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Phase 3a General Practice and Community > New GP Derm > Flashcards

New GP Derm Flashcards

1
Q

What is the medical term for acne?

A

Acne vulgaris

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1
Q

What is acne caused by?

A

Chronic inflammation
+/- localised infection in pockets within the skin (pilosebaceous unit)

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2
Q

What is a pilosebaceous unit?

A

Tiny dimpes in the skin containing haor follicles + sebaceous glands

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3
Q

What do the sebaceous glands produce?

A

Natural skin oils + sebum (waxy substance)

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4
Q

How does acne develop?

A

Acne results from:
* Increased sebum production → trapping of keratin (dead skin cells) → blockage of the pilosebaceous unit
* → Swelling + inflammation in the pilosebaceous unit

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5
Q

What increases and decreases the production of sebum?

A
  • Androgenic hormones = increase sebum production (hence why acne is exacerbated by puberty)
  • Anti-androgenic hormonal contraception = decreases sebum production
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6
Q

What type of acne does bacteria play a major role in?

A

Propionibacterium acnes
(Bacteria colonises the skin → excessive bacteria growth = can exacerbate acne)
(Treatments = aim to reduce these bacteria)

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7
Q

Define macules

A

Flat marks on the skin

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8
Q

Define papules

A

Small lumps on the skin

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9
Q

Define pustules

A

Small lumps containing yellow pus

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10
Q

Define comedones

A

Skin coloured papules representing blocked pilosebaceous units

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11
Q

Define blackheads

A

Open comedones with black pigmentation in the centre

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12
Q

Define ice pick scars

A

Small indentations in the skin that remain after acne lesions heal

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13
Q

Define hypertrophic scars

A

Small lumps in the skin that remain after acne lesions heal

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14
Q

Define rolling scars

A

Irregular wave-like irregularities of the skin that remain after acne lesions heal

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15
Q

What are the aims of acne vulgaris treatment?

A
  • Reduce symptoms
  • Reduce risk of scarring
  • Minimise the psychosocial impact
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16
Q

Name the options for the management for acne and what order is the stepwise fashion (based on severity + response to treatment)?

A
  • No treatment (if mild)
  • Topical benzoyl peroxide (↓ inflammation, unblock skin, toxic to P. acnes bacteria)
  • Topical retinoids (chemicals related to vitamin A; ↓ sebum production)
  • Topical antibiotics (clindamycin) + benzoyl peroxide (↓ antibiotic resistance)
  • **Oral antibiotics (lymecycline) **
  • Oral contraceptive pill (stabilse hormones + ↓ sebum production) (Dianette = most effective combined contraceptive pill)
  • Oral retinoids (isotretinoin) (highly teratogenic)
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17
Q

What is an effective last-line option for severe acne?

A

Oral retinoids e.g. isotretinoin
* Prescribed by specialist after other methods fail
* Follow-up + reliable contraception
* ** = Highly teratogenic**

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18
Q

What is the most effective combined contraceptive pill for acne treatment?

A

Co-cyprindiol (Dianette)
= Most effective due to its anti-androgenic effects
= High thromboembolism risk → discontinued after acne is controlled (not prescribed long-term)

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19
Q

How are oral retinoids (isotretinoin) (e.g. Roaccutane) effective?

A
  • Reduce sebum production
  • Reduce inflammation
  • Reduce bacterial growth
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20
Q

Name a side effect of oral isotretinoin?

A
  • Dry skin and lips
  • Photosensitivity of the skin to sunlight
  • Depression, anxiety, aggression and suicidal ideation (patients should be screened for mental health issues prior to starting treatment)
  • Rarely Stevens-Johnson syndrome and toxic epidermal necrolysis
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21
Q

What is psoriasis

A

A chronic autoimmune condition that causes recurrent symptoms of psoriatic skin lesions

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22
Q

Is psoriasis genetic?

A

Clear genetic component - but no clear genetic inheritance

Approx. 1/3 patients have a first degree relative with psoriasis

Symptoms start in childhood in a 1/3 of patients

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23
Q

In basic terms, how does psoriasis present?

A

Patches of psoriasis are dry, falky, scaly, faintly erythematous skin lesions in raised + rough plaques - commonly over extensor surfaces of the elbows + knees + scalp

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24
Q

Simple pathophysiology of psoriasis

A

Skin changes = caused by the rapid generation of new skin cells → resulting in an abnormal buildup thickening of skin in those areas

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25
Q

What are the types of psoriasis?

