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BRS missed out > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Examples of conditions where folliculitis may be seen

A

HIV- esinophillic foliculitis
Recurrent nasal s.aureus

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2
Q

Treatment for folliculitis

A

Antibiotics e.g eryhtromycin or flucloxacillin
Incision or drainage

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3
Q

Difference between furuncle and carbuncle

A

Furuncle - deep follicular abscess
Carbuncle - involvement with adjacent connected follicles

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4
Q

Features of Panton Valentine Staphylococcus

A
  • B pore forming exotoxin, leukocyte destruction and tissue necrosis
    -Higher morbidity, mortality tand transmissability
  • Recurrent and painful abscesses, folliculitis, celluliti, often painful more than one site
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5
Q

Extracutaneous features of Panton Valentine Leukocidin Staphylococcus

A
  • Necrotising pneumonia
    Necrotising fascitis
    Purpura fulminans
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6
Q

What are the 5Cs for risk of aquiring Panton Valentine Leukocidin Staphylococcus

A

Close contact
Crowded space
Contaminated items
Cleanliness
Cuts and grazes

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7
Q

Treatment for Panton Valentine Leukocidin Staphylococcus

A

Consult local microbiologist
Antibiotics
Chlorhexidine body wash 7 days
Nasal application of mupirocin ointment
Treatment of close contacts

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8
Q

Cellulits:
1. infection involving which layers of the skin
2. Presentation
3. Common bacterial causes
4. Predisposing factor
5. Treatment

A
  1. Lower dermis and subcutaneous tissue
  2. blanching eythema or oedema, tender swelling, ill defined
  3. strep pyogenes, staph aureus
  4. oedema
  5. Systemic antibiotics
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9
Q

Impetigo:
1. Presentation
2. Common bacterial causes
3. Often affects
Treatment

A
  1. honey crusted superficial bacteria infection, overlying an erosion
  2. streptococci (non- bullous), staphylococci(bollous)
  3. face, perioral, ears, nares,
  4. Topical +/- systemic antibiotics
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10
Q

What is the gold crusted skin feature , caused by staph aureus that occurs in atopic dermatitis called?

A

Impetiginisation

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11
Q

Lyme disease aka

A

Borreliosis

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12
Q

Lyme disease:
1. Skin presentation
2. Systemic presentation
3. Diagnosis

A
  1. Erythema migrans and erythema papulae, everntually annular erythema>20 cm. Progression : smaller secondary lesions develop
  2. Carditis, meningitis, fever, headaches, arthritis, facial palsy , polyradiculitis
  3. Histopathology non specific, serology non specific, clincial
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13
Q

Primary Syphilis:
1. Bacterial cause
2. Primary infection presentation:
3. after 1 week presentation:

A

1.Treponema pallidum
2. Chancre - painless ulcer with firm indurated borders
3. Lymphadenopathy - painless - regional

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14
Q

Secondary syphilis:
1. Onset
2. Symptoms:
3. Skin symptoms:
4. Rare manifestations

A
  1. 50 days after primary chancre
  2. Malaise, Fever, Pruritus, iritis, headache
  3. Lymphadenopathy, hepatosplenomegaly, rash, mucous patches, alopecia
  4. Lues maligna
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15
Q

Treatment of syphilis

A

IM benzylpenicilin or oral tetracycline

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16
Q

Melanoma -
cancer of what?
Often found where?

A

Melanocytes

Mucosal surfaces - Oral, Vagina, Conjunctival and within uveal tract of eye

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17
Q

Melanoma Risk Factors

A

Genetic
Pale skin
Red hair

Environmental
Sun exposure - intermittant or chronic
Sun beds
Immunosuppression

Phenotypic
>100 Melanocytic nevi

Atypical melanocytic nevi

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18
Q

Subtypes of Melanoma

A

Superficial spreading

Nodular

Lentigo maligna

Acral lentiginous

Unclassifiable

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19
Q

Superficial spreading (melanoma)
1.Where is it most commonly found?
2. How does it normally arise?
3. What is visible in 2/3 of tumours?
4. How does it spread?

A
  1. Trunk of men, legs of women
  2. From Nevus or de novo
  3. Regression - greyish centre or
    hypo/ de pigmentation (due to host response)
  4. Horizontally then vertically
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20
Q

Nodular (Melanoma)
1. where does it most ocmmonly affect?
2. Does it affect male or females more?

