DYP Survival guide Dermatology

Table of contents :
dyp 1 part 1......Page 1
dyp 1 part 2......Page 159
dyp 2 -1......Page 370
dyp 2 -2......Page 415
dyp 2 -3......Page 442
dyp 2 -4......Page 526
dyp 2 -5......Page 540

Citation preview


• Editors • Nitin Nadkarni

Sharmila Patil

Kiran Godse

THE EDITORS • Dr. Nitin Nadkarni (MD, DVD, DDV) Professor, Department Of Dermatology, Dr. D Y Patil Medical College and Research Center, Nerul, Navi Mumbai. • Dr. Sharmila Patil (MD, DDV) Professor and Head, Department Of Dermatology, Dr. D Y Patil Medical College and Research Center, Nerul, Navi Mumbai. • Dr. Kiran Godse (MD, DDV) Associate Professor, Department Of Dermatology, Dr. D Y Patil Medical College and Research Center, Nerul, Navi Mumbai.

CONTRIBUTORS • Dr. Mrs. Manjyot Gautam (MD Dermatology), Associate Professor, Department Of Dermatology, Dr. D Y Patil Medical College and Research Center, Nerul, Navi Mumbai. • Dr. Nanma Nikalji (MD Dermatology), Assistant Professor, Department Of Dermatology, Dr. D Y Patil Medical College and Research Center, Nerul, Navi Mumbai. • Dr. Shweta Agarwal (MD Dermatology), Assistant Professor, Department Of Dermatology, Dr. D Y Patil Medical College And Research Center, Nerul, Navi Mumbai. II

Notice Medical knowledge is a constantly changing science. Changes in treatment and drug therapy are essential as new research and clinical experiences enlighten our knowledge. The authors and publisher of this work have checked with sources which are believed to provide reliable and complete information in compliance with the standards, at the time of publication. Readers are encouraged to confirm with other sources the information that is provided in this work. As the possibility of human error exists and due to the everchanging advances in medical sciences, neither the author nor the publisher nor any other party involved in preparation or publication of this work assume any liability for any injury and/or damage to persons or property arising from this publication.


Foreword One of the most challenging tasks for a student is to prepare for an examination. Laborious years of study, hard work in the outpatients, wards, regular attendance at lectures, symposia and conferences finally culminating in the all important test of knowledge assimilation – the examination. However appearing for an examination requires a skill which an astute mind can develop only by a steadfast focus and intense preparation which will ultimately decide success or failure. It is not unusual to find one amongst equally diligent students to flounder while the others sail through an examination. It is often the big match temperament that helps one score over the other, but overall it is the preparedness that distinguishes the two. This book is compiled by a group of dedicated teachers, ably led by Dr. Nitin Nadkarni, who have kept their students on their toes by a daily exercise of case presentation followed by a viva grilling. Their experience has helped them understand common deficiencies in students which they have attempted to rectify in this book. The book gives the student a comprehensive approach to preparation for the practical examination and discusses long, short and spot cases, as well as answers a number of viva questions It is my pleasure to write this brief foreword to this wonderful book so thoughtfully prepared by Dr. Nadkarni and his colleagues. I have no doubt that it will be of great help to both students and teachers in Dermatology.

Dr. Rui Fernandes, MD, DVD, DDV Professor Emeritus Department of Dermatology, Seth GS Medical College and KEM Hospital, Mumbai. Former President, IADVL.



Preface Examinations are a test, not only of knowledge and competence, but of technique and temperament. Having (collectively) appeared for more than a dozen examinations, and having been examiners for a lot more, we are only too aware of the foibles of examiners (including ourselves) and the follies of examinees. This book is a humble attempt to guide the unwary candidate through the pitfalls of dermatology post graduate examinations at various levels (M.D., D.N.B., D.V.D., F.C.P.S., etc). This book is intended for the examination going candidate who is appearing (hopefully for the first and last time) for an important PG examination. We aim to give reliable advice on both simple and tricky questions asked by examiners in different clinical situations. We have divided the book into various sections, including long cases, short cases (and spots) as well as viva. We have collected common questions asked in the examinations, through “chatting up” our examiner friends, as well as quizzing candidates who have recently appeared for examinations (when their traumatic experiences are still fresh!). We have included lots of questions but have purposely omitted any references, for the sake of brevity. Some of the questions (and the answers) reflect our own personal preferences and idiosyncrasies, but we think that is to be expected in a book of this nature. We are extremely thankful to our teacher Dr. Rui Fernandez, who went through the entire draft of this book and gave valuable suggestions, besides consenting to write the foreword.We gratefully acknowledge the help and cooperation given by the Director of the D.Y.Patil Group of Hospitals, Mr. Vijay D. Patil as well as Dr. Shirish Patil, Dean of our Hospital. We thank Torrent Pharmaceuticals for printing and distributing this book and making it possible for us to reach the target audience in all parts of India. Lastly we would like to thank the residents of our department, who helped with the nitty-gritty of preparing this book. Special mention must be made of Dr. Aditya Mahajan and Dr. Zubin Mandlewala, whose contribution to proof reading was invaluable. Many thanks to both of them. – Editors VI


Contents 1. 2.

Hints for asppearing in examination Signs in Dermatology

1 5

LONG CASES 1. 2. 3 4 5 6 7 8 9 10 11 12 13 14

Anogenital Warts Chancroid Dermatomyositis Erythroderma Genital ulcer Gonorrhoea Hansens Disease Leg ulcers Lymphogranuloma Venerum Pellagra Psoriasis Systemic Lupuserythematosus Scleroderma Vesicobullous diseases

17 24 30 45 65 112 123 152 172 179 188 212 229 257

SHORT CASES 1. 2. 3. 4. 5. 6.

