DERM Revision 4

Question 2

Describe the pathophysiology of rosacea [3]

Answer 2

Vascular dysregulation:
- Increased reactivity of capillaries to heat, results in flushing and telangiectasia

Inflammation

Ultraviolet radiation:
- Sun exposure may exacerbate rosacea by causing oxidative stress and inducing inflammation.

Question 3

Name and describe this association of rosacea [1]

Answer 3

Rhinophyma
* Men
* Nose enlarges, reddens and becomes rugose

Question 4

Describe the tx for rosacea
- simple measures
- for predominant erythema or flushing? [2]
- Mild/moderate papules [2]
- Moderate/severe papules [2]
- Telangiectasia that hasn’t resolved despite treatment [1]

Answer 4

Simple:
- recommend daily application of a high-factor sunscreen
- camouflage creams may help conceal redness

Flushing:
- Topical brimonidine gel (alpha adrenergic agonist) - as required basis’ to temporarily reduce redness’

Mild/moderate papules:
- topical ivermectin is first-line (CKS)
- alternatives include: topical metronidazole or topical azelaic acid

Moderate / severe papules:
- combination of topical ivermectin + oral doxycycline
- isotretinoin

refractory, prominent telangiectasia:
- laser therapy

NB: steroids not used in rosacea

Question 6

What are the 4 subtypes of rosacea? [4]

Answer 6

Erythematotelangiectatic rosacea (ETR):
- Characterized by facial redness, flushing, and visible blood vessels (telangiectasias).

Papulopustular rosacea:
- Presents with acne-like breakouts, including papules and pustules, along with facial redness and swelling.

Phymatous rosacea:
- Associated with skin thickening, especially around the nose (rhinophyma), and can also affect the chin, forehead, cheeks, and ears.

Ocular rosacea:
- Involves the eyes, causing redness, burning, itching, and the sensation of a foreign body. It can lead to complications such as blepharitis, conjunctivitis, and keratitis if not treated promptly.

Question 7

Which subtype of rosacea is shown? [1]

Answer 7

Phymatous rosacea: Associated with skin thickening, especially around the nose (rhinophyma), and can also affect the chin, forehead, cheeks, and ears.

Question 8

How do you differentiate rosacea to seborrhoeic dermatitis? [1]

Answer 8

Yellow greasy scales on an erythematous base in a seborrhoeic distribution (peri-orificial and on the scalp). Usually scaly.

Question 9

Answer 9

topical ivermectin

Question 10

Answer 10

Epistaxis

Question 11

Answer 11

topical brimonidine

Question 12

Answer 12

topical ivermectin + oral doxycycline

Question 13

What are the different classes of cellulitis

Answer 13

Class I:
- There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities

Class II:
- The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection

Class III:
- The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize

Class IV:
- The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

Question 14

Which patients do you admit for cellulitis? [6]

Answer 14

• Has Eron Class III or Class IV cellulitis.
• Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
• Is very young (under 1 year of age) or frail.
• Is immunocompromized.
• Has significant lymphoedema.
• Has facial cellulitis (unless very mild) or periorbital cellulitis.

Question 15

How do you manage Class III/IV Cellulitis? [2]

Answer 15

Eron Class III-IV
* admit
* NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone

General points
* mark the area of erythema to detect spreading cellulitis
* if possible elevate the leg
* consider paracetamol or ibuprofen for pain or fever

Question 16

Answer 16

Co-amoxiclav

Question 17

Describe the pathophysiology of pressure sores [3]

Answer 17

sequence of events initiated by unrelieved pressure:
- Ischaemia: when external pressure exceeds capillary closing pressure, it leads to occlusion of blood vessels causing ischaemia in the affected area. This deprives tissues of oxygen and nutrients leading to cell death and necrosis.
- Reperfusion injury: Upon relief from sustained pressure, reperfusion occurs. However, this sudden influx of blood can cause further damage due to oxidative stress and inflammation.
- Tissue distortion: Continuous mechanical stress can distort and damage cells directly.

Question 18

Describe the stages in the development of pressure sores [4]

Answer 18

Non-blanchable erythema::
- Initial presentation involves reddening of the skin that does not turn white (non-blanchable) when pressed.
- The affected area may feel differently than surrounding skin – warmer or cooler, firmer or softer.

Partial-thickness skin loss:
- With continued pressure, there is partial-thickness loss involving epidermis or dermis.
- It presents as a shallow open ulcer with a red-pink wound bed without sloughing.

Full-thickness skin loss:
- Prolonged unrelieved pressure results in full-thickness tissue loss exposing subcutaneous fat but not muscle or bone. Slough may be present along with undermining or tunneling.

Full-thickness tissue loss with exposed bone, muscle or tendon:
- This is the most severe form of pressure sore where there is extensive destruction and necrosis extending to underlying structures.

Question 19

Beyond the 4 stages of pressure sores, what two categories of pressure sore exist? [2]

Answer 19

Unstageable Pressure Sores:
- This classification is used when the base of the ulcer is covered by slough (yellow, tan, grey, green or brown) and/or eschar (tan, brown or black) in the wound bed, making it impossible to determine its depth.

Suspected Deep Tissue Injury (SDTI):
- SDTI is characterised by a purple or maroon localised area of discoloured intact skin or a blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.

Question 20

How do you prevent / manage pressure sores [4]

Answer 20

Regular repositioning every 2 hours for bed-bound patients and hourly for those in chairs.

Maintain skin integrity by keeping skin clean and dry. Use mild soap and warm (not hot) water for cleaning

Dressings:
- Alginate dressings are useful for exuding wounds;
- Hydrocolloid dressings can be used for non-exuding wounds.

Administer analgesics as required. Regularly reassess pain levels.

Question 21

Describe the basic pathophysiology of follicultiis

Answer 21

1. Bacterial colonisation within the hair follicle (especially if there is any damage or disruption to skin barrier)
2. An inflammatory response is triggered; leads to follicular wall rupture causing it to break down and release its contents (including bacteria) into the surrounding dermis.
3. Leads to a cycle of ongoing tissue damage and repair

Question 22

Asides from pain, itching and small red inflamed papules, what is a key localised symptom seen in folliculitis? p[1]

Answer 22

Follicular hyperkeratosis: This describes thickening or roughness of the skin surrounding the hair follicle, which can be a feature in chronic cases.

Question 23

Name this subtype of folliculitis [1]

Answer 23

Pseudofolliculitis barbae: This is a specific type of folliculitis that commonly affects men with curly hair.
- It presents as inflammation and bumps in the beard area due to ingrown hairs.

Question 24

What is the name for this form of folliculitis? [1]

Answer 24

Folliculitis decalvans
- A chronic form of deep folliculitis that leads to scarring and permanent hair loss, usually on the scalp. Patients may present with painful, red plaques containing pustules around hair follicles.

Question 25

How do you differentiate acne vulgaris to folliculitis?

Answer 25

Acne vulgaris predominantly affects the face and upper trunk where there is a high density of sebaceous glands.

folliculitis can occur anywhere on the body where hair follicles are present.

Question 26

Treatment algorithm for folliculitis? [2]

Answer 26

Topical treatments
* Mild cases can often be managed with topical antiseptics (e.g., chlorhexidine) or antibiotics (e.g., fusidic acid).
* If fungal infection suspected (e.g., Pityrosporum folliculitis), consider antifungal creams or shampoos containing ketoconazole.

Systemtic treatments:
- In severe or recurrent cases, consider oral antibiotics that cover Staphylococcus aureus (e.g., flucloxacillin).

Question 27

Why might reoccurring folliculitis occur? [2]

Answer 27

Antibiotic resistance or due to an an underlying disease such as diabetes

Question 28

Name these complications of folliculitis [1]

Answer 28

Question 29

Name for this? [1]

Answer 29

Sycosis barbae
- A specific type of deep folliculitis affecting the beard area in men, leading to scarring and hair loss if left untreated.

Question 30

A patient has a PMH of HIV.

Present with what appears to be folliculitis.

Which type of folliculitis is this most likely to be? [1]

Answer 30

Eosinophilic folliculitis: A variant seen in immunocompromised patients (e.g., HIV/AIDS) presenting with recurrent itchy papules and pustules predominantly on the face and upper body.

Question 31

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Describe the difference between irritant and allergic contact dermatitis

Answer 31

Irritant Contact Dermatitis
- The process commences when an irritant breaches the stratum corneum, the outermost layer of the skin. This occurs because of direct physical or toxic damage to skin cells.

Allergic contact dermatitis:
- involves skin inflammation via an underlying allergic process (type 4 delayed hypersensitivity reaction). Allergy usually develops after an initial sensitisation event.

Question 32

How do you differentiate atopic dermatitis to contact determatitis? [1]

Answer 32

Atopic dermatitis frequently has an early onset in childhood and may be associated with a personal or family history of atopy.

Atopic dermatitis typically affects the flexural surfaces such as the antecubital and popliteal fossa; this contrasts with contact dermatitis where lesions tend to localise to areas of direct exposure.

Question 33

Management of contact dermatitis?

Answer 33

Avoiding allergens

Topical corticosteroids are first-line treatment for acute flares.

Question 34

What clinical sign often helps to distinguish that a patient is suffering from irritant contact dermatitis c.f allergic?

Answer 34

the sentinel sign - and is commonly caused by prolonged contact with water.

Question 35

Urticaria is which type HS reaction? [1]

Answer 35

Type 1 (IgE mediated)

Question 36

How do you manage urticaria? [3]

Answer 36

It is critical that all patients presenting with urticaria are assessed for a more systemic allergic reaction (e.g. anaphylaxis) or angio-oedema affecting the airway due to laryngeal oedema

non-sedating antihistamines (e.g. loratadine or cetirizine) are first-line
- NICE Clinical Knowledge Summaries suggest continuing these for up to 6 weeks following an episode of acute urticaria CKS

a sedating antihistamine (e.g. chlorphenamine) may be considered for night-time use (in addition to day-time non-sedating antihistamine) for troublesome sleep symptoms CKS

prednisolone is used for severe or resistant episodes

Question 37

Answer 37

Generalised hyperpigmentation - Addisons disease