Alavert

By O. Ingvar. Presbyterian College. 2018.

Palatal and gag reflex Relatively well preserved reflex: absent gag is a severe sign generic alavert 10 mg mastercard. Corneal reflex Needs localizing if unilaterally absent discount 10 mg alavert otc. Bilateral absence is not a sign of a structural lesion, but of metabolic or toxic encephalopathy. Pain Pain can be elicited in the trigeminal nerve distribution. Pain in the limbs and body may induce mimic changes and ipsilateral dilatation of the pupil. Acoustic startle reflex The acoustic startle reflex is usually present in superficial coma. Exaggerated acoustic startle reflex can be a sign of disinhibition, as observed in hypoxic brain damage. Plum F, Posner JB (1980) The diagnosis of stupor and coma. Davies, Philadelphia References Young GB (1998) Initial assessment and management of the patient with impaired alert- ness. In: Young GB, Ropper AH, Bolton CF (eds) Coma and impaired consciousness. McGraw Hill, New York, pp 79–115 82 Pupil Genetic testing NCV/EMG Laboratory Imaging Biopsy Pharmacologic testing + Fig. Horner’s syndrome: A Shows a Horner syndrome of l0 years duration, characterized by mild ptosis and enophthal- mos, compared to normal side B. C Shows a Horner syndrome with mild ptosis, and miosis (cause: carotid artery dissec- tion) Innervation: 2 antagonistic muscles: circular muscle of iris (cervical sympathetic) and pupillary sphincter (CN III) Paralysis of sphincter pupillae: Between Edinger-Westphal nucleus and the eye: widens due to unantagonized action of sympathetic iris dilator muscle. Paralysis of dilatator pupillae: Ocular sympathetic paralysis, as in Horner’s syndrome Paralysis of accommodation: Drugs: pilocarbin, eserin Atropine, homatropine, psychotropics and antidepressants Cocaine causes dilatation by stimulating sympathetic nerve endings Pupillary size and equality: Anisocoria indicates an inequality in pupil size between the right and left pupils. Botulism: Foodborne: Cranial nerve duction appears first, then dilated fixed pupils (not always present) Reflex iridioplegia: Argyll Robertson pupils Optic nerve lesions: (swinging flashlight test) – MS Adie tonic pupils Unilateral dilatation: Raised intracranial pressure Chadwick D (1993) The cranial nerves and special senses. In: Walton J (ed) Brain’s diseases References of the nervous system. Oxford University Press, Oxford, pp 76–126 Shintani RS, Tsuruoka S, Shiigai T (2000) Carotid cavernous fistula with brainstem conges- tion mimicking tumor on MRI. Neurology 55: 1229–1931 84 Multiple and combined oculomotor nerve palsies Fig. The optomotor nerves: 1 Oculomotor nerve, 2 Trochle- ar nerve, 3 Abducens nerve Fig. Optomotor nerves and relation to vessels and brain- stem: 1 Trigeminal ganglion, 2 Trochlear nerve, 3 Abducens nerve, 4 Oculomotor nerve, 5 Optic nerve, 6 Internal carotid artery 85 Fig. Orbital metastasis: A Atypical optomotor function; B Exophthalmos, best seen from above; C CT scan of orbital me- tastases 86 III, IV, VI Site of lesion Cause Associated findings Brainstem: Infarction Associated Leigh syndrome brainstem signs Tumor Wernicke’s disease Subarachnoid space Aneurysm Other cranial Clivus tumor nerve palsies Meningeal carcinomatosis Meningitis Trauma Cavernous sinus Aneurysm Ophthalmic division Carotid-cavernous of trigeminal nerve Fistula involved, Herpes zoster orbital swelling Infection pain Mucormycosis Mucocele Nasopharyngeal Carcinoma Pituitary apoplexy Tolosa Hunt syndrome Tumor: meningeoma Orbital Thyroid eye disease Proptosis Orbital cellulitis Pseudotumor Trauma Tumor Uncertain Cranial arteritis Pain, polymyalgia Miller Fisher syndrome Ataxia Diabetes Vincristine Toxic Differential diagnosis: orbital muscle disease including thyroid disease, MG, rare ocular myopathies Reference Garcia-Rivera CA, Zhou D, Allahyari P, et al (2001) Miller Fisher syndrome: MRI findings. Neurology 57: 1755–1769 87 Plexopathies 89 Cervical plexus and cervical spinal nerves Genetic testing NCV/EMG Laboratory Imaging Biopsy + The ventral rami of the upper cervical nerves (C1–4) form the cervical plexus. Anatomy The plexus lies close to the upper four vertebrae. The dorsal rami of C1–4 innervate the paraspinal muscles and the skin at the back of neck. Greater auricular Cutaneous nerves Greater occipital Lesser occipital Supraclavicular Transversus colli Transverse cutaneous nerve of the neck Intertransversarii cervicis (C2–C7) Muscle branches Rectus capitis anterior (C1–3) Rectus capitis lateralis (C1) Rectus capitis longus (C1–3) M. Other communicating branches exist with caudal cranial nerves and auto- nomic fibers, cervical vertebrae and joints, and nerve roots/spinal nerves (C1/C2 and C3–8). Complete cervical plexus injury: Clinical picture Sensory loss in the upper cervical dermatomes. Clinical or radiological evi- dence of diaphragmatic paralysis. High cervical radiculopathies: Less common, affected by facet joint. C2/3: site for Herpes Zoster, with post-herpetic neuralgia possible. C2 dorsal ramus spinal nerve (or greater occipital nerve) irritation is better labeled “occipital neuropathy”.

