Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine - GP > Basic Derm 1 > Flashcards

Basic Derm 1 Flashcards

1
Q

Basic history for a rash?

A

WHISPer Fart in MECCa

  1. Where is rash and where did it start?
  2. How long? (Acute/subacute/chronic)
  3. Itchy? Severity of itch
  4. Supplementary: contacts, meds, new clothes or exposures, PHX (rash, asthma, eczema), FHX

Clinical questions you’re trying to answer:

  • Is this a drug rash?
  • Has the rash been modified by treatment?
  • Any contacts with a similar rash?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is cellulitis?

A

Acute spreading skin infection
Indistinct borders
Mainly involves dermis and subcutaneous tissue

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

Cause of cellulitis?

A

Mostly Strep pyogenes
S. Aureus secondly, can be more severe
Break in skin

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

Principles of Management of cellulitis?

A 
Rest in bed and limb elevation at all times
Basic analgesia
Wound cleansing
Dressing with non stick saline dressings
Antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Antibiotics for cellulitis?

A

Empiric or known S. aureus:
Flu/dicloxicillin
days
Penicillin allergy: Keflex

Confirmed S. pyogenes: phenoxymethylpenicillin

All doses are 500mg q6h PO 7-10 days

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

What is erysipelas?

A

Form of superficial cellulitis
Raised, sharply demarcated borders from uninvolved skin
Lymphatic involvement

Causes and management is as per cellulitis

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

What is impetigo?

A

Superficial, contagious, blistering infection of skin caused by S. aureus / S. pyogenes. Can be bullous or vesiculopustular.

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

Causes of impetigo?

A

S. Aureus
S. Pyogenes
Skin trauma, but 30% cases (bullous) occurs on intact skin

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

Distinguish between bullous and non bullous impetigo.

A

Bullae: fluid filled lesions >0.5cm diameter
Vesicles: fluid filled lesions <0.5cm diameter

Non bullous (vesiculopustular) is more common (70% cases) and occurs at skin trauma. Can be caused by either or both S aureus and S pyogenes.

Bullous is less common and occurs on intact skin.

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

Principles of managing impetigo?

A
  1. Topic antiseptic and cleansing to remove crusts
  2. Topical antibiotic
  3. Minimise recurrence and transmission
  4. Antibiotics for extensive lesions or systemic features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prescribe your topical therapy for impetigo.

A

Antibacterial soap (saline chlorhexidine or povidone iodine) cleansing to gently remove crusts.

Follow with 2% Mupirocin (bactroban) small amount TDS x 10 days

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

Describe measures to reduce recurrence and transmission of impetigo.

A

Daily bath with Oilatum Plus bath oil for 2 weeks

Hot water wash for clothes, towel and linen for 2-4 weeks

Regular hand washing

Exclude from childcare settings until sores fully healed

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

A child with impetigo has extensive lesions and shows systemic features. What antibiotics will you use?

A

Fluclox/dicloxicillin 6.25mg/kg up to 250mg q6h PO x 10 days

If allergic then Keflex (same dose)

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

Basic examination for lumps and bumps?

A 
Look
Feel
Move
Measure
Auscultate
Transilluminate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Approach to describing lumps and bumps?

A

A number with poor eyesight is eating shapes - he changes size then falls into another position onto a stony hard rock, which is a cyst. It turns out to be mobile, which goes to buy a surface with lots of special features.

Ie
Number, site, shape, position, consistency (soft v hard), solid v cystic, mobility, surface, special features

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

What anatomical questions are you trying to answer when examining lumps and bumps?

A

Skin / SC tissue / muscle / tendon or joint / bone

In Skin: moves with skin
In SC tissue: skin moves over lump, slipping sign
In muscle: movable when muscle relaxed, limited movement when contracted
In tendon/joint: movement of these may change mobility or shape
In bone: immobile, best outlined when muscle relaxed

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

Define an epidermoid cyst

A

Aka sebaceous cyst
Benign cyst arising from ectodermal tissue
Results from proliferation of epidermal cells in circumscribed space of the dermis

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

Clinical features of an epidermoid cyst?

