Si può desiderare di provare un trattamento naturale disfunzione erettile come un diverso per i problemi di costruzione. Al giorno d oggi ci sono diverse terapie sul mercato, ma un trattamento naturale disfunzione erettile è stato confermato qualche ora e ora di nuovo per dare risultati efficienti e permanenti. Cos è la disfunzione sessuale? L incapacità di sviluppare o sostenere una costruzione abbastanza lungo per fare l amore è chiamato disfunzione erettile, ED https://farmacia-senzaricetta.it/ o (maschio) problemi di erezione. Tutti gli uomini possono avere problemi di costruzione di volta in volta e gli scienziati considerano ED essere presenti se si verificano problemi di costruzione almeno il 25% del tempo. Alcuni fatti duri: ED Può essere dovuto a problemi emotivi. Stress, pressione, giltiness, depressione, bassa autostima e ansia prestazioni può essere la causa dei vostri problemi di costruzione. La ricerca ha confermato che il 90 per cento della disfunzione erettile è fisica in origine, non emotiva. L impotenza colpisce la maggior parte degli uomini durante la loro vita e può essere dovuto a troppo colesterolo, problemi cardiaci, diabete, ipertensione, fumo o alcol. Alcuni rimedi possono essere la ragione. Le questioni legate al movimento sono collegate. Se ti occupi dei tuoi problemi di movimento, hai piu possibilita di risolvere questo problema. Qui ci sono 5 consigli facili su come aumentare la circolazione: 1. Mangia i pasti giusti. Questo ti rendera il flusso sanguigno ovvio. Una grande parte di rimanere sani e anche mantenere il flusso sanguigno ovvio è legato al vostro piano di alimentazione quotidiana e quello che si mangia. Una buona cura per la disfunzione erettile è mangiare un piano a basso contenuto di grassi e grande alimentazione di fibre. Mangiare fibre tutti i giorni e questo viene scoperto in prodotti cerealicoli cereali integrali, frutta e verdura. Evitare il più possibile pasti pronti o pasti non sani. 2. Wonder herbal rimedi. Molti rimedi vegetali per ED eseguire bene come possono migliorare il movimento. Hanno molto meno reazioni avverse rispetto ai farmaci convenzionali e si svolgono in modo efficiente per migliorare hardons e la forza, troppo. Erbe naturali come Ginkgo Biloba sono utilizzati come una strategia per ED. Gli specialisti di erboristeria credono anche che le spezie o le erbe come noce moscata, portano al movimento intorno al corpo, tra cui il pene. 3. Vitamine naturali vitali. Gli scienziati sanitari hanno scoperto che una mancanza di supplemento è tipico tra gli uomini con ED in particolare vitamina A. Se si ha una mancanza del nutriente ossido di zinco, Questo è stato confermato per portare alla disfunzione erettile. Queste inadeguatezze derivano dal fatto che molti valori nutrizionali in quello che mangiamo piano non sono sufficienti. Aggiungere al vostro fabbisogno di nutrienti aumenterà la circolazione del sistema e migliorare questa condizione. Gli integratori alimentari sono completamente naturali, quindi non dovrete preoccuparvi dei rischi di reazioni avverse. Inoltre, queste vitamine naturali sono utili per il vostro benessere over-all. Oltre a questi vantaggi benessere, disfunzione erettile vitamine naturali e integratori costano molto meno di farmaci rimedi. 4. Esercitare. Fai una mossa e non un tablet vibrante. Camminare farà di più per migliorare e sostenere hardons di qualsiasi altra compressa chimica nel lungo periodo. Il fitness fisico manterrà bassi livelli di pressione e mantenere grandi stadi di movimento. Andando per un 20-30 minuti di movimento rapido ogni giorno, può affrontare questo problema e può sostenere la vostra libido senza l uso di qualsiasi farmaco. 5. Sottolineare. Questo è il peggior attaccante per problemi di erezione. Scopri diversi metodi per riposare. Alcuni metodi tipici per riposare includono la lettura di un libro, la meditazione, un bagno rilassante o allenamenti di respirazione. Sto solo imparando alcuni semplici allenamenti di respirazione che possono migliorare significativamente il movimento nel reparto pantaloni. Una naturale disfunzione erettile soluzioni di trattamento stanno diventando sempre più popolare con gli uomini. Questi rimedi a base di erbe sono preferiti perché non hanno reazioni avverse e sono confermati essere efficiente come il farmaco. La maggior parte degli uomini combattere parlano dei loro problemi, in particolare la disfunzione erettile come c è poca discussione sui problemi di erezione. La verita e che ED ha un impatto su piu di dieci milioni di uomini solo negli Stati Uniti. Non siete soli e l aiuto è disponibile.