Scott DG: Acute ulcerative acne conglobata 12 Motoyoshi K: Enhanced comedo formation in 26 Pepall LM discount 10mg alavert mastercard, Cosgrove MP 10mg alavert otc, Cunliffe WJ: Abla- (acne fulminans) with erythema nodosum. Clin rabbit ear skin by squalene and oleic acid per- tion of whiteheads by cautery under topical Exp Dermatol 1977;2:351–354. Br J Dermatol 1991;125:256– 42 Quigley JW, Bucks DAW: Reduced skin irrita- 13 Downing DT, Stewart ME, Wertz PW, et al: 259. J Am Acad Der- 27 Yip J, Pepall LM, Gawkrodger DJ, Cunliffe er-2, a new topical tretinoin delivery system: A matol 1986;14:221–225. WJ: Light cautery and EMLA® in the treat- summary of preclinical and clinical investiga- 14 Thiboutot DM, Knaggs H, Gilliland K, Hagari ment of chloracne lesions. S: Activity of type 1 5·-reductase is greater in 128:313–316. Br J Dermatol 1997;136: Treatment of closed comedones – Compari- reduced irritancy incorporating multiple trig- 166–167. J 15 Stewart ME, Greenwood R, Cunliffe WJ, et al: electrocautery with fulguration. Effect of cyproterone acetate-ethinyl oestradiol 1993;186:253–257. Thus, cuta- vous system such as emotional stress can influence the neous neurogenic factors should contribute to onset course of acne. We examined possible participation of and/or exacerbation of acne inflammation. Karger AG, Basel neuropeptide-degrading enzymes and neurotrophic fac- tors, in association with inflammation in the pathogene- sis of acne. Immunohistochemical studies revealed that Acne vulgaris is a skin disorder of the sebaceous folli- substance P (SP)-immunoreactive nerve fibers were in cles that commonly occurs in adolescence and young close apposition to the sebaceous glands, and that neu- adulthood. Many lines of clinical evidence suggest that tral endopeptidase (NEP) was expressed in the germina- components of the nervous system, such as psychological tive cells of the sebaceous glands in the skin from acne and neurogenic factors, can influence the course of acne patients. The disease has been reported to be initiated and/or only within the germinative cells. In addition, an increase exacerbated as a result of emotional or psychosocial in the number of mast cells and a strong expression of stress. However, the nature of the association between endothelial leukocyte adhesion molecule-1 on the post- stress and acne remains unclear, due in part to a lack of capillary venules were observed in adjacent areas to the substantial evidence regarding the participation of cuta- sebaceous glands. In vitro, the levels and the expression neous neurogenic factors in the pathogenesis of acne. When organ-cultured normal skin specimens were ex- posed to SP, we observed significant increases in the Cutaneous Innervation and Neuropeptides sizes of the sebaceous glands and in the number of sebum vacuoles in sebaceous cells. Furthermore, sup- The skin is innervated by primary afferent sensory plementation of SP to organ-cultured skin induced ex- nerves, postganglionic cholinergic parasympathetic pression of NEP, and we demonstrated the subcellular nerves and postganglionic adrenergic and cholinergic © 2003 S. The cutaneous sensory nervous sys- Nevertheless, none of those previous studies addressed tem comprises a network of fine C fibers within the skin the effects of SP on the sebaceous glands or on the disease that innervate multiple cell types and play an important process of acne. Various stimuli may direct- ly activate peripheral nerve endings of primary sensory neurons and impulses are conveyed centrally as well as, SP-Containing Nerves in Acne through antidromic axon reflexes, peripherally. Upon re- lease of neuropeptides (NPs) from sensory terminals, im- Nerve fibers showing immunoreactivity for SP were portant visceromotor inflammation and trophic effects rarely observed in skin specimens from the face devoid of occur in the peripheral tissues. This proinflammatory acne lesions in healthy subjects. On the other hand, speci- NPs release causes the set of changes collectively referred mens from acne patients showed a strong immunoreactiv- to as neurogenic inflammation [6–8]. Some of them were invading into the seba- tivity, and they contribute to the cross-talk between the ceous glands and were located in close apposition to the nervous system and the immune system in the skin [8– sebocytes. NPs are a heterogeneous group of several hundred biologically active peptides, present in neurons of both the central and the peripheral nervous system and in- Effects of SP on the Sebaceous Glands volved the transmission of signals not only between nerve cells, but also with the immune system where they appear To examine whether cutaneous neurogenic factors af- to be critical mediators of different processes. Normal fect the morphology of sebaceous glands, we used electron human skin expresses a variety of NPs that are either microscopy to observe alterations of the sebaceous glands directly derived from sensory neurons or from skin cells in organ culture by several kinds of NPs and nerve growth such as keratinocytes. In addition, immune cells that ei- factor (NGF), the best-characterized member of the neu- ther constitutively resides in the skin such as mast cells rotrophin family. The ultrastructure of the sebaceous (MCs) or infiltrating cells into the skin under inflammato- glands with medium alone was identical to that of intact ry conditions have been reported to produce NPs.

Even then cheap 10mg alavert overnight delivery, it is very difficult to analyze the information process involved buy alavert 10mg amex. The results of all of the neuronal and muscular activity in unknown anatomical sites are transmitted using a homogenous medium. The electrical signals moni- tored on the surface of the skin are of enormous clinical and physiological importance. Electroencephalograms, electrocardiograms, electromyograms, and other signals are already being used in clinical medicine to measure the activity of muscular and neuronal systems. The way in which the information supplied by these systems is interpreted is based principally on statistical experience built up over the years. The plasma cell mem- brane is a medium that separates the intercellular fluids from the extracellular ones. These two types of fluids have different ions concentrations, and the membrane has different levels of permeability for the different ions dissolved in the solution. A membrane poten- tial is generated by the ion transfer, principally as a function of diffusion mechanisms. If we take into consideration the effects of the three main ions alone, potassium, sodium, and chlorine, we obtain the membrane potential via the following equation: þ þ À þ þ À E ¼ ln RTPX½K ŠþPNa½Na ŠþPC½Cl Š FPX½K ŠþPNa½Na ŠþPC½Cl Š where R, T and F are the universal gas constant, the absolute temperature, and Faraday’s constant, respectively; PX is the permeability of the remaining membrane to X ions and Xo and Xi are the concentrations of X ions in the extracellular and intracellular fluids. The remaining membrane potential calculated in this way is approximately 80 mV; the interior of the cell becomes negative in relation to the exterior. Some membranes have different levels of excitability. When the membrane is excited by an electrical or mechanical signal or by a chemical stimulus, its permeability changes in relation to the ion transfer. These changes in turn cause an increase in the remaining potentials of the membrane, which become positive for a short period of time and then, when the membrane changes its sign, return to the resting potential. The type and duration of the action potential differs from one cell type to another. The membrane only becomes excited when the stimulus exceeds a threshold level of around 20 mV. Once this threshold has been exceeded and the action potential appears, there is also a change in the sensitivity of the threshold. After the potential has been acti- vated, there is a period of time (approximately 1 or 2 msec) during which the threshold becomes infinite. This period is called the period of total refractoriness during which no new action potential can be activated. The threshold thus returns to its nominal value in accordance with the computation of the decay function. The period during which the threshold falls to its normal level is known as the relative refractoriness period. In that per- iod, a new action potential can be activated by a stimulus that is sufficiently large to cross the relatively high threshold. The source of electrical signals is the action potential generated by individual neurons and muscle fibers. The current density generated by the membrane activity can give rise to a change in the surrounding medium. The surrounding tissue in which the current change took place is called the conduction volume. In many clinical and neurophysiological applications, we can monitor the conduction volume field but not the bioelectrical sources that generate it. BEAUTYTEK1 IN COSMETIC MEDICINE & 157 This is definitely the case when electrodes are attached to the skin to monitor the electrical activity of the heart and brain. It is therefore extremely important to be able to precisely deduce the underlying bioelectric source producing the conduction volume activity. This operation involves a very complex computation, especially if the characteristics of the biological medium are taken into consideration. Mathematical models of flow fields of currents in the conduction volumes have been developed with varying degrees of success. If, for example, the two electrodes are situated in a position that will permit a reading of the sys- tem in an inflamed area, the machine performs a very fast physiochemical analysis of the 1 tissue once the circuit is closed.