A 
Fixed to skin but not other structures
Regular lump, usually round
Mainly scalp, also face, neck, trunk, scrotum
Soft to firm
Cystic
Moves with skin
Special features:
- usually fluctuant with sebaceous material
- tends to get inflamed
- +/- central punctum with keratin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Management options for epidermoid cyst?

A

If before puberty: consider polyposis coli
Can leave alone if small and not bothersome
Surgical:
Method 1: incision into cyst
Method 2: incision over cyst and blunt dissection
Method 3: standard dissection

Infected cysts: incise and drain purulent material. When inflammation completely resolved remove cyst by method 1 or 3

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

What is seborrhoeic keratosis?

A

Common benign skin tumour, usually multiple
Most commonly on torso, face, but can be found anywhere
Age > 40 (number + pigmentation tends to increase)

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

What age does seborrhoeic keratosis tend to present?

A

Age >40

80-100% people over age 50 are affected

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

Clinical features of seborrhoeic keratosis?

A 
Pt age >40
Number: Multiple
Site: Sits on skin, torso or head but can be anywhere
Shape: "Sultana pressed into skin", well defined border
Size: <1cm diameter usually
Surface: Pitted
Special features: get-brown to black
Usually asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is solar Lentigo?

A

Aka actinic keratoses, sunspots
Intraepidermal keratinocytic dysplasia with potential for malignant change (especially on ears)
Reddened scaly hyperkeratotic thickenings occurring on light exposed areas

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

Clinical features of solar lentigo?

A

Site: Sun exposed fair skin (face, ears, scalp if balding, forearms, dorsum of hands)
Size: Variable (2-20mm diameter)
Surface: Dry and rough, adherent scale
Special features:
Usually asymptomatic, might have discomfort on rubbing with towel
Scale can separate to leave oozing surface
Small proportion will undergo malignant change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

You are suspecting an infectious cause of your patients rash. What are the common infectious conditions of the skin?

A

An IMP in a CELL finds a TIN CAN full of tomatoes - he has a TOMATO-FIGHT with the guard who PITYs him and gives him ROSES. He says PHEW.

Bacterial: Impetigo, cellulitis
Fungal: Tinea, Candidiasis, Dermatophytes, Pityriasis versicolor
Viral: Pityriasis rosacea, HSV/HZV, Exanthema, Warts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Definition of Dermatophytes?

A

Dermatophytes are fungal organisms that require keratin for growth.
They cause superficial infections of hair, skin and nails.
Spread by direct contact from people, animal, soils, clothes, utensils and furniture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Types of Dermatophyte infections?

A

By site: hair, hair follicles, perifollicular skin, keritanized epidermal skin, nail apparatus
By species: Microsporum, Trichophyton, Epidermophyton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Definition of Tinea Cruris?

A

Tinea cruris is a common dermatophyte infection of the groin area caused by Tinea infection
Usually young men esp. athletes
Transmitted by towels and objects in locker rooms, saunas ad communal showers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Clinical features of Tinea cruris?

A

Young males
Groin area (untreated spreads to inner upper thighs, butt), usually scrotum spared
Acute onset itchy rash. Scaling, especially at the margin. Well-defined margin.
Clothing (tight pants, nylon jock straps)
Hot months
Physically active people

30
Q

Management of Tinea cruris?

A

Soak area in arm bath and dry ++
Topical imidazole (Miconazole or Clotrimazole) BD for 3-4 weeks on rash and 2cm beyond border
Prevent recurrence: Tolnaftate dusting powder BD when almost healed
Consider skin scrapings from scaly area for microscopy, Woods light to differentiate from Erythrasma

31
Q

Definition of Tinea pedis?

A

Tinea pedis is a dermatophyte infection of the skin of the feet
It is the most common fungal infection in humans
Usually caused by Trichophyton rubrum
Transmitted by walking barefoot in warm damp places or direct skin contact with someone else

32
Q

Clinical features of Tinea pedis?

