Final Derm II Flashcards

(46 cards)

1
Q

Describe what is meant by bullous pemphigoid [1]

It is caused by antibodies agaisnt which basement membrane proteins? [2]

Which patients is it commonly found in?

A

In frail patients
Autoimmune blistering condition
Antibodies against basement membrane proteins which are key components of hemidesmosomes
* BP 180
* BP 230

NB:
“The Bull and the Basement”
* Picture a big, angry bull (bullous pemphigoid).
* Instead of running on the ground, this bull is smashing through the basement (hemidesmosomes are at the base of epithelial cells, anchoring them to the basement membrane).
* Since the bull is attacking the basement, it’s causing subepidermal blisters—which is exactly what happens in bullous pemphigoid!

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2
Q
A
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3
Q

Describe the topical treatments [4] and systemic therapy [5] used to treat Bullous Pemphigoid

A

Topical Treatments
* Super potent topical steroid
* Non adhesive dressings
* Potassium per manganate soaks
* Pop large blisters

Systemic therapy
* Antihistamines
* Tetracycline antibiotic vs oral steroid (BLISTER trial)
* Methotrexate
* Mycophenolate Mofetil
* Biologic therapy - Rituxumab

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4
Q

Describe the pathophysiology of Pemphigus Vulgaris [1]

A

Autoimmune blistering condition
- Autoantibodies to Desmoglein-3 (and sometimes also Desmoglein-1) which are found in desmosomes
- The autoantibodies belong to the IgG class, specifically IgG4

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5
Q

Which drugs can induce PV? [2]

A

Penicillamine
ACE-inhibitors

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6
Q

Tx of Pemphigus Vulgaris? [4]

A

First-Line Treatment
- oral corticosteroid ± azathioprine or mycophenolate

Second line:
- Rituximab

Intravenous immunoglobulin (IVIG) and plasmapheresis are adjunctive therapies for severe or refractory cases.

Patients on high-dose steroids or other immunosuppressants should receive prophylaxis against Pneumocystis jirovecii pneumonia with co-trimoxazole.

Notes: BMJ BP

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7
Q

Define erythroderma [1]

Name 5 causes

A

Widespread erythema of skin (over 90% of body surface area)

Causes
* Idiopathic (30%)
* Adverse drug reaction (gold)
* Known inflammatory skin disease (eczema, psoriasis)
* Cutaneous lymphoma

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8
Q

Tx for Eczema Herpeticum? [2]

A

Acyclovir
Flucoxacillin

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9
Q

Describe the clinical presentation of eczema herpticum [6]

A

The skin lesions of eczema herpeticum typically present as painful clusters of blisters, fluid-filled elevations of the skin

Areas of rapidly worsening, painful eczema

The blisters appear widely over the body but are most common on the face, neck, and trunk.

Older blisters that have burst and dried commonly form “punched out” erosions, which are circular breaks in the continuity of the skin that may bleed or produce pus.

Possible fever, lethargy, lymphadenopathy or distress

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10
Q

A patient takes penicillin for an infection.

They come out in targetoid lesions.

What type of hypersensitivty reaction is this?

Type 1
Type 2
Type 3
Type 4

A

Type 1
Type 2
Type 3
Type 4

EM is considered a cell-mediated (type IV) hypersensitivity reaction, which is an abnormal cell-mediated reaction initiated by T cells.

The exact mechanism leading to EM is incompletely understood, but it appears to be an abnormal immune reaction to a drug metabolite or viral antigen that becomes expressed by keratinocytes within the skin

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11
Q

What is the management for EM? [3]

A

Management

  • EM typically develops over 3-5 days and improves over 2 weeks. Some patients may get persistent or recurrent episodes.
  • Stop the drug
  • Treat the underlying infection
  • Treat with a week of oral prednisolone if severe mucosal pain/ difficulty eating
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12
Q

Describe what is meant by SJS [1]

Describe the presentation of SJS [3]

A

Stevens-Johnson syndrome is a severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction.

Presentation:
* Patients usually start with non-specific symptoms of fever, cough, sore throat, sore mouth, sore eyes and itchy skin.
* They then develop a purple or red rash that spreads across the skin and starts to blister.
* Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently

NB: Nikolsky sign = where very gentle rubbing of the skin causes it to peel away

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13
Q

Which drugs cause SJS? [7]
Which infection can also can? [1]

A

SPANLOC
* Sulphonamide
* Penicillin
* Phenytoin
* Allopurinol
* NSAIDS
* Lamotrigine
* OCP
* Carbamazepine

Most commonly caused by drugs. Less commonly infection eg Mycoplasma

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14
Q

How do you dx SJS / TEN? [1]
What score is used for to classifiy the severity of SJS / TEN? [1]

A

Dx:
- skin biopsy

Severity:
- SCORTEN

sum of five points or more indicates a mortality risk of over 90%

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15
Q

Clinical presentation of SSSS? [5]

A

Fever:
- High fever (>38.9°C)

Rash:
- A diffuse, blanching erythroderma resembling sunburn usually appears early in the disease course.
- Desquamation, particularly on the palms and soles, typically occurs one to two weeks after the onset of illness

Myalgias and arthralgias are frequently reported;

Hypotension:
- Hypotension or shock may be present, often manifesting as systolic blood pressure less than 90 mmHg.

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16
Q

Management for SSSS? [1]

A
  • Admit
  • Fluids
  • IV flucloxacillin and clindamycin Clindamycin suppresses toxin production, while flucloxacillin targets the bacterial cell wall.
  • If methicillin-resistant Staphylococcus aureus (MRSA) is suspected, vancomycin or daptomycin can replace flucloxacillin.
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17
Q

What are the four types / causes of necrotising fasciitis? [4]

A

Type 1 – Polymicrobial (anaerobes + aerobes)
Type 2 – Group A beta-haemolytic streptococci
Type 3 – Clostridium perfringens; also associated with Vibrio species infection from seafood ingestion or water contamination of wounds.
Type 4 - Fungal infection

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18
Q

Erythrasma is a superficial bacterial skin infection caused by [1]

How do you dx erythrasma? [1]

What is the treatment? [1]

A

Erythrasma is a superficial bacterial skin infection caused by Corynebacterium minutissimum

Examination with Wood’s light reveals a coral-red fluorescence.

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection

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19
Q

Which drugs are used for fungal nail infection, for both fingernails and nails, if:

  • Limited involvement
  • Extensive involvement
  • Extensive involvement due to Candida infection
A

Limited involvement: - Topical treatment with amorolfine 5% nail lacquer
- Fingernails: 6 months
- Toe nails: 9-12 months

Extensive involvement - : oral terbinafin
- Fingernails: 6 weeks-3 months
- Toe nails: 3-6 months

Candida:
- oral itraconazole is recommended first-line;
- ‘pulsed’ weekly therapy is recommended

20
Q

Which four factors are in the criteria for hereditary haemorrhagic telangiectasia? [4]

A

epistaxis :
- spontaneous, recurrent nosebleeds

telangiectases:
- multiple at characteristic sites (lips, oral cavity, fingers, nose)

visceral lesions:
- for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM

family history:
- a first-degree relative with HHT

NB only 3 are needed for a definite diagnosis; 2 is a possible diagnosis

21
Q

Describe what is meant by Hidradenitis suppurativa

A

Hidradenitis suppurativa
* Chronic, painful, inflammatory skin disorder.
* It is characterized by the development of inflammatory nodules, pustules, sinus tracts, and scars in intertriginous areas
* The axilla is the most common site
* Coalescence of nodules can result in plaques, sinus tracts and ‘rope-like’ scarring.

22
Q

Treatment of acute and chronic Hidradenitis suppurativa?

A

Acute flares:
- can be treated with steroids (intra-lesional or oral) or flucloxacillin.
- Surgical incision and drainage may be needed in some cases.

Long-term disease:
- can be treated with topical (clindamycin) or oral (lymecycline or clindamycin and rifampicin) antibiotics.

23
Q

Hyperhidrosis describes the excessive production of sweat.

What are 4 managment options? [4]

A
  1. topical aluminium chloride preparations are first-line. Main side effect is skin irritation
  2. iontophoresis: particularly useful for patients with palmar, plantar and axillary hyperhidrosis
  3. botulinum toxin: currently licensed for axillary symptoms
  4. surgery: e.g. Endoscopic transthoracic sympathectomy. Patients should be made aware of the risk of compensatory sweating
24
Q

What is the treatment algorithm for impetigo? [3]

A

Tx:
- Hydrogen peroxide 1% cream for ‘people who are not systemically unwell or at a high risk of complications’
- topical antibiotic creams: topical fusidic acid; topical mupirocin should be used if fusidic acid resistance is suspected
- Extensive disease: oral flucloxacillin; oral erythromycin if penicillin-allergic

25
Management of LP? [2]
**potent topical steroids** are the mainstay of treatment **benzydamine mouthwash** or spray is recommended for oral lichen planus
26
How do you treat lichen sclerosus? [2] Why do you follow up patients? [1]
**Treatment**: * super potent topical steroids and emollients Follow up due to risk of **vulval cancer**
27
What is mycosis fungoides? [1]
Mycosis fungoides is a **rare form of T-cell** **lymphoma** that affects the **skin**.
28
How do you differentiate mycosis fungoides from eczema and psoriasis?
lesions tend to be of **different colours** in contrast to eczema/psoriasis where there is greater homogenicity
29
This patient is suffering from dermatitis due a deficiency in a vitamin - which one? [1]
**Pellegra - B3 deficiency** The classical features are the **3 D's - dermatitis, diarrhoea and dementia.** Dermatitis (brown scaly rash on sun-exposed sites - termed Casal's necklace if around neck)
30
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.
31
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** ## Footnote NB: steroids not used in rosacea
32
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.
33
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**
34
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.
35
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
36
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.
37
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.
38
Treatment algorithm for folliculitis? [2]
**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**).
39
Name these complications of folliculitis [1]
40
Management of contact dermatitis?
Avoiding allergens **Topical corticosteroids** are first-line treatment for **acute flares.**
41
How do you manage urticaria? [3]
I**t 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
42
Rubella poses a serious risk to unvaccinated pregnant women. Congenital rubella infection (especially in the first 20 weeks of pregnancy) can lead to congenital rubella syndrome, which can cause severe fetal abnormalities such as: [4]
* Cataracts * Deafness * Patent ductus arteriosus * Brain damage
43
How can measles be prevented in someone who has had close contact with a confirmed case of measles? [2]
**Prompt vaccination or a dose of immunoglobulin** within a few days of contact.
44
What are Pastia’s lines? [1]
Red creases in the skin folds (e.g. armpits) associated with scarlet fever.
45
Deficiency of which vitamin is a risk factor for measles? [1]
Vitamin A
46
What is Telogen effluvium? [1]
excessive shedding of resting or telogen hair after some metabolic stress, hormonal changes, or medication.