A
  • Plaque psoriasis
  • Guttate psoriasis
  • Pustular psoriasis
  • Erythrodermic psoriasis
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26
Q

How does plaque psoriasis present?

A
  • Thickened erythematous plaques with silver scales
  • Commonly seen on the extensor surfaces + scalp
  • Plaques are 1-10cm diameter

(Most common form of psoriasis in adults)

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27
Q

How guttate psoriasis present? And how in?

A

Guttate psoriasis = 2nd most common form of psoriasis, commonly presents in children

  • Many small raised papules across the trunk + limbs
  • Papules = mildy erythematous + can be slightly scaly
  • Over time, the papules → turn into plaques
  • Guttate psoriasis = often triggered by a streptococcal infection, stress or medications
  • Often resolves spontaneously within 3-4 months
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28
Q

What is guttate psoriasis often triggered by?

A

Streptococcal throat infection

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29
Q

What is pustular psoriasis?

A
  • Rare severe form of psoriasis
  • Pustules = form under areas of erythematous skin
  • The pus in these areas = not infectious
  • Can be systemically unwell
  • Treated as medical emergency - require hospital admission
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30
Q

What is erytherodermic psoriasis?

A
  • Rare severe form of psoriasis
  • Extensive erythematous inflamed areas - covering most of the surface of the skin
  • The skin = comes away in large pathches (exfoliation) → resulting in raw exposed areas
  • Medical emergency - requires hopsital admission
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31
Q

What form of psoriasis is most common in children, that is often triggered by a throat infection?

A

Guttate psoriasis

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32
Q

How might psoriasis present differently in children from adults?

A

In children - psoriasis plaques may be smaller, softer and less prominent

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33
Q

What are the 3 specific signs suggestive of psoriasis?

A
  • Auspitz sign → small points of bleeding when plaques are scraped off
  • Koebner phenomenon → development of psoriatic lesions to areas of skin affectsed by trauma
  • Residual pigmentation of the skin after lesions resolve
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34
Q

How can a diagnosis of psoriasis be made?

A

Clinical diagnosis - based on the appearance of the lesions

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35
Q

What is the management for psoriasis?

A
  • **Topical steroids **
  • Topical vitamin D analogues (calcipotriol)
  • Topical dithranol
  • Topical calcineurin inhibitors (tacrolimus) are usually only used in adults
  • Phototherapy with narrow band ultraviolet B light is particularly useful in extensive guttate psoriasis
  • Severe + difficult to treat:** Methotrexate, cyclosporine, retinoids, biologic medications**
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36
Q

What are the two commonly used products prescribed for psoriasis?
(They contain a potent steroid + vitamin D analogue)

A
  • Dovobet
  • Enstilar
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37
Q

What are some associations of psoriasis?

A
  • Nail psoriasis (nail changes that occur in psoriasis) → nail pitting, thickening, discolouration, ridging, onycholysis (separation of the nail from bed)
  • Psoriatic arthritis (10-20%) → usually occurs within 10 years of skin changes - middle age
  • Psychosocial → mood, self-esteem, social acceptance → depression + anxiety
  • Other co-morbidities that increase the risk of cardiovascular disease are associated with psoriasis, particularly obesity, hyperlipidaemia, hypertension and type 2 diabetes.
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38
Q

What is impetigo?

A

A superficial bacterial skin infection - usually caused by a staphylococcus skin infection
Occurs when bacteria enter via a break in the skin

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39
Q

What are the 2 common causative organisms of impetigo?

A
  • Staphylococcus aureus (most common)
  • Streptococcus pyogenes
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40
Q

What is the characteristic feature of impetigo caused by a staphylococcus skin infection?

A

A ‘golden crust’

41
Q

What are two classifications of impetigo?

A
  • Non-bullous
  • Bullous
42
Q

Is impetigo contagious?

A

Yes very!
(Keep kids off of school)

43
Q

How does non-bullous present?

A
  • Non-bullous impetigo = typically occurs around the nose or mouth
  • Exudate from the lesions → dries to form a ‘golden crust’
  • Do not usually cause systemic symptoms or make the person unwell
44
Q

Management of non-bullous impetigo?

A
  • First line: Topical fusidic acid or hydrogen peroxide topical (1%)
  • Second line: Oral flucloxacillin (more widespread or severe impetigo)
45
Q

What is bullous impetigo caused by?

A

Staphylococcus aureus bacteria

46
Q

What is the pathophysiology of bullous impetigo?

