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Coumadin

By W. Kalan. Loyola University, New Orleans. 2018.

TABLE 12–2 Typical Vitamins Provided in 1 L of TPN by Adding 2 Vials of Standard MVI–12 Ascorbic acid 100 mg Pyridoxine (B6) 4 mg Vitamin A 3300 IU Dexpanthenol 15 mg Vitamin D 200 IU Vitamin E (α tocopherol) 10 IU Biotin 60 µg Thiamine (B1) 3 mg Folic acid 400 µg Riboflavin (B2) 3 purchase coumadin 5mg amex pulse pressure widening. Insulin generic coumadin 5 mg with visa hypertension jnc 8, when required, can be given subcutaneously as regular insulin using a sliding scale, as shown in Table 12–4. This allows a constant infusion of insulin along with the infusion of dex- trose, which avoids the peaks and valleys in blood glucose that occur when the sliding scale is used. Insulin drips are not advised because TPN can be tem- porarily or permanently discontinued, which would then stop the insulin. This could be done with minimal supplementation; as little as 4% of total calories per day would prevent the syndrome of EFAD. Most clinicians prescribe 500 mL of 10% lipid emulsion three times weekly to prevent this syndrome. The signs and symptoms of this deficiency include scaling skin rash, alopecia, and wound healing failure. TABLE 12–4 Sliding Scale for Insulin Orders Regular Insulin Dose Urine Glucose* (Units, given SQ) 0–1+ 0 2+ 5 3+ 10 4+ 15 Any acetone: call house officer *Should be checked every 6 h as part of standing TPN orders. Once data became available establishing the problems associated with overfeeding of carbohydrate calories, the use of lipid for caloric supplementation became more recognized. Commercially available intravenous fat emulsions are derived from soybean oil, with one product (Liposyn II) combining both soybean and safflower oil. Pediatricians often prefer the Liposyn II product because of its higher percentage of linolenic acid. Because the particle size of these emulsions closely approximates naturally occurring chylomicrons, parenteral infusion is possible. In addition, the emulsions are cleared from the bloodstream in a manner and rate similar to that for chylomicrons. Before beginning the IV fat emulsion, the serum triglyceride level should be checked to ensure that hypertriglyceridemia is not present. Provided that the serum triglyceride level is below 400 mg/dL, the fat emulsion can be given over a 6–12-h period. The first bottle should be given slowly (1 mL/min for 15 min to check for hypersensitivity reaction). Adverse reactions can include dyspnea, fever, chills, chest tight- ness, wheezing, headaches, and nausea. Currently, the only absolute contraindication to the use of IV fat emulsion is type IV hy- pertriglyceridemia, although isolated cases of nontype IV intolerance to the solution have been reported. To monitor for the clearing of the fat from the bloodstream, a trough serum triglyceride level should be tested 8–12 h following the daily infusion of the fat emulsion. Because fat emulsions are primarily composed of triglycerides (essentially cholesterol free), if the blood is mistakenly drawn while the fat is being infused or shortly thereafter, the serum triglyceride level will be markedly elevated. Other possible contraindications include lipoid nephrosis, severe hepatic failure, and allergy to eggs (egg phosphatides are used as the emulsifying agent). For this reason, it is usually recommended that the fat emulsion be infused into the central line under strict aseptic technique via a ster- ile Y-connector. As mentioned earlier, some institutions combine the lipid with the TPN for- mula in one bag for 24-h administration. This limits the clinicians ability to validate fat clearance from the blood and makes baseline triglyceride data extremely important. STARTING TPN In general, TPN should not be started until a patient has a stable fluid and electrolyte profile. It is usually unwise to begin TPN in a patient who requires large amounts of fluid, may need resuscitation for trauma, or is septic. Placement of a deep line must be done aseptically, as outlined in Chapter 13, page 253. Infection (bacteremia, fungemia) arising from the catheter or the catheter–skin interface is the most common complication of TPN. SMA-7 and SMA-12; in particular check phosphate, glucose, and routine elec- trolytes (Na, K, Cl) d. Medications are generally not added to TPN solutions except insulin and H2 receptor blockers. Check urine for sugar and acetone every 6-8 h, house officer should be called if sugar is >2+ or acetone is present.

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A1) 2 mg coumadin with mastercard blood pressure chart in hindi,“rapid”voltage-gatedNa+ Na+ channels in depolarized membranes can- channels are activated (! This is followed by a This results in increased Na+ conductance safe 5mg coumadin hypertension vs hypotension, gNa relative refractory period during which only ac- (! If the threshold potential is not of rise can be generated, even by strong reached, this process remains a local (sub- stimuli. Large numbers of The activation of the Na+ channels reaches a Na+ channels are activated, and the influxing maximum at resting potentials of ca. As mals, Na+ channels can no longer be activated a result, the Em rapidly collapses (0. This is the reason for the abso- sweep)andtemporarilyreachespositivelevels lute and relative refractory periods (see above) (overshooting, +20 to +30mV). The gNa drops and the non-excitability of cells after the ad- before overshooting occurs (! A2) because ministrationofcontinuouslydepolarizingsub- the Na+ channels are inactivated within 0. The potential therefore reverses, increased extracellular Ca2+ concentration and restoration of the resting potential, the re- makesitmoredifficulttostimulatethecellbe- polarization phase of the action potential, cause the threshold potential becomes less begins. On the other hand, excitability in- slowly) the open-probability of voltage-gated creases (lower threshold) in hypocalcemic K+ channels. This increases the potassium con- states, as in muscle spasms in tetany ductance, gK, thereby accelerating repolariza- (! The special features of action potentials in Inmanycases,potassiumconductance,gKis cardiac and smooth muscle fibers are de- still increased after the original resting poten- scribed on pages 192, 70 and 59A. Action potential (1) and ion conductivity (2) (nerve and skeletal muscle) 1 2 + “Overshoot” + (20–30mV) 0 0 – Action – potential gNa Action potential gK Threshold After-hyper- polarization Resting Pre- GK depolari- sation Resting GNa 0 Time Time ca. Closed, [mV] activatable + Depolarization 0 – –90mV [mV] Resting potential Na+ + 0 2. Closed, inactivated + 0 – Reversal of potential and start of repolarization In 47 Despopoulos, Color Atlas of Physiology © 2003 Thieme All rights reserved. Propagation of Action Potentials in Action potentials normally run forward (or- thodromic) because each segment of nerve Nerve Fiber fiber becomes refractory when an action Electrical current flows through a cable when potentialpasses(! The metal wire inside the impulses are conducted backwards (anti- the cable is well insulated and has very low- dromic)due,forexample,toelectricalstimula- level resistance, reducing current loss to a tion of nerve fibers from an external source minimum. C) conduct much faster (up to 80 m/s = 180 Propagation of action potentials: The start mph in humans). In the internode regions, a ofanactionpotentialisaccompaniedbyabrief myelin sheath (! The fibers from the surroundings; thus, longitudi- cell membrane that previously was inside nal currents strong enough to generate action negative now becomes positive ( +20 to potentials can travel further down the axon +30mV), thus creating a longitudinal poten- (ca. This results in more rapid tial difference with respect to the adjacent, conduction because the action potentials are still unstimulated nerve segments (internal generated only at the unmyelinated nodes of –70 to –90mV;! This is followed by a Ranvier, where there is a high density of Na+ passive electrotonic withdrawal of charge from channels. This results in rapid, jump-like pas- the adjacent segment of the nerve fiber, caus- sage of the action potential from node to node ing its depolarization. Thesaltatorylengthis another action potential is created in the adja- limited since the longitudinal current (1 to cent segment and the action potential in the 2nA) grows weaker with increasing distance previous segment dissipates (! Before it drops below the threshold Because the membrane acts as a capacitor, level,thesignalmustthereforeberefreshedby the withdrawal of charge represents a capaci- a new action potential, with a time loss of tating (depolarizing) flow of charge that be- 0. Because of the rela- fiber limits the spread of depolarization, as de- tively high Ri of nerve fiber, the outward loops scribed above, the axon diameter (2r) also af- of current cross the membrane relatively close fectstheconductionvelocity,θ(! R ispro-i to the site of excitation, and the longitudinal portional to the cross-sectional area of the current decreases as it proceeds towards the nerve fiber (πr ),2 i. Atthesametime,depolarizationin- therefore require fewer new APs per unit of creasesthedrivingforce(=Em–EK;! K+ fluxing out of the cell therefore fiberdiameterareaccompaniedbyan increase accelerates repolarization.

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Coumadin
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