Tips from short courses, lectures, journals & podcasts

Question 1

Jameson, a 35-year-old mortgage broker, presents to his GP regarding a progressive growth on his right upper eyelid. The lesion began six months ago as a flat purplish patch of skin. Jameson reports that it became more like a “raised fleshy bump” two months ago. The initial lesion was painless, but it is now quite sore, which prompted him to seek medical attention. He reports that it is not impacting his vision and there is no history of trauma. Jameson was diagnosed with HIV 12 months ago. After some deliberation, he decided to start antiretroviral therapy one month ago, along with his partner, Gareth. He has no other significant medical history.

a) What is it and what are the ddx?
b) What is the aetiology?
c) *asked in answer section
d) Describe Dx and Rx.

Answer 1

a) Kaposi Sarcoma
ddx: Haemangioma, BBC, Pyogenic Granuloma, SCC
b) Kaposi sarcoma (KS) is a connective tissue cancer caused by human herpesvirus 8 (HHV-8), now known as Kaposi’s sarcoma-associated herpesvirus (KSHV)
c) What are the 4 types?

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Classic or European KS: Elderley males of european heritage. Classically occurs on the legs but can occur in lymph nodes and abdominal viscera. Slowly progressive.

African-endemic KS: Young adults ~35 and young children ~3. Four clinical patterns (Nodular/Florid/Infiltrative/Lymphadenopathic)

Iatrogenic immunosuppression associated KS: Most common in solid organ transplant recipients ~16.5 months post-op.

HIV/AIDS associated KS: Risk is >20,000x the general population & >300 x immunosuppressed population.

d) Dx is best completed with biopsy. Rx is aimed at symptom control, not sure. Classic KS responds well to radiotherapy, African-endemic KS responds best to systemic chemotherapy. Immunosuppressive assoc KS responds to lowering of culprit drugs & HIV assoc responds to local therapies however extensive involvement may require chemotherapy.

ADDITIONALLY: Cryosurgery, Laser surgery, PDT, excisional surgery, intralesional cytotoxic chemotherapy.

Question 2

a) What percentage of patients with psoriasis have undiagnosed PsA?
b) What are the hallmark features of PsA?
c) Name comorbidities assoc with psoriasis
d) Is psoriasis related to renal function?
e) Does psoriasis affect BP?
f) Comment on mood, skin cancer and myocardial infarction in patients with psoriasis.

Answer 2

a) 20% of patients with psoriasis have undiagnosed PsA
b) Joint or entheseal inflammation and extra-articular manifestations.

NB: Prevalence of PsA increases with psoriasis severity, but severity of psoriasis is only weakly associated with severity of joint disease.

c) Irritable bowel disease, Crohn’s disease, nonalcoholic fatty liver disease, increased risk of respiratory, abdominal and skin infections.
d) Severe, not mild, psoriasis has been linked to increased risk of CKD & ESRD.
e) HTN is more prevalent in patients with psoriasis than in those without it. Men more than women
f) Patients with psoriasis have increased risk for mood disorders, skin cancers and MI.

Question 3

a) What is the name of this lesion?

Patrick, a 14-year-old budding basketball player, presents complaining of an expanding brown patch on the back of his left shoulder. The lesion appeared a year ago and, over the past few months, has developed some coarse, long hairs. He has also started to experience some anxiety regarding the patch; a few teammates have mocked him, and he finds the area unsightly. Patrick has no other significant medical history and takes no medications. He reports that he has always utilised good sun protection measures when at the beach.

b) Are females or males more likely to have it?
c) When does it develop?
d) What can happen over this lesion?
e) What are some theories on the underlying pathogenesis?

Answer 3

a) Becker’s naevus, a commonly encountered benign cutaneous hamartoma.
b) Males 5:1
c) It may be present at birth, or it may develop around the onset of puberty, commonly on th eupper torso.
d) Excessive hair growth (hypertrichosis) and acne vulgaris.
e) Androgenic stimulation has been suggested due to it’s appearance during puberty and lightening in older adulthood.

Question 4

1-Describe the features of this lesion

Note: The lesion is rough on palpation

2-Name the lesion

Answer 4

1-Asymmetric lesion on the inside (i.e colours etc), could be considered symmetric if considering the outside border only. There is pigmentation surrounding some hair follicles however not tightly, there is also some white circles surrounding hair follicles (this gives a hint that there is keratin being produced).