A

Feet (soles and inbetween toes)
Acute onset
Itchy (especially between toes)
Contacts: barefoot exposure in warm damp places or skin of affected person
Examination: White and soggy top layer of skin. Scaling, maceration and fissuring of skin between toes 3/4/5

33
Q

Management of Tinea pedis?

A

Education: dry feet, remove flaky skin and improve air circulation and reduce sweating
Change shoes and socks daily
Antifungal cream BD/TDS for 2-3 weeks

34
Q

Definition of pityriasis versicolor?

A

Pityriasis versicolor (aka Tinea versicolor) is a mild, chronic superficial yeast infection of the skin caused by Malassezia sp.
Characterised by discrete or confluent, scale, discoloured or depigmented areas, mainly on the upper trunk
It is NOT a dermatophyte infection
Present worldwide, but more common in tropical climates
Has 2 distinct presentations (red brown/hypopigmented area)

35
Q

Clinical features of pityriasis versicolor?

A

Young-middle aged adult (late teens, peaks early twenties)
Mainly upper trunk, may involve neck, upper arms, face and groin
Patches may coalesce
Recurrent, especially in summer
Mild irritation sometimes - sometimes itchy
2 distinct presentations:
- Reddish brown, slightly scaly patches on upper trunk
- Hypopigmented area that won’t tan, especially in suntanned skin
On examination: Brown on pale skin or white on tanned skin

36
Q

Management of pityriasis versicolor?

A

First line treatment is topical antifungal therapy
1st line:
Topical azoles BD for 2-3 weeks or
Terbinafine cream 1% BD for 2-3 weeks or
Ketoconazole shampoo twice weekly for 2-3 weeks or
Selsun (25% selenium shampoo) 2nd daily for 2-3 weeks

37
Q

Definition of candidiasis?

A

Candidiasis is a fungal (yeast) infection due to any type of candida
Most commonly it is a superficial infection of the skin and mucous membranes, but can also cause systemic disease

38
Q

Clinical features of candidiasis of the skin?

A

Rash in skin folds or where occlusion from clothing/dressings causes abnormally moist conditions
Areas close to body orifices, fingers

39
Q

General management principles of candidiasis?

A

Oral candidiasis: Mouthwash, topical antifungal

Skin: Careful drying of affected areas, topical antifungal

40
Q

Definition of candidiasis intertrigo?

A 
Candidiasis intertrigo (aka flexural candidiasis) is a superinfection of simple intertrigo with Candida albicans.
It tends to affect obese or bedridden patients, especially if incontinent
41
Q

Clinical features of candidiasis intertrigo?

A

Affects men and women equally
Erythematous scale rash in the groin (margins are less well defined than Tinea)
Satellite lesions

42
Q

Management of candidiasis intertrigo?

A

Treat underlying problem
Imadazole (miconazole, clotrimazole) until 2 weeks after symptoms resolve
Burow’s solution 1:40 compresses to dry weeping area
Short term hydrocortisone cream for itch or inflammation

43
Q

Define atopy

A

Atopy is a hereditary or tendency to develop a group of conditions: allergic rhinitis, asthma, eczema, skin sensitivities and urticaria
Allergic rhinitis is the most common manifestation
Common (10% of population)

44
Q

Define eczema

A 
Eczema (aka dermatitis, atopic dermatitis) is an inflammatory epidermal rash characterised by vesicles (acute stage), redness, weeping, oozing, crusting, scaling and itch.
Can be acute or chronic
Multifactorial causes (not always allergic)
45
Q

Cases of eczema?

A 
Exogenous vs endogenous
"A SUN CONTACTS an ANVil with a LISP"
Exogenous:
- Light (photoallergic or phototoxic)
- Contact: Allergens, irritant
Endogenous:
- Atopic, nummular (discoid), vesicular (hand/foot)
- Lichen simplex chronicus
- Seborrhoeic
- Pityriasis alba
46
Q

Clinical features of atopic dermatitis in infants?

