Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

4th year everything > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is cellulitis?

A

A spreading infection of the deep subcutaneous layer of the skin. It is the most common skin infection leading to admission to hospital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What preferential anatomical distribution does cellulitis demonstrate?

A

Cellulitis preferentially involves the lower limbs and extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is erysipleas? What anatomical proclivity does it show?

A

Similar to cellulitis; it is an infection of the deep dermis and subcutaneous tissues and has a proclivity for involvement of the face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the most common bacterias causing cellulitis/erysipleas?

A

Streptococcus spp. most commonly

Rarely staphylococcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the clinical presentation of cellulitis?

A

Tender erythematous patch with poorly demarcated borders, swelling, warmth and potentially a low grade fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the clinical presentation of erysipleas?

A

Raised erythematous area with sharply demarcated borders, warmth, tenderness and potentially a low grade fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the major differential diagnosis to be ruled out in the case of suspected cellulitis of the lower limb?

A

Deep vein thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the antibiotic of choice for treatment of cellulitis/erysipleas?

A

Flucloxacillin (erythromycin if penicillin allergic)

If disease is diffuse then intravenous therapy for 3-5 days followed by at least two weeks of oral therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is necrotising fasciitis?

A

A deep-seated infection of the subcutaneous tissue that results in fulminant and spreading destruction of the fascia and fat.

May initially spare the skin, leading to delayed diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the clinical features of necrotising fasciitis?

A

Spreading erythema and underlying crepitus with severe pain and system toxicity (disproportionate to skin findings)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Outline the difference between type 1 and type 2 necrotising fasciitis

A

Type 1 - mixed anaerobic and aerobic bacteria

Type 2 - mono-microbial (group A streptococci)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What profile of people are most likely to get type 1 necrotising fasciitis? (2)

A

Patients who have had recent abdominal surgery

Type 2 diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is necrotising fasciitis managed?

A

Surgical debridement followed by aggressive use of broad-spectrum antibiotics (usually benzylpenicillin and clindamycin)

With the addition of metronidazole in type 1 to cover anaerobic microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is gas gangrene?

A

A specific deep-seated infection with clostridium spp. (especially clostridium perfringens) contaminating penetrating wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What clinical picture does gas gangrene present with?

A

Muscle necrosis with severe pain and swelling and crepitus on deep palpation (due to gas in subcutaneous tissue as a result of necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is gas gangrene treated?

A

Surgical debridement and combination antimicrobial therapy of benzylpenicillin and clindamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does the dermamatophytes refer to?

A

Three types of fungi commonly responsible for infections of the superficial skin layers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How are dermatophytes transmissible?

A

Direct contact with infected humans/animals or by indirect contact with exfoliated hair/skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of dermatophyte infection affects the body?

A

Tinea corporis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of dermatophyte infection affects the face?

A

Tinea faciei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of dermatophyte infection affects the groin?

A

Tinea cruris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What type of dermatophyte infection affects the feet?

A

Tinea pedis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What type of dermatophyte infection affects the hands?

A

Tinea manuum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of dermatophyte infection affects the nailbed?