The bone mar- row picture in the RA with 5q– syndrome is characterized by the presence of monolobu- lated and bilobulated micromegakaryocytes purchase alavert 10mg with mastercard. Two thirds of these patients have RA or RA with ringed sideroblasts (RARS) generic 10 mg alavert otc, and the remainder have RAEB (RA with excess of blasts). In those patients who have a del(5q) as their sole cytogenetic abnormality, MDS tends to follow a more benign course, although progression to acute myeloid leukemia (AML) may occur. A 62-year-old woman well known to you comes to see you in clinic. Since the last time you saw her, she was admitted to the hospital and diagnosed with acute leukemia. She has been followed by a local hema- tologist and has undergone remission-induction chemotherapy. She is scheduled to begin postinduction consolidation therapy. She explains that she and the specialist are working toward a “complete remis- sion” (CR) and wants to know if that means she will be cured. Which of the following definitions of CR is most accurate? Full recovery of normal peripheral blood counts; blast cells are unde- tectable in the bone marrow B. Full recovery of normal peripheral blood counts; bone marrow cellu- larity with less than 5% residual blast cells C. Full recovery of normal peripheral blood counts; bone marrow cellu- larity with less than 10% residual blast cells D. Full recovery of normal peripheral blood counts; bone marrow cellu- larity with less than 10% residual blast cells for a minimum of 1 year Key Concept/Objective: To understand the concept of CR in leukemia patients The goal of remission-induction chemotherapy is the rapid restoration of normal bone marrow function. The term complete remission is reserved for patients who have full recovery of normal peripheral blood counts and bone marrow cellularity with less than 5% residual blast cells. Induction therapy aims to reduce the total-body leukemia cell pop- ulation from approximately 1012 cells to below the cytologically detectable level of about 109 cells. The leukemia cells in some patients have high levels of primary drug resistance and will be refractory to courses of remission-induction chemotherapy. It is assumed, how- ever, that even in CR a substantial burden of leukemia cells persists undetected, leading to relapse within a few weeks or months if no further therapy is administered. Postinduction or remission consolidation therapy, usually comprising several additional courses of 40 BOARD REVIEW chemotherapy, is designed to eradicate residual leukemia, allowing the possibility of cure. A 52-year-old man presents to you in clinic as a new patient. It has been several years since he has seen a physician. He comes to you today because he has not been feeling well and he thinks something is wrong. He reports that for the past several weeks, he has been experiencing malaise, subjective weight loss, and fevers. Physical examination is notable for lymphadenopathy and splenomegaly. Laboratory data reveal a moderately decreased hemoglobin level, thrombocytopenia, and a moderate leukocytosis. Which of the following statements is the most accurate regarding cure of ALL? A combination of vincristine, prednisone, and daunorubicin cures about one third of patients with Philadelphia positive (Ph+) ALL B. A combination of L-asparaginase and cyclophosphamide cures about one third of patients with Ph+ ALL C. Allogeneic stem cell transplantation cures about one third of patients with Ph+ ALL D. There are currently no regimens that are known to cure this disease Key Concept/Objective: To know the regimen that is associated with cure of Ph+ ALL Ph+ ALL is identified by the t(9;22)(q34;q22) or the bcr-abl fusion gene.