  1. How does it spread?
A
  1. Trunk, Head, neck
  2. Males
  3. Vertical growth only
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21
Q

Lentigo Maligna +/- Melanoma
1. Difference between + and -
2. What are the common risk factors specifc to this?
3.Where does it most commonly affect?
4. How does it look?

A
  1. Whether or not it is invasive or just in situ
  2. Age > 60 and chronically sun damaged skin
  3. Face
  4. Asymmetrical brown/black macule with colour variation and irregular indented borders
22
Q

Acral lentigous (melanoma)
1. Age most ocmmonly found in
2. Location most commonly affected
3. Disproportionally represented in which group?

A
  1. 7th decade
  2. Palms and soles of feet, around nail apparatus
  3. Afro caribean and asian
23
Q

Melanoma self detection

A

Asymmetry

Border irregularity

Colour varieation

Diameter greater than 5mm

Evolving

24
Q

GArbe’s rule

A

If a patient is worried about a single lesion, dont ignore it, test it , low threshold for biopsy

25
Q

Poor prognostic factors for Melanoma

A

Increased Breslow thickness >1mm

Ulceration

Age

Male gender

Anatomical site – trunk, nhead, neck

Lymph node involvement

26
Q

How do you measure the length from granular layer to bottom of tumour?

A

Breslow thickness

Use dermascope first, and if in doubt take it out (for histiological examination)

27
Q

Management of Melanoma

A
  1. Primary excision down to subcutaneous fat
    2mm peripheral margin
    Wide excision
    • Margin determined by Breslow depth
      - 5mm for in situ
    • 10mm for </=1mm
  2. Sentinel lymphoma node biopsy
    Currently offered for pT1b+
    Extracapsular spread on lymph node biopsy – needs lymph node dissection

3.Imaging
Stage III, IV
And Stage IIc without SLNB
PET-CT
MRI Brain
LDH – major prognostic indicator in melanoma

  1. Unresectable or metastatic
    Mutated oncogene targeted therapy
    Immunotherapy
28
Q

What is involved in Melanoma staging?
TNM

A

Thickness
Ulceration
In situ

29
Q

Types of Keratinocyte Dysplasia

A

Basal cell carcinoma ( Virtually never metastisis)
Actinic Keratoses ( Dysplastic keratinocytes)
Bowens disease (Squamous cell carcinoma in situ)
Squamous cell carcinoma ( potential for metastesis/ death)

30
Q

Basal cell carcinoma
1. What is a significant risk factor?
2. Cross talk between what and what explains the pathogenesis of BCC and how
3. What is the impact BCC having proteolytic activity?
4. Loss of function in which chromosome and gene is associated with the pathogenesis of BCC?

A
  1. UV radiation
  2. Tumour and Mesenchymal cells of stroma, there is an upregulation of PDGF receptors on mesenchymal cells and an unpregulation of PDGF production from tumour cells
  3. Metalloproteinases and collagenases breakdown - degrade pre existing dermal tissues and facilitate spread of tumour
  4. 8q of PTCH gene and p53 missense
31
Q

Squamous cell carcinoma
1. What is a significant risk factor?
2. Alteration in which genes are most common

A
  1. UV radiation
    2.P53 then CDKN2A then NOTCH 1 & 2
32
Q

HSV:
What is it summarised by?
Where is it typically presents?
What are the types and differences?

A
  1. Primary and recurrent vesicular eruptions
  2. Orolabial and genital region
  3. HSV1 - direct contact with saliva and other secretions
    HSV2 - sexual contact
33
Q

HSV:
When do symptoms start?
What are the initial symptoms?
What then occurs?
What are the systemic manifestations?
When does it resolve?
What causes it to reactivate?

A
  1. 3 -7 days after exposure
  2. Malaise, Fever, Tender lymphadenopathy +/- burning/ tingling
  3. Painful rouped vesicles on erythematous base → ulceration / pustules / erosions with scalloped border
    Orolabial lesions – often asymptomatic
    Genital involvement – often excruciatingly painful→ urinary retention
  4. 10% Atypical meningitis
  5. Within 2-6 weeks
  6. Spontaneous, UV, fever, local tissue damage, stress
34
Q

HSV emergency:
What is it called?
Presentation?

A

Eczema herpeticum

Monomorphic, punched out erosions (excoriated vesicles)

35
Q

HSV: Herpetic whitlow
What population is it often found in?