A

Age of onset can be in any age group, but most it will start <5 years old
Infants: Head (cheeks, neck, scalp), limbs (extensor surfaces, can spread to flexures, groin)
Affects 3% of infants
Chronic relapsing course - signs appear between 3 months - 2 years
Family history of atopy
Dry skin

47
Q

Clinical features of atopic dermatitis in children?

A 
Children: cubital and popliteal fossae, hands and feet. Face often clears up if they had it as an infant.
Chronic relapsing course, most start <5 years old
Itchy
Family history of atopy
Evident trigger factors
Dry skin
Lichenification if chronic
Flexures usually
48
Q

Clinical features of atopic dermatitis in adults?

A 
Adults: Neck, groom, dorsum of hands, ankles, feet
Chronic relapsing course. Onset is mostly <5 years old but can occur at any age
Itchy
Family history of atopy
Evident trigger factors
Dry skin
Lichenifcation in chronic cases
Usually affects flexures
49
Q

Diagnostic criteria for atopic dermatitis?

A

ITCHy-Dick

  • Itch
  • Typical morphology and distribution
  • Chronic relapsing
  • History of atopy
  • Dry skin
50
Q

Trigger factors of atopic dermatitis?

A

Endogenous vs Exogenous
Endogenous: a stressed emotional sweaty person with poor general health, scratching and rubbing themselves because of allergies
Exogenous: A Micro-man made his skin irritated by being in a hot bubble bath full of sand and food

51
Q

Management principles of atopic dermatitis?

A 
Education and reassurance
Keep skin moist
Pharmacological therapies
Depends on stage of dermatitis:
- Acute weeping: wet dressings
- Acute: creams
- Chronic: ointments +/- occlusion
- Lichenified: Ointments under occlusion
- Infection: Antibiotics Topical 2% mupirocin or oral ABx if unresponsive)
- Moisturisers: use LOTIONS not creams
52
Q

Education for a patient with atopic dermatitis?

A

Reassure: does not normally scar or disfigure
Avoid triggers: endogenous, exogenous (microbiological, manmade, irritants, environmental, food)
Clothing: Wear light soft loose clothes (Cotton) and avoid people with sores

53
Q

Measures to keep skin moist in a patient with eczema?

A

Soap substitute (Aqueous cream) and BD emollient (bath oil, aqueous cream, sir Ilene, paraffin cream)

54
Q

Pharmacological Management of eczema in the acute phase?

A

Creams

  • Mild: +/- weak steroid (1% hydrocortisone)
  • Moderate: Moderate steroid to trunk and limbs, weak steroid to face and flexures. NSAID cream (pimecromilus) can be used for facial flares. Nocte antihistamine.
  • Severe: Potent steroids to worse areas, otherwise as above. Consider occlusive dressings and hospitalisation in very severe cases.
  • Weeping: crusts are often present due to exudate. Burow’s solution 1:20 to soak affected areas, or saline dressings
55
Q

Pharmacological management of eczema in the chronic phase?

A

OINTMENTS

  • Mild: +- weak steroid ointment (1% hydrocortisone)
  • Moderate: Moderate strength ointment to trunk and Limbs, weak to face and flexures. Regimen of 10 days on 4 days off. Nocte antihistamine.
  • Severe: Potent steroids to worse areas. Consider occlusive dressings, hospitalisation.
56
Q

Briefly describe the hair growth cycle.

A

3 stages: Anagen, Catagen and Telogen.

  • Anagen: active growth phase (3-5 years)
  • Catagen: Transition phase (2 weeks)
  • Telogen: Dormant phase and shedding of club hair (2-4 months). Once the club hair is shed the follicle then re-enters anagen. This results in every hair on the scalp being shed and replaced every 3-5 years.
57
Q

How much hair must be shed before there is a noticeable difference in density?

A

25%

58
Q

Define alopecia and its variants.

A

Alopecia is a generic term for hair loss.
Alopecia areata: aka spot baldness. Hair follicle disorder causing sudden onset of localised or diffuse hair loss. It is an autoimmune disorder with genetic component.
Alopecia totalis: alopecia which extends over the whole scalp
Alopecia universalis: alopecia includes eyebrows and eyelids

59
Q

Causes of alopecia?

A 
PAT the balding PANDA
Post-febrile state
Anagen effluvium
Telogen effluvium
Postpartum Telogen effluvium
Androgenetic alopecia
Nutritional (Zinc or iron deficiency, crash dieting or malnutrition)
Drugs (eg. Cytotoxic)
Alopecia areata
60
Q

Clinical features of alopecia areata?

A

Triad of:
- Patch of complete hair loss (small patch or can be diffuse)
- Clean scalp
- Exclamation mark hairs (esp around periphery)
Pigmented hairs lost first
Clean normal scalp
Minimal to no inflammation
Associated with loss of facial or body hair, as well as nail changes (dystrophy, pitting)

61
Q

Management of alopecia areata?

A

Depends if localised patches or extensive (50%)

  • Localised patches: topical steroids (potent class III) especially for children, topical irritants, intralesional steroids, minoxidil (once hair growing), DNCB antigen
  • Extensive loss: Counselling and support groups, cosmetic aids. Topic steroids are ineffective. Consider specialist referral for topical immunotherapy or psoralen and ultra violent A (PUVA) phototherapy. Systemic steroids only for active and progressive cases.
62
Q

Describe the natural course and prognosis of alopecia areata.

A
  • Small patches: 80% may spontaneously recover (1/3 in 6 months, 1/2 in 12 months, 1/3 never recover). Most patients relapse.
  • Alopecia totalis: 50% recovery in fit adults
  • Poor prognosis if: multiple patches, alopecia unversalis, or if alopecia develops in childhood
63
Q

Define Telogen effluvium.

A

Telogen effluvium is inreased shedding of hair in the Telogen phase. It is triggered by stressors, and one of the most common causes of diffuse hair loss.

64
Q

What are the causes of Telogen effluvium?

A

Stressful insult –> Shunts hair follicles into premature Telogen phase (cessation of anagen and transition through Catagen) –> 2-3 month delay before shedding occurs.
Any severe stress can cause it, but common ones include:
- Childbirth
- High fever
- Weight loss, crash dieting, malnutrition
- Trauma (inc. surgery, haemorrhage)
- OCP cessation

65
Q

Clinical features of Telogen effluvium?

A 
Triad of:
- Stress event 2-3 months prior
- Diffuse hair loss
- White bulbs
Patients may describe large clumps of hair with white bulbs going out with gentle shampooing or tugging
66
Q

Natural course of Telogen effluvium?

A

Spontaneous recovery occurs within 6 months
Chronic idiopathic form persists longer - episodes of dramatic shedding that recover but recur weeks-months later - is self limiting and does not usually require treatment. Consider androgenetic alopecia in these patients.

67
Q

Management of Telogen effluvium?

A

Education (esp. if <6 months since hair loss)
Correction of stress factors
Pharmacotherapy (if concerned) - Topical minoxidil x 4 months
Specialist referral if relapsing or incomplete recovery

68
Q

Define Anagen effluvium

A

Hair loss during the anagen phase. It is caused by immediate metabolic arrest of hair follicles in the anagen phase, which can be caused by chemotherapy or radiotherapy to the scalp.

69
Q

Clinical features of anagen effluvium?

A

Triad of:

  • Recent chemotherapy/radiotherapy
  • Diffuse hair loss
  • Long pigmented hair bulb
70
Q

By what general mechanisms do drugs cause alopecia?

A

Drugs cause alopecia by either:

  • Telogen effluvium
  • Anagen effluvium
  • Acceleration of androgenetic alopecia
71
Q

What is the most common form of alopecia?

A

Androgenetic alopecia

Medicine - GP (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions