Dermatology Flashcards
1
Q
Describe how a patient with urticaria would present.
A
Itchy wheals
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
3
Q
Describe how you would manage a patient with urticaria.
A
- Antihistamines
- Corticosteroids is severe
4
Q
Describe the potential complications of urticaria.
A
Normally uncomplicated
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.
6
Q
Describe how a patient with angioedema would present.
A
Swelling of tongue and lips
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
8
Q
Describe how you would manage a patient with angioedema.
A
Corticosteroids
9
Q
Describe the pathophysiology behind angioedema.
A
Deeper swelling involving the dermis and subcutaneous tissues
10
Q
Describe the potential complications of angioedema.
A
- Asphyxia (unconsciousness)
- Cardiac arrest
- Death
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)
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
13
Q
Describe how you would manage a patient with anaphylaxis.
A
- Adrenaline
- Corticosteroids
- Antihistamine
14
Q
Describe the potential complications of anaphylaxis.
A
- Asphyxia (unconsciousness)
- Cardiac arrest
- Death
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
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
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
18
Q
Describe the pathophysiology behind erythema nodosum.
A
A hypersensitivity response to a variety of stimuli
19
Q
Describe how a patient with erythema multiforme would present.
A
Mucosal involvement is absent or limited to only one mucosal surface
20
Q
Describe the pathophysiology behind erythema multiforme.
A
Acute self- limiting inflammatory condition with herpes simplex virus being the main precipitating factor
21
Q
Describe the causes of erythema multiforme.
A
- Often unknown
- Herpes simplex virus
- Drugs
22
Q
Describe how you would manage a patient with erythema multiforme.
A
- Early recognition and call for help
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.
24
Q
What can be seen on the histopathology of a patient with Stevens-Johnson syndrome?
A
Epithelial necrosis with few inflammatory cells
25
Describe the pathophysiology behind toxic epidermal necrosis.
Usually drug-induced
26
Describe how a patient with toxic epidermal necrosis would present.
Extensive skin and mucosal necrosis accompanied by systemic toxicity
27
What can be seen on the histopathology of a patient with toxic epidermal necrosis?
Full thickness epidermal necrosis with sub-epidermal detachment
28
What are the morality rates of Stevens-Johnson syndrome?
5-12%
29
What are the morality rates of toxic epidermal necrosis?
>30%
30
Why do patients with Stevens-Johnson syndrome or toxic epidermal necrosis often die?
- Sepsis
- Electrolyte imbalance
- Multi-system organ failure
31
What is the microbial cause of acute meningococcaemia?
Gram negative diplococcus - Neisseria meningitides
32
Describe how a patient with acute meningococcaemia would present.
- Headache
- Fever
- Neck stiffness
- Hypotension
- Fever
- Myalgia
- Rash
33
Describe the characteristic rash of acute meningococcaemia.
Non-blanching purpuric rash on the trunk and extremities, which may be preceded by a blanching maculopapular rash
34
Describe how to manage a patient with acute meningococcaemia.
- Antibiotics (e.g. benzylpenicillin)
| - Prophylactic antibiotics (e.g. rifampicin) for close contacts (ideally within 14 days of exposure)
35
Name 4 complications of acute meningococcaemia.
1. Septicaemic shock
2. Disseminated intravascular coagulation
3. Multi-organ failure
4. Death
36
Describe the appearance of Erythroderma (‘red skin’).
Exfoliative dermatitis involving at least 90% of the skin surface
37
Name some causes of erythroderma (‘red skin’).
- Previous skin disease (e.g. eczema, psoriasis)
- Lymphoma
- Drugs (e.g.sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril)
- Idiopathic
38
Describe how a patient with erythroderma (‘red skin’) would present.
Skin appears inflamed, oedematous and scaly and patients are systemically unwell with lymphadenopathy and malaise
39
Describe how a patient with erythroderma (‘red skin’) would be managed.
- Treat the underlying cause
- Emollients and wet-wraps to maintain skin moisture
- Topical steroids may help to relieve inflammation
40
Name 5 complications of erythroderma (‘red skin’).
1. Secondary infection
2. Fluid loss and electrolyte imbalance
3. Hypothermia
4. High-output cardiac failure
5. Capillary leak syndrome (most severe)
41
Describe how a patient with eczema herpeticum would present.
- Extensive crusted papules, blisters and erosions
| - Systemically unwell with fever and malaise
42
What microbe causes eczema herpeticum?
Herpes simplex virus
43
Describe how a patient with eczema herpeticum would be managed.
