s e s a e s i d T N E 1 Many give steroids \200\230to reduce oedema \200\231 (esp. if <6 days since onset). Help ful studies: Hat & Shafshak217 showing that bene \201 t of steroids may be con \201 ned t o those treated in 24h of onset. Spontaneous recovery is good-ish anyway. For every 3 peopl e treated with steroids within 24h, 1 extra had a good recovery compared with no treatment; for ethical reasons, this study was not randomized. Older randomized stud- ies were inconc lusive, but did not look speci \201 cally at early treatment. Meta-analyzes support steroi ds. 218 575 s e s a e s i d T N E 8 Sphenopalatine ganglion 9 Superior maxillary nrv 10 Lacrimal gland 11 Large deep petrosal nrv 12 Vidian nerve 13 Nose & palate gland nrvs 14 Small petrosal nerve at geniculate gang lion 17 Auricular branch 18 Stylomastoid foramen 19 Lingual nerve \200\224visceral motor VII & t aste VII & general sensory to tongue (V3) 1 Facial nerve nucleus, deep in the reticular formation of lower pons 2 Spinal nucleus of V 3 Superior salivary nucleus 4 Solitary tract 5 Porus acusticus internus 6 Meatal foramen 7 Large petrosal nerve 20 Submandibular ganglion 21 Submandibular gland 22 Sublingual gland 15 Stapedial nerve 16 Chorda tympani Fig 1. Facial nerve branches. Reproduced from Oxford Handbook of Clinical Medicine, with permission Fig 2. Bell \200\231s palsy: the patient is trying to smile, but his right lower lid is dro oping, the naso-labial fold is slack, and the lips do not move. OUP data bank \200\207Wh enever you see someone with Bell \200\231s palsy within 3 days of its starting, ask about p reced- ing pain in the ear, stiff neck, or a reddish auricle: if these are associated with severe paralysis, the cause is likely to be zoster (without vesicles: zoster sine herpete) \200\224and high-dose antivirals eg valaciclovir 1g/8h PO for 7 are indicated, days 219 (+p rednisolone). If there are no prodromal features, zoster is less likely and lower doses of antivirals may be used (eg valaciclovir 500mg/12h PO for 5 days). Lumps in the neck \200\207Don \200\231t biopsy neck lumps! Refer any possibly malignant ne ck lump to ENT, where thorough assessment and search for a primary can be done, eg in a ded icated fast-track \200\2302-week rule \200\231 neck lump clinic220 with access to \201 n e- needle aspiration (FNA for cytology \200\224beware pulsatile lumps!) and CT/MRI (MRI is better). \200\207Culture any specimens for TB: don \200\231t put it all in formalin. Diagn osis \200 How long has the lump been present? If <3 weeks, lymphadenopathy from 576 \200 a self-limiting infection is likely, and extensive investigation is unwise. Which tissue layer is the lump? Is it intradermal? (eg from sebaceous cyst with a central punctum, or a lipoma.) If the lump is not intradermal, and not of recent onset, allow yourself to feel the intoxic ating pleasure of a hunt beginning over complex terrain. But remember \200\224you are vastl y outnumbered by a pack of diseases, so be cunning. The first step in this process is a pro per appreciation of anatomy. Midline lumps In patients <20yrs old, the likely diagnosis is a dermoid cyst, or, if it moves on protruding the tongue and is below the hyoid, a thyroglo s- sal cyst (a \202 uctuant lump developing in cell rests in thyroid \200\231s migration path; treated by surgery). If over 20, it \200\231s probably a thyroid mass, unless it is b ony hard, when the diagnosis may be a chondroma.221 Submandibular triangle (Below jaw; abov e anterior belly of digastric.) If <20yrs, self-limiting lymphadenopathy is likely. If >20, exclude malignant lym- phadenopathy (eg \201 rm and non-tender). \200\207Is TB likely? If it \200\231s not a node, think of submandibular salivary stone, tumor, or sialadenitis.2 22 Anterior triangle (Below digastric and in front of sternomastoid.) Nodes are common (see above): remember to examine the areas which they drain (is the spleen enlarged? \200\224th is may indicate lymphoma). Branchial cysts emerge under the anterior border of sternomastoi d where the upper \205\223 meets the middle \205\223; age <20. The popular theory is that they are due to non-disappear- ance of the cervical sinus (where the 2nd branchial arch gr ows down over 3rd and 4th) but this is not universally accepted. Lined by squamous epitheli um, their \202 uid contains cholesterol crystals. Treat by excision. Cystic hygromas (mac rocystic lymphatic malformations) arise from the jugular lymph sac and transilluminate brig htly. Treat by surgery or hypertonic saline sclerosant. Ca- rotid body paraganglionomas are very rare, move from side-to-side, but not up and down, and splay out the carotid bifurcat ion. They are \201 rm (softness is rare) and pulsatile, and do not usually cause bruits. They may be bilateral, familial, and malignant (5%). This tumor should be suspected in tumo rs just anterior to the upper third of sternomastoid. Diagnose by MRI. Treatment: extirpati on by vascular surgeon. If the lump is in the superoposterior area of the anterior triangle , is it a parotid tumor? (more likely if >40yrs). A laryn- gocele is an uncommon cause of a lump in the anterior triangle: it is painless, more common in males, and is made worse by blowing.223 Posterior triangle (Behind sternomastoid, in front of trapezius, and above the clavicle.) If there are many small lumps, think of nodes \200\224TB or viruses, eg HIV or E BV (infectious mononucleosis) or, if over 20yrs, consider lymphoma or metastases. The prima ry may be head and neck (eg tongue base, posterior nasal space, tonsils, etc) or bronchus, gut, breast, or gonad (in that order of likelihood). Cervical ribs may intrude here.224 Tes ts Ultrasound shows lump consistency. CT de \201 nes masses in relation to their anatomica l neighbors. Do virology and Mantoux test. CXR may show malignancy or reveal bilateral hila r lymphadenopathy, when you should con- sider sarcoidosis. Fine-needle aspiration (FNA, \201 g 7). s e s a e s i d T N E 577 Fig 1. Branchial cyst. Fig 2. Goiter. Fig 3. Infected cyst. s e s a e s i d T N E Fig 4. Deep cervical abscess. Figs 1 \200\2236 Bechara Ghorayeb. Fig 5. Lymph node metastases. Fig 6. Submandibular abscess. Suspicious neck node Fig 7. Pivotal role of \201 ne needle aspiration cytology (FNAC).225 Fig 8. Procedure for suspicious node if FNAC +ve. \201\205 EGA: examination under GA \201\205 LCUC: large cel l undiff erentiated ca \201\205 MDT: multidiscipli- nary team \201\205 SCC: squamous cell ca \201\205 US: ultrasound Reproduced from Balm et al Int J Surg Oncol, 2010. ENT mirror and/or endoscopic examination skin and thyroid examination Primary tumor FNAC 1 Negative Staging and treatment FNAC 2 Negative Positive Cystic \202uid Biopsy \200 Incisional \200 Excisional \200 True cut See \201gure below US-FNAC FNAC Positive SCC/LCUC Melanoma Thyroid carcinoma Lymphoma Merkel cell carcinoma Adenoca Skin cancer MDT ENT examination Skin cancer MDT Ultrasound thyroid Excision \200\223 \200\223 MRI/PET CT scan* EGA \200 Tonsillectomy + directed biopsies \200 Tonsillectomy + blinded biopsies (Nasop harynx, base of tongue, piriform sinus) The salivary glands \200\207Refer all patients with unexplained salivary gland masses. The 3 major pairs of salivary glands are: parotid, submandibular, and sublin- gual. 800 small er glands are distributed through the upper aerodigestive tract. History and examination Dr y mouth/eyes; lumps; swelling related to food; pain. Look for external swellings, secretion s (in mouth \201 rst), do bimanual pal- pation for stones, test VII nerve, any regional n odes? In \202 ammation is usually due to infection or an obstructing calculus (calcium pho sphates and carbonates form around a nidus of cells and organisms). Classi \201 cation Are symptoms unilateral, or bilateral? Acute or chronic? Acute bilateral symptoms are usually due to mumps (eg if young/unvacci- nated, p142). \201\231 \201\231: staphs, TB, HIV, ALL, Heerfordt \200\231s syndrome (acute sarcoidosis, with uveitis, fever and salivary/lacrimal gland swelling, ie uveoparotid fever). Acute unilateral symptoms are also likely to be due to mumps but acute parotitis may occur by ascending oral infection. This occurs post-op but is now rare, unless dehydrated or poor oral hygiene; it is managed by oral hygiene, heat, massage, hydration, antibiotics (depends on culture and sensitivities). If the duct stops d raining pus, or there is increasing pain and pyrexia, think of abscess formation which need s draining through the skin, in theater. Recurrent unilateral symptoms are often from stone s (submandibular in 80%. Pain/swelling is worse on eating). The gland may be red, swollen, and tender (not always infected). \201\231: plain radiography; sialography. Treatment: Rem ove distal stones via the mouth; excise the gland if it contains the stone. Chronic bilater al symptoms may be associated with dry eyes and mouth Sj gren \200\231s or Mikulicz \200\231s syndromes (OHCM p698). Treatment is hard. If chronic infection is the cause, simp le antibiotics will fail: what is needed is prolonged treatment with oxytetracycline 250mg/ 12h 1h ac PO. Fixed swellings may be malignant, idiopathic or due to sarcoidosis. Tumors \200\23080% are in the parotid, 80% of these are benign pleomorphic ad- enomas, 80% of thes e are in the super \201 cial lobe \200\231. 10% are submandibular (50% are malignant here) . \200\207Remove any salivary gland swelling if present for >1 month (or examine cells by \201 ne-needle aspiration: this does not lead to seeding along its track; exception: prov en pleomorphic adenoma if elderly: safe to ob- serve for years). VIIth nerve paresis sugges ts malignancy. As tumors grow by budding and have no capsule, lumpectomy leads to seedling deposits, so par- tial parotidectomy is needed. NB: sialograms (OHCM p597) + CT are useful pre-op. 578 s e s a e s i d T N E Malignant: Intermediate: Classi \201 cation Benign: Pleomorphic (mixed parotid) adenoma Mucoepidermoid tumor Adenoi d cystic cancer Adenolymphoma (Warthin \200\231s tumor) Acinic cell cancer Haemangioma/lymp hangioma (child) Oncocytoma Adenocarcinoma Squamous cell cancer Pleomorphic adenoma: Middle age; slow growth; removed by super \201 cial parot- Radiothera py has a role if there was intraoperative idectomy or enucleation. spillage, or in residual disease, or recurrences (seen in 1 \200\2232% at 12-yr follow-up). Adenolymphoma: Usually elderly men; soft. Surgery: Partial parotidectomy. Carcinomas: Rapid growth; hard \201 x ed mass; pain & VIIth nerve palsy. \201\227: Sur- gery + radiotherapy. PET scan is better than CT and MRI for staging, detecting local recurrence and regional lymph node and distant metastases. 226 Adenoid cystic ca: Rare tumor of exocrine mucous glands (salivary, lacrima l, lid). Painful slow growing mass + late recurrences + perineural in \201 ltration + dis - tant mets. Survival: 88%, 69% and 52% at 5, 10 and 15yrs. 227 Follow-up: \200\207for lif e. Complications of surgery: VIIth palsy; salivary \201 stula; Frey \200\231s syndrome (B OX 3). 579 Assessing salivary lumps Note size, mobility, and extent of the mass, as well as \201 xity to surroundings. Any te nderness? Bimanually palpate the lateral pharyngeal wall for deep parotid tumors (any parap haryngeal space extension?). Also bimanually examine submandibular and sublingual masses. \200 Assess surrounding skin as regional metastases from skin or mucosal ma- lignancies may present as salivary gland masses. \200 Cranial nerve examination may show neural in \201 ltration.228 The dry mouth (xerostomia) Signs Dry, atrophic, \201 ssured oral mucosa; also: \200 Dis comfort, causing diffi culty eating, speaking, Typical causes \200 Hypnotics & tricyclics \200 Antipsychotics \200 \200 -blockers; diuretics \200 Mouth breathing \200 Dehydration \200 ENT radiotherapy \200 Sj gren \200\231s syndrome \200 SLE and scleroderma \200 Sarcoidosis \200 HIV/AIDS \200 Pa rotid sialoliths; 40% are radio-opaque vs >80% if submandibular s e s a e s i d T N E and wearing dentures. No saliva pooling in \202 oor of mouth. \200 Diffi culty in expressing saliva from majo r ducts. Complications Dental caries; candida infection. Management229 \200 Increase oral \202 uids; take frequent sips. \200 Good dental hygiene; no acidic drinks and foods that demineralize teeth. Try a saliva substitute, eg SST tablets (contain polyethylene and cottonseed oil). \200 \230Allow a tab- let to dissolve in the mouth \200\224while moving it around with your tong ue. \200\231 Up to 16 tablets per day may be needed. \200 Chewing sugar-free gum or sweet s may \200\200salivary \202 ow.230 \200 Pilocarpine (Salagen ) is rarely satisfactory .231,232 Cholinergic SE: sweating, lacrimation, rhinitis, amblyopia, diarrhea, urinary freq uency. Pilocarpine mouth washes may obviate these (diffi cult to obtain, but may be made by diluting pilocarpine eye-drops in water).233 N=40 \200 Irradiation xerostomia: Acupunctu re may help, eg as an 8-needle regimen of 3 weekly sessions followed by monthly sessions.23 4 n=50 \201ucja Frey and her misconnection syndrome ( \201 g 1) \200\234Doctor when I eat, or even just think of food, a sweaty rash crops up on my cheek. \200\235 Duphe- nix \201 rs t described gustatory sweating in 1757. Its cause was mysterious until 1923, when a soldier presented to \201ucja Frey, a pioneering Polish neurologist (the \201 rst female neurol o- gist we know of, and the most tragic). Her soldier had a bullet in his parotid, and gus- tatory sweating. Frey \200\231s brilliant dissections showed how the auriculo-temporal bra nch of the trigeminal nerve sends parasympathetic \201 bres to the parotid and sympatheti c \201 bres to facial sweat glands. During resprouting after injury, \201 bres switch c ourse to cause gustatory sweating. How misguided . 2 4 9 1 n i o t t e h g w w L e h t n i s t n e i t a p r e h l l a h t i w You don \200\231t have to be shot to get Frey \200\231s syn- drome. Other causes: birth tra uma; parotid surgery (in 23%, so pre-op counseling is vital but only understood fully by ne uroanatomists; NB: +ve Minor \200\231s iodine starch tests that detect subclinical cases ar e seen post-op in 62%). Management is hard, but not always needed. Botulinum toxin has been tried. s i z a N y b Fig 1. Frey \200\231s syndrome before and after eating. Reproduced from Frey \200\231s synd rome: a masquerader of food allegy, Nahin Hus- sain, Muthu Dhanarass, William White- house, Postgrad Med J 86 (1011), with permission (BMJ Publishing Group Ltd). d e r e d r u m s a w y e r F Dentistry for doctors Other oral diseases: OHCM p238. \200\207Any oral ulcer which has not healed in 3 weeks should receive specialist as- sessment for biopsy to exclude malignancy (OHCM p238). Causes of facial pain Tooth pathology, sinusitis, temporomandibular joint (TMJ ) dysfunction, salivary pathology, migraine, trigeminal neuralgia, atypi- cal facial pain ( no clear cause), trauma, cluster headache (OHCM p461), angina, frontal bone osteomyelitis ( post sinusitis), ENT tumors. \200\207When helping a patient with a dental infection pay at tention to these fea- tures \200\224before consulting a maxillofacial surgeon, or a dentist (GDP). 580 1 Is it the teeth? History: Is the pain \200 Worse with sugar and heat?} \200\207 Tooth is alive (pulpitis) Worse or better with cold? \200 Intermittent? Is the pain \200 \200 Worse with percussion? \200 Constant/uninterrupted? Is the pain \200 \200 Exacerbated by movement } \200\207 Tooth dead (osteitis/abscess) s e s a e s i d T N E between \201 nger and thumb } \200\207 Abscess Radiography (usually helpful): Orthopantogram (OPT) is useful for imaging molars and pre-mo lars. If incisors are suspected, request periapical radio- graphs of the tooth in question. Interpretation of radiograph \200 \200 Abscess (Tooth tender to percussion) Periodontal disease (Tooth mobile) Fig 1. Distinguishing between (a) absess of the tooth and (b) periodontal disease. 2 Trismu s: (Opening mouth is diffi cult because of spasm or pain.) This is a sign of severe infecti on. Ask the patient to open mouth wide and measure how many \201 ngers breadth between th e incisor teeth. Trismus always re- quires maxillofacial advice. Other causes: tetanus; neo plasia. 3 Facial swellings due to dental infection: Usually subside with oral an- tibiotics. \200 \207If swelling is related to the lower jaw, assess for airways ob- struction; if spreading to the eye, assess the second cranial nerve. If in any doubt, refer to a maxillofacial sur geon. 4 Bedside observations: Temperature (very important), pulse and blood pressure. This inform ation must be to hand prior to referral. Systemically unwell patients require maxillofacial advice/admission. 5 Systemic disease complicating dental infection: Any immunocompro- mise (eg HIV, leukemia, diabetics, those on steroids); patients at risk of endocarditis; coagulopathy (eg hemophil ia or warfarin). Seek specialist advice. In one HIV study, lesions included: candidiasis (2 9%), ulcers (15%), salivary gland disease (9%), necrotizing ulcerative gingivitis/periodont itis (5%), linear gingival erythema (4%), labial molluscum contagiosum (3%), oral warts (2% ), hairy leukoplakia (2%), and herpes zoster (1%).235 Dental caries Although on the decline in the West due primarily to \202 uoride, this condition is increasing exponentially in developing countries. Causes: bac- teria (esp . S. mutans), substrate (sugars) and susceptible tooth surface. In otherwise healthy indivi duals it is an entirely preventable disease. Rampant caries is a variant found in children exposed to excessive sucrose in the forms of coated dummies, \200\230health \200\231 drink s, and prescribed medicines. Radiation caries (eg post head & neck radiotherapy, eg with ja w osteoradio- necrosis). Treatment and complications: Pain infection. Toothache pain re- sponds best to NSAIDs, eg ibuprofen 200 \200\223400mg/8h PO after food (can buy it from ph armacists), and dental infection to penicillin and metronidazole, but drug treatment is nev er de \201 nitive, and a dental referral is required. Periodontal disease Virtually all de ntate adults have gingivitis, caused by bacterial and polysaccharide com- plexes at the too th \200\223gingival interface (=plaque). Toothbrushing is the only an- swer. Pathogens: her pes; streps.et al Vincent \200\231s angina is a smoking or HIV associated, painful, foul-sm elling, ul- Fig 2. Periodonitis with damange to sup- cerative gingivitis, caused by anaerob es porting tissue including bone. BMJ. (Fusobacteria) spirochetes (Borellia vincentii ). \201\227: penicillin 250mg/6h PO + metronidazole 200mg/8h PO. Causes of gingival swelli ng: Fibrous hyperplasia (congenital or from pheny- toin, ciclosporin, nifedipine); pregnanc y, HIV, scurvy, leukaemic deposits. Periodontitis (pyorrhoea) is a progression of localized in \202 ammation from the gums into the ligament supporting a tooth. Associations: anaero bes; calci- \201 ed bacterial deposits (calculi, tartar); poor oral hygiene. It needs a d entist. HIV and periodontal disease: HIV causes linear gingival erythema, necrotizing ulcer ative gingivitis and necrotizing ulcerative periodontitis. Causes of juvenile periodontitis : Poor nutrition; immunosuppression; wcc \200\201; neutrophil dysfunction (leucocyte adhesi on de \201 ciency, Chediak \200\223Higashi or Papillon \200\223Lefevre syndrome, with palm ar keratosis), granulomatous disease.236 Malocclusion Inappropriate positioning of the teet h in the jaws or between the jaws themselves is common. Those with prominent upper teeth ar e par- ticularly prone to trauma, and those children at risk (eg in epilepsy) or those invo lved in contact sports should be referred to an orthodontist. Those with severe facial or j aw disharmony who may be unable to chew or have psycho- logical diffi culty with their appe arance may be amenable to surgical correc- tion by an oral or maxillofacial surgeon. Wisdom teeth These declare them- selves in early adult life. Like the appen- dix, they are someth ing of a vestigial organ. Impaction can cause pain ( \201 g 3). They account for an enormo us number of inpatient operations. If asymptomat- ic and not exposed to contamination by th e mouth, they don \200\231t usually need removal. Complications are pain and infection and they may be involved in fractures of the mandible. Post-op recovery is often complicated by pain and swelling; pain responds well to NSAIDs and poorly to opiates (eg dihydroco- deine . Infection complicates up to 30% not receiving antibiotics. Penicillin and metronidazole ( as above) are standbys. Teething An acute sore mouth during tooth eruption is often caused by viral infections (eg herpetic). The onset of eruption of \201 rst deciduous teeth ( \201 g 1, p221) correlates with the fall-off in transferred maternal antibody. 581 s e s a e s i d T N E Fig 3. Impacting wisdom teeth. 582 8 Dermatology History and examination 584 Creams and ointments 585 Patterns of skin disease 586 Itch 586 Skin signs in systemic disease 588 Skin diagnoses not to miss 590 Mole or melanoma? 592 Pso riasis 594 Eczema (dermatitis) 596 Skin infections: fungi 598 Single nerve \201bre Capsule Myelin sheath Fig 1. Under pressure: the right Pacinian cor- puscle is feeling the strain. Filippo Pacini , the Italian anatomist, born in 1812, saw the corpus- cles that now bear his name in a han d he was dissecting as a medical student in an anatomy class in Pistoia hospital in 1831, w hen he was 19. 1 These corpuscles ( 1mm in diameter) transmit pressure sensations. We can f eel our clothes as soon as we put them on \200\224whereupon we stop feeling them, as these corpuscles only respond to changes in pressure. No one took his observations seriously, and Pa- cini heads our list of brilliant medical students ignored by their narrow-mined profes sors. For example, he discovered the cause of cholera in 1854, 30 years before Koch \200 \231s \200\230 \201 rst \200\231 description. 2 Pacini was the \201 rst medical student to un- derstand what it is to feel pressure, without buckling. In his case, his chief pres sure was the need to look after his two sick sisters. These duties eventually bankrupted hi m, and he died in a poorhouse in Florence in 1883. 2 We dedicate this chapter to him, and e very- one else feeling the strain. bacteria 598 viruses 599 Acne vulgaris 600 Acne rosacea 600 Drug eruptions 601 Speci \201 c skin disorders 602 Blistering disorders: pemphigus, pemphigoid et al Strawberry naevus Pyogenic granuloma Lichen planus; Haemangiomas Pityriasi s rosea; Alopecia Photosensitivity; Urticaria The skin in old age 604 \200\2235 (leg ulcers & pressure sores, etc) Skin disorders and HIV 606 Infestations 608 Mast cell disorders 610 Lasers in dermatology 6 10 Psychodermatoses 611 a ir p t o r s ) a t g l a e c ticle w t a n t s S l o e r e ff C a e l s d is c s o r e H d n e w c S M e r k e ( m n a h c Corneal layer Basal layer s i m r e d p E i Piloerector muscle Sebaceous gland and hair follicle (pilosebaceous unit) Meisser corpuscle (for light touch) Artery Vein Pacinian corpuscle Fat cells s i m r e D r e y a l s u o e n a t u c b u S Fig 2. The anatomy of pleasure. All pleasure is sensory, and as our skin is our largest org an, let us rejoice in our unmyelinated tactile C aff erents which mediate all tactile pleas ure by sending impulses to our insular cortex rather than to mundane somatotosensory areas. 3 \201\201 Holistic approaches to dermatology Because our skin is our most super \201 cial organ, dermatology is never given due weight; but the skin is also our heaviest organ, and although its wounds only ever seem skin deep, their eff ects cast long shadows over the psy che because people judge our health and beauty by the condition of our skin. 4,5 583 ? p e e d n i k s Our skin displays a more varied range of signs and reaction patterns than any other organ. Recognizing these may allow diagnosis of unsuspected systemic diseases (see p588). Primaril y skin conditions such as eczema and psoriasis (p594) are not only the domain of dermatolog ists but are likely to be encountered by us all, regardless of our \201 eld of practice. A practical knowledge and clinical con \201 dence in diagnosing skin disease is thus a mos t valuable asset \200\224and we all need to know how the dermatological aspects of our pati ents \200\231 lives interact to form those complex social and biological matrices that are the lives of our patient with chronic skin conditions. y l n o s i y g o l o t a m r e D y g o o t a m r e D l Dermatologists do not con \201 ne themselves to the skin. Skin symptoms are features of ma ny medical (p588) and psychiatric illnesses, eg body im- age problems, dermatitis artefacta , neurotic excoriations, and trichotillo- mania (neurotic pulling out of one \200\231s hair ). 6 Psychocutaneous events There is an association between depression/ social phobia and p soriasis, and between obsessive \200\223compulsive disorder, stress, and acne. If you doubt the relevance of psychocutaneous phenom- ena, look no further than Dennis Potter \200\231s Singing Detective, Philip Marlow. 7 The psycho-physiology of acne is instructive. Sebaceou s glands and their secretions are involved in a pathway like the hypothalamic \200\223pitui tary \200\223adre- nal axis, mediating a direct link between oily skin and the stress hormo ne CRH (corticotrophin releasing hormone) which acts on sebaceous glands. So think of CRH a s an autocrine hormone for human sebocytes that exerts hom- eostatic lipogenic activity, wi th testosterone and growth hormone inducing CRH negative feedback. These \201 ndings impl icate CRH (hence stress) in medi- ating acne, seborrhoea, androgenic alopecia, skin ageing, and xerosis. Sub- stance P is another route connecting stress, seborrhoea, and acne. 8,9 T elemedicine, virtual outreach, and dermatology delivery Traditionally, dermatologists see p atients on wards and in central clinics: convenient for them, but less convenient for patie nts who live far away, and this paradigm does not allow for useful interaction between the re- ferring doctor and the specialist. Also, urgency cannot be assessed until the patient p resents (unless a photograph is sent with the referral letter; this simple idea requires e- mail, digital cameras, and technical commit- ment). Telemedicine uses high-quality video li nks and computer equipment to form a virtual consultation. Is the expense entailed worth it ? Are there problems \200\224even for this, the most visual of specialties? Disadvantages10,11 N=3170 Expense is not outweighed by \200\201travel time No proper shari ng of patients \200\231 problems Advantages Travel times are less Fewer tests ordered Teaching referring GPs Technical probl ems can waste whole sessions Patient satisfaction Fewer follow-ups Extra time needed from GPs and consultants Important clinical cues are lost in telemedicine We thank our Specialist Reader, Dr Jonathan Bowling, and our Junior Reader, William Hunt, f or their help with this chapter. Dermatology basics History Duration of rash/lesions; site of onset, spread, and distributio n of lesions; symptoms (itch, pain); aggravating factors (sunlight, heat); previous treatme nts; medical conditions and medications; family history (psoriasis, atopy); occupation (ind ustrial chemicals); pets. Family and personal history of allergy/atopy (eg to animal dander s), migraine. Examination Examine all the skin, the hair, and nails. To communicate with a dermatologist, it is customary to translate your \201 ndings into rather garbled Latin or Greek (see below \200\224but English will usually do just as well). Distribution Symmetric al \202 exural (atopic eczema, \201 g 1 on p596); contact with jewelry or cosmetics (al lergic contact dermatitis); areas exposed to sun, eg backs of hands, face, neck (photosensi tivity); grouped lesions (herpes virus); symmetrical extensor surfaces (psoriasis, p594). A re there crops of le- sions? Monomorphic (Greek for all taking one form or shape) or polymo rphic? Pattern Ring (fungal \200\224active edge with healing center, p598); linear (K bner phenomenon, below), targetoid (erythema multiforme). 584 Terms used to describe lesions and processes in dermatology Alopecia Atopy/ atopic Atrophy Autosens- itization y g o o t a m r e D Hair loss Prone to allergic eczema, asthma, or rhinitis; typical patient: city- based child in a 1-child family of high socio-economic class.1 12 Thinning and loss of skin substance General lowering of the irritation threshold triggered by intense local in \202 ammation, eg a fungal foot infection or a local area of contact dermatitis may produce a generalized itchy rash (=autoeczematization= \200\230id reaction \200\231) Blister larger than a vesicl e (see below, ie >0.5cm diameter) Dried brownish exudate Super \201 cial break in epiderma l surface; heals without scarring l . e c n a t r o p m Bulla Crust Erosion Erythema Reddening of the skin which blanches on pressure Excoriation A scratch which has broken the surface of the skin Filiform i - f l e s r u o Long, irregular projections, which may be threadlike, or broader, like close-packed tombsto nes on a mound (seen in warts) Crack, often through keratin s e t a l f n i Fissure Induration An area of cutaneous or subcutaneous hardening or thickening Skin lesion s which develop at sites of injury \200\224seen in psoriasis K bner (p594), lichen planus, plane warts, and vitiligo phenomena Skin thickening with exaggerated skin markings, as a r esult of Licheni \201 - repeated trauma (eg in response to itch). See \201 g 1, p585 cat ion De \201 ned, \202 at area of altered pigmentation; big macules are patches Macule So lid lump >0.5cm in diameter; subcutaneous or intradermal Nodule Raised well-de \201 ned le sion, usually less than 0.5cm in diameter Papule Raised \202 at-topped lesion, usually ov er 2cm in diameter Plaque Purplish lesion resulting from free red blood cells in the skin; it Purpura doesn \200\231t blanch on pressure, and may be nodular (vasculitis) n o g r a j t a h t t i m d a d n a s e l u t s u p r u o g n i t a i r o c x e Pustule Well-de \201 ned, pus- \201 lled lesion Scale Scar Ulcer Vesicle Weals/ urticaria Fragment of dry skin Permanent replacement of skin area with connective tissue Loss of epid ermis and dermis resulting in a scar (unlike erosions) Blister less than 0.5cm in diameter Transient pale papules with pink margins, eg \200\230nettle rash \200\231 (=hives) p o t s s \200\231 t e L 1 Allergic conjunctivitis and urticaria are other features. 585 Ointments, creams, lotions: 3 ends of a spectrum \200\207Ointments are for dry skin, and c reams are for moist ar- eas. Any topical compound is more or less like an idealized ointmen t (greasy as has no added water), cream (oil-in-water or water-in-oil emulsions) or lotion (water-based; typically made from powders). Lotions are less common (used as a coolant, eg calamine lotion). If a large area of skin is involved, a large volume of cream or ointment is needed, eg 500g. Use clean procedures when getting creams out of pots, eg remove cream w ith a clean spoon \201 rst. Close tubs of ointment after use. Pump dispensers are a good way around bacterial contamination. Regimens may be complex, and you may get annoyed at the patient \200\231s \200\230poor compli- ance \200\231 \200\224until you reframe this as lo ss of concordance (compliance is when the doctor and the patient share the same view as to what is important 13). Then you may get annoyed with yourself (just as bad). Avoid both by get- ting a nurse to help plan treatment through dialog, and understanding lifestyle constr aints. \200\207Dermatology/practice nurses are invaluable in teach- ing topical therapies, and in optimizing concordance. \200\207Topical treatment is not enough: take steps to imp rove coping behavior and quality of life. 14 . g n o s e m a s e h t g n i g n i s y g o o t a m r e D \211\210 y n o m r a h l \211\210 e c n a d r o c n o C LatinL & GreekG for dermatologists AlbaL=white (as in albino). CutisL=skin (subL=under, eg subcutaneous). DermaG \200\210e \200 =skin (intraL=within, hence intradermal=within the skin). EczemaG , from ekzein, to break out, boil over: ek, out; (zein=to boil). ErythemaG= redness (eg of the skin). ImpetereL = to attack (as in impetigo). IndurareL =to harden (as in induration). LichenL = tree moss; licheni \201 cation to dermat- ologist mea ns like Morocco leather, a condition caused by scratching ( \201 g 1). LivedoL livid (furi ous, red/blue); retic- ulumL = netL. Livedo reticularis, p588. Fig 1. Licheni \201 cation. LupusL=wolf. MaculaL=stain/spot (immaculate; without st - ain; macula peccati=the stain of original sin). Mens/mentemL=mind; nature; temper; men- tum=chin (submental=below the jaw). Muto (mutat)L=I (he) change(s)/mutate(s). PapillaL=nipple or teat (so papule; papilloma). P ilus/piliL=hair (hence fur coat; pelt)/hairs. PityriasisG=grain husk, scale; pityuron=bran. PsoriasisG=to have the itch (psora=itch; NB: psoriasis often does not itch). PurpuraL=purple (imperial) color; porphyra. G RoseaL=pink; akmeG=acne (summit; acme; pimple); 15 acne rosacea=pink pimples, p600). Seborrhoeic=making sebumL (suet, grease). Sen exL=old man. Tel G \200 telos=end+angeion=+vessel+ekstasis Fig 2. Purpura: on warfarin. Check her INR now! Is vitamin K needed? =extension, hence telangiectasia. TopicosG=surface (hence topography; creams are topical). VesicaL=purse, bladder ( \202 uid - \201 lled blister). VitellusL=spotted calf (vitiligo). So \200 try translating lupus pil um mutat, non mentem (the wolf can change his coat but not his nature); but it is unkind to think of dermatologists as wolves: think of them as leopards who can change their (and our ) spots. Possible causes of patterns of skin disease White lesions \200 Pityriasis versicolor: sup er \201 cial slightly scaly infection with the yeast Malassezia furfur; appears depigmente d on darker skins; \201\227: p598. \200 Pityriasis alba: post-eczema hypopigmentation, o ften on children \200\231s faces. \200 Vitiligo (vitellus is Latin for spotted calf ): wh ite patches hyperpigmented borders. Sunlight causes itch. Associations: Autoimmunity: pe rnicious an- aemia, thyroid or Addison \200\231s, DM, alopecia areata. \201\227: (unsatisf actory): try cos- metic camou \202 age, narrowband UVB PUVA (p595) 16 potent topical st eroids. 586 Ring-shaped lesions \200 Basal cell cancer (rodent ulcer; p590): pearly papule + central ulcer. \200 Tinea: active red scaly edge + central healing. \200 Granuloma annulare ( \201 g 1; 1cm ring on hand). \200 Erythema multiforme: target-like lesions, eg on extensor limb surfaces ( \201 g 2 p588). Fig 1. Granuloma annulare. Rarely, leprosy. Brown pigmented lesions Apart from sun-related freckles there are: \200 Lentigos: persistent brown macules, often larger than freckles ( \201 g 2). \200 Caf -a u-lait spots: faint brown macules; if >5, consider neuro \201 bromatosis. 17,18 \200 Seb orrhoeic keratoses/warts: benign greasy-brown warty lesions usually on Dr Jonathan Bowling. y g o o t a m r e D l the back, chest, and face; very common in the elderly. Chloasma (melasma) are brown patches especially on the face, related to pregnancy or Pill use. The condition may respond to topical azelaic acid. Systemic diseases: Addison \200\231s (palmar creases, oral mucosa, scars); haemo- chromatosis; porphyria cutanea tarda (+ skin fragility and blisters). Round, oval, or coin- shaped (discoid) lesions \200 Bowen \200\231s disease ( \201 g 7). \200 Discoid eczema ( \201 g 5 & p602): itchy, crusted/scaly eczema, worsened by heat. \200 Psoriasis: well -de \201 ned scaly red/pink plaques (p594). Distribution on exten- sor surfaces, scalp and natal cleft distinguishes it from discoid eczema (also, scales are thicker, get silvery on rubbing, and bleed on lifting). Pityriasis rosea: herald patch; oval red lesions with scaly edge, eg on trunk. \200 Eryth ema chronicum migrans ( \201 g 3). See p588. \200 Impetigo: well-de \201 ned red patche s, covered with honey-colored crust, \201 g 6. Linear lesions \200 K bner phenomenon: psoriasis, lichen planus. \200 Dermatitis artefacta: linear or bizarre-shaped lesions, in duced by patient. \200 Herpes zoster: polymorphous vesicles/pustules in dermatomal distri bution. \200 Scabies burrows ( \201 g 8, the mite is visible as a speck just above the r ed area). \200 Cutaneous larval migrans ( \201 g 4), eg from strongyloidiasis (OHCM p442 ). Subcutaneous nodules Rheumatoid nodules, rheumatic fever, PAN, xanthe- lasma, tuberous s clerosis, neuro \201 broma, sarcoidosis, granuloma annulare. Itch (pruritus) \200\207Itch can be very distressing. Skin will usually be scratched or rubbed and a number of secondar y skin signs are seen: excoriations (scratch marks); licheni \201 cation (skin thickening, \201 g 1 on p585); papules or nodules (lo- cal skin thickening). Causes: Dry (and older) skin tends to itch. Determine if there is a primary skin disease or is itch due to systemi c disease. \200 Itchy lesions: scabies (burrows in \201 nger-webs, wrists, groin, butto ck); urti- caria (transient wheals, dermatographism); atopic eczema ( \202 exural eruption , licheni \201 cation, \201 g 1 on p596); dermatitis herpetiformis (very itchy blisters on elbows, shoulders); lichen planus ( \202 at violet wrist papules). \200 In 22%, itch is caused by a systemic disease: 19 Fe \200\201 (koilonychia, pale); lym- phoma (nodes, he patosplenomegaly); hypo/hyperthyroidism; liver disease (jaundice, spider naevi); chronic re nal failure (dry sallow skin); malignancy (clubbing, masses); drugs. Do FBC, ESR, ferritin, LFT, U&E, glucose, TSH, CXR. Treatment: Treat any primary disease; bland emollients (eg Diprobase ) to soothe dry skin; emollient bath oils; sedative antihistamines at night. Lentigos are brown macules/patch- es. Some are premalignant. Fig 2: lentigo maligna (melano ma in situ) \200\224 precursor to invasive lentigo maligna melanoma. Typical patient: Cauca sian >40yrs. It develops in sun-damaged skin. It is \202 at, irregular, and variably pigm ented (darker areas may be in- vasive). Not all show ABCDE signs of malignancy.1 Use dermos copes2 biopsy in equivocal lesions. 20 Excision is best (>5mm margins); if impos- sible, try radiotherapy or topical 5% imiquimod \211\210 5/wk (typical time to clear: 9 wks; do repeated biopsy over the next years 21 to spot dangerously common occult recurrence). 22 587 y g o o t a m r e D l Fig 2. Lentigo maligna. Dr Suzannah Baron. Fig 3. Erythema chronicum migrans. Fig 4. Cutaneous larval migrans. Courtesy of Dr Jonathan Bowling. Courtesy of Dr Jonathan Bowling. Fig 5. Discoid/nummular eczema (p602). Fig 6. Impetigo (honey-colored crusts). Dr Jonathan Bowling (& \201 gs 7 & 8). Courtesy of Dr Samuel Da Silva. Fig 7. Bowen \200\231s disease. Fig 8. Scabies burrow (and mite, top).