Microsoft word - neuro-ophthalmic disease cases.doc
Neuro-Ophthalmic Disease Cases
● The content of this COPE Accredited CE activity was prepared independently by Kelly A. Malloy without input from members of the optometric community. ● Kelly A. Malloy has no direct financial or proprietary interest in any companies, products or services mention in this presentation. ●The content and format of this course is presented without commercial bias and does not claim superiority of any commercial product or service.
Course Description: Clinical cases will be used to demonstrate the varied presentations related to neuro-ophthalmic disease. These will include both afferent and efferent manifestations of neuro-ophthalmic disease, as well as associated ocular health and neurologic manifestations. Conditions that may be demonstrated through clinical cases are included in the outline below. Course Learning Objectives:
1. To emphasize the importance of the optometrist’s role in identifying signs and symptoms
which suggest a neuro-ophthalmic disease process.
2. To understand how to conduct an examination oriented to the detection of neuro-ophthalmic
3. To discern the differential diagnoses for a variety of clinical neuro-ophthalmic presentations. 4. To become familiar with the necessary diagnostic testing for a variety of neuro-ophthalmic
5. To emphasize the need to promptly identify and refer patients presenting with emergent
6. To have a better understanding of the work-up, management, and treatment of neuro-
Neuro – Ophthalmic Disease Cases - OUTLINE
Conditions that may be demonstrated through actual clinical cases are included in the outline below.
Papilledema - Bilateral/Asymmetric (anatomic difference in lamina) RARELY Unilateral ICP (Intracranial pressure) greater than 200 - 250 mm H2O Features of edema Axoplasmic stasis in pre-laminar optic nerve Obscuration of retinal vessels coursing over the disc margin Paton’s lines temporally Symptoms of Increased Intra-Cranial Pressure Headache Nausea Vomiting Diplopia (Abduction deficit – CN VI) Pulsatile tinnitus Transient Visual Obscurations (TVOs) Last few seconds (uni or bi-lateral) Transient optic nerve ischemia
Pattern of Edema Corresponds with NFL thickness Superior, Inferior > Nasal > Temp Superior and Inferior NFL swell first Last to swell is Temporal NFL NFL swelling blurs disc margins and obscures underlying vessels Spontaneous Venous Pulsation Presence of SVP means ICP normal (at that moment - can fluctuate) 10-20 % of normals may not have SVP PSEUDOTUMOR CEREBRI IMPOSTERS Tumor Cerebri Anomalous Discs, Obesity, Migraine Venous Sinus Thrombosis Arteriovenous Malformation Spinal Cord Tumors Meningitis PSEUDOTUMOR CEREBRI IS A SYNDROME BASED UPON: MODIFIED DANDY’S DIAGNOSTIC CRITERIA PATIENT MUST BE AWAKE & ALERT SIGNS & SYMPTOMS OF INCREASED ICP NO NEUROLOGIC SIGNS EXCEPT CN VI PARESIS CSF OPENING PRESSURE > 200MM. H20 & NORMAL COMPOSITION NORMAL MRI, CT PSEUDOTUMOR CEREBRI - EPIDEMIOLOGY 92% Women Ages 11-58 No Racial Bias 13/100,000 In Women - 10% Above Ideal Body Weight 19/100,000 - 20% Above Ideal Body Weight PSEUDOTUMOR CEREBRI INVESTIGATIONS MRI and MRV (MRA) LUMBAR PUNCTURE with opening pressure and analysis of CSF TREATMENT WEIGHT LOSS (6-10%) CARBONIC ANHYDRASE INHIBITORS acetazolamide (diamox); up to 1000 mg. reduces CSF by 50% but may be unsustained! Contraindicated in renal disease SURGICAL TREATMENT Lumboperitoneal Shunt Optic Nerve Sheath Fenestration Gastric Bypass Surgery PROGNOSIS 49% Have Some Visual Loss (Corbett 1982; Orcutt 1984)
