By K. Fraser. Northern State University. 2018.
The deposition is the most important event for the defendant physician before trial (1–7) generic depakote 250mg amex facial treatment. However depakote 250 mg with amex symptoms detached retina, one can ask to have it in a setting in which the pathologist feels more com- fortable, such as in the hospital. The deposition is typically attended by a court reporter, who will record everything. There may be other defense attorneys present if they represent other parties within the lawsuit, such as code- fendant physicians or the hospital. The possibility exists that the plaintiff’s family could also be present. The deposition is taken under oath and can be read to the jury at trial. The format of the deposition is for the opposing (plaintiff’s) attorney to pose a series of questions (cross- examination). Your defense attorney will follow, typically with fewer questions, to clarify certain points raised during cross-examination. Bring your curriculum vitae, but do not bring literature or notes because they will be discoverable. Plaintiff’s Goal: To Be Educated About Your Strategies and Information The defendant’s or physician’s role is not to educate the opposing attorneys, but rather just to answer their questions: • Do not volunteer unnecessary information. If you provide them with information they did not request, it may deprive your attorney of determining when certain information will be disclosed for maximal impact. Providing a lengthy discourse may open up fur- ther questions or opinions that may be detrimental to your case. The attorney Chapter 5 / Discovery and Deposition 55 may be waiting for you to offer additional information that could eventually be damaging to your case. Plaintiff’s Goal: To Impeach Your Credibility What you answer at deposition is sworn testimony and can be read back at trial to make you look bad if there are certain internal incon- sistencies or differences in trial testimony. The role of the physician in this regard is to tell the truth and to be consistent. Assume that any misstatement will be discovered, and it will be made to look like nothing that you say can be trusted. This allows you to think carefully before answering, and it allows time for your attorney to raise objections. Do not panic, because these mistakes can be rehabilitated at trial or when your attorney follows up with questions. The following are some specific ploys used by plaintiff lawyers to ruin your credibility. Plaintiff attorney: Asks specifically ambiguous questions so that you will answer them in an incriminating manner. Defending physician: Do not help the plaintiff attorney by saying, “Do you mean X or Y? Defending physician: Respond by saying, “There are two points raised by your question, and let me answer each one of them separately. Defending physician: Ask for the statement to be clarified without the use of double negatives or carefully try to dissect the question and answer it correctly. Often, a hypothetical question will include facts different than you believe to be true for your case. If you just answer the question, then it can be used out of context at trial in a damaging fashion. Defending physician: Answer a hypothetical question in this way: “Although this hypotheti- cal question does not apply to the current case, if I assume the facts in your hypothetical question, then I would answer as follows. Asks what textbooks to which you commonly refer or recommend, so that if something is found within that text that conflicts with your testimony, you can be made to look bad. The correct way to respond to this question is, “Nothing in its entirety is authoritative, but I would have to see specifically the sentence or sec- tion on a specific issue to see if I agree with that statement. Defending physician: Watch out for phrases such as, “Is it fair to say,” or, “Do you mean to say this? Specifically clarify any inaccuracies that he or she made in his or her summary.
Human Cardiovascular Con- mm Hg central blood volume with standing trol order 250 mg depakote with mastercard xanax medications for anxiety. Venules collect blood from the capillaries and act as reser- is a major determinant of capillary hydrostatic voirs for blood volume buy depakote 500 mg line symptoms 5dp5dt fet. Myogenic arteriolar regulation is a response to increased cules from the interstitial space between cells. By-products of metabolism cause the dilation of adjacent endothelial cells. The concentration difference of solutes across the capillary norepinephrine, which constricts the arterioles and wall is the energy source for capillary exchange. Autoregulation of blood flow allows some organs to main- primary forces for fluid filtration and absorption across tain nearly constant blood flow when arterial blood pres- capillary walls. If all microvessels were to dilate are exchanged between the blood and cells. The microcir- fully because of relaxation of their smooth muscle cells, the culation minimizes diffusion distances, facilitating ex- arterial blood pressure would plummet. Virtually every cell in flow in a standing individual would be inadequate, resulting the body is in close contact with a microvessel. Regulation of vascular resistance in cells are in direct contact with at least one microvessel. The lens and cornea are exceptions be- cular resistance to preserve the arterial pressure and simulta- cause their nutrients are supplied by the fluids in the eye. The compromise is to preserve the regulate vascular resistance and thereby interact with car- mean arterial pressure by increasing arterial resistance at the diac output to maintain the arterial blood pressure (see expense of reduced blood flow to most organs other than the Chapter 12). The organs survive this conflict by increas- 262 CHAPTER 16 The Microcirculation and the Lymphatic System 263 ing their extraction of oxygen and nutrients from blood in the microvessels as the blood flow is decreased. The microvasculature is considered to begin where the smallest arteries enter the organs and to