Presentation:

Misdiagosed as:

A

Children

infection of digits – pain, swelling and vesicles

paronychia or dactylitis

36
Q

HSV: Neonatal HSV infection
1.How do neonates get exposed?
2.Which type of HSV?
3.When is the onset?
4.where is it localised?
5.How does it present?
6. Treatment:
If not treated?

A
  1. vaginal birth
  2. HSV 1 & 2
  3. Birth to 2 weeks
  4. Scalp and Trunk
  5. Vesicles
  6. IV antivirals
  7. Encephalitis 50%, Neurplogical impairments may still be present once treated
37
Q

HSV:
Diagnosis
Treatment

A
  1. PCR of swab
    2.Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection

Intravenous 10mg/kg TDS X 7-19 days

38
Q

Pityriasis versicolor

Species
Presentation
Onset
Management

A

Malassezia spp.

Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale

Begins during adolescence (when sebaceous glands become active)
Flares when temperatures and humidity are high – Immunosuppression

Topical Azole

39
Q

Dermatophytes

A

fungi that live on keratin

40
Q

Kerion

A

an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp; scalp is tender and patient usually has posterior cervical lymphadenopathy

41
Q

Tinea capitis
aka
often caused by

A

Trichophyton tonsurans

42
Q

Most fungal infections caused by

A

Trichophyton rubrum

43
Q

Mucormycosis

Presentation

Associations:

Treatment

A

oedema, then pain, then eschar
fever, headache proptosis, facial pain, orbital cellulitis ± cranial nerve dysfunction

Diabetes mellitus (1/3 of patients - DKA very high risk ,Malnutrition ,Uraemia, Neutropaenia, Medications: Steroids / antibiotics / desferoxamine , Burns, HIV

Treatment: aggressive debridement & antifungal therapy amphoteracin

44
Q

Id reaction

Aka

Description

A

Dermatophytid reactions

Inflammatory reactions at sites distant from the associated dermatophyte infection

May include urticaria, hand dermatitis, or erythema nodosum

Likely secondary to a strong host immunologic response against fungal antigens

45
Q

Candida albicans

Predisposed by

Presentation

A common cause of what

A

occlusion, moisture, warm temperature, diabetes mellitus

erythema oedema, thin purulent discharge
Usually an intertriginous infection (skin folds) or of oral mucosa.

A common cause of vulvovaginitis

46
Q

Scabies

caused by?

Pathophysiology

Presentation

Diagnostic criteria

Areas affected

Treatment

A

Sarcoptes species

Female mates, burrows into upper epidermis, lays her eggs and dies after one month.

Insidious onset of red to flesh-coloured pruritic papules

diagnostic burrow consisting of fine white scale

Affects interdigital areas of digits, volar wrists, axillary areas, genitalia

permethrin, oral ivermectin

- Two cycles of treatment are required
47
Q

Deficiencies in staph aureus

A
  • Hypogammaglobulinaemia
  • HyperIgE syndrome – deficiency
48
Q

Actinic Keratoses
What is it confined to?
What is a major risk factor?
Where is it seen?
How to distinguish with SCC?
Presentation

A
  1. Atypical keratinocytes confined to epidermis
  2. Develop on sun-damaged skin - usually head, neck, upper trunk and extremities
  3. Distinction from squamous cell carcinoma sometimes difficult – requiring biopsy
  4. Macules or papules
    Red or pink
    Usually some scale – may be thick scale
49
Q

Bowen’s disease
Description
Presentation
Arise from

A

Squamous cell carcinoma in situ

Erythematous scaly patch or slightly elevated plaque

de novo or from pre-existing AK

50
Q

Actinic Keratoses & Bowen’s Disease: Treatment

A

5-fluorouracil cream

Cryotherapy

Imiquimod cream

Photodynamic therapy

Curettage and cautery

Excision

51
Q

Squamous cell carcinoma
Presentation

A

Erythematous to skin coloured, Papule, Plaque-like , Exophytic, Hyperkeratotic, Ulceration

52
Q

Squamous Cell Carcinoma: High Risk Features

A

Clinical features

Localisation and size:
- Trunk and limbs > 2cm
- Head / neck > 1cm
- Periorificial zones
Margins: Ill-defined
Rapidly growing
Immunosuppressed patients
Previous radiotherapy or site of chronic inflammation

  • Tumour thickness - Clark level: >6mm, Clark IV, V
    • Invasion beyond subcutaneous fat

BRS missed out (10 decks)

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