25% Severe & Permanent Visual Loss (Folley 1955; Boddle 1974) 80% Improve In 8 Months (Corbett 1982) 10% Recurrence Rate
NEUROMUSCULAR DISORDER WEAKNESS & FATIGABILITY OF VOLUNTARY MUSCLE DECREASE OF Ach RECEPTORS AUTOIMMUNE ATTACK PEAK INCIDENCE YOUNGER WOMEN (15-20) OLDER MEN (50-60) OVERALL F:M 2:1 UNDER 3O: F:M 4.5:1 23% HAVE AN ASSOCIATED IMMUNOLOGIC DISORDER 60% INITIAL PRESENTING SIGN IS AN OCULAR MANIFESTATION 90% WILL DEVELOP EYE SIGNS 15% WILL DEVELOP ONLY EYE SIGNS MG WORK-UP AChR ANTIBODY ASSAY (binding, blocking & modulating) MuSK Antibody TSH, T4, T3, thyroid antibodies (to r/o associated thyroid dysfunction) EMG (SINGLE FIBER) CHEST CT (to r/o thymoma in MG) PROGNOSIS IN 5 YEARS 40% STAY OCULAR 40% CONVERT TO GENERALIZED 11% SPONTANEOUS REMISSION 85% CONVERT TO GENERALIZED SYMPTOMATIC THERAPIES ACh ESTERASE INHIBITORS (MESTINON (pyridostigmine) / PROSTIGMIN (neostigmine)) IMMUNOTHERAPIES ANTICYTOKINE AGENTS CORTICOSTEROIDS, CYCLOSPORIN CYTOTOXIC: IMMURAN (azathioprine) HUMORAL THERAPY PLASMAPHERESIS, INTRAVENOUS GAMMA GLOBULIN SURGICAL THERAPY THYMECTOMY DRUGS TO AVOID IN MG IODINATED CONTRAST AGENTS
CALCIUM CHANNEL BLOCKERS BETA-BLOCKERS: PROPRANOLOL, TIMOPTIC NEUROMUSCULAR BLOCKING AGENTS SUCCINLYCHOLINE, VECURONIUM QUININE, QUINIDINE, PROCAINAMIDE SELECTED ANTIBIOTICS AMINOGLYCOSIDES, CIPROFLOXACIN
DISORDER OF IMMUNE REGULATIONS CYTOTOXICITY DIRECTED AT THYROID GLAND & EOM HYPERTHYROIDISM INFILTRATIVE ORBITOPATHY INFILTRATIVE DERMOPATHY GRAVES’ DISEASE - WOMEN 5:1 GRAVES’ ORBITOPATHY - WOMEN 3:2 GR
TUMOR (exophthalmos; eyelid edema) LOSS OF FUNCTION (eyelid retraction; motility defect; optic neuropathy) REDNESS PRO
RARELY AN ISOLATED FINDING ABSENCE MAY MEAN POSTERIOR DECOMPRESSION EYE
“JELLY ROLL” “FINGER-LIKE” DIURNAL IMPROVEMENT LO
DIURNAL VARIATION GAZE INDUCED IOP RISE Thy
TSH T3 T4 Thyroid Stimulating Immunoglobulin Thyroperoxidase Antibody Thyroglobulin Antibody
BLEPHAROPLASTY _______________________________________________________________________
F ABDUCTION DEFICIT CN VI PALSY KEY POINTS - Measure At DistanceImposters – Abduction Deficits Graves Disease / Thyroid Orbitopathy, Myasthenia Gravis, Loss Of Fusional Reserves, Spasm Of The Near Reflex, Duane’s Retraction Syndrome “THE SIGNATURE OF CN VI PARESIS” At Distance: Eso Which Increases In The Action Of The Palsied Eye CN VI PALSY - ANSWER BY MOTILITY Duction > Version, “Glissades” (Slowed Saccades), Asymmetric OKN (Optokinetic Nystagmus), Negative Forced Duction ANATOMIC LOCALIZATION FASICULAR CN VI + Contralateral Hemiplegia = (Raymond’s) VII + Contralateral Hemiplegia = (Millard-Gubler) Etiology: Infarction, Demyelination, Tumor SUBARACHNOID Increased Intracranial Pressure (Papilledema), AICA Aneurysm, Subarachnoid Hemorrhage, Trauma, Meningitis, Clivus Tumor, Post Infectious, Neurosurgical PETROUS Petrous Apex/ Mastoid Infection, Inferior Petrosal Sinus Infection, Petrous Bone Fracture, Trigeminal Schwannoma, Lumbar Puncture, Myelography, Spinal/ Epidural Anesthesia CAVERNOUS SINUS/ SOF Aneurysm, Thrombosis, CCF (Carotid Cavernous Fistula), Dural AVM (Arterio-venous Malformation), Tumor, Tolossa-Hunt, Herpes Zoster WORK-UP? CBC (Complete Blood Count), BS (Blood Sugar) / HEMOGLOBIN A1c, LYME TITER, RPR/ FTA-ABS (tests for syphilis), ANA (Anti-Nuclear Antibody), ESR (Erythrocyte Sedimentation Rate), C-REACTIVE PROTEIN, PLATELETS, & HEMOGLOBIN (tests for Giant Cell Arteritis), Exclude Trauma, MRI With Gadolinium, Lumbar Puncture CHRONIC CNVI PALSY (= OR > 6 months) – Harbingers of Serious Intracranial Disease __________________________________________________________________________