- Antivirals (e.g. aciclovir)
| - Antibiotics for bacterial secondary infection
44
Name 4 complications of eczema herpeticum.
1. Herpes hepatitis
2. Encephalitis
3. Disseminated intravascular coagulation (DIC)
4. Death
45
Describe the pathology necrotising fasciitis.
A rapidly spreading infection of the deep fascia with secondary tissue necrosis
46
Name the cause of necrotising fasciitis.
Group A haemolytic streptococcus
47
Name 3 risk factors of necrotising fasciitis.
1. Abdo surgery
2. Diabetes
3. Malignancy
48
Describe how a patient with necrotising fasciitis would present.
- 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
Describe how a patient with necrotising fasciitis would be managed.
- Urgent referral for extensive surgical debridement
| - Intravenous antibiotics
50
What is Erysipelas?
Erysipelas is an acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue
51
What layer of the skin does cellulitis involve?
Deep subcutaneous tissue
52
Name 2 microbial causes of erysipelas and cellulitis.
1. Streptococcus pyogenes
| 2. Staphylococcus aureus
53
Name some risk factors of erysipelas and cellulitis.
- Immunosuppression
- Wounds
- Leg ulcers
- Toe-web intertrigo
- Minor skin injury
54
Describe how a patient with erysipelas/ cellulitis would present.
- Local signs of inflammation
- May be associated with lymphangitis
- Systemically unwell with fever, malaise or rigors (particularly with erysipelas)
55
How is erysipelas distinguished from cellulitis?
Erysipelas is distinguished from cellulitis by a well-defined, red raised border
56
Describe how a patient with erysipelas/ cellulitis would be managed.
- Antibiotics (e.g. flucloxacillin or benzylpenicillin)
| - Supportive care: rest, leg elevation, sterile dressings and analgesia
57
Name 3 complications of erysipelas/ cellulitis.
1. Local necrosis
2. Abscess
3. Septicaemia
58
Describe how a patient with staphylococcal scalded skin syndrome would present.
- 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
Describe the pathophysiology of staphylococcal scalded skin syndrome.
Production of a circulating epidermolytic toxin from phage group II, benzylpenicillin-resistant (coagulase positive) staphylococci
60
Describe how a patient with staphylococcal scalded skin syndrome would be managed.
- Antibiotics (e.g. a systemic penicillinase-resistant penicillin, fusidic acid, erythromycin or appropriate cephalosporin)
- Analgesia
61
Describe the 3 main groups of superficial fungal infections.
1. Dermatophytes (tinea/ringworm)
2. Yeasts (e.g. candidiasis, malassezia),
3. Moulds (e.g. aspergillus)
62
Describe the presentation of tinea corporis.
Tinea infection of the trunk and limbs.
Itchy, circular or annular lesions with a clearly defined, raised and scaly edge is typical.
63
Describe the presentation of tinea cruris.
Tinea infection of the groin and natal cleft. Very itchy.
64
Describe the presentation of tinea pedis.
Athlete’s foot.
Moist scaling and fissuring in toe-webs, spreading to the sole and dorsal aspect of the foot.
65
Describe the presentation of tinea capitis.
Scalp ringworm. Patches of broken hair, scaling and inflammation.
66
Describe the presentation of tinea unguium.
Tinea infection of the nail. Yellow discolouration, thickened and crumbly nail.
67
Describe the presentation of tinea manuum.
Tinea infection of the hand. Scaling and dryness in the palmar creases.
68
Describe the presentation of tinea incognito.
Inappropriate treatment of tinea infection with topical or systemic corticosteroids. Ill-defined and less scaly lesions.
69
Describe the presentation of candidiasis skin infection.
White plaques on mucosal areas, erythema with satellite lesions in flexures.
70
Describe how to manage patients with fungal skin infections.
- 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
Describe the presentation of a patient with a BCC.
- 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
Name 6 morphological types of BCCs.
1. Nodular (most common)
2. Superficial (plaque-like)
3. Cystic
4. Morphoeic (sclerosing),
5. Keratotic
6. Pigmented
73
Name some risk factors for BCCs.
- 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
Describe the management of BCCs.
- 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
Describe the pathology of BCCs.
A slow-growing, locally invasive malignant tumour of the epidermal keratinocytes normally in older individuals, only rarely metastasises.
76
Describe the pathology of SCCs.
A locally invasive malignant tumour of the epidermal keratinocytes or its appendages, which has the potential to metastasise
77
Name some risk factors for SCCs.