A

Tinea unguium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What type of dermatophyte infection affects the scalp?
Tinea capitis
26
How does tinea corporis present?
Mildly itchy patches with central clearing and an advancing, scaly edge
27
How does tinea faciei present?
Erythematous annular lesion on the face; may or may not be itchy
28
How does tinea cruris present?
Intensely itchy rash in the groin with scaly edges and often extends on the inner thigh
29
How does tinea pedis present?
White, macerated/fissured skin around toe clefts with more scaly erythema extending onto the soles and sides of the feet
30
How does tinea manuum present?
Diffuse erythematous scaling of the palmar surface of the hands
31
How does tinea capitis present?
A spectrum of presentation from mild scaling and no hair loss to circular patches of scale and alopecia
32
How does tinea unguium present?
Asymmetrical white/yellow/black discolouration of the nails with nail plate thickening and white residue under the nail.
33
How are dermatophyte infections treated differently on a local and more diffuse scale?
Local disease - topical antifungal creams (e.g. clotrimazole) Diffuse disease - oral antifungal therapy (e.g. terbinafine)
34
Where can cutaneous candida infection present on the body?
Can occur in the groin, interdigital/toe clefts or around nails
35
What are the clinical features of acne vulgaris?
Increased sebum production Blockage of pilosabaceous units Follicular epidermal hyperproliferation All leading to formation of open/closed comedones, inflammatory papulaes/pustules, hypertrophic/keloidal scarring and hyperpigmentation
36
What is the first line therapy for acne vulgaris?
Topical agents; e.g. Keratolytics (benzyl peroxide) Topical retinoids (isotretinoin) Antibiotics (clindamycin)
37
What is the second line therapy for acne vulgaris?
``` Low-dose oral antibiotics for 3-4 months (e.g. erythromycin) Hormonal treatment (e.g. cyproterone acetate) ```
38
What is the third line therapy for acne vulgaris?
Oral retinoid (isotretinoin)
39
What is the absolute contraindication of using retinoids?
Teratogenicity therefore contraindicated in pregnancy
40
What is psoriasis?
A chronic hyperproliferative disorder typically characterised by well-defined scaly plaques on extensor surfaces of the body
41
What are the two peak age ranges for psoriasis?
16-22 years old | 55-60 years old
42
What four different entities of psoriasis are there?
1. Chronic plaque psoriasis 2. Flexural psoriasis 3. Guttae 4. Erythrodermic and pustular
43
Outline the features of chronic plaque psoriasis
Most common form. Erythematous and scaly plaques form on extensor surfaces . Scalp involvement is also common
44
Outline the features of flexural psoriasis
Erythematous non-sclay plaques confined to flexures such as the groin and under breasts
45
Outline the features of guttae
Most commonly in children Explosive eruption of small discoid plaques over the trunk proceeding after a streptococcal throat infection
46
Outline the features of erythrodermic and pustular psoriasis
Most severe form Widespread intense inflammation and systemic upset including malaise, pyrexia and potentially haemodynamic instability
47
Outline the different treatment modalities for psoriasis?
Topical treatement - emmolients, vitamin D3 analogues, corticosteroids Phototherpay - UVA with photosensitising agent Systemic therapy - oral retinoid, biologics
48
What is eczema (dermatitis)?
A condition characterised by superficial skin inflammation with vesicles in the acute phase; along with erythema, oedema, scaling and intense itching
49
What is the primary defect in skin function in eczema?
Abnormal barrier function of skin leading to antigenic presentation to immune cells causing an immune reaction leading to inflammation
50
How is eczema managed?
Known irritants should be avoided Regular use of emollients Topical steroids are the mainstay of treatment. Mild steroids (e.g. hydrocortisone) used for face and more potent steroids (e.g. betamethasone) for the body. Topical immunomodulators e.g. tacrolimus are particularly useful for treatment of sensitive areas such as face and eyelids
51
What is contact dermatitis? What clinical features would make you think of it as a diagnosis?
Sharply demarcated inflammation (both acute and chronic) produced by substances which irritate the skin (irritants) Unusually sharply defined borders to the lesions should rouse suspicion
52
What is erythema nodosum?
