By J. Marius. California Institute for Human Science.
Endothelial impairment and hence dysfunction has been proven to result from smoking motilium 10mg low price gastritis blood test, and nicotine is under discussion as a factor favoring the progression of arteriosclerosis. By releasing epinephrine, it elevates plas- ma levels of glucose and free fatty acids in the absence of an immediate physio- logical need for these energy-rich me- tabolites. Furthermore, it promotes platelet aggregability, lowers fibrinolyt- ic activity of blood, and enhances coag- ulability. The health risks of tobacco smoking are, however, attributable not only to nicotine, but also to various other ingre- dients of tobacco smoke, some of which Lüllmann, Color Atlas of Pharmacology © 2000 Thieme All rights reserved. Nicotine 113 Nicotine Nicotiana tabacum "Tar" Nitrosamines, acrolein, polycyclic hydrocarbons e. Sequelae of tobacco smoking Lüllmann, Color Atlas of Pharmacology © 2000 Thieme All rights reserved. In the CNS, dopamine itself serves antihypertensive agents, reserpine (ob- as a neuromediator and is implicated in solete) and "-methyldopa, deplete neu- neostriatal motor programming (p. A common ad- the elicitation of emesis at the level of verse effect of dopamine antagonists or the area postrema (p. It Dopamine receptors are coupled to G- plays a role in inflammatory and allergic proteins and exist as different subtypes. The aforemen- creased permeability of small blood ves- tioned actions are mediated mainly by sels. When given by infusion, from enterochromaffin-like cells and dopamine causes dilation of renal and stimulates acid secretion by the parietal splanchnic arteries. In the CNS, it acts as a neuromod- ed by D1 receptors and is utilized in the ulator. Two receptor subtypes (G-pro- treatment of cardiovascular shock and tein-coupled), H1 and H2, are of thera- hypertensive emergencies by infusion of peutic importance; both mediate vascu- dopamine and fenoldopam, respective- lar responses. Most of the so-called evidenced by cardiac stimulation and H1-antihistamines also block other re- vasoconstriction, respectively. Administra- pheniramine); as antiemetics (mecli- tion of the precursor L-dopa promotes zine, dimenhydrinate, p. The ergolides, bromocriptine, sents the transition to the neuroleptic pergolide, and lisuride, are ligands at D- phenothiazines (p. Unwanted ef- receptors whose therapeutic effects are fects of most H1-antihistamines are las- probably due to stimulation of D2 recep- situde (impaired driving skills) and atro- tors (indications: parkinsonism, sup- pine-like reactions (e. Typical adverse effects of es, astemizole, cetrizine, fexofenadine, these substances are nausea and vomit- and loratidine are practically devoid of ing. H2- amphetamine and ritaline augment do- antihistamines (cimetidine, ranitidine, pamine release.
Typical inf dose: 2–20 µg/kg/min Dopamine (Intropin) INDICATIONS: Second line for symptomatic bradycardia purchase motilium 10mg otc gastritis symptoms upper right quadrant pain. Hypotension (BP <70–100 mm Hg) with signs of symptoms of shock SUPPLIED: 40 mg/mL or 160 mg/mL. Initial, 5–10 µg/kg/min; typical: 2–20 µg/kg/min Note: If >20 µg/kg/min is required, consider use of alternative adrenergic agent (eg, epinephrine) Epinephrine INDICATIONS: Cardiac arrest: VF, pulseless VT, asystole, PEA. Anaphylaxis, severe allergic reactions: Combine with large fluid volumes, corticosteroids, antihistamines. Inf: 30 mg epinephrine (30 mL of 1:1000 solution) to 250 mL NS or D5W, run at 100 mL/h, titrate. Profound bradycardia/hy- potension: 2–10 µg/min (1 mg of 1:1000 in 500 mL NS, infuse 1–5 mL/min). Do NOT use with history of active bleeding or surgery within 30 d or if platelets <150,000/mm3. Continue 12 IU/kg/h (max 1000 IU/h for patients >70 kg) round to the nearest 50 IU. Heparin (Low Molecular Weight) (Fragmin, Lovenox) INDICATIONS: ACS with non-Q wave or unstable angina SUPPLIED: Dalteparin (Fragmin), Enoxaparin (Lovenox) DOSAGE: 1 mg/kg bid SQ for 2–8 d with aspirin Ibutilide INDICATIONS: Supraventricular arrhythmias (AFiB, A flutter); short-acting SUPPLIED: 1 mg/10 mL DOSAGE: 1 mg IV over 10 min (if <60 kg 0. Stable VT, wide-complex tachycardias of uncertain type, wide-complex PSVT SUPPLIED: 20 mg/mL in preloaded 5-mL syringe, 10 mg/mL in 5-mL vial. Perfusing arrhythmia: For stable VT, wide-complex tachycardia or uncertain type, signifi- cant ectopy, use as follows: 1. Maintenance inf: 1–4 mg/min (30–50 µg/min) Magnesium Sulfate INDICATIONS: Cardiac arrest associated with torsades de pointes or suspected hypomagnesemic state, refractory VF, life-threatening ventricular arrhythmias due to digitalis toxicity, tricyclic over- dose. Torsades de pointes: Loading dose