- UV exposure
- Pre-malignant skin conditions (e.g. actinic keratoses)
- Chronic inflammation (e.g. leg ulcers, wound scars)
- Immunosuppression
- Genetic predisposition
78
Describe the presentation of a patient with a SCC.
Keratotic (e.g. scaly, crusty), ill-defined nodule which may ulcerate
79
Describe the management of SCCs.
- Surgical excision
| - Radiotherapy (for large, non-resectable tumours)
80
Describe the pathology of a malignant melanoma.
An invasive malignant tumour of the epidermal melanocytes, which has the potential to metastasise
81
Name some risk factors for malignant melanomas.
- Excessive UV exposure
- Skin type I (always burns, never tans)
- History of multiple moles or atypical moles
- Family history
- Previous history of melanoma
82
Describe the presentation of a patient with malignant melanoma.
```
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
Name 4 types of malignant melanoma.
1. Superficial spreading melanoma
2. Nodular melanoma
3. Lentigo maligna melanoma
4. Acral lentiginous melanoma
84
Describe the common site, demographics and causes of the subtype nodular melanoma.
- Common on the trunk
- Young and middle-aged adults
- Related to intermittent high-intensity UV exposure
85
Describe the common site, demographics and causes of the subtype lentigo maligna melanoma.
- Common on the face
- Elderly population
- Related to long-term cumulative UV exposure
86
Describe the common site, demographics and causes of the subtype acral lentiginous melanoma.
- Common on the palms, soles and nail beds
- Elderly population
- No clear relation with UV exposure
87
Describe the common site, demographics and causes of the subtype superficial spreading melanoma.
- Common on the lower limbs
- Young and middle-aged adults
- Related to intermittent high-intensity UV exposure
88
What is the current staging system for melanoma in the UK?
2009 American Joint Committee of Cancer Staging System (AJCC)
89
Describe the management of malignant melanoma.
- 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
Describe the presentation of a patient with atopic eczema.
- 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
Describe the pathophysiology of atopic eczema.
A primary genetic defect in skin barrier function (loss of function variants of the protein filaggrin)
92
Name 5 exacerbating factors involved with atopic eczema.
1. Infections
2. Allergens (e.g. chemicals, food, dust, pet fur),
3. Sweating
4. Heat
5. Severe stress
93
Describe the potential nail changes in a patient with atopic eczema.
Pitting/ ridging
94
Describe the management of atopic eczema.
- 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
Name 2 complications of atopic eczema.
1. Secondary bacterial infection (crusted weepy lesions)
2. Secondary viral infection - molluscum contagiosum (pearly papules with central umbilication), viral warts and eczema herpeticum
96
Describe the pathophysiology of acne vulgaris.
An inflammatory disease of the pilosebaceous follicle
97
Describe the presentation of a patient with acne vulgaris.
- 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
Describe the management of acne vulgaris.
- 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
Describe the complications of acne vulgaris.
- Post-inflammatory hyperpigmentation
- Scarring
- Deformity
- Psychological and social effects
100
Describe the pathophysiology of psoriasis.
Hyperproliferation of keratinocytes and inflammatory cell infiltration
101
Describe the presentation of a patient with psoriasis.
- 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
Describe the management of psoriasis.
- 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
Describe the complications of psoriasis.
- Erythroderma
| - Psychological and social effects
104
Name 6 types of psoriasis.
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
Name 5 potential precipitating factors in a patient with psoriasis.
1. Trauma
2. Infection
3. Drugs
4. Stress
5. Alcohol
106
Name 2 associated pathological changes that some patients with psoriasis experience.
1. 50% have associated nail changes (e.g. pitting, onycholysis)
2. 5-8% suffer from associated psoriatic arthropathy
107
Name 7 common causes of blisters.
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
What is bullous pemphigoid?
A blistering skin disorder which usually affects the elderly
109
Describe the pathophysiology of bullous pemphigoid.
Autoantibodies against antigens between the epidermis and dermis causing a sub-epidermal split in the skin
110
Describe the presentation of a patient with bullous pemphigoid.
- 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
Describe the management of bullous pemphigoid.
- 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
What is pemphigus vulgaris?
A blistering skin disorder which usually affects the middle-aged
113
Describe the pathophysiology of pemphigus vulgaris.
Autoantibodies against antigens within the epidermis causing an intra-epidermal split in the skin
114
Describe how a patient with pemphigus vulgaris would present.
- Flaccid, easily ruptured blisters forming erosions and crusts
- Lesions are often painful
- Usually affects the mucosal areas (can precede skin involvement)
115
Describe how to manage a patient with pemphigus vulgaris.
- 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)