Acanthosis Nigricans (AN) Acrochordon Acna Acne Excotiée Acquired Melanocytic Nevus Aceokeratosis verruciformis of Hopf VIII

303 307 309 321 322 326

7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34.

Actinic Keratosis Alopecia Areata (AA) Aphthous Stomatitis Astratotic Eczema Atopic Dermatitis Bacterial Infections Questions Becker’s Nevus Café–Au-Lait Macules (CALM) Callus Carcinomas Congenital Melanocytic Nevus Contactdermatitis CORN (clavus) Cutaneous Tuberculosis Darier’s Disease Dermatofibroma Dermatitis Artefacta Dowling – Degos Disease Epidermal Nevi Erythema multiforme Erythema Nodosum (EN) Fixed Drug Eruptions Freckles Fox Fordyce disease Granuloma Annulare Haemangiona’s Hailey – Hailey disease Halo Nevi IX

329 333 341 346 350 357 384 387 389 391 397 399 404 407 412 415 417 419 421 425 430 435 441 443 444 447 456 459

35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59. 60. 61. 62. 63.

Henoch–schönlein purpura (HSP) Herpes simplex virus Hidradenitis Suppurativa Ichthyosis Idiopathic Guttate Hypomelanosis Incontinentia Pigmenti Keloid and Hypertrophic Scar Keratolysis exfoliativa Keratosis Pilaris Lentigo Lichen Planus (LP) Lichen Planus Pigmentosus Lichen Simplex Chronicus (LSC) Lichen Spinulosus Lichen Sclerosus Et Atrophicus Lichen striatus Linear and Whorled Nevoid Hyoeroigmentation Lipoma Lipodermatosclerosis Macular and Lichen Amyloidosis Miliaria Milium Melasma Morphea Mycetoma Nevus Comedonicus Nevus Depigmentosus Nevus of Ota and Nevus of Ito Nevus sebaceous X

461 468 479 482 485 487 490 493 494 495 501 512 514 516 517 522 525 527 530 532 536 541 544 548 553 565 568 570 573

64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. 78. 79. 80. 81. 82. 83. 84. 85. 86. 87. 88. 89. 90. 91. 92.

Nevus spilus Neurofibromatosis Nipple eczema, hand eczema and pompholyx Nummular Eczema Other Deep Fungal Infections Parapsoriasis Palmoplantar Keratoderma Paronychia Parry Romberg Syndrome Pearly Penile Papules - Hirsute Penis Pediculosis Perioral Dermatitis Phrynoderma Piebaldism Pigmented Purpuric Dermatosis Pityriasis Alba Pityriasis Rosea Pityriasis Rubra Pilaris (PRP) Prurigo Nodularis Pseudo Xanthoma Elasticum (PXE) Pyoderma Faciale Pyogenic Granuloma Reticulate Acropigmentation of Kitamura Rosaces Scabies Sebaceous Hyperplasia Striae Superficial Fungal Infection Tattoo XI

575 577 587 591 595 601 610 615 618 619 620 628 630 633 635 638 640 644 647 651 655 656 658 659 661 670 672 674 690

93. 94. 95. 96. 97. 98. 99.

Trichotillomania Tuberous sclerosis Twenty Nail Dystrophy Urticaria Xanthomas Xeroderma Pigmentosum

693 697 704 706 711 714

Yellow Nail Syndrome


100. M olluscum Contagiosum


101. Chickenpox



1. HINTS FOR APPEARING IN THE EXAMINATION In our opinion, spots are the “make or break” section of the practical’s. First impression is the last impression. Since the examiner encounters the candidate for the first time during the spots, what impression he gets will have a bearing on the final result. Hence it is imperative that a candidate does reasonably well in this section. If you get through the spots comfortably, for all practical purposes, you have passed! Important Tips: 1. The candidate should be well equipped. He should be wearing a clean (not tattered) apron with multiple pockets without any name on it. The pockets should contain: Pen, Magnifying lens (illuminated), Small Pen torch, Measuring tape, Glass slide, Pin, Cotton piece and a blotting paper (to demonstrate Auspitz sign). However, there is absolutely NO need to carry a mobile (actually, it is banned!). 2. Since most of the candidates are females, it is advisable (please accept our apologies if we sound sexist) that they should avoid the following items: Heavy makeup, streaked hair, painted and untrimmed nails, mehendi, jewellery, dangling ear rings and prominent nose rings, pencil heels (they make a distracting noise). Both males and females should wear modest clothes. You should fit in the crowd and not stand out (for the wrong reasons!). 3. Greet the examiners respectfully during the first interaction. The following instructions are targeted towards the spots. 1




Make the patient comfortable and take his permission before examining


Keep both your hands free. All the accessories should be kept in the pocket s of your apron.


Look at the lesion through a magnifying glass (which you should carry and not borrow from the examiner!).


Touch the lesion. You cannot make out whether the lesion is flat or raised by just looking. If you suspect erythema or purpura, do a diascopy. If you suspect psoriasis, or pityriasis versicolor, do grattage. Remove the scale to see the “carpet tacking” if you suspect lupus erythematosus. Spots do not mean you take a cursory glance at the patient and give your diagnosis. Please do not put your hands in your pockets or fold them. This implies you have already become a consultant (which you have not become yet).


If you want to look at other sites besides the one you are asked to see, ask the permission of the examiner before doing so.


If you want to ask questions of the patient, seek the permission of the examiner (some examiners do not allow it, but no harm in asking!).


If you suspect any infectious or neoplastic process, palpate the regional nodes (after taking permission).


As far as possible, give a single diagnosis, which is SIMPLE and COMMON. DON’T use short forms like LP, LE, PLE, (though they are used in this book for sake of brevity). Spots test your ability to come out with a single diagnosis. Try not to impress the examiner with “rare” diagnosis. We know of a candidate who came into trouble by giving a diagnosis of “porokeratosis palmaris et plantaris” when it was a



case of palmo-plantar warts. Remember, sounds of hoofs imply approaching horses and not zebras. 12. Usually the question asked is “how will you treat”? The examiner wants ONE treatment for the “SPECIFIC” patient sitting before you. Do not impress the examiner with a long list of possible treatments. First say the most common treatment you would give, with the dose (or concentration and frequency, in case of a topical medication) and duration. Also mention the general measures you would advice the patient (after talking about the specific treatment). If there is no satisfactory or specific treatment for a condition, say it, BUT immediately come out with SOME treatment or at least some general measures you would advice in case of an absolutely untreatable condition. Don’t say, there is no satisfactory treatment and stop. In a series of cases of viral infections (warts, molluscum, etc.), a candidate said, there is no specific treatment at least 3 consecutive times, without saying anything more. The examiner asked him why he was trying to become a dermatologist when he didn’t want to treat patients. Such embarrassing encounters should be avoided. We will try to discuss the common “spots” which are kept in the examination. The list is NOT inclusive, since potentially any lesion on the skin (including a tattoo) is worthy of being kept as a spot! In case of short and long cases, following hints will be helpful: 1. Write down all the history and examination findings as you would write in the ward notes. Many examiners look at them and criticize them. 2. Take a targeted history in short cases but a detailed history in long cases.




When time is limited, try to do the history taking and examination at the same time. This is especially true of leprosy cases, where you will be really pressed for time. 4. Give a specific yet detailed diagnosis. For example, in psoriasis, tell about the type of psoriasis, extent of involvement, stable or unstable, etc. 5. When examiner asks “how will you manage”, start with investigations; when he asks how you will treat, start with the treatment. 6. Always talk about counseling and advice to the patient in the beginning of your treatment. 7. DON’T use trade names of medications. Always mention the dose or concentration of the medications even without being asked. 8. Do not forget to look at special sites: genitals, palms, soles, mouth, peri-anal areas, scalp, nails. 9. In case a patient refuses to allow you to examine a particular site, do not forcibly make him/her strip, but just inform the supervisor about it. 10. Ask for a tongue retractor, vaginal speculum but do not insist that the patient allows you to use it. In case of any controversy, inform the supervisor. In general, please remember, DO NOT ARGUE WITH THE EXAMINERS. They are INFALLIBLE during the course of the examinations. As one of my respected teachers said, if the examiner says that the sun rises in the west, nod respectfully and say that it has been reported. Do NOT however, quote textbooks at the examiners to quote your point. Remember, there is such a thing as winning the battle and losing the war!




The scales are completely scraped off, seen as a moist red surface (membrane of Bulkeley) through which dilated capillaries at the tip of elongated dermal papillae are torn leading to multiple bleeding points. Parakeratosis, suprapapillary thinning of the stratum malpighii, elongation of dermal papillae and dilation and tortuosity of the papillary capillaries, psoriasis, darier’s disease and actinic keratosis 2.


Also called cat’s tongue sign and tin tack sign in DLE, partially adherent scales entering a patulous follicle. When the scale is removed, its undersurface shows horny plugs that had occupied follicles. Seborrheic dermatitis and pemphigus foliaceous 3.


Also called coup d’ongle sign, besnier’s sign, stroke of the nail sign. Seen in Pityriasis versicolor and is an important diagnostic tool. Occurs may be due to the loosing of barely perceptible scale with a fingernail. Scale is usually white or light tan and flakes off rather easily. 4.


Refers to the urtication and erythematous halo that are produced in response to rubbing or scratching of lesions of cutaneous mastocytosis. Named after the French dermatologist Ferdinand-Jean Darier. 5



Conditions associated with Darier’s sign: Cutaneous mastocytosis, leukemia cutis, juvenile xanthogranuloma, histocytosis and lymphoma. A transient piloerection and elevation or increased induration of a lesion induced by rubbing and is observed in congenital smooth muscle harmartomas. 6. DERMATOGRAPHISM A form of physical urticaria that consists of local erythema due to capillary vasodilation, followed by edema and a surrounding flare due to axon reflex induced dilation of arterioles, which is observed after the firm stroking of skin. 7. MARFAN SYNDROME: Unusually tall habitus, long, thin extremities, arachnodactyly, joint hypermobility, excessive length of the lower extremities, armspan exceeding the individual’s length. 8. WRIST SIGN: Wrist sign is the overlapping of the thumb and fifth fingers when these encircle the opposite wrist. 9. THUMB SIGN Also called Steinberg sign Is the extension of the thumb past the ulnar border of the hand when apposed to the palm 10. EHLERS-DANLOS SYNDROME Joint hypermobility limited to the digits and hyperextensible skin 11. BEIGHTON SIGN Is the passive apposition of the thumb to the flexor aspect of the forearm. India-rubber man: Hyperextensibility of the skin and



give rise to gaping ‘fish mouth wounds’ over bony prominences like shins, knees and elbows. Wide, thin, papyraceous scars over the knees and elbows are called ‘cigarette paper scars’. 12. GORLIN’S SIGN Is the ability to touch the tip of the nose by extension of the tongue. Seen in pseudoxanthomaelasticum. 13. ANTENNA SIGN It is seen in keratosis pilaris in which individual follicles show a long strand of keratin glinting when examined in tangentially incident light. 14. ASBOE-HANSEN SIGN (BLISTER SPREAD SIGN) Gustav Asboe Hansen first described it in 1960. He demonstrated enlargement of bulla by applying finger pressure to small, intact, and tense bulla in patients with pemphigus and bullous pemphigoid. In the traditional bulla spread sign, pressure is applied to the blister from one side, whereas in Asboe-Hansen sign pressure is applied at the center of the blister and perpendicular to the surface due to smaller size of the lesion. 15. BARNETT’S SIGN (SCLERODERMA NECK SIGN) It is ridging and tightening of the skin of the neck on extending the head with a visible and palpable tight band over platysma in the hyperextended neck. 16. BRANHAM’S SIGN (Nicoladoni sign) It is to be elicited in cases of arterio-venous fistula where there is slowing of the heart rate in response to (manual) compression.




“BREAKFAST, LUNCH, AND DINNER” SIGN The bites of bed bugs (Cimex lectularius) usually follow a linear pathway in a group of three to five blood meals and are often referred to as “Breakfast, lunch, and dinner” or “Breakfast, lunch, and supper” sign. 18. BUSCHKE-OLLENDORFF SIGN This is a sign to be elicited in case of secondary syphilis and cutaneous vasculitis, where there is deep dermal tenderness on pressing the lesion (e.g., papular lesions of syphilis) with a pinhead. 19. BUTTERFLY SIGN This refers to sparing of the mid scapular region in patients having prurigo nodularis with neurodermatitis as they are unable to reach the region for scratching. 20. BUTTONHOLE SIGN In type 1 neurofibromatosis (Von-Recklinghausen’s disease), neurofibromas can be invaginated with the tip of index finger back into the subcutis and again reappear after release of pressure. Other condition where one can find positive buttonhole sign are anetoderma and dermatofibroma. 21. CORAL BEAD SIGN Papules seen around the nail fold in multicentric reticulohistiocytosis are called as coral bead sign. 22. CHAGAS-MAZZA-ROMAÑA’S SIGN In about eighty percent of cases of Chagas’ disease (American trypanosomiasis), conjunctiva is the portal of entry for TrypanosomaCruzi Unilateral swelling of eyelids and orbit after conjunctival inoculation is called as eye-sign or ChagasMazza-Romaña’s sign or Romaña’s sign.




COUDABILITY SIGN It was first described by Shuster in cases of alopecia areata in 1984. Coudability sign is normal-looking hairs tapered at the proximal end in the perilesional hair-bearing scalp and can easily be made to kink when bent or pushed inward. 24. CULLEN’S SIGN Periumbilical ecchymosis in cases of acute hemorrhagic pancreatitis and ruptured ectopic pregnancy is termed Cullen’s sign. Similar changes in the flank is called as Grey-Turner sign. 25. DECK-CHAIR SIGN It was classically described in Papulo-erythroderma of Ofuji, wherein there are flat-topped red papules that become generalized erythrodermic plaques without the involvement of abdominal skin folds. 26. DIMPLE SIGN (FITZPATRICK SIGN) Squeezing the skin adjacent to a dermatofibroma causes a dimpled appearance on its surface, also termed a positive “pinch sign” or “dimple sign”. 27. DORY-FLOP SIGN It is described in relation to syphilitic chancre on the coronal border of the prepucial skin in an uncircumscribed male, whereupon on retracting the foreskin the entire ulcer flips out all at once because it is too hard to bend due to underlying button like induration. 28. FORSCHEIMER’S SIGN Seen in 20% of rubella patients, where there is an enanthem of dull-red macules or petechiae confined to the soft palate during the prodromal period or on the first day of the rash. Can also be seen in infectious mononucleosis.




FRANK’S SIGN Diagonal crease in the earlobes of adults has been associated with an increased risk for atherosclerotic heart disease. 30. FRIAR TUCK SIGN Friar tuck was a companion of Robin Hood in the legendary stories who had alopecia of the vertex with sparing of occipital region. This is described in relation to trichotillomania, where patient plucks his own hair either in a wave like pattern across the scalp or centrifugally from a single starting point. Hairs over the occipital area are mostly spared in trichotillomania and is referred as Friar Tuck sign. 31. GOTTRON’S SIGN It is a characteristic finding in dermatomyositis typified by scaly erythematous eruption seen on the dorsa of hands, metacarpophalangeal joints, and proximal interphalangeal joints. 32. HAIR COLLAR SIGN It is a marker of cranial dysraphism, including encephalocele, meningocele, and heterotropic brain tissue. Ectopic neural tissue in the occipital and parietal areas takes the form of smooth dome-shaped hairless nodules and sometimes a collar of hypertrichosis surrounds them, this is called as hair-collar sign. 33. HAIRY PALM SIGN It is a characteristic histopathological finding seen in prurigo nodularis, where there is a presence of thick compact orthohyperkeratosis; the hairy palm sign (folliculosebaceous units seen with a thick and compact cornified layer, seems like that biopsy has been taken from palm, i.e., volar skin but contains pilosebaceous unit).




HAMBURGER SIGN This sign has been described in relation to trichotillomania, wherein there is vertically oriented split of hair shafts and proteinaceous material and erythrocytes are present in the split resembling a hamburger within a bun. 35. HERTOGHE’S SIGN (QUEEN ANNE’S SIGN) It is defined as loss of lateral one third of eye-brows (superciliary madarosis). It is seen in leprosy, myxedema, follicular mucinosis, atopic dermatitis, trichotillomania, ectodermal dysplasia, discoid lupus erythematosus, alopecia areata, syphilis, ulerythema ophryogenes, systemic sclerosis, HIV infection, and hypothyroidism. 36. HANGING CURTAIN SIGN It is seen in patients with pityriasis rosea. When the skin is stretched across the long axis of the herald patch, the scale is noted to be finer, lighter, and attached at one end, which tends to fold across the line of stretch. 37. HOLSTER SIGN OF DERMATOMYOSITIS Literally, holster means an extra pocket made from various materials to hold something where it can quickly be taken out for use (e.g., Gun holster). Confluent macular violaceous erythema present on the lateral side of hip and thighs is called as “Holster sign” corresponding to the site of hanging a holster. 38. HYPOPYON SIGN Hypopyon sign describes the presence of small, discrete, vesicles either flaccid or tense that become secondarily infected and pus accumulates in the lower half of the pustule. It is a clinical sign seen in pyodermas and secondarily infected vesicobullous disorders (e. g.,



pemphigus, bullous pemphigoid, and linear IgA dermatosis), where there is a transverse fluid level comprising of purulent material at the bottom when the patient is in a standing position and is called hypopyon sign. 39. INGRAM’S SIGN Inability to retract the lower eye-lid in patients of progressive systemic sclerosis due to underlying sclerosis is called Ingram’s sign. 40. KAPOSI-STEMMER SIGN Inability to pinch or pick up a fold of skin at the base of the second toe because of its thickness. It is seen in chronic lymphedema. 41. LESER-TRELAT SIGN First described by Edmund Leser and Ulysse Trelat, characterized by sudden eruption of numerous seborrhoeic keratosis, usually associated with pruritus and is considered as a marker of internal malignancy. 42. LOVE’S SIGN Exact localization of tenderness with the help of pin head in glomus tumor is called as Love’s sign. 43. MATCHBOX SIGN Patient having delusions of parasitosis (acarophobia, entomophobia) collects skin debris with mistaken belief that such collected material contains alleged parasite in a matchbox, tissue paper, or small container. This whole exercise executed by the patient is referred to as “matchbox sign.” 44. MEFFERT’S SIGN It is described in Fordyce’s disease, characterized by presence of ectopically located sebaceous glands on the lips, oral mucosa and less commonly on gums. Prominent lip



involvement can result in a lipstick like mark left on the rim of a glass mug after consuming a hot beverage (Meffert’s sign). 45. MILIAN’S EAR SIGN Erysipelas and cellulitis have traditionally been defined as acute inflammatory processes of infectious origin that primarily affect the dermis (in the case of erysipelas) or deeper dermis and subcutaneous tissue in cellulitis. It is a sign used to distinguish between erysipelas and cellulitis of the facial region, where there is involvement of ear in erysipelas and sparing in cellulitis, as there is no deeper dermal tissue and subcutaneous fat. 46. MIZUTANI’S SIGN (ROUND FINGER PAD SIGN) It is seen in Raynaud’s phenomenon associated with systemic sclerosis. This sign refers to disappearance of the peaked contour on fingerpads and replacement with a hemisphere-like fingertip contour especially on ring fingers. 47. NAZZARO’S SIGN Follicular hairy hyperkeratosis (horny follicular spicules) commonly located on the face which shows compact follicle bound hyperkeratosis is a rare but typical clinical finding in multiple myeloma and is termed as Nazzaro’s sign. 48. PASTIA’S SIGN Linear petechial eruption in the skin folds especially on the ante-cubital fossa and axillary fold seen in streptococcal scarlet fever is called Pastia’s sign. 49. PATRICK YESUDIAN SIGN Palmar melanotic macules (palmar freckling) seen in type 1 neurofibromatosis was first reported by Patrick Yesudian and hence the name.




PRAYER SIGN It is described in relation to diabetic cheiroarthropathy, wherein the patient is requested to bring both the palmar surface of the hands together as at prayer. Prayer sign is said to be positive when patient is unable to bring both the palmar surface together completely and it indicates limited joint mobility. Limited joint mobility is secondary to nonenzymatic glycosylation of collagen and its deposition in the small joints of the hand. 51. PUNSHI’S SIGN In young women and girls having from vitiligo the original white color of vitiligo macules turns to red-pink during menstruation and after the menstruation, it turns to the original colour 52. PUP-TENT SIGN It is seen in nail lichen planus, in which the nail splits and elevates longitudinally with downward angle of lateral nail edge. 53. REVERSE NAMASKAR SIGN Namaskar’ is the typical Indian way of greeting people, where the forearms are folded in front of the chest and the palms are closely approximated together. In patients with hyperextensible joints as seen in Ehler Danlos syndrome, they are able to fold their forearms at the back and oppose their palms to say “Namaskar,” demonstrating the hyper extensible joints. 54. ROPE SIGN It refers to the thick indurated inflammatory cord like structure that extends from the lateral trunk to the axillae and said to be a classical finding of interstitial granulomatous dermatitis (Ackerman’s syndrome) with arthritis.




RUSSELL’S SIGN Crusted callosity on the knuckles of dominant hand due to repeated self-induced vomiting in patients of bulimia. 56. SANDWICH SIGN In dermatophytosis, fungi are present in the horny layer between two zones of cornified cells, the upper being orthokeratotic and lower consisting partially parakeratotic cells. 57. SHUSTER’S SIGN Scarring of the concha due to lesions of discoid lupus erythematosus is called as Shuster’s sign and it can be present in 30% of the cases. 58. SHAWL SIGN Confluent macular violaceous erythema on the posterior neck and shoulders in patients of dermatomyositis is called Shawl sign. 59. UGLY DUCKLING SIGN In 1998, Grob and Bonerandi introduced the “ugly duckling” concept to demonstrate that nevi in the same individual tend to resemble one another and that atypical mole often deviates from the individual’s nevus pattern. In other words, nevus that does not resemble other nevi is more likely to be suspicious of melanoma. 60. VOLCANO SIGN It is descriptive term for the morphologic feature of Old World cutaneous leishmaniasis. The lesion starts as a small nontender papule, which enlarges in size and ulcerates in the centre. The border of the crusted ulcer often has an erythematous rim and is called as “Volcano sign.”.



What are Anogenital Warts?


Anogenital Warts are the most common manifestations of sexually transmissible infection caused by Human Papilloma Virus(HPV 6, HPV 11).


What are the genital lesion associated with HPV infections?



Condyloma acuminata- HPV-6, 11


Non-condylomatous lesions and/or intraepithelial neoplasia- HPV 6, 11, 16, 18, 30, 31, 33, 34, 35, 39, 40, 42, 43, 45, 51, 52, 56, 57, 59, 61, 62,64.


Carcinoma- HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 66, 68


Vulvar Papilloma - HPV 70


Busckhe Lowenstein tumor - HPV 6,11




How are anogenital HPV subdivided?



Low or no oncogenic risk - HPV types 6, 11, 42, 43 and 44.


Intermediate risk - HPV types- 31, 33, 35, 51 and 52.


High risk - HPV types-16, 18, 45 and 46.


What are the types clinical types of genital warts?



Condyloma acuminata.


Papular warts.


Macular warts.


Verruca vulgaris or Keratotic Warts.


Sessile Warts.


Flat Warts. 17




Q. A.

Intraepithelial Neoplasia (Bowenoid Papulosis and Bowen's disease) 8] Giant Condyloma (Buschke Lowenstein tumor). How anogenital warts are transmitted? ADULTS - Mostly sexual transmission. Perianal warts may accompany genital warts, either due to local spread of infection or to direct contact during anal coitus. CHILDREN- Anogenital warts are uncommon in children, but their occurrence frequently stimulates the possibility of sexual transmission and sexual abuse. Infection from the mother's genital tract at delivery is regarded as a frequent source of childhood anogenital warts, probably including those presenting up to 2 years of age.


Postnatally, transmission from adults with genital warts may occur nonsexually such as by sharing a bath with an infected adult. Q.

Describe the clinical appearance of Condyloma acuminata(acuminate warts)?


(condyloma = knuckle, acuminatum= pointed; plural condylomata acuminata). Soft, Pink, Pedunculated papilliferous masses (cauliflower like) with fingerlike peduncles and an irregular surface. Does not bleed on touch. Site-Labia minora, introitus, vagina, cervix, anus, prepuce, frenulum, glans penis, urinary meatus.


What is Giant Condyloma Acuminata?


Giant Condyloma acuminata, also known as Buschke Lowenstein tumor is a rare, aggressive wart-like


growth that is verrucous carcinoma. This is caused by HPV-6 and 11. Site-Glans and prepuce of an uncircumscribed male; less often in perianal skin and vulva. It may invade deeply into the underlying dermal structures. Q.

Describe the clinical appearance of flat warts?


Flat warts are slightly raised, may exhibit an undulating wavy surface. Located anywhere on genital epithelium. On vulval vestibule - velvety, granular, or cobblestone-like surface known as ''vulval papillomatosis''. On colposcopic examination, these lesions are described as ''Arizona cactus-like projections'', ''Camel hump like projections'' and ''Stony colonial pavement-like projections''.


Describe about papular warts?


Protruberant, non-pedunculated, dome-shaped, or hemispherical masses, about 1-4mm in diameter and are located in fully keratinized epithelium.


Describe about Macular variants?


Macular lesions are usually found on mucosal surfaces, characterized by subtle changes in the colour of mucosa, a greyish-white colour being most common manifestation. Occassionally, there may be slight capillary punctuation and slight elevation at the edges of the lesion may be present. To visualize them, 3-5% acetic acid is applied and the affected area is covered with a gauze piece soaked in acetic acid for 5 mins. Macular lesion are stained grayish white. This whitish appearance is attributed




to an overexpression of cytokeratin 10 in suprabasal cells. Q.

Describe the histopathology of warts?


Hyperkeratosis of stratum corneum, papillomatosis and acanthosis of stratum malpighii and thickening and elongation of rete ridges. Most characteristic feature is presence of epithelial cells with perinuclear vacoulization known as Koilocytes. There is peripheral rim of condensed cytoplasm with hyperchromatic and large nucleus.


What is the treatment of external genital warts?



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Podofilox 0.5% solution or gel OR Imiquimod 5% cream OR Sinecatechins 15% ointment Provider-Administered: Cryotherapy with liquid nitrogen or cryoprobe. Repeat applications every 1-2 weeks. OR Podophyllin resin 10%-25% in a compound tincture of benzoin OR Trichloroacetic acid (TCA) or Bichloroacetic acid (BCA) 80%-90% OR Surgical removal either by tangential scissor excision, tangential shave excision, curettage, or electrosurgery. Therapies not generally recommended: used only in

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special situation, includes interferons, 5-flurouracil, Bleomycin, cidofovir, retinoids, gluteraldehyde, formaldehyde, cantharidin etc. Are any vaccine available for HPV infections? Yes. Two HPV vaccines are available, both of which offer protection against the HPV types that cause 70% of cervical cancers (i.e., types 16 and 18); 1] The quadrivalent vaccine(Gardasil) protects against the types 6, 11, 16 and 18 of HPV. Contains recombinant virus-like particles from the L1 proteins of HPV-6, 11, 16, and 18. Recommended to be given to females between 9-26years. Given in arm muscle in three doses. Dose 1, Dose 2- 1 month after dose 1, Dose-36months after dose 1. 2] The bivalent vaccine(Cervarix) protects against HPV 16, 18 types. Contains L-1 protein of viral capsid. Vaccine has no live virus so do not infect the patient. Given to females between 10-45 years of age. Cervarix is more effective against HPV than Gardasil. How podophyllotoxin is applied? Podophyllotoxin is a purified extract of Podophyllum plant which binds to cellular microtubules, inhibits mitotic division at metaphase, and induces necrosis of warts that is 3-5 days after administration. Podofilox solution(0.5%) or 0.15% cream should be applied with a cotton swab, or podofilox gel with a finger, to visible genital warts twice a day for 3 days, followed by 4 days of no therapy. This cycle can be repeated, as necessary, for up to four cycles. The total



wart area treated should not exceed 10 cm2, and the total volume of podofilox should be limited to 0.5 mL per day. Mild to moderate pain or local irritation might develop after treatment. The safety of podofilox during pregnancy has not been established. Q. A.

How imiquimod is applied? Imiquimod is a topically active immune enhancer that stimulates production of interferon and other cytokines. Imiquimod cream should be applied once daily at bedtime, three times a week for up to 16 weeks. The treatment area should be washed with soap and water 6-10 hours after the application. Local inflammatory reactions, including redness, irritation, induration, ulceration/erosions, and vesicles, are common with the use of imiquimod, and hypopigmentation has also been described.

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How is Sinecatechin ointment applied? Sinecatechin ointment, a green-tea extract with an active product (catechins), should be applied three times daily (0.5cm strand of ointment to each wart) using a finger to ensure coverage with a thin layer of ointment until complete clearance of warts. This product should not be continued for longer than 16 weeks. The medication should not be washed off after use. Sexual (i.e., genital, anal, or oral) contact should be avoided while the ointment is on the skin. The most common side effects of sinecatechins 15% are erythema, pruritus/burning, pain, ulceration, edema, induration, and vesicular rash. This medication may weaken condoms and diaphragms. The medication is not recommended for HIV-infected


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persons, immunocompromised persons, or persons with clinical genital herpes. How Podophyllin resin is applied? Podophyllin resin 10%-25% should be applied to each wart and allowed to air-dry before the treated area comes into contact with clothing; overapplication or failure to air dry causes local irritation caused by spread of the compound to adjacent areas. The treatment can be repeated weekly, if necessary. To avoid the possibility of complications associated with systemic absorption and toxicity, two guidelines should be followed: 1) Application should be limited to 5 cells/cubic mm) then it is suggestive of active neurosyphilis in which case retreatment is essential even if VDRL is negative. While if the protein count is high with the cell count being low then it is not significant. Q. Stigmata of syphilis? Syphilitic facies Frontal bossing, saddle nose, short maxilla, protuberant mandible Ophthalmologic Interstitial keratitis, chorioretinitis, secondary glaucoma, corneal scarring, optic atrophy Ears Sensorineural hearing loss Oropharynx Hutchinson teeth, mulberry molars, perforation of hard palate Cutaneous Rhagades, gummas Central nervous system Intellectual disability, arrested hydrocephalus, seizures, optic atrophy, juvenile general paresis Skeletal Saber shins (anterior bowing of the tibia), Higoumenakis sign (enlargement of the sternoclavicular portion of the clavicle), Clutton joints (painless arthritis), scaphoid scapula




What are the differentiating features of various STD ulcers?







Incubation Period Primary lesion

9-90 days

2-7 days

1-14 days

3 days-6 weeks

1-4 weeks (up to 6 months)


Vesicle (erosion)

Papule/Pust ule

Papule, pustule,or vesicle Usually one


Number of lesions

Usually one

Multiple , may coalesce


Erythematous, Cratered


Sharp, Well demarcated, Round or Oval Deep or Superficial Smooth, Nonpurulent , Relatively nonvascular Indurated

Pain Lymph nodes Fluctuance


Multiple , may coalesce Ragged, Undermined , Irregular Excavated

Serous, Erythematous, Nonvascular

Purulent, Vascular, Friable



Occasionall y firm



Often Tender

Very tender





May suppurate

Tenderness None



May suppurate Tender

Distributio n

Bilateral with primary infection

Usually Unilateral

Usually Unilateral

None; pseudobuboes None; pseudobuboes None; pseudobuboes

Depth Base



Elevated, round, or oval

Elevated, irregular

Superficial or deep Variable, nonvascular

Superficial or deep Red and velvety, bleeds Readily


What does the word HERPES means?


The word Herpes is derived from Greek word which means to creep.


What is the causative organism for Herpes genitalis?


Human herpes virus-2 is the most common organism implicated in Herpes Genitalis. However HHV 1 can cause the same in case of oral intercourse.


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What is Primary Herpes infection, First Episode Infection and what is recurrent herpes infection? Primary Herpes Infection- 'Primary infection' denotes initial HSV infection in individuals without preexisting antibodies to HSV-1 or HSV-2. First episode infection denotes initial clinical attack of HSV in individuals with pre existing antibodies to HSV 1 or HSV 2 due to previous subclinical infection with the virus Recurrent Herpes Infection- The reactivation of HSV after the establishment of latency. Non Primary genital infection- refers to an infection with one HSV type in an individual who already has pre-existing antibodies to the other HSV type. What are the risk factor for transmission of genital herpes? Risk factors associated with the transmission of genital herpes include 1] an age of 15-30 years (period of greatest sexual activity), 2] an increased number of sexual partners, 3] black or Hispanic race, 4] lower income levels and education, 5] female gender, 6] homosexuality and 7] HIV positivity. Describe the pathogenesis of Herpes infection? The causative organism of Herpes genitalis, HSV-2 spreads primarily by sexual contact.



Virus will replicate at the site of infection (i.e. the mucocutaneous surface), PRIMARY HERPES INFECTION

Virus then travel by retrograde axonal flow to the dorsal root ganglia and establish latency. Latency enables the virus to exist in a relatively non-infectious state for varying periods of time in its host. LATENCY Stress, UV light, Fever, Tissue damage, Immunosuppression.


How do you differentiate primary and recurrent herpes genitalis?


Prodromal symptoms Number of lesions Severity(Pain and extent) Time taken for resolution Complications Regional lymph nodes Scarring

Primary More severe more more 2-6 weeks More common Enlarged and tender Sometimes

Recurrent Less severe Limited Less 1 week Uncommon Not involved Never


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Why does Non-Primary Genital Herpes lesion heal faster? Patients with non-primary first episode have neutralising antibodies to HSV-1 which interrupts the spread of HSV infection. Thus they have lower frequencies of systemic symptoms, shorter duration of pain, fewer lesions and shorter healing time compared to true primary infections. What are the atypical presentations of genital herpes? 1] vaginal discharge(unrelated to candidiasis) 2] genitourinary pain 3] nonspecific vulvar erythema 4] prostatitis and lower back pain 5] itching, burning, soreness, pain over genital area( without obvious lesions) 6] unexplained systemic symptoms- fever, malaise, myalgia 7] vulvar, penile or perianal fissures 8] folliculitis. How does Herpes in HIV present? 1] hyperkeratotic, verrucous lesions 2] vegetating plaques 3] chronic, persistent ulceration 4] generalised papular eruptions How will you investigate the case of genital HSV ? 1] Collection of specimen - A large vesicle should be chosen and fluid should be aspirated with a tuberculin syringe. If large vesicle is not present, then exudates of a small vesicle or open lesion is


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collected by vigorously rubbing with a cottontipped swab on a wire shaft and sent for culture. To collect cervical specimens, swabs should be taken from ectocervix and the entry of the endocervical canal, as the HSV involves squamous rather than columnar epithelium. The specimen should be placed immediately into vials containing 1ml of viral transport medium and should be kept at 4 degree until cultured. 2] Culture- Gold Standard for diagnosis of acute HSV infections. Human diploid fibroblast cell lines is used- HSV takes 12-18 hrs for replication. 3] Confirmatory tests- Neutralization with type specific antisera, Immunological assays, Nucleic acid hybridization. Describe the bedside test for Herpes infection? Tzanck test is the bedside investigation for herpes Infection. Specimen collected. Slide is air-dried.

Slide is covered with Giemsa stain (which is diluted 1:10 with distilled water) for 15 mins. Wash with water. Air dry the slide and examine under oil immersion.



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What will you see in Tzanck smear? Acantholytic cells(secondary acantholysis) with multinucleated gaint cell. What is the significance of HSV antibody titres? HSV IgG- Past infection. HSV IgM- Recent infection. What are the sequelae of genital herpes? 1] Psychological morbidity associated with recurrences. 2] Psychological morbidity related to fear of transmission to partner or fetus or newborn. 3] Systemic complication. 4] Increased risk of acquiring or transmitting HIV infections. What are the systemic complications associated with Herpes Infections? 1] Aseptic meningitis. 2] Radiculomyelopathy- urinary retention, numbness, paresthesias, neuralgic pain of buttocks, constipation, impotency. 3] HSV encephalitis. 4] Disseminated infections 5] Transmission to newborn. 6] Secondary microbial infection. 7] Pelvic inflammatory disease 8] extragenital lesions What measures can be helpful for prevention of HSV infections? 1] Abstinence.

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2] 3]

Limiting number of sexual partners. Avoiding partners who have a history of genital herpes. 4] Consistent and correct condom use. 5] Vaginal and rectal microbicides. 6] Antiviral therapy. 7] Vaccines. Q. How will you manage genital herpes infections? A. General Measures1] Counselling 2] Maintainence of local hygiene. 3] Sietz bath. Topical TreatmentTopical antibiotics to avoid secondary infection. Systemic TreatmentParacetamol- 500mg, 4 hourly may relief pain. Anti-Virals (Acyclovir, Valacyclovir, and famciclovir) reduce viral shedding, itching, average healing time, and frequency of new lesion formation. CDC GUIDELINES-2010 FIRST EPISODE

Acyclovir 400 mg orally three times a day for 7–10 days OR Acyclovir 200 mg orally five times a day for 7–10 days

EPISODIC THERAPY FOR RECURRENT GENITAL HERPES Acyclovir 400 mg orally three times a day for 5 days OR Acyclovir 800 mg orally twice a day for 5 days OR

SUPPRESSIVE THERAPY FOR RECURRENT GENITAL HERPES Acyclovir 400 mg orally twice a day OR Famiciclovir 250 mg orally twice a day OR Valacy clovir 1 g orally once a day

GENITAL HERPES IN HIV INFECTED INDIVIDUALS AND OTHER IMMUNOCOMPROMISED EPISODIC TREATMENT-Acyclovir 400 mg orally three times a day for 5–10 days OR Famciclovir 500 mg orally twice a day for 5 – 10 days



OR Famciclovir 250 mg orally three times a day for 7–10 days OR Valacyclovir 1 g orally twice a day for 7–10 days *Treatment can be extended if healing is incomplete after 10 days of therapy.

Famciclovir 125 mg orally twice daily for 5 days. OR Valacyclovir 1 g orally once a day for 5 days

OR Valacyclovir 1 g orally twice a day for 5–10 days SUPPRESSIVE TREATMENTAcyclovir 400–800 mg orally twice to three times a day OR Famciclovir 500 mg orally twice a day OR Valacyclovir 500 mg orally twice a day.


What are the indications of IV acyclovir?


Immunocompromised patient with disseminated herpes.


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CNS complications (Herpetic meningoencephalitis) pneumonitis, or hepatitis Severe initial clinical episodes in immunocompetent patient. Neonatal Herpes simplex virus infections. Varicella zoster infection in immunocompromised infections. Patient is unable to swallow or tolerate oral acyclovir because of vomiting. Q.

How is IV Acyclovir administered?


5-10 mg/kg, 8 hourly infused at a constant rate over 1 hour for 3-7 days or until clinical improvement observed, followed by oral antiviral therapy to complete at least 10 days of total therapy. Acyclovir dose adjustment is required in renal failure.

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How is Acyclovir injection available? It is available as sterile solution containing acyclovir containing 25mg/ml (as 20ml and 40ml vials). How will you manage asymptomatic sex partners of patients with genital herpes? Asymptomatic sex partners of patients who have genital herpes should be questioned concerning histories of genital lesions and offered type-specific serologic testing for HSV infection. What is the risk of transmission of genital herpes from mother to neonate? The risk for transmission to the neonate from an infected mother is high (30%-50%) among women who acquire genital herpes near the time of delivery and low (