Most common acute monocular vision loss in young and middle-aged 3rd and 4th decades, Females Association with Multiple Sclerosis Typical ON Unilateral Painful (with eye movements) Visual loss progressing over one week Young / middle age adult Normal fundus or minimal ON edema Atypical OPTIC Neuruitis NLP vision Optic disc or retinal hemes Severe disc swelling Macular exudates No pain Uveitis Bilateral vision loss (adults) DDX of Optic Neuritis Inflammatory / Autoimmunine Diseasesn ( SLE, Antiphospholipid Syndrome, Primary Sjogren’s Syndrome, Neurosarcoidosis, Neuro-Bechet’s Disease, Wegener’s Granulomatosis) Infectious Etiologies ( Lyme , Neurosyphilis, HIV-related disorders of the CNS) Genetic / Hereditary Disorders Demyelinating Disorders 50% of MS pts develop ON at some point ON is 1st clinical symptom of MS in 20% Work-Up lab testing to R/O other etiologies ACE, ANA, Lyme titer, FTA-ABS, RPR MRI of brain and orbits with contrast Spinal tap ? Recommended ON Tx IV Methylprednisolone 250 mg q 6 hr x 3 days Oral prednisone taper 1 mg/kg/day x 11 days, 4 day taper [20 mg day 1; 10 mg days 2 and 4] MS TREATMENTS High-risk ON and 2 or more lesions on MRI Immunomodulators
Interferon beta-1a (Avonex or Rebif) Interferon beta-1b (Betaseron)
Lower risk of further demyelinating events Reduce MRI activity
New Oral MS Medication – Fingolimod (may cause macular edema) OPTIC NEURITIS (CLINICAL PROFILE) F (77.2%)
IDIOPATHIC OPTIC NEURITIS FUNDUS EXAM RETROBULBAR OPTIC NEURITIS 65%
IDIOPATHIC OPTIC NEURITIS VISUAL RECOVERY RECOVERY BEGINS WITHIN 3 WEEKS OF ONSET OF SYMPTOMS PLATEAU’S @ 6 WEEKS; IMPROVES UP TO 1 YEAR @ 5 YEARS: 87%: > 20/25 94%:> 20/40 VISUAL RECOVERY IS WORSE IN PATIENTS WITH FC/LP RECURRING OF 20% IN 5 YEARS ONTT(Beck 1992) Optic Neuritis= MS (Relapsing/ remitting) DxMS: Clinical Diagnosis + MRI findings Oral steroids double risk of recurrence (30%) Treatment affects course of disease (IV sol medrol halves risk of CDMS at 2 years in patients with + MRI). IV steroids speed visual recovery MRI can predict CDMS ONTT TREATMENT RECOMMENTATIONS FOR IDIOPATHIC OPTIC NEURITIS 8 DAYS OF ONSET MRI SHOULD BE PERFORMED ASSESS CRITICAL NUMBER OF WHITE MATTER LESIONS IV METHYLPREDNISOLONE X 3 DAYS (short course of prednisone) ONTT – 10 year results Overall risk of MS in 10 yrs = 38% CDMS One or more brain lesions = 56% CDMS > 40% with one or more lesions did NOT develop CDMS in 10 yrs No brain lesions = 22% CDMS 78% with no lesions did NOT develop CDMS in 10 yrs Risk significantly higher with 1 lesion
No increased risk with greater number of lesions
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Neuromyelitis optica is, like Multiple Sclerosis an inflammatory, demyelinating syndrome of the Central Nervous System Whereas MS affects the entire CNS (optic nerve , Brain, spinal cord), NMO preferentially affects the optic nerve and spinal cord.