2-Pigmented actinic keratosis

Question 5

1-Describe the features of this lesion

Note: Smooth and flat (not rough)

2-Name this lesion

Answer 5

1-Asymmetry in the inner structures of the lesion, tight pigmentation around some hair follicles (patchy in areas)

2-Lentigo Maligna

Question 6

1-Describe the deramtoscopic features of this fast growing lesion.

2-What are the ddx?

Answer 6

1-Featureless areas with white lines on the dermatoscope

2-Pyogenic granuloma or amelanotic melanoma

NB: In this case after bx it was pyogenic granuloma

Question 7

1-Describe the features of this lesion

Answer 7

1-Symmetrical exophytic lesion. Chaotic vessels with no symmetry, small amount of pigment on the lateral side.

NB: This lesion had been treated multiple times with laser and hence the dermatoscopic anatomy is distorted.

Note: This lesion was a melanoma >10mm on biopsy.

Question 8

1-What are some differential diagnosis to blistering dermatoses

2-What is the most common age for blistering disease to occur?

3-What is the most common type of pemphigus in much of the world?

3a) Why/how does it occur?
3b) What areas of the body can it involve?
3c) Is it serious?
3d) What are the variants of this disease?

Answer 8

1-Blistering allergic contact dermatitis, bullous impetigo, pemphigus vulgaris, bullous pemphigoid, bullous lupus, linear IgA bullous dermatoses

2-Older patients 50+ are the most likely to get pemphigus and pemphigoid disorders

3-Pemphigus vulgaris

3a? Pemphigus vulgaris occurs due to autoantibodies directed at desmoglein proteins, which make up desmosomes holding keratinocytes together in the skin.

3b? Pemphigus vulgaris can involve the mucous membrane (i.e eye, gum, genitals, oesophagus).

3c? Pemphigus vulgaris can be life-threatening if the blisters are widespread (issues with fluid loss and infections).

3d? Variants include pemphigus foliaceous, paraneoplastic pemphigus, and mucous membrane pemphigus

Question 9

1-How do you diagnose pemphigus?

2) What are the clinical signs of paraneoplastic pemphigus?
2a) What underlying condition does it represent?

Answer 9

1) Skin biopsy for direct immunofluorescence. If positive, serum testing for circulating autoantibodies can be helpful for monitoring treatment response.
2) Severe mucositis, eye involvement with scarring, and blistering of palms and soles. NB: This condition has a high mortality rate.
2a) It represents underlying lymphoma and requires urgent work-up for underlying haematologic or solid tumour malignancy.

Question 10

1-What is the most common autoimmune blistering disorder?

2) How can you differentiate pemphigus vulgaris (PV) and bullous pemphigoid (BP)?
3) What is the pathogenesis of bullous BP?

Answer 10

1) Bullous pemphigoid
2) BP: -Blisters and tense and fluid filled (splits below basement membrane (BM) of the epidermis)

PV: Flaccid blisters (splits within the epidermis)

NB: Where the blister splits is an important differentiating indicator seen on biopsy. Some patients have lesions in their mouth, but this occurs much less often than pemphigus patients.

3) BP is caused by autoantibodies targeted to proteins that make up hemidesmosomes, which anchor the epidermis to the dermis in our skin.

Question 11

1) How is bullous pemphigoid diagnosed?
2) What is the treatment for PV and BP?
3) What are the most common drugs causing drug-induced BP or PV?

Answer 11

1) Direct (DIF) or indirect immunofluorescence (IIF) to detect antibodies in either serum or skin specimens. ELISA techniques offer a serum test to detect serum autoantibodies, this method can also be used to monitor treatment response i.e serum levels of circulating autoantibodies.
2) First line treatment for both involves PO steroids with a taper to a steroid-sparing immunosuppressant. Mild cases may be managed with tetracycline antibiotics in combination with nicotinamide. If drug induced, cessation of the offending drug.
3) Penicillamine (used for severe RA, Wilsons disease, heavy metal poisoning, cystinuria), ACE-I, furosemide, and some ABs.