A
  • Staphylococcus aureus = produce epidermolytic toxins that break down proteins that hold skin cells together → causes 1-2cm fluid filled vesicles to form → grow → burst → form ‘golden crust’ → heal without scarring
  • Lesions = can be painful + itchy
47
Q

Who does bullous impetigo typically present in?

A
  • Neonates + children (under 2) (most common)
  • Older children
  • Adults
48
Q

Which type of impetigo is likely to cause patients to have systemic symptoms (feverish + generally unwell)?

A

Bullous impetigo

49
Q

What is the condition called in which bullous impetigo becomes widespread?

A

Staphylococcus scalded skin syndrome

50
Q

What are the Ix for impetigo?

A
  • First line: Clinical diagnosis
  • Gold standard: Bacterial skin culture
51
Q

What is the management for bullous impetigo?

A

Oral or IV flucloxacillin

IV if very unwell or at risk of complications

52
Q

Name two complications of impetigo

A
  • Cellulitis if the infection gets deeper in the skin
  • Sepsis
  • Scarring
  • Post streptococcal glomerulonephritis
  • Staphylococcus scalded skin syndrome
  • Scarlet fever
53
Q

What is folliculitis?

A

Folliculitis = an inflammatory process involving any part of the hair follicle

Folliculitis = most commonly secondary to infection

54
Q

Causative organisms of follicultitis

A
  • Bacterial (most commonly staphylococcus aureua)
  • Fungal
  • Viral
  • Parasitic
55
Q

What subset of patients can folliculitis particulary develop in?

A

Folliculitis can occur in patients with acne undergoing long-term oral antibiotic therapy and may mimic an acne flare.

56
Q

Risk factors for folliculitis

A
  • Trauma (shaving + extraction)
  • Topical corticosteroid preparations
  • Diabetes mellitus
  • Immunosuppression (can cause eosinophilic folliculitis)
  • Hot-tub use (‘hot-tub folliculitis - caused by Pseudomonas aeruginosa)
  • Chronic inflammatory skin disease
57
Q

A 26-year-old woman presents to the GP complaining of an erythema on her left leg. She admits to shaving the area 2-3 days ago. On examination, there is a small cluster of erythematous papules. A short course of oral antibiotics completely resolves the issue. Possible diagnosis?

A

Folliculitis

58
Q
A
59
Q
A
60
Q

Signs and symptoms of folliculitis

A

Signs:
* Localised to shaving area
* Blistering (if severe)
* Subdermal mass (abscess formation if can occur in severe disease)
* Raised eosinophils

Symptoms:
* Erythema
* Papules (small, clusters)
* Pustules (small, white-headed)
* Pruritus (localised to affected area)

61
Q

Investigations for folliculitis

A

Uncomplicated, superficial folliculitis is often managed in General Practice without the need for further investigation.

However, severe, persistent or recurrent episodes may warrant further tests:
* Bacterial skin swab: gram-positive cocci in Staphylococcus aureus infection
* Viral skin swab: moulding and clustering of keratinocytes is suggestive of Herpes simplex infection
* Skin scraping for mycology: hyphal forms seen in dermatophyte infection
* Skin biopsy: neutrophilic infiltrate in bacterial and fungal disease, lymphocytic in viral

62
Q

Management of folliculitis

A

Conservative:
* Using clean, sterile razors for shaving
* Wearing loose clothing
* Antibacterial soap use
* Avoiding hot-tub use

Medical:
* Mild (all organisms): self limiting, no treatment required or trial of topical antibiotics
* Moderate (bacterial): oral flucloxacillin (Staph aureus) or oral ciprofloxacin (Pseudomonas spp.)
* Moderate (viral): oral aciclovir
* Moderate (fungal): ketoconazole, fluconazole, itraconazole

Surgical:
* Incision + drainage
* IV antibiotics

63
Q

Complications of folliculitis

A
  • Abscess formation (in severe infection)
  • Sepsis (in severe infection)
  • Scarring
64
Q

A 10-year-old child presents with multiple small, firm, rough bumps on his hands. The lesions are skin coloured and have been present for a couple of months and are slowly increasing in size. They are not painful but the child is concerned about their appearance. Possible diagnosis?

A

Cutaneous warts

65
Q

What virus are cutaneous (common warts) caused by?

A

Human papillomavirus (HPV) type 2 and 4
(Genital warts HPV 6 and 11)

The virus invades the skin through small cuts or abrasions and causes rapid growth of cells on the outer layer of the skin, leading to the formation of a war

66
Q

Signs and symptoms of cutaneous warts

A

Signs:
* Firm, rough papules or nodules
* Interrupted skin lines over the warts
* Black dots within the wart (thrombosed capillaries)

Symptoms:
* Often asymptomatic
* Ocassionaly tender (particularly verrucas)

67
Q

Investigations for cutaneous warts

A

Warts = typically diagnosed based on their characteristic clinical appearance

Investigations to consider:
* Biopsy

68
Q

Management of cuatneous warts (common warts)

A

First-line:
* Watchful waiting (especially children)
* Topical salicylic acid

Second-line:
* Cryotherapy (involves freezing the wart with liquid nitrogen and is typically used if topical salicylic acid is ineffective)
* Immunotherapy

69
Q

A 34-year-old farmer attends his GP due to persistent erythema and pruritus on his hands following the use of certain weedkillers. A skin-patch test reveals the particular allergen and subsequent avoidance of the substance has improved his symptoms. Possible diagnosis?

A

Contact dermatitis

70
Q

Info: Pathophysiology of contact dermatitis

A

Contact dermatitis is a skin reaction caused by an external agent [1]. Contact dermatitis can be either:

  • Irritant contact dermatitis (ICD)
  • Allergic contact dermatitis (ACD)

ICD is caused by direct toxicity by an agent, whereas ACD is a delayed hypersensitivity reaction

71
Q

Risk factors for contact dermatitis

A
  • Occupation with frequent exposure to water and caustic material: compromise of the epidermal barrier allows penetration by allergens, e.g. labourers, farmors, chefs
  • History of atopic eczema
72
Q

Signs and symptoms of contact dermatitis

A

Signs:
* Acute onset: ICD (minutes to hours for severe irritants) ACD (24-72 hours if previously sensitised)
* Affecting hands + face
* Sparing of non-exposed areas
* Persistence of symptoms: ICD can take 3-6 weeks to resolve, ACD usually resolves within a few days
* Scaling: chronic contact dermititis
* Lichenification: chronic contact dermatitis

Symptoms:
* Erythema
* Pruritis (more in ACD than ICD)
* Burning (more in ICD than ACD)
* Vesicles (more common in ACD than ICD)

73
Q

Investigations for contact dermatitis

A
  • Skin patch testing: to identify allergen
  • Repeated open application test: to reproduce ACD at application site
74
Q

Management of contact dermatitis

A

IRRITANT CONTACT DERMITITIS:
* First-line: Avoidance of irritant + skin emollients (simple moisturisers)
* Second-line: Topical corticosteroids (hydrocortisone, betamethasone)

ALLERGIC CONTACT DERMITITIS
* First-line: Avoidance of allergen + topical corticosteroids (hydrocortisone, betamethasone)
* Second-line: Topical calcineurin inhibitors: tacrolimus, pimecrolimus
* Third-line (or severe disease): oral corticosteroids (prednisolone, dexamethasone); phototherapy; immunosuppressants (azathioprine, ciclosporin)

75
Q

Complications of contact dermatitis

A
  • Secondary impetigo: bacterial infection due to compromised skin barrier
  • Post-inflammatory hyperpigmentation
76
Q

What is an ‘exanthem’?

A

An exanthem = an eruptive widespread rash

77
Q

What are the 6 viral exanthemas?

A

First disease: Measles
Second disease: Scarlet Fever
Third disease: Rubella (AKA German Measles)
Fourth disease: Dukes’ Disease
Fifth disease: Parvovirus B19
Sixth disease: Roseola Infantum

“My Sister Really Doesn’t Pick Rashes.”

78
Q

What are the clinical features of measles?

A
  • Fever
  • Coryzal
  • Conjunctivitis
  • Koplik spots (greyish white spots on the buccal mucosa) → appear 2 days after feber → pathognomic for measles
  • RASH (erythematous macular rash with flat lesions): starts on face (classically behind the ears) (3-5 days after fever) → spreads to rest of body

Koplik spots = pathognomonic for measles, meaning if a patient has Koplik spots, you can diagnose measles.

79
Q

Treatment of measles

A
  • Measles = self resolving after 7 – 10 days of symptoms.
  • Children should be isolated until 4 days after their symptoms resolve.
  • Measles = a notifiable disease and all cases need to be reported to public health.
  • 30% of patients with measles develop a complication.
80
Q

Complications of measles

A
  • Pneumonia
  • Diarrhoea
  • Dehydration
  • Encephalitis
  • Meningitis
  • Hearing loss
  • Vision loss
  • Death
81
Q

What is scarlet fever caused by?

A

Scarlet fever = caused by Group A streptococcus infection → usually tonsilitis (not caused by a virus)

Specifically an endotoxin produced by streptococcus pyogenes (group A strep) bacteria

82
Q

Characteristic features of Scarlet fever

A
  • Strawberry tongue
  • Red-pink blotchy, macular rash with ‘sandpaper’ skin (trunk → spreads outwards)
  • Red flushed cheeks (usually)
83
Q

Clinical features of Scarlet fever

A
  • Strawberry tongue
  • Red-pink blotchy, macular rash with ‘sandpaper’ skin (trunk → spreads outwards)
  • Red flushed cheeks (usually)
  • Cervical lymphadenopathy
  • Sore throat
  • Fever
  • Lethargy
84
Q

Treatment of Scarlet fever

A

Phenoxymethylpenicillin (penicillin V) for 10 days

(To treat the underlying streptococcal bacterial infection)

85
Q

Is Scarlet fever a notifiable disease?

A

Yes

Children should be kept off school until 24 hours after starting antibiotics.

86
Q

Apart from Scarlet fever, what other conditions can group A streptococcus cause?

A
  • Post-streptococcal glomerulonephritis
  • Acute rheumatic fever
87
Q

Clinical features of Rubella

A
  • Milder erythematous macular rash (face → rest of body) (more mild than measles) - lasts 3 days
  • Mild fever
  • Joint pain
  • Sore throat
  • Lymphadenopathy (behind ears + back of neck)
88
Q

Management of Rubella

A
  • Supportive + self-limiting
  • Notifiable disease to public health
  • Children should stay off school for at least 5 days after the rash appears.
  • Children should avoid pregnant women.
89
Q

Complications of Rubella

A

Rare:
* Thrombocytopenia
* Encephalitis

90
Q

Why is rubella so dangerous in pregnancy?

A

Rubella in pregnancy → can lead to congenital rubella syndrome

Rubella syndrome (triad):
* Deafness
* Blindness
* Congenital heart disease

91
Q

What is Duke’s disease?

A

No specific organism has been found

It is very common for children to get non-specific “viral rashes”. It is likely that “fourth disease” was used to describe these non-specific viral rashes that are now understood to be caused by many potential viruses

BS really?

92
Q

What virus causes slapped cheek syndrome (erythema infectiosum)?

A

Parvovirus B19 virus

93
Q

Clinical features of slapped cheek syndrome (erythema infectiosum)

A

Starts:
* Mild fever
* Coryza
* Non-specific viral symptoms (muscle aches, lethargy)

After 2-5 days:
* Rash appears rapidly: bright red rash on both cheeks

Few days later:
* Reticular midly erythematous rash (trunk + limbs) - can be raised + itchy

94
Q

Treatment for slapped cheek syndrome

A
  • Supportive (plenty of fluids + simple analgesia)

It is infectious prior to the rash forming, but once the rash has formed they are no longer infectious and do not need to stay off school.

95
Q

Which patients are at risk of developing complications when infected with parvovirus B19 (slapped cheek syndrome)?

A
  • Immunocompromised patients
  • Pregnant women

Patients with haemoatological conditions:
* Sickle cell anaemia
* Thalassaemia
* Hereditary spherocytosis
* Haemolytic anaemia

These patients need:
* Serology testing → to confirm diagnosis
* Full blood count + reticulocyte count → check for aplastic anaemia

People that would be at risk of complications that have come in contact with someone with parvovirus prior to the rash forming, should be informed and may need investigations.

96
Q

What are some major complications parvovirus B19 infection?

A
  • APLASTIC ANAEMIA
  • Encephalitis or meningitis
  • Pregnancy complications including fetal death
  • Rarely hepatitis, myocarditis or nephritis
97
Q

What viruses cause Roseola Infantum?

A

Human herpes virus 6 (HHV-6) and less frequently by human herpes virus 7 (HHV-7)

98
Q

Clinical features of Roseola Infantum

A

Infection → 1-2 weeks → high fever (up to 40C) comes on suddenly - lasts for 3-5 days → disappears suddenly

  • Coryzal symptoms
  • Sore throat
  • Swollen lymph nodes
  • When the fever settles → rash appears for 1-2 days
  • Rash = mild erythematous macular rash across arms + legs + trunk + face → not itchy
99
Q

Main complication of Roseola Infantum

A

Febrile convulsions - due to the high temperature

Immunocompromised patients = may be at risk of rare complications:
* Myocarditis
* Thrombocytopnia
* Guillain-Barre syndrome

Phase 3a General Practice and Community (14 decks)

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