Within 5 years of disease onset, more than 50% of patients with relapsing neuromyelitis optica are blind in one or both eyes or require ambulatory help. Typical features are optic neuritis and myelitis (muscle weakness, sensory dysfunction, bladder dysfunction) Serious neurogenic respiratory failure can occur (not common in MS) Work-up: MRI of brain and spine neuromyelitis optica immunoglobulin G (NMO-IgG)
an autoantibody, in the serum of patients with neuromyelitis optica, distinguishes neuromyelitis optica from other demyelinating disorders
the main channel that regulates water homoeostasis in the CNS
NMO –Ig G binds to aquaporin-4 channels on astrocytes, and is toxic, leading to demyelination
This process is different than what happens in MS
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90% WOMEN MORE COMMON IN BLACKS SYSTEMIC SYMPTOMS – FATIGUE, MALAISE, FEVER, WEIGHT LOSS ARHTRALGIAS, MYALGIAS, ARTHRITIS RASH HAIR LOSS EDEMA KIDNEY PROBLEMS + ANA IN 98%
MANY OTHER AUTO ANTIBODIES CAN BE ASSOCIATED AS WELL
MAINLY WOMEN, MAINLY MIDDLE-AGED, BUT CAN ALSO OCCUR IN CHILDHOOD MAY BE ASSOCIATED WITH OTHER AUTOIMMUNE DISEASES DIMINSIHED LACRIMATION AND SALIVATION, ARTHRALGIAS / ARTHRITIS CAN BE ASSOCIATED WITH LYMPHOMA, MENINGITIS, AND MULTIPLE SCLEROSIS Has been associated with optic neuropathy Lab Tests: ANA, SSA & SSB Antibodies
LYME TITER WESTERN BLOT IgG AND IgM STUDIES NEURO-LYME – Optic neuropathy, Diplopia, Disc edema
10-20 x MORE PREVALENT IN African Americans & Scandinavians OCULAR INVOLVEMENT: 22% NEUROSARCOIDOSIS: 5% FEATURES OF ANY OPTIC NEUROPATHY OPTIC DISC PALLOR DECREASED COLOR VISION (DYSCHROMATOPSIA) VISUAL FIELD LOSS RELATIVE AFFERENT PUPILLARY DEFECT SA
LYMPHADENOPATHY ERYTHEMA NODOSUM, SKIN NODULES, MACULOPAPULAR RASH, LUPUS PERNIO NASOPHARNGITIS HEPATOMEGALY, SPENOMEGALY, PORTAL HYPERTENSION, BONE CYSTS, POLYARTHRALGIAS SA
ELEVATED SERUM LYSOZYME LIVER FUNCTION TESTS (+SERUM ALKALINE PHOSPHATASE) CSF: NORMAL OR PLEOCYTOSIS SA
BRONCOALVEOLAR LAVAGE FIBEROPTIC BRONCHOSCOPY WITH TRANSBRONCHIAL BIOPSY BIOPSY (conjuntiva, lung, skin, lymph node, optic nerve sheath) SA
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BARTONELLA TITERS (Henselae and Quintana) Transmitted by a cat (typically a kitten) can be transmitted by scratch or even a lick Usually occurs in patient’s under age 20 Disc Edema – occurs prior to development of the macular star Neuro-retinitis – macular star Treatment: Antibiotics – Rifampin, Azithromycin, Bactrim
[email protected] 42434143 Uw informatie en instructie voor het VCE -onderzoek Onderzoekdag: ddU wordt thuis bezocht rond . uur door . Met vragen voor, tijdens of na het onderzoek kunt u zn bel en:06 42 43 41 43 Erik Herdes / / 06 25021595 Jos LablansBijgevoegd uw recept voor de Colofort® laxans. Zorg dat u optijd naar uw apotheek gaat. De camerapil brengen wij op de da
No. 12 • September 2007 Reform without Reason: What’s Wrong with the FDA Amendments Act of 2007 By John E. Calfee The recently passed Food and Drug Administration Amendments Act (FDAAA) actually combines atleast two laws. One renews the Prescription Drug User Fee Act (PDUFA), which sets deadlines forFDA action on new drug applications and assesses user fees to cover the salaries of extr