Question 12

1) Describe the histologic detail of the images provided

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2) State the tumour suppressor gene involved
3) State the cellular matrix proteins which might be involved with neoplasm formation?
4) What is a Spiroadenoma and what is the clinical course?
5) Once it has turned malignant, what are some important markers to investigate?

Answer 12

1) A dense basophilic adnexal proliferation with nuclear pleomorphism, atypia, and mitoses. Additional tissue from the outside institution (image not available) revealed this arose from a spiradenoma, enabling us to confirm the diagnosis of spiradenocarcinoma (hematoxylin-eosin, original magnification ×100).
2) CYLD, also responsible for responsible for Brooke-Spiegler syndrome, trichoepitheliomas, and cylindromas
3) Claudin-4, cadherin, and β-catenin
4) Spiroadenomas are rare adnexal tumours (usually benign) that appear in early adulthood. Some can degenerate into aggressive spiradenocarcinomas (SCs). The process of which is still debated and there are only 117 malignant cases in the literature.
5) PD-L1 expression in immunohistochemistry, oestrogen receptor (ER) and progesterone receptor expression,

Question 13

1) How many skin types are there?
2) Describe each skin skin type

Answer 13

1) 6
2) Type I: Pale white skin that never tans and always burns. High potential risk of UV damage. These people usually have blue or green eyes and blonde or red hair.

Type II: Fair skin that may tan but easily burns. Fair skin people usually have blue eyes and a high risk of UV-related skin damage

Type III: Darker white skin that burns initially but tans later.

Type IV: Light brown skin that tans easily but amy also burn.

Type V: Brown skin that tans intensely and burns rarely

Type VI: Dark skin that never burns and always tans intensely

Question 14

1) What is the risk of actinic keratosis?

Answer 14

1) Actinic keratosis is a pre-disposing factor of SCC, this risk increases in severe actinic keratosis.

Question 15

1-What is Pembrolizumab?

2-How was Pembro used in the SWOG S1801 trial?

3-What does this mean for future practice?

Answer 15

1-Pembrolizumab (KEYTRUDA) is an immunotherapy treatment which has an anti-PD-1 action.

2-Showed that patients with high-risk melanoma who received pembrolizumab both before and after surgery had significantly longer event-free survival than patients who received pembrolizumab after surgery only.

**Suggested explanation for the findings was that “inhibiting the PD-1/PD-L1 immune checkpoints before surgery gives an antitumor response at local and distant sites, and this occurs before resection of the tumor bed. This approach tends to leave behind a larger number of anti-tumor T cells, these T cells can be activated and circulated systematically to recognize and attack micro-metastatic melanoma tumors.”

3-Further survival data is needed to really change the standard of practice in high-risk melanoma and demonstrate whether there is a superior sequence of therapy and surgery.

Question 16

1-What are the main differences between Axial Psoriatic Arthritis (PsA) and Axial Ankylosing Spondylitis (AS)?

2-What should be considered with medications?

Answer 16

1-Patients with isolated axial PsA were older at diagnosis, more likely to have psoriatic nail lesions.

-Patients with axial AS and accompanying psoriasis were more likely to have inflammatory back pain and were younger in age at diagnosis

2-Medications for psoriasis, including those targeting the interleukin-23 cytokine, may not be effective for AS, but patients with axial PsA may not get them because of the association with axial AS.

Question 17

1-What questionnaires are used to define psoriasis severity?

2-How are these scored in terms of severity?

3-Does severe psoriasis affect mortality?

4-When switching biologics in severe psoriasis, when is a treatment interval required?

5-In relation to live vaccines and biologics, how long after a live vaccine has been given can a biologic be started, and how long should a biologic be stopped prior to giving a live vaccine?

Answer 17

1-Psoriasis Area Severity Index (PASI) and Dermatology Life Quality Index (DLQI)

2-PASI <5% mild, 5-10% moderate, >10% severe

DLQI <5% mild, 5-10% moderate, >10% severe

NB: When face, scalp, hands, and/or nails are involved, systemic treatment may also be condifered despite not meeting BSA %.

3-Yes, psoriasis is independently associated with increased mortality in both men and women (3.5% and 4.4% respectively)

4-When switching biologics due to lack of efficacy, no treatment free interval is required, when switching biologics for a safety reason, a treatment free interval may be required.