end where the smallest veins, the venules, exit the organs. In between are microscopic arteries, the arterioles, and the capillaries. De- pending on an animal’s size, the largest arterioles have an inner diameter of 100 to 400 m, and the largest venules have a diameter of 200 to 800 m. The arterioles divide into progressively smaller vessels to the extent that each section of the tissue has its own specific microvessels. The branching pattern typical of the microvasculature of differ- ent major organs and how it relates to organ function are discussed in Chapter 17. THE ARTERIAL MICROVASCULATURE Large arteries have a low resistance to blood flow and func- tion primarily as conduits (see Chapter 15). As arteries ap- proach the organ they supply, they divide into many small FIGURE 16. In most or- muscle cells wrapping around arterioles of gans, these small arteries, which are 500 to 1,000 m in di- various sizes. Each cell only partially passes around large-diame- ameter, control about 30 to 40% of the total vascular re- ter (1A) and intermediate-diameter (2A) arterioles, but com- sistance. These smallest of arteries, combined with the pletely encircles the smaller arterioles (3A, 4A). The en- blood vessels; together they regulate about 70 to 80% of larged views of 3A and 4A are at 4-times-greater magnification. Constriction of these vessels maintains the rel- testine during maturation. Constriction re- sults from the release of norepinephrine by the sympathetic larger vessel, but may encircle a smaller vessel almost 2 nervous system, from the myogenic mechanism (to be dis- times (see Fig. Vessel Wall Tension and Intravascular Pressure Arterioles Regulate Resistance by the Contraction Interact to Determine Vessel Diameter of Vascular Smooth Muscle The smallest arteries and all arterioles are primarily respon- The vast majority of arterioles, whether large or small, are sible for regulating vascular resistance and blood flow. Ves- tubes of endothelial cells surrounded by a connective tissue sel radius is determined by the transmural pressure gradient basement membrane, a single or double layer of vascular and wall tension, as expressed by Laplace’s law (see Chap- smooth muscle cells, and a thin outer layer of connective ter 14). Changes in wall tension developed by arteriolar tissue cells, nerve axons, and mast cells (Fig. Most arte- cular smooth muscle cells around the arterioles are 70 to 90 rioles can dilate 60 to 100% from their resting diameter and m long when fully relaxed.
This has the It was predicted that the flawed gene in patients with advantage of restoring both the known and unknown cystic fibrosis would normally encode either a chloride functions of the gene order depakote 500 mg with visa symptoms 8dpiui. The field of gene therapy is in its channel protein or a membrane protein that regulates infancy order depakote 250 mg online medicine 0552, and although there have been no “cures” for chloride channels. The gene was identified in 1989 and en- cystic fibrosis, much has been learned about the prob- codes a protein of 1,480 amino acids, the cystic fibrosis lems presented by the inefficient and short-lived transfer transmembrane conductance regulator (CFTR). The next phase of gene therapy will fo- dence indicates that CFTR contains both a chloride channel cus on improving the technology for gene delivery. Although it functions as an ion therapy may become a reality for many lung diseases channel, it has structural similarities to adenosine triphos- during this century. Sodium ions are that directly use metabolic energy to transport ions against transported out of the cell and potassium ions are brought a gradient of concentration or electrical potential are in. It is known as a P-type ATPase because the protein is known as ion pumps. The direct use of metabolic energy to phosphorylated during the transport cycle (Fig. The carry out transport defines a primary active transport pump counterbalances the tendency of sodium ions to en- mechanism. The source of metabolic energy is ATP syn- ter the cell passively and the tendency of potassium ions to thesized by mitochondria, and the different ion pumps hy- leave passively. It maintains a high intracellular potassium drolyze ATP to ADP and use the energy stored in the third concentration necessary for protein synthesis. Because of this abil- a role in the resting membrane potential by maintaining ion ity to hydrolyze ATP, ion pumps also are called ATPases. The sodium-potassium pump can be inhibited ei- The most abundant ion pump in higher organisms is the ther by metabolic poisons that stop the synthesis and sup- sodium-potassium pump or Na /K -ATPase. It is found ply of ATP or by specific pump blockers, such as the car- in the plasma membrane of practically every eukaryotic cell diac glycoside digitalis. The sodium- plasma membrane, in the membrane of the endoplasmic potassium pump is an integral membrane protein consisting reticulum, and, in muscle cells, in the sarcoplasmic reticu- 28 PART I CELLULAR PHYSIOLOGY lum membrane. They pump Mitochondria have F-type ATPases located in the inner calcium ions from the cytosol of the cell either into the ex- mitochondrial membrane. This type of proton pump nor- tracellular space or into the lumen of these organelles. Instead of using the energy organelles store calcium and, as a result, help maintain a stored in ATP molecules to pump protons, its principal low cytosolic concentration of this ion (see Chapter 1). It is present in the luminal membrane of the parietal the respiratory chain. By pumping protons into the lumen of the stomach in exchange Secondary Active Transport. The net effect of ion for potassium ions, this pump maintains the low pH in the pumps is maintenance of the various environments needed stomach that is necessary for proper digestion (see Chapter for the proper functioning of organelles, cells, and organs. It is also found in the colon and in the collecting ducts Metabolic energy is expended by the pumps to create and of the kidney. Its role in the kidney is to secrete H ions