mucosal involvement less common)
111
Q

Describe the management of bullous pemphigoid.

A
  • General measures: wound dressings where required, monitor for signs of infection
  • Topical therapies for localised disease - topical steroids
  • Oral therapies for widespread disease: oral steroids, combination of oral tetracycline and nicotinamide, immunosuppressive agents (e.g. azathioprine, mycophenolate mofetil, methotrexate, and other)
112
Q

What is pemphigus vulgaris?

A

A blistering skin disorder which usually affects the middle-aged

113
Q

Describe the pathophysiology of pemphigus vulgaris.

A

Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin

114
Q

Describe how a patient with pemphigus vulgaris would present.

A
  • Flaccid, easily ruptured blisters forming erosions and crusts
  • Lesions are often painful
  • Usually affects the mucosal areas (can precede skin involvement)
115
Q

Describe how to manage a patient with pemphigus vulgaris.

A
  • General measures: wound dressings where required, monitor for signs of infection, good oral care (if oral mucosa is involved)
  • Oral therapies: high-dose oral steroids, immunosuppressive agents (e.g. methotrexate, azathioprine, cyclophosphamide, mycophenolate mofetil, and other)

Year 4: Special Senses (6 decks)

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