5-Biologic therapy can be started 4 weeks after administration of a live vaccine. Biologic therapy should be stopped for at least 6 months before giving live vaccines; in the case of the herpes zoster (shingles) vaccine, it should be stopped for 12 months.

Question 18

1-What is melasma?

2-What are the topical options for management?

Answer 18

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122278/pdf/jcad_15_5_19.pdf

Question 19

1-What is Pyoderma Gangrenosum

2-How is it diagnosed?

3-What are the current suggested treatments?

Answer 19

https://link.springer.com/content/pdf/10.1007/s40257-022-00699-8.pdf

Question 20

1-What are the pertinent CV screening tests that should be completed when assessing as adult with psoriasis?

2-What are the treatment considerations for children with psoriasis?

3-What can individualised psoriasis treatment for children be based on?

4-What can complicate decisions about treatment initiation and continuation of systemic therapy?

5-What main co-morbidities should a child with psoriasis be screened for?

Answer 20

1-Cholesterol (incl total, HDL, LDL), BP, wt and smoking status.

2-Measures of severity, presence of psoriatic arthritis, optimising well-being, ensuring shared decision making

3-Patient age, type of psoriasis, comorbidities, triggers, psychological and physical impact, safety, family preference, feasibility and cost

4-The tendency for psoriasis to be unpredictable with periods of remisson and relapse

5-Obesity (high BP, cholesterol and Diabetes[metabolic syndrome]), arthritis (physical examination) and mood disorders (anxiety and depression)

Question 21

1-What is the main ddx for generalised pustular psoriasis?

2-What parts of the history help to divide the ddx?

3-Does pregnancy make a difference to ddx?

4-How can a biopsy change the differential, what are common histological findings and what are different?

Answer 21

1-Acute generalised exanthematous pustulosis (AGEP), or a drug eruption.

2-History of psoriasis, prolonged fever, longer duration of eruption, hypocalcaemia and lack of precipitating drug (commonly antibiotic) favours pustular psoriasis over AGEP.

3-Pregnancy can precipitate generalised pustular flares

4-Both entities show subcorneal pustule formation. AGEP, or drug eruption, has eosinophilia in the dermis, eosinophilic spongiosis, interface change and papillary dermal oedema. Absence of those features suggests pustular psoriasis

Question 22

1-What are the areas affected on the body which can increase the perceived severity of psoriasis?

2-Why are these areas related to severity?

Answer 22

1-Face, scalp, nails, palms, soles, genitalia

2-Despite the fact there may not be a large surface area affected, psoriasis in these sites can increase the patients perceived severity because it affects activities of daily living and may be visible to other people.

e.g scalp scaling, pruritus and bleeding

Question 23

1-What is the name for an accumulation of neutrophils under the stratum corneum?

2-What histologic findings accompany these in generalised pustular psoriasis?

3-What are the 3 general diagnostic criteria for GPP?

4-What are 5 ddx of pustular rash?

5-What are 3 possible triggers for GPP?

6-What is considered to be the IL driver of GPP?

Answer 23

1-Kogoj’s spongiform pustules

2-Parakeratosis, acanthosis, elongation of rete ridges, diminished stratum granulosum, hyperkeratosis and superficial perivascular mononuclear cell infiltrations

NB: presence of eosinophils and nectrotic keratinocytes is NOT associated with GPP.

3-(1)Macroscopic sterile pustules on non-acral skin and not within psoriasis plaques (2) Should only be dx if it has relapsed at least once or if it has persisted for at least 3/12. (3) Drug reactions such as AGEP have been ruled out.

4-Subcorneal pustular dermatoses (Sneddon Wilkinson disease), Pustular psoriasis, drug induced (AGEP), IgA pemphigus (ruled out with negative DIF), TEN/impetigo, Steven Johnson syndrome

5-Respiratory virusus (incl. COVID-19)Stress, Pregnancy and corticosteroid treatment withdrawal

6-IL-36

Question 24

1-What is the most common nail sign of PsA?

2-What is the first line-treatment for plaque psoriasis and how long does it take to see an effect?

3-When topical treatment starts, what is the first and second change noted in the psoriatic rash?

4-How long can erythema take to fully resolve after topical treatment starts?

5-What is Anthralin aka Dithranol and how does is treat psoriasis?

6-What is Calcipotriol and what should not be used with it?

