DERM Revision 4 Flashcards
Kaposi’s sarcoma is a vascular tumour that often presents as purple-red macules or nodules on the skin, commonly affecting the lower extremities. This form of Kaposi’s sarcoma is typically seen in elderly men of [] or [] descent.
Kaposi’s sarcoma is a vascular tumour that often presents as purple-red macules or nodules on the skin, commonly affecting the lower extremities. This form of Kaposi’s sarcoma is typically seen in elderly men of Mediterranean or Eastern European descent.
Describe the pathophysiology of rosacea [3]
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.
Name and describe this association of rosacea [1]
Rhinophyma
* Men
* Nose enlarges, reddens and becomes rugose
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]
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
What are the 4 subtypes of rosacea? [4]
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.
Which subtype of rosacea is shown? [1]
Phymatous rosacea: Associated with skin thickening, especially around the nose (rhinophyma), and can also affect the chin, forehead, cheeks, and ears.
How do you differentiate rosacea to seborrhoeic dermatitis? [1]
Yellow greasy scales on an erythematous base in a seborrhoeic distribution (peri-orificial and on the scalp). Usually scaly.
topical ivermectin
Epistaxis
topical brimonidine
topical ivermectin + oral doxycycline
What are the different classes of cellulitis
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
Which patients do you admit for cellulitis? [6]
- 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.
How do you manage Class III/IV Cellulitis? [2]
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
Co-amoxiclav
Describe the pathophysiology of pressure sores [3]
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.
Describe the stages in the development of pressure sores [4]
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.
Beyond the 4 stages of pressure sores, what two categories of pressure sore exist? [2]
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.
How do you prevent / manage pressure sores [4]
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.
Describe the basic pathophysiology of follicultiis
- Bacterial colonisation within the hair follicle (especially if there is any damage or disruption to skin barrier)
- 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.
- Leads to a cycle of ongoing tissue damage and repair
Asides from pain, itching and small red inflamed papules, what is a key localised symptom seen in folliculitis? p[1]
Follicular hyperkeratosis: This describes thickening or roughness of the skin surrounding the hair follicle, which can be a feature in chronic cases.
Name this subtype of folliculitis [1]
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.
What is the name for this form of folliculitis? [1]
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.