Acute panniculitis (inflammation of subcutaneous adipose tissues) producing painful blue/red nodules over the limbs
53
What systemic features are often seen concurrently with erythema nodosum?
Malaise, fever and arthralgia
54
How is non-resistant erythema nodosum treated?
NSAIDs Light compression and bedrest for up to a number of weeks.
55
How is resistant erythema nodosum treated?
Dapsone (antibiotic cream) or Colchicine or Oral prednisolone
56
List some common causes of erythema nodosum (5)
``` Inflammatory bowel disease Sarcoidosis Tuberculosis Streptococcal infection Drugs (e.g. oral contraceptive pill) ```
57
What is erythema multiforme?
An acute, self-limiting rash characterised by multiple 'target lesions' on the distal limbs
58
What is the most common cause of erythema multiforme?
Herpes simplex infection Other causes include herpes simplex or autoimmune conditions such as lupus
59
What is pyodermic gangrenosum? What is the classical presentation?
Ulcerating condition presenting with erythematous nodules/ pustules which go on to ulcerate. The ulcers typically have a blue/black appearance and a purulent surface.
60
What are the main causes of pyodermic gangrenosum?
Inflammatory bowel disease, rheumatoid arthritis, haematological malignancy and biliary cirrhosis
61
How is pyrodermic gangrenosum managed?
High-dose topical and/or oral steroids to prevent further ulceration Debridement is contraindicated as it worsens the condition
62
What is acthanosis nigrans?
Thickened and hyperpigmented skin of flexures associated with obesity, diabetes, underlying malignancy (especially gastrointestinal) and hyperandrogenism in females
63
Outline the genetics of Type 1 Neurofibromatosis (Von Ricklinghausen's Disease)
Autosomal dominant condition caused by an NF1 gene mutation on chromosome 17
64
Outline the genetics of Type 2 Neurofibromatosis
Autosomal dominant condition caused by an merlin/schwannonin conding gene mutation on chromosome 22
65
What are the features indicative of Type 1 Neurofibromatosis?
Multiple fleshy skin tags and deeper soft tissue tumours (neurofibromas) Café-au-lait spots (light brown macules) Scoliosis Increased incidence of meningiomas or gliomas
66
What are the features indicative of Type2 Neurofibromatosis?
Presents with bilateral acoustic neuromas and cutaneous neurofibromas
67
What is the inheritance pattern demonstrated in tuberous sclerosis?
Autosomal dominant Due to mutations in either the TSC1 or TSC2 gene coding for hamartin or tuberin respectively
68
What are the clinical features of tuberous sclerosis?
Mental retardation, epilepsy and cutaneous abnormalities including adenoma sebaceum (red papules around the nose), periungual fibroma and café-au-lait spots
69
What is Ehlers-Danlos Syndrome?
Inherited defect in collagen leading to hyperelastic skin, hypermobile joints and progressive gut/aorta wall weakening
70
What is pemphigus vulgaris?
Autoimmune condition leading to formation of cutaneous and mucosal blisters which evolve into erosions. Can be fatal. Treatment with high-dose oral prednisolone and immunosuppression
71
What is bullous pemphigoid?
Autoimmune condition leading to the formation of large tense blisters on limbs and torso. It is a disease of the elderly and is treated with high-dose oral prednisolone and immunosuppression
72
What is the most common form of skin malignancy?
Basal Cell Carcinoma
73
How do Basal Cell Carcinomas present?
Shiny, pearly nodule typically on sun exposed areas which may go on to ulcerate They rarely metastasise but are locally invasive Treated by surgical excision or topical immunomodulators e.g. imiquimod
74
How do Squamous Cell Carcinomas present?
More aggressive than BCCs. Poorly-defined nodules that can grow rapidly and ulcerate Treated with wide margin excision or radiotherapy (less commonly)
75
What is the most severe form of skin malignancy?
Malignant melanoma
76
Why is melanoma the most severe form of skin malignancy?
It can metastasise early to sites such as the bones, lung and brain
77
What are the four clinical entities of malignant melanoma?
1. Lentigo meligna melanoma 2. Superficial spreading melanoma 3. Nodule malignant melanoma 4. Acral lentiginous malignant melanoma
78
What is Kaposi sarcoma?
A tumour of vascular and lymphatic endothelium presenting as purple nodules/plaques in elderly males
79
What groups of people are more disposed to developing Kaposi sarcoma?
Ashkenazi Jews Central African natives Patients with HIV infection

4th year everything (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions