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By T. Rune. Lincoln University of Pennsylvania.

Type 1 5α-reductase isoenzyme converts testosterone to dihy- drotestosterone preferentially in the prostate D generic 20 gm betnovate fast delivery skin care experts. Peptide growth factors such as fibroblast growth factors buy betnovate 20 gm visa acne natural treatment, insulinlike growth factors, and epidermal growth factors are felt to be the local forces that determine prostate growth Key Concept/Objective: To understand the basic pathophysiology involved in BPH BPH involves hyperplasia of both the epithelial and the stromal compartments. The hyperplastic process begins in the periurethral and transition zones of the prostate; in contrast, prostate cancer preferentially develops in the peripheral zones. At least three types of alpha2-adrenergic receptors have been identified in the lower urinary tract. The type 1 5α-reductase isoenzyme has low activity in the prostate and is expressed pre- dominantly in the skin and liver. The pathophysiologic mechanisms underlying the development and progression of BPH are incompletely understood. Clearly, BPH involves prolonged exposure of the prostate gland to androgens. In the prostate, inter- actions between epithelial and stromal cells and the extracellular matrix, mediated pri- marily by locally produced (intrinsic) growth factors, appear important. These peptide growth factors, which include fibroblast growth factors, insulinlike growth factors, and epidermal growth factors, are felt to be the local forces that determine prostate growth. A 57-year-old man presents for evaluation of urinary frequency. On review of symptoms, the patient also reports occasional hesitancy and dribbling. Results of physical examination, including digital rectal examination, are normal. Which of the following statements regarding the diagnosis of BPH is false? Systemic diseases that can mimic BPH include diabetes, heart fail- ure, and hyperparathyroidism B. It is important to ask about over-the-counter medications because they can contain anticholinergic and sympathomimetic agents that can cause or exacerbate symptoms C. Abdominal and pelvic ultrasound are indicated in the initial workup of BPH D. A urinalysis is a part of the workup of BPH to screen for hematuria or infection Key Concept/Objective: To understand the differential diagnosis and diagnostic workup of BPH Symptoms of bladder emptying in men with BPH include straining, hesitancy, inter- mittency, a weak stream, terminal dribbling, and a sensation of incomplete emptying. Bladder filling symptoms include daytime frequency, nocturia, urgency, and urge incontinence. The physician should look for evidence of systemic diseases that can pres- ent with lower urinary tract symptoms, particularly urinary frequency and nocturia. Examples of such diseases include diabetes, heart failure, and hyperparathyroidism. Routine tests performed on men with lower urinary tract symptoms should generally include a urinalysis to screen for hematuria and infection. Pyuria suggests infection, either primary or superimposed on bladder outlet obstruction. Microscopic hematuria may indicate simply that the prostate is enlarged and vascular, but it should prompt further evaluation for genitourinary malignancy. Upper urinary tract imaging (by ultra- sonography, computed tomography, or intravenous pyelography) and urethrocys- toscopy are not indicated for routine cases of lower urinary tract symptoms attributa- ble to BPH. A patient of yours whom you follow for BPH, hypertension, and osteoarthritis presents to your office. He has had symptoms of BPH for 3 years now, but over the past 2 to 3 months, his symptoms of hesi- tancy and straining have worsened to the point that he wishes to pursue therapy. Which of the following statements regarding the medical management of BPH is true? Alpha1-adrenergic blockers work primarily through relaxation of the detrusor muscle of the bladder B. Alpha1-adrenergic blockers reduce prostate size and lower prostate- specific antigen (PSA) levels C. The 5α-reductase inhibitors reduce prostate size and lower PSA levels D.

Ann Neurol 14: 696–697 Kissel JR buy betnovate 20gm lowest price acne treatments that work, Burde RM generic betnovate 20gm online skin care yang terbaik, Klingele TG, et al (1983) Pupil sparing oculomotor palsies with internal carotid-posterior communicating aneurysms. Ann Neurol 13: 149–154 Richards BW, Jones FRI, Young BR (1992) Causes and prognosis in 4278 cases of paralysis of oculomotor, trochlear and abducens cranial nerve. Am J Ophthalmol 113: 489–496 43 Trochlear nerve Genetic testing NCV/EMG Laboratory Imaging Biopsy + Somatic motor to the superior oblique muscle. Qualities The trochlear nucleus is located in the tegmentum of the midbrain at the Anatomy inferior colliculus, near the midline and ventral to the aqueduct. Axons leave the nucleus and course dorsally around the aqueduct and decussate within the superior medullary velum (thus, each superior oblique muscle is innervated by the contralateral trochlear nucleus). The axons exit from the midbrain on its dorsal surface and travel around the cerebral peduncle, emerging between the posterior cerebral and superior cerebellar arteries with the oculomotor nerve. The trochlear nerve pierces the dura at the angle between the free and attached borders of the tentorium cerebelli. It then enters the lateral wall of the cavern- ous sinus, along with the ophthalmic nerve (V1), CN III, and sometimes the maxillary nerve (V2). It enters the superior orbital fissure, passes above the tendinous ring, crossing medially along the roof of the orbit, then diagonally across the levator palpebrae. The nerve breaks into three or more branches as it enters the superior oblique muscle. Lesion sites include the midbrain, subarachnoid space, cavernous sinus, supe- Topographical rior orbital fissure, or orbit. The affected eye is sometimes extorted (although this may not be apparent to Signs the observer) and exhibits poor depression during adduction. Isolated lesion of the trochlear nerve is rare, although it is the most common Pathogenesis cause of vertical diplopia. More often trochlear nerve dysfunction is observed in association with lesions of CN III and CN VI. Metabolic: Diabetes Vascular: Hypertension Subarachnoid hemorrhage 44 Uncertain: microvascular infarction Vascular arteriosclerosis, diabetes (painless diplopia) Infection: Mastoiditis Meningitis Inflammatory: Ophthalmoplegia or diplopia associated with giant cell arteritis Compression: Cavernous sinus, orbital fissure lesions Inflammatory aneurysms ( posterior cerebral artery, anterior superior cerebellar artery) Trauma: Head trauma causing compression at the tentorial edge Lumbar puncture or spinal anesthesia Surgery The trochlear nerve is the most commonly injured cranial nerve in head trauma. Neoplastic: Carcinomatous meningitis Cerebellar hemangioblastoma Ependymoma Meningioma Metastasis Neurilemmoma Pineal tumors Trochlear nerve sheath tumors Others: Superior oblique myokymia Pediatric: congenital, traumatic and idiopathic are the most frequent causes. Diagnosis Diagnosis can be facilitated by the Bielschowsky test: 1. Diplopia is exacerbated when the affected eye is turned nasally 3. Diplopia is improved by tilting the head away from the affected eye Also, when viewing a horizontal line, the patient sees two lines. The lower line is tilted and comes closest to the upper line on the side towards to the affected eye. Subtle diagnosis: “Cross over” or Maddox rod techniques Differential diagnosis Skew deviation, a disparity in the vertical positioning of the eyes of supra- nuclear origin, can mimic trochlear palsy. Myasthenia gravis, disorders of the extraocular muscles, thyroid disease, and oculomotor palsy that affects the superior rectus can also cause similar effects. Surgery could be indicated to remove compression or repair trauma. The recovery rate over 6 months was observed to be higher in cases of diabetic Prognosis etiology than other non-selected cases. Berlit P (1991) Isolated and combined pareses of cranial nerves III, IV, and VI. J Neurol Sci 103: 10–15 Jacobson DM, Marshfield DI, Moster ML, et al (2000) Isolated trochlear nerve palsy in patients with multiple sclerosis. Neurology 55: 321–322 Keane JR (1993) Fourth nerve palsy: historical review and study of 215 inpatients. Neurol- ogy 43: 2439–2443 Rush JA, Younge BR (1981) Paralysis of cranial nerves III, IV, and VI. Arch Ophthalmol 99: 76–79 46 Trigeminal nerve Genetic testing NCV/EMG Laboratory Imaging Biopsy + Somatosensory evoked potentials Reflexes: masseteric, corneal reflex, EMG Fig. General sensory: Face, scalp, conjunctiva, bulb of eye, mucous membranes of paranasal sinus, nasal and oral cavity, tongue, teeth, part of external aspect of tympanic mem- brane, meninges of anterior, and middle cranial fossa. Anatomy The trigeminal nuclei consist of a motor nucleus, a large sensory nucleus, a mesencephalic nucleus, the pontine trigeminal nucleus, and the nucleus of the spinal tract.

In the case of carboxytherapy generic betnovate 20 gm on line acne jensen boots sale, either the micropercutaneous approach or direct infiltrations may be used discount betnovate 20gm online acne home remedies. Normally, there is a control visit and a therapist meeting after each six- or eight-session cycle in order to adjust diagnosis and thera- peutic conditions. These meetings and the physiotherapist’s appraisal are of utmost importance, because ultimately the therapist perceives the patient’s sensations and symptomatology as the cellulite therapy progresses. In fact, it is a chronic therapy for a disease that is frequently evolutive and gets worse, due to perpetuation and worsening of intestinal flora alterations and endocrine–metabolic disorders, not to mention today’s lifestyle, usually sedentary and reckless from a nutritional or environ- mental point of view. Medical history should include the patient’s structural diagram, details of the cel- lulite areas, a possible therapeutic strategy, and photographs from different angles taken 96 & LEIBASCHOFF during the first visit, halfway through therapy, and at the end of treatment. Maintenance therapy may vary, being just dietary–hygienic and physical (diet and cycles of monthly ses- 1 sions of Endermologie ), or medical–physical (monthly sessions of carboxytherapy or mesotherapy plus subdermal therapy) (2). As for the measurement of bitrochanteric, knee, and calf circumference, we believe they are not important. We know, in fact, that frequently circumference reduction is com- bined with tissue alterations and loose tissue. Circumference reduction due to a decrease in excessive adipose tissue––subcutaneous or steatomeric––is different from circumference reduction in the cellulite pathology. This difference should be thoroughly explained to patients to discredit false popular beliefs. Non-invasive assessment of the effectiveness of cellasene in patients with oedematous fibrosclerotic panniculopathy (cellulitis): a double-blind prospective study. Int J Cosmet Surg Aesthet Dermatol 2001; 3(4):265–273. Atti 1 Congr Multid Chir Plast e Invecch, Roma, Italy, 1989. Valutazione clinica controllata in doppio cieco di prodotti fitocomposti nel trattamento della cosiddetta cellulite. Efficacy of a multifunctional plant complex in the treatment of a localised fat-lobular hypertrophy. Echodoppler coleur et exploration veineuse superficielle. Physiological effects of endermologie: a preliminary report. Valutazione sull’attivita` microcircolatoria della tecnica endermologie LPG in paziente con PEFS (1997). TYPICAL MEDICAL HISTORY INTAKE FORM City: Date: Mr/Mrs: Address: Tel. Hormones: EXAMINATION ARTERIAL SYSTEM: VENOUS SYSTEM: R (Right): L (Left): LYMPHOADIPOSE SYSTEM: CUTANEOUS SYSTEM: LOCOMOTOR SYSTEM AND FEET: Notes: ROM test: Cellulitic pathology Localization: Type: Echography Videocapillaroscopy ROM test VEGA expert test 100 & LEIBASCHOFF CLINICAL INSTRUMENT CLASSIFICATION OF CELLULITE PATHOLOGY: Cellulite pathology code // // // Clinical instrument examination: THERAPEUTIC STRATEGY: Suggested: Medical therapy: Phase 1: Cleansing: Phase 2: Maintenance: SPECIFIC THERAPY: Carboxytherapy Endermologie1 Mesotherapy Diet SURGICAL THERAPY: LOCAL THERAPY: LIFESTYLE: DIAGNOSIS & 101 B. EXAMPLE OF MEDICAL HISTORY City: Arezzo Date: January 2, 2000 Mr/Mrs: PAOLA ROSSI Address: Florence Tel. Past medical history: Noncontributory Family history: Positive to vasculopathy Allergies: & Yes &ü No Smoker: &ü Yes & No Hepatitis: & Yes &ü No Diabetes: & Yes &ü No Exercise: & Yes &ü No MEDICAL HISTORY: Deliveries: Two Surgeries: Appendectomy; tonsillitis episodes Diseases: Mild overweight Therapies: Current Medical History: 1. Hormones: Estro-progestagens since 3 years ago 102 & LEIBASCHOFF EXAMINATION ARTERIAL SYSTEM: No lower limb arteriopathy VENOUS SYSTEM: Normal deep veins, with normal valves R (Right): NO Varicosis saphena—small saphenous vein normal L (Left): NO Varicosis saphena—telangiectasia due to knee hyperextension—small saphe- nous vein normal LYMPHOADIPOSE SYSTEM: Mixed adipoedematous hypodermatosis with adiposity in flanks and culotte de cheval. LOCOMOTOR SYSTEM AND FEET: Lower limbs dysmetria þ pes varus valgus to the left with thrust deficit and takeoff alteration. Typical primary lymphedema observed that started unexpectedly in summer, as usual. Adi- poedematous cellulitis with localized adiposity and true bitrochanteric culotte de cheval–knee lymphedema. Cellulitic pathology Localization: Type: Echography Videocapillaroscopy ROM test VEGA expert test CLINICAL INSTRUMENT CLASSIFICATION OF CELLULITE PATHOLOGY: Cellulite pathology code: G1a/S2/V3/A1a-b Clinical instrument examination: Photoplethysmography-podoscopy-videocapillaroscopy DIAGNOSIS & 103 THERAPEUTIC STRATEGY: Suggested: Medical therapy: Phase 1: Cleansing: Cellulase gold 3 per day Phase 2: Maintenance: Cellulase gold 2 tablets/day + SPECIFIC THERAPY: Carboxytherapy Carboxytherapy six sessions one/week Endermologie1 Endermologie1 twice a week during one month Mesotherapy Mesotherapy once a week in calves Control within 30 days Diet Hyperprotein 15 days SURGICAL THERAPY: Liposculpture in culotte de cheval and knees LOCAL THERAPY: Functional plantar þ panty hose 15 mm/Hg LIFESTYLE: Walk frequently Pay attention to stypsis and control weight 6 Cellulite Characterization by High-Frequency Ultrasound and High-Resolution agnetic Resonance Im aging Bernard Querleux Department of Physics, L’Oreal´ Recherche, Aulnay-sous-bois, France & INTRODUCTION Cellulite is an accepted term for describing an aesthetic problem called the ‘‘orange peel effect,’’ which causes some dimpling of the skin. Cellulite, which affects about 90% of women, is usually associated with lipodystrophy, localized on the thigh, buttock, and hip (1,2). Histologically, some authors report modifications of the dermal–hypodermal interface, and describe different patterns of the architecture of fibrous septae in adipose tissue in women with cellulite (3,4). Also an increase in the volume of adipocytes in women with cellulite as well as alterations of the lymph vessels and blood circulation has been reported (5). Few studies have been performed in vivo with noninvasive methods. In this chapter, we will present a comparison of the skin and adipose tissue properties in women with cellulite compared to normal women without visible signs of cellulite.