of 1–2 g mixed in 50–100 mL of D5W, over 5–60 min IV. Mannitol INDICATIONS: Increased intracranial pressure in management of neurologic emergencies SUPPLIED: 150-, 250-, and 1000-mL IV containers (strengths: 5%, 10%, 15%, 20%, and 25%). Morphine Sulfate INDICATIONS: Chest pain and anxiety associated with AMI or cardiac ischemia, acute cardiogenic pulmonary edema (if blood pressure is adequate) SUPPLIED: 2–10 mg/mL in a 1-mL syringe DOSAGE: Adults. Bolus IV dose: For total reversal of narcotic effects (smaller doses may be used if total reversal not required), as fol- lows: Birth–5 y (≤ 10 kg): 0. Use infusion pump; hemodynamic monitor- ing for optimal safety Norepinephrine INDICATIONS: Severe cardiogenic shock and significant hypotension. Procainamide (Pronestyl) INDICATIONS: Recurrent VT not controlled by lidocaine, refractory PSVT, refractory VF/pulseless VT, stable wide-complex tachycardia of unknown origin, AF with rapid rate in WPW SUPPLIED: 100 mg/mL in 10-mL vial, 500 mg/mL in 2-mL vial DOSAGE: Adults. Other indications: 20 mg/min IV until one of the following occurs: arrhythmia suppression, hypotension, QRS widens by more than 50%, total dose of 17 mg/kg is given.
The • The gene(s) responsible for DD have not yet been exact role of telethonin is not known buy discount motilium 10 mg online gastritis diet 30. The autosomal dominant LGMD genes merosin, which is made by a gene called laminin. These merosin protein usually lies outside muscle cells and types of LGMD are considered quite rare. When merosin is not produced, the muscle fibers degenerate soon after The genes causing these types of LGMD, their chro- birth. A second gene called integrin is responsible for mosomal location, and the proteins they code for (when CMD in a few individuals but alterations in this gene known) are listed below: are a rare cause of CMD. The gene responsible for • LGMD1A (chromosome 5): myotilin Fukuyama CMD is FCMD and it is responsible for • LGMD1B (chromosome 1): laminin making a protein called fukutin whose function is not clear. The distribution of • COL6A2 (chromosome 21): collagen VI alpha 2 symptoms, age of onset, and progression differ signifi- cantly. Pain is sometimes a symptom of each, usually due • COL6A3 (chromosome 2): collagen VI alpha 3 to the effects of weakness on joint position. The causes of the other muscular dystrophies are not DUCHENNE MUSCULAR DYSTROPHY (DMD) A boy as well understood: with Duchenne muscular dystrophy usually begins to • EDMD is due to a alteration in the gene for a protein show symptoms as a pre-schooler. Most patients walk three to six months later than expected and have difficulty running. Later on, a boy with • Myotonic dystrophy is caused by alterations in a gene DMD will push his hands against his knees to rise to a on chromosome 19 for an enzyme called myotonin pro- standing position, to compensate for leg weakness. About tein kinase that may control the flow of charged parti- the same time, his calves will begin to enlarge, though cles within muscle cells. This gene alteration is called a with fibrous tissue rather than with muscle, and feel firm triple repeat, meaning it contains extra triplets of DNA and rubbery; this condition gives DMD one of its alter- code. It is possible that this alteration affects nearby nate names, pseudohypertrophic muscular dystrophy. He genes as well, and that the widespread symptoms of will widen his stance to maintain balance, and walk with myotonic dystrophy are due to a range of genetic dis- a waddling gait to advance his weakened legs. Contractures (permanent muscle tightening) usually • The gene for OPMD appears to also be altered with a begin by age five or six, most severely in the calf muscles. Nearly all cases of this age often leads to scoliosis (a side-to-side spine cur- FSH are associated with a deletion (missing piece) of vature) and kyphosis (a front-to-back curvature). Researchers are investi- gating the molecular connection of this deletion and The most serious weakness of DMD is weakness of FSH. It is not yet certain whether the deleted material the diaphragm, the sheet of muscles at the top of the contains an active gene or changes the regulation or abdomen that perform the main work of breathing and activity of a nearby FSH gene. Diaphragm weakness leads to reduced energy 772 GALE ENCYCLOPEDIA OF GENETIC DISORDERS and stamina, and increased lung infection because of the shortened. Symptoms most commonly begin in the teens or early twenties, though Among males with DMD, the incidence of car- infant or childhood onset is possible. Symptoms tend to diomyopathy (weakness of the heart muscle), increases be more severe in those with earlier onset.
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