Jonathan Gleadle - How to Pass the FRACP Written Examination

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How to Pass the FRACP Written Examination More than a simple practice exam, this guide provides clear and complete explanations of each answer, a mini-review of the subject, and links to the most recent or relevant articles on the topic. Complementing the main body of questions are a number of ‘teaching’ and two-step questions—designed to strengthen clinical reasoning skills, highlight important issues, and expand knowledge of contemporary ‘hot’ topics. Written by an experienced team of physicians and educators, this must-have book: 
Provides a thorough review of the latest FRACP basic training syllabus Features QR codes embedded in the text to enable quick access to all references Offers tips, hints, advice, and examination strategies from previous candidates Provides numerous questions grounded in clinically relevant cases Covers of areas of medicine that are new, contemporary, and evolving Covering both the ‘Basic Sciences’ and ‘Clinical Practice’ of the latest exam
 is an essential companion for FRACP candidates as well as those looking to refresh, improve, or update their knowledge of the FRACP syllabus.

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8 8. A 42‐year‐old woman presents with a 9‐month history of repeated facial flushing, often precipitated by sun exposure. She reports that the flushing occurs on the nose, both cheeks, and the central forehead. On examination, she has multiple telangiectasia on both malar surfaces, but no evidence of inflamed papules or pustules. There are no features suggestive of systemic lupus erythematosus.Which of the following treatments is most likely to be helpful in reducing her symptoms?Oral doxycycline.Oral isotretinoin.Topical brimonidine.Topical metronidazole.

9 9. An 82‐year‐old man with vascular dementia is constantly scratching his hands and elbows. There are diffuse scaly rashes on hands, elbows, and scrotum with several vesicles and scratch marks. A clinical diagnosis of scabies is made.Which of the following statements is true in regard to this patient?A skin biopsy should be performed prior to the treatment.He is at risk of having highly contagious crusted scabies.His pruritus is caused by direct irritation from mites and eggs.The mite can survive on bedding, clothes for more than one week.

10 10. A 40‐year‐old woman who received a heart transplant two years ago is seeking your advice regarding sunscreen usage to prevent skin cancers.Which of the following do you advise her?High‐number SPF (Sun Protection Factor) sunscreen allows longer time intervals between application.SPF 30 sunscreen blocks 60% of the sun's UVB rays.SPF 30 sunscreen decrease the skin’s production of vitamin D.UVA rays mainly cause sunburn and UVB rays cause skin cancers.

11 11. A 66‐year‐old man has a skin lesion on his right shoulder which is suspicious for a BCC. He has a history of ischaemic heart disease with a coronary artery stent and hypertension. His dermatologist excises the lesion without stopping clopidogrel and causes profuse bleeding.Which layer of the skin has the dermatologist most likely transversed to cause this bleeding?Papillary dermis.Reticular dermis.Stratum basale.Stratum granulosum.

12 12. A 60‐year‐old man presents with a 2‐week history of flu‐like symptoms including malaise, sore throat, and fever. His GP had commenced him on amoxicillin, but he did not respond to this treatment. On examination, he has an erythematous, desquamating rash over his torso with injected conjunctivae.Which of the following has the most benefit on mortality in this condition?Etanercept.High dose systemic steroids.Intravenous Immunoglobulin (IVIG).Supportive care.

QUESTIONS (13–17) REFER TO THE FOLLOWING INFORMATION

Match each of the clinical scenarios with the best fitting dermatological emergency:

1 Drug rash with eosinophilia and systemic symptoms.

2 Meningococcaemia.

3 Necrotising fasciitis.

4 Disseminated candidiasis.

5 Staphylococcal scalded skin syndrome.

6 Stevens‐Johnson syndrome.

7 Acute generalised exanthematous pustulosis.

8 Toxic epidermal necrolysis.

1 13. A 21‐year‐old woman presents with a 6‐hour history of fever and rash over her body. She was started on oral trimethoprim for UTI 7 days ago. She takes no other medication and has no known allergies. On examination, she is febrile and other vital signs are in normal range. There are erythematous, urticarial, targetoid rashes studded with small, tense blisters on the shoulders, back, palms but less than 10% of body surface area involved. There are also small vesicles and crusts on the upper and lower lips, but there are no lesions are present on the soles or genitalia. Nikolsky’s sign is positive. Her FBE, LFTs, and renal function are normal.

2 14. A 25‐year‐old woman with a history of epilepsy, depression, and diabetes presents with fever (39oC ), a morbilliform eruption and facial swelling. Her GP had commenced her on paracetamol, carbamazepine and metformin 6 weeks ago. On examination, the rash has varying morphology with targetoid lesions, pustules and blisters, however she is Nikolsky sign negative. She has WCC of 16 × 109/L, eosinophil of 4 × 109/L, deranged LFTs and a serum creatinine of 300 μmol/L [45‐85]. The skin biopsy shows lichenoid infiltrate with focal necrotic keratinocytes.

3 15. A 58‐year‐old man presents with fever, malaise, and conjunctivitis progressing to a tender erythematous rash in the face, neck, axilla, and groin with mucous membranes spared. Nikolsky’s sign is positive and flaccid bullae develop in areas of erythema.

4 16. A 42‐year‐old woman presents with fever and examination showswidespread erythema worse on the skin folds progressing to widespread small coalescing pustules.

5 17. A 56‐year‐old man presents with a 3‐day history of worsening skin erythema, blistering and pain. He is known to have smoking related COPD. He was started with allopurinol 7 days ago, because of frequent acute gout attack. On examination, he is febrile, HR is 110 bpm, there is confluent erythema of the entire trunk and all extremities with blistering and erosions affecting >30% of the body surface. On palpation, mild pressure causes several non‐blistered skins to slough. There is mild neutrophilia, slight elevation in liver aminotransferase levels.

Answers

1. Answer: C

Bullous pemphigoid is a rare autoimmune skin condition with an increasing incidence over the last two decades. It is caused by autoantibody‐mediated damage to the epithelial basement membrane of the epidermis. IgG +/‐ IgE antibody and activated T cells attack the protein BP180 (Type XVII collagen), or less frequently BP230 (a plakin), in the basement membrane.

There are HLA associations to suggest genetic predisposition to the disease. It most commonly affects elderly patients over the age of 70. However, drug‐induced bullous pemphigoid is linked to patients who are younger than 70 years of age and has a male predominance. The risk of developing bullous pemphigoid is greater in elderly patients with neurological disease, such as stroke, dementia, Parkinson’s disease, unipolar disorder, bipolar disease, and multiple sclerosis. The risk of developing bullous pemphigoid is also increased in patients with psoriasis and in patients treated with phototherapy. A medication, trauma, or skin infection can trigger the onset of bullous pemphigoid. Medications which are associated with bullous pemphigoid include penicillamine, frusemide, spironolactone, captopril, penicillin and its derivative, sulfasalazine, salicylazosulfapyridine, phenacetin, nalidixic acid, topical fluorouracil, neuroleptics, and dipeptidyl‐peptidase 4 (DPP‐4) inhibitors. Bullous pemphigoid is associated with underlying malignancy and appropriate screening is important.

Schmidt E Zillikens D Pemphigoid diseases The Lancet - фото 76

Schmidt E, Zillikens D. Pemphigoid diseases. The Lancet. 2013;381(9863):320–332.

https://www.ncbi.nlm.nih.gov/pubmed/23237497

2. Answer: C

This patient is likely to have coeliac disease. Classically, patients with coeliac disease present with steatorrhea, weight loss, nutrient deficiency, and resolution of the mucosal lesions (villous atrophy) and symptoms upon withdrawal of gluten‐containing foods. The malabsorption may cause weight loss, severe anaemia, neurologic disorders from deficiencies of B vitamins, and osteopenia from deficiency of vitamin D and calcium. Coeliac disease can exist in a very mild form and go largely undetected.

Dermatitis herpetiformis (DH) is a rare but persistent immunobullous disease associated with coeliac disease. It develops in 15 to 25% of patients with coeliac disease. There is a genetic predisposition with an association with HLA, DQ2, and DQ8. Some patients have a personal or family history of other autoimmune diseases including thyroid disease, pernicious anaemia, type 1 diabetes, vitiligo, and Addison disease.

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