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Phase 3a - GP > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is atopic dermatitis?

A

aka eczema. Chronic, autoimmune, pruritic inflammatory skin condition.

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2
Q

What is the atopic triad and how are they linked?

A
  1. Atopic dermatitis
  2. Allergic rhinitis
  3. Asthma

Associated cdtns have an increased IgE and if someone has atopic dermatitis they’re more likely to develop either allergic rhinitis or asthma or both.

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3
Q

RF for atopic dermatitis

A
  1. Family history
  2. Allergies
  3. Environmental triggers - changes in temperature, certain dietary products, washing powders, cleaning products and emotional events or stresses
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4
Q

What inherited abnormality causes eczema?

A

Loss of filaggrin gene

Note: Filaggrins are filament-associated proteins which bind to keratin fibres in the epidermal cells and therefore a loss of this can cause disordered barrier function.

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5
Q

Sx of atopic dermatitis

A

Acute:
red (erythematous)
weeping/crusted (exudative)
blisters (vesicles or bullae)

Chronic:
skin becomes less red but thickened (lichenified) and scaly
cracking of the skin (fissures)

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6
Q

Tx for atopic dermatitis

A

Emollients (thin or thick)
Topical steroids
Wet wraps

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7
Q

What is measles and is it a notifiable disease?

A

aka rubeola. A highly contagious viral infection.

Measles is a notifiable disease.

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8
Q

How is measles spread?

A

Airborne respiratory droplets

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9
Q

Who is at risk of measles?

A
  1. Infants who lost passive immunity from mother
  2. Unvaccinated traveller
  3. Immunodeficient travellers
  4. Pregnant women
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10
Q

Sx of measles

A

Prodrome (initial flu-like Sx):
Fever (40c)
Malaise
Loss of appetite
Conjunctivitis (red eyes)
Cough
Coryza (blocked or runny nose)
Exanthem (rash) - flat red spots appear 4th or 5th day after Sx start. Non-itchy rash begins on the face and behind the ears. Within 24hrs it spreads over the entire trunk and extremities.

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11
Q

Ix of measles

A

PCR - viral nasopharyngeal or throat swab
Blood and urine samples

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12
Q

Tx of measles

A

Mild: self limiting, supportive
If immunocompromised: ribavirin (antiviral)

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13
Q

How can measles and mumps be prevented?

A

Combined measles, mumps and rubella (MMR) vaccination with live attenuated vaccine.
Two dose vaccine strategy.

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14
Q

What is mumps and how is it spread?

A

A viral infection spread by respiratory droplets.
Notifiable disease

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15
Q

Sx of mumps

A

Prodrome (initial flu-like Sx):
Fever
Muscle aches
Lethargy
Reduced appetite
Headache
Dry mouth

Specific mumps Sx: Parotid gland swelling, either unilateral or bilateral

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16
Q

Ix of mumps

A

PCR testing - saliva swab

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17
Q

Tx of mumps

A

Self limiting, supportive tx

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18
Q

Describe pathophysiology of acne vulgaris

A
  1. Chronic inflammation in pockets within skin = pilosebaceous unit.
  2. Pilosebaceous units = tiny dimples containing hair follicles and sebaceous glands (produces sebum)
  3. Inc. sebum = trapped keratin (dead skin cells) = blockage pilosebaceous units = inc. swelling and inflammation (aka comedones)
  4. Androgenic hormones inc. sebum production = inc. sebum during puberty
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19
Q

What is the name of the bacteria that plays a role in acne vulgaris?

A

Propionibacterium acnes bacteria

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20
Q

Describe the appearance of lesions and scars in acne vulgaris

A

Macules - flat marks on skin
Papules - small, tender red pumps
Pustules - small lumps containing yellow pus
Comedones - skin coloured papules
Blackheads - open comedones w/ black pigmentation
Nodules - large painful red lumps

Ice pick scars - small indentations in skin that remain after acne lesions heal
Hypertrophic scars - small lumps in skin that remain after acne lesions heal
Rolling scars - irregular wave-like irregularities in skin that remain after acne lesions heal

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21
Q

Term to describe oily skin

A

Seborrhoea

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22
Q

Term to describe increased hair growth

A

Hirsutism

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23
Q

Tx of acne vulgaris

A

Topical benzoyl peroxide - reduce infl. + unblock skin
Topical retinoids - slow sebum production
Topical antibiotics - clindamycin
Oral abx - i.e. lymecycline
OCP - i.e. Co-cyprindiol (Dianette) stabilise hormone + dec. sebum production

Last line (if very severe) - oral retinoids i.e. isotretinoin

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24
Q

Why is it imp. to monitor oral retinoid intake?

A

Retinoids are highly teratogenic.

Needs careful follow-up and monitoring and reliable contraception in females.

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25
Q

Side effects of isotretinoin (oral retinoid)?

A

Dry skin and lips
Photosensitivity of the skin to sunlight
Depression, anxiety, aggression and suicidal ideation.

26
Q

What is impetigo?

A

A superficial, highly contagious bacterial skin infection.

27
Q

What 2 bacteria usually cause impetigo?

A

MC - Staphylococcus aureus

Less commonly - Streptococcus pyogenes

28
Q

What are RF for developing impetigo?

A
  1. Skin conditions: atopic dermatitis, contact dermatitis, scabies, chickenpox
  2. Skin trauma: lacerations, insect bites, thermal burns, abrasions
  3. Immunosuppression
  4. Warm, humid climate
  5. Poor hygiene
  6. Crowded environments.
29
Q

How is impetigo usually transmitted?

A

Through direct contact

30
Q

What are the two different types of impetigo?

A

Non-bullous

Bullous - more common in neonates and children under 2, always caused by staph aureus bacteria.