Answer 24

1-Nail pitting

2-Topical therapy is the first line treatment and takes 2-3 weeks to notice full effect.

3-First change noted is the clearing of scale, then flattening of treated plaques

4-Erythema can take 6-8 weeks to clear

5-A keratolytic medication which restores the normal rate of epidermal cell proliferation by reducing the mitotic activity of the hyperplastic epidermis. May be applied while in hospital for a few hours each day, or at home for ~10mins p/day prior to shower. Can stain the skin. NB: Must be mixed with a salicylic acid for chemical stability.

6-Calcipotriol suppresses proliferation of keratinocytes. Should not be used with Salicylic acid which destabilises calcipotriol molecule. Apply them at different times of the day.

Question 25

1-When should phototherapy be considered in plaque psoriasis?

2-Is the burning risk lower or higher in narrowband UVB?

*PUVA can be combined with oral retinoid derivatives to reduce the cumulative dose of UVA radiation to the skin.

*UVB phototherapy is very effective for the treatment of moderate to severe plaque psoriasis and should be considered in appropriate patients.

3-What is the cardiovascular benefit that biologics appear to provide?

Answer 25

1-When there is resistance to topical treatment or in the case of extensive and widespread disease.

2-Narrow-band UVB phototherapy may convey a lower risk for burning than broadband UVB.

3-Improve coronary arteries by reducing noncalcified plaque and the necrotic core of plaque and increasing its fibrous cap, making it harder for plaques to rupture.

Question 26

1-What drugs are linked to Lupus?

Answer 26

1-PPI

Question 27

1) Cemiplimab for SCC

Answer 27

1) Immunotherapy for SCC. Provisional TGA approval, not yet PBS listed. Can apply for it for adult patients with metastatic or locally advanced SCC. 350mg IV every 21/7. Further studies occurring.

Question 28

1) Which of the following does NOT involve cutaneous manifestations? Acute leukaemias, chronic leukaemias, B-call non-hodgkins lymphoma (NHL), multiple myeloma, myelofibrosis, myeloproliferative disorders
2) In what haematologic malignancies can skin manifestations be the first sign of the disease?
3) What haematologic condition has a hallmark overexpression of CD123
4) In what other haematologic malignancies is CD123 over-expressed?
5) In what haemotologic malignancy is CD123 not expressed?
6) What methods can be used to test CD123?
7) What skin manifestations can present in Blastic plasmacytoid dendritic cell neoplasm?

Answer 28

1) Multiple myeloma does NOT have skin manifestations. Skin manifestations can be seen in all other haematologic malignancies mentioned. Due to hematologic skin infiltration, immune-mediated reactions, or treatment-related adverse events (AEs)
2) Blastic plasmacytoid dendritic cell neoplasm (BPDCN), & some aggressive NHLs e.g primary cutaneous T-cell, B-cell, or natural killer (NK) cell lymphomas.
3) BPDCN
4) Multiple hematologic malignancies, i.e AML, acute lymphoblastic leukemia (ALL), hairy cell leukemia, Hodgkin lymphoma, chronic myelogenous leukemia (CML), and myeloproliferative disorders (eg, myelofibrosis, chronic myelomonocytic leukemia [CMML], mastocytosis)
5) Multiple myeloma
6) Skin biopsy, bone marrow sample, blood sample, or any cellular suspension (eg, cerebrospinal fluid, pleural effusion, ascites) depending on the patient’s specific symptoms.
7) Solitary or multiple manifestations and typically present as nonpruritic nodules, plaques, or bruises. Skin manifestations are often followed by bone marrow involvement and cytopenias.

Question 29

1) BPDCN occurs in what age most often?
2) What organ systems does BPDCN involve?
3) In addition to CD123 overexpression, what biomarkers are observed in BPDCN?
4) What is an important consideration for biopsies when suspecting BPDCN?
5) How is a diagnosis of BPDCN confirmed?
6) What are the guidelines and treatments for BPDCN? Are there any targeted therapies available?

Answer 29

1) Men in their 60s
2) Lymph nodes, spleen, CNS & Liver.

NB: Does NOT involve stomach

3) CD4 and CD56
4) Biopsy samples must go to the lab ASAP and should NOT be fixed in formalin. They require specific fixation methods to maintain IHC sensitivity.
5) If an atypical skin lesion is biopsied and shows CD123 overexpression, a bone marrow biopsy should also be evaluated to look for potential hematologic involvement.

NB: CD123 overexpression in a skin biopsy alone is not enough due to the number of other malignancies that have CD123 overexpression. NB: CD123 overexpression is present in 100% of BPDCN cases

6) Currently there are no international guidelines, treat with AML based chemotherapy regimens. FDA and european medicines agency has approved Tagraxofusp (CD123-targeted cytotoxin)

Question 30

1) What is the prognosis of BPDCN?
2) What membrane markers are associated with BPDCN?
3) What is the history of this haematologic cancer classification?
4) How do the skin manifestations of BPDCN present?
5) What is the lag time between lesion development and diagnosis? & what is an important tip for the skin biopsy?
6) What is the most important ddx of BPDCN?

Answer 30

1) Poor prognosis of ~12-14 months
2) CD123, CD4, CD56
3) Previously it has been known by many other names as seen in the picture. In 2008 WHO named BPDCN as a sub-classification of AML, in 2016 BPDCN was re-classified into a distinct category.
4) They can present as solitary, purple violaceous nodues, or diffuse, bruise like hyperpigmented brown nodules. They may become scaly and can be atypical or subtle
5) The lag time can be up to 6 months! Skin biopsy needs to include deep dermis as the epidermis is often spared.
6) Acute myeloid leukaemia

Question 31

1) What antigen markers confirm BPDCN and what markers exclude it?
2) What is the primary treatment of choice for BPDCN and what is the main side-effect? What signs indicate that a side-effect may be occurring?
3) What is another option for treatment available?

Answer 31

1) Confirmatory markers: CD4, CD123, CD56, TCL1, TCF4, CD303 (BDCA2). NB: These markers CAN rarely be expressed in AML, it is usually the combination that confirms BPDCN. Excuding markers: CD3 (pan T-cell), CD79a, CD20 (pan b-cell), CD11c, CD163, Lysozyme, Myeloperoxidase, CD34, CD17
2) Tagraxofusp (targets CD123 aka IL-3Ra). The main side-effect of concern is capillary leak syndrome (CLS), which can present as hypoalbuminaemia, fluid shift and hypotension.

NB: Patients with CLS, once recovered can be re-challenged successully with Tagraxofusp.

3) Venetoclax (BCL-2 antagonist). On it’s own it shows modest results, however combined with chemotherapy results are more encouraging.

NB: BPDCN also affects the CNS in up to 22% of cases which further complicates management options.

Question 32

1) What is Monkey pox, who is most likely to transmit it and where geographically is it known to have arisen?
2) Which animals can it affect?
3) How does transmission occur and can you be born with it?

Answer 32

1) Monkey pox is a DNA viral zoonosis that is transmitted between humans and from animals. It is first known to have occurred in tropical rainforest areas of central and west Africa.

NB: Central african virus considered more transmissible

2) Tree squirrels, Gambian pouched rats, dormice and monkeys
3) Transmission occurs via direct contact with lesions, or blood/bodily fluid. Transmission can also occur through respiratory droplets and or via bed linen that can bodily fluid/respiratory droplets on it. Placental transmission is possible and therefore a child could be born with congenital monkey pox.

Question 33

1) How long is the incubation period and what are the symptoms?
2) Does Monkey pox affect mucous membranes?
3) How does the rash evolve over time?
4) How long is the patient contagious?
5) How long does it last and what are the complications?
6) What is the ddx?
7) How is Monkey pox diagnosed?

Answer 33

1) Incubation may be up to 3/52. Then initially present with fever, myalgia, headaches and lymphadenopathy. Then after 1-3 days, facial rash and a rash affecting the limbs can occur.
2) In most cases oral mucous membranes are affected. Genital involvement occurs in ~1/3 of cases.
3) Rash may initially present as maculopapular, then evolve into vesicles and pustules that crust over; these lesions may be numerous. Lesions may have an umbilicated appearance and be up to 1cm in diameter.
4) The patient is contagious until all scabs fall off and the underlying skin is intact
5) Symptoms are self-limiting and can last up to 4/52. Secondary infection leading to sepsis and corneal involvement leading to blindess are the main complications.
6) Chickenpox, syphilis, bacterial skin infections and a rash associated with HIV seroconversion. Lymphadenopathy makes Monkey more likely over chicken pox.
7) PCR testing from skin lesions. Antigen and antibody testing are less reliable as orthopoxviruses are serologically cross-reactive

Question 34

1-Describe Rosacea in basic terms

2-What antibacterial peptide is common in Rosacea?

3-What mites are found to have increased growth on skin of people with rosacea?

4-What are common Rosecea triggers (4 overall areas)?

Answer 34

1-Rosacea is an inflammatory condition involving abnormal neurological, vascular and lymphatic signalling.

2-Cathelidicin LL-37

3-Demodex folliculorum

4-Environmental: Sun exposure, windy, hot temp, pollution, face masks. Diet: Hot food and beverages, Capcaisin in chilli and spices, Cinnamaldehyde in tomatoes, cinnamon and chocolate, alcohol (red wine and hard liquor). Activities such as exercise, hot showers, cooking over hot stove. Stress and emotion e.g. anger/embarrassment.

Question 35

4 overall product goals e.g. Skin barrier repair

1-What is an ideal skincare regimen for Rocasea?

Answer 35

1- (1)Skin barrier repair and hydration: Glycerin, ceramides, squalene, lipids, niacinamide, panthenol, hyaluronic acid. (2) Anti-inflammatory: Niacinamide, ambophenol, bisabolol. (3) Anti-oxidants: Vitamin C, Vitamin E. (NB: These can sting)(4) SPF50+ sunscreen: Physical or chemical + protective clothes.

Question 36

1-What are the 4 Rocacea subtypes?

2-What are the main ways to differentiate between Acne vulgaris, perioral dermatitis and papulopustular rosacea? (pic attached)

3-What topical treatment should be avoided in Rosacea?

4-What treatment is advised for mild/moderate papulopustular rosacea?

5-What is the next step following mind/mod rosacea treatment?

Answer 36

1-Erythematotelangiectatic rosacea, Papulopustular rosacea, Ocular rosacea, Rhinophyma

2-Acne Vulgaris: Polymorphic (papules, pustules, nodules). Affects forehead cheeks and jawline, greasy skin, trunkal acne common (50%).

Perioral dermatitis: Monomorphic (papules +/- pustules). No comedones or nodules. Stinging skin with mild flaking and irritation around nasolabial and peri-alar skin.

Papulopustular rosacea: Monomorphic (papules + pustules). No comedones or nodules. Persistent centrofacial erythema and telangiectasia. Ocular symptoms in 50%.

3-Topical steroids MUST be AVOIDED in Rosacea.

4-Topicals-Metronidazole (0.75%) aka Rozex, Ivermectin (1%) aka Soolantra, Acelaic acid (15 or 20%) aka Finacea, and Clindamycin (1%) Clindatech (topical liquid) and Dalacin (lotion).

Oral ABs: Mino/doxycycline 50mg BD (caution Minocycline is preferred as it does not cause as much photosensitivity as doxy). Erythromycin 250-500mg (NB: PBS only for the 250mg, need authority for the 500mg). Be aware of liver dysfunctin and monitor. Treat for total of 3-6 months.

5-After 3-6months lack of treatment response, consideration of isotretinoin and/or vascular laser

Question 37

1-What are 4 important treatment points when starting isotretinoin for rosacea?

2-What are the signs of erythematotelangiectatic rosacea? (picture)

3-What is a temporary medication for erythematotelangiectatic rosacea and what is the side effect to look out for?

Answer 37

1-(1) It is effective for persistent or extensive papulopustular rosacea. (2) 6-12 month treatment course, repeated courses often needed. (3) hormonal contraception for sexually active females (4) Bloods incl. pregnancy test, fasting lipids, LFTs.

2-Diffuse bright erythema and telangiectatic matting +/- flushing (intensity varies).

• Periocular sparing. Affects nasolabial folds.
• Lateral neck and decolletage commonly involved

NB: May see overlap with other facial erythema causes.

3- Topical brimonidine (Mirvaso): alpha-2 agonist which causes vasocontriction. Can help for once off events, not recommended for regular use due to rebound erythema.

Question 38

1-What are 4 conditions that can mimic rosacea, or could be ddx?

Answer 38

1-(1) Actinic erythema: Actinic keratoses (solar keratosis), lentigines (solar lentigo), dyschromia (melanocytic discolouration).

(2) Keratosis pilaris rubra faceii: Keratotic papules on cheeks and eyebrows +/- brow loss. Diffuse erythema, NO telangiectasia. Check outer arms!
(3) Seborrhoec dermatitis: Yellow crusts & erythema. Affects nasolabial folds. Check scalp and beard!
(4) Malar rash of lupus: Spares nasolabial folds.

Question 39

1-What are the signs of Ocular rosacea and what is the treatment?

2-What are the treatment options for Rhinophyma?

3-What is the treatment for persistent centrofacial oedema (Morbihan disease)? (pictured in ans)

Answer 39

1-Sensitive, gritty eyes, blepharitis, styes, chalazion. Treatment includes eyedrops, doxycycline 50mg BD. If no response, consider referral to ophthalmologist for ?ocular IPL

2-First line requires isotretinoin, second line ablative laser resurfacing (limited role of topical retinoids). NB: Caution nostil narrowing and difficulty breathing.

3-Responds to high dose isotretinoin, daily facial massage.

Question 40

1-Describe a dermatologic emergency associated with rosacea?

2-How is it treated?

Answer 40

1-Rosacea Fulminans, or Pyoderma Faciale. Affects young adult women (not men) without a prior history of rosacea. Rapid onset of painful nodules, papules, pustules with centrofacial erythema>high scarring risk

2-Requires urgent dermatology review. Usually requires prednisolone (20mg for 7/7 then 10mg for another 7/7), antibiotics (not as effective ?bactrim), and isotretinoin (0.5-1mg/kg daily for 4-6/12).

Question 41

1-What is the treatment recommendations for rosacea during pregnancy?

Answer 41

1-Skincare WITHOUT retinoids are safe. For erythematotelangiectatic rosacea, lasers and light based treatments are safe. In papulopustular rosacea: Mild/mod-Topical ivermectin, azelaic acid, metronidazole and clindamycin (Cat B). Mod/severe-Oral erythromycin (Cat A) NB: Balance risks with benefits and some caution with macrolides and CV malformations if used in first trimester.

Question 42

1-What part of the skin structure does acne affect

2-What are the 4 main issues that contribute to acne?

3-What is the distribution of acne?

Answer 42

1-Acne affects the pilosebaceous unit structure composed of the hair follicle and sebaceous gland.

2-(1) Follicular hyperkeratosis (prevents the sebum from flowing out, causing blockage).

(2) Seborrhoea, i.e increased sebum production caused by the action of androgens on the sebaceous gland
(3) Bacterial colonisation (p.acnes and s.aureus overgrowth)

3-Distribution reflects the areas of highest density pilosebaceous units, i.e face, neck, chest, shoulders, back.

(4) Post-inflammatory hyperpigmentation

Question 43

1-What are the likely causative factors associated with acne?

Answer 43

1-Family history, medication, stress, gender, hormones, oil based cosmetics.

Question 44

When examining pink tumours/lesions, what are some important considerations? e.g amelanotic melanoma, BCC, SCC, spitz naeveus

Answer 44

• Combine clinical + dermoscopy:
• Look for prevalent features, don’t waste time on insignificant features
• If you cannot clearly define it as benign, you need to excise it (flat or nodular). Do NOT monitor, if there is suspicion, excise.

Question 45

Describe the most prominent feature of the 3 lesions in the picture, and therefore the diagnosis.

Answer 45

Left: Sharply focussed vessels. BCC

Middle: White colour due to keratinising process. SCC

Right: Polymorphic vessels (not hugely specific to melanoma however makes you consider it). Amelanotic melanoma

Question 46

Menzies score

In the menzies score, what are the 4 non-suspicious criteria and the 7 suspicious criteria?

Answer 46

Non-Suss (-1 point)

1-Multiple (>3) milia-like cysts

2-Symmetrical pigmentation pattern

3-Comma vessels in regular distribution

4-Multiple brown dots

Suss (+1 point) >/= 0 means malignant)

1-Depigmentation

2-Small diameter arborising vessels

3-Leak-like areas

4-Ulceration

5-Irregularly sized or distributed blue-grey globules

6-Grey colour

7-Large diameter vessels