31
Q

Which part of the body are non-bullous and bullous impetigo commonly found?

A

Non-bullous - face (nose or mouth) or extremities

Bullous - face, trunk, extremities, buttocks, and perineal regions.

32
Q

Main clinical features of impetigo?

A

Both: The exudate from the lesions dries to form a “golden crust”

Non-bullous: no systemic sx
Bullous: Systemic sx, feverish and unwell.

33
Q

Tx of impetigo?

A

Non-bullous:
Topical fusidic acid
Antiseptic cream (hydrogen peroxide 1% cream)
If severe - Oral flucloxacillin

Bullous:
Oral flucloxacillin

Px should be advised to ISOLATE!!! It’s very CONTAGIOUS!!!

34
Q

Complications of impetigo? (2)

A

Cellulitis if the infection gets deeper in the skin
Sepsis
Scarring
Post streptococcal glomerulonephritis
Staphylococcus scalded skin syndrome
Scarlet fever

35
Q

What is shingles?

A

aka herpes zoster, viral infection caused by the varicella-zoster virus, which is the same virus that causes chickenpox.

The virus remains dormant in nerve tissues near spinal cord and can reactivate years later.

36
Q

Sx of shingles

A

Tingling or burning sensation in specific area of skin followed by development of painful rash (red band or cluster of fluid-filled blisters, usually on one side of the body or face)

Fever
Headache
Fatigue
Sensitivity to light

37
Q

Tx of shingles

A

Antiviral medication - e.g. acyclovir
Analgesia or NSAIDs
Topical treatments - e.g. lidocaine patches

38
Q

What is contact dermatitis?

A

aka contact eczema, group of skin disorders in which skin reaction is due to direct contact with the causative agent.
Dermatitis = outer layers of skin affected.

39
Q

What are features of contact dermatitis?

A

Erythema
Blisters - small (vesicles) or large (bullae)
Oedema
Dryness or scaling
Cracks (fissuring)
Lichenification (thickened, lined skin)
Pigmentation increased (hyperpigmentation) or reduced (hypopigmentation).

40
Q

Tx of contact dermatitis?

A

Avoid soap
Dry skin after washing
Short course of topical corticosteroid creams

If severe:
Oral corticosteroids e.g. oral prednisone
Phototherapy

41
Q

Define and describe each of the following cutaneous fungal infections:
1. Tinea corporis
2. Tinea pedis
3. Tinea cruris
4. Candida intertrigo

A
  1. Ringworm - Presents as round, erythematous, scaly lesions on the body.
  2. Athlete’s foot - erythema, scaling, and maceration, typically between the toes.
  3. Jock itch - erythematous, well-demarcated lesions in the groin area.
  4. erythematous, macerated patches in skin folds.
42
Q

What are warts?

A

Elevated, round, hyperkeratotic skin papules with a rough greyish-white or light brown surface. Although lesions may occur anywhere, they have a tendency to occur at sites prone to trauma, such as knees and elbows.

43
Q

Describe appearance of filiform warts

A

stalk-like appearance with multiple spikes

44
Q

RF of warts (3)

A

Human papillomavirus infection
water immersion
occupations involving handling of meat or fish
nail biting
age under 35 years

45
Q

What is folliculitis?

A

Inflammatory process involving any part of the hair follicle; it is most commonly secondary to infection.

46
Q

Where does folliculitis most commonly found on the body?

A

Areas with terminal hair growth, such as the head and neck region, axillae, groin and buttocks

47
Q

Which organism is folliculitis most commonly caused by?

A

Staphylococcus aureus
If hot tub - Pseudomonas aeruginosa

48
Q

What are the RF for developing folliculitis?

A

Recent hx of immersion in spa water
Medications - corticosteroids or lithium
Shaving
DM or immunosuppression

49
Q

Sx of folliculitis?

A

Umbilicated, flesh-coloured papules

50
Q

Ix for folliculitis?

A

Skin swab
Skin scraping
Tissue culture

51
Q

Tx of folliculitis?

A

If uncomplicated - self-limiting
If recurrent:
1. by staph aureus - oral cefalexin (abx) or topical therapy
2. MRSA - oral clindamycin
If hot tub folliculitis - topical benzoyl peroxide and if severe - ciprofloxacin

52
Q

Where does psoriasis commonly occur?

A

Extensor surfaces of the elbows and knees and on the scalp.

53
Q

Describe how skin changes occur in psoriasis.

A

Rapid generation of new skin cells, results in an abnormal build up and thickening of the skin in those areas - psoriatic skin lesions

54
Q

What kind of psoriasis are more common in children and how does it present?

A

Guttate psoriasis

** triggered by strep throat infection

Appearance:
- Many small raised papules across the trunk and limbs.
- The papules are mildly erythematous and can be slightly scaly.
- Overtime, papules turn into plaques

55
Q

Describe appearance of psoriatic patches + specific Sx that suggest psoriasis

A

Dry, flaky, scaly, faintly erythematous skin lesions that appear in raised and rough plaques.

Auspitz sign - small points of bleeding when plaques are scraped off
Residual pigmentation - after the lesions resolve

56
Q

Tx of psoriasis

A

Topical steroids
Topical vitamin D analogues (calcipotriol)
Topical dithranol
Topical calcineurin inhibitors (tacrolimus) - only used in adults

57
Q

What is urticaria?

A

aka hives. Small itchy lumps that appear on the skin. They may be associated with a patchy erythematous rash. This can be localised to a specific area or widespread.

58
Q

The release of what chemical causes urticaria?

A

Histamines

59
Q

RF of urticaria (2)

A

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites

60
Q

Tx of urticaria?

A

Antihistamines - fexofenadine

If severe - oral steroids

Phase 3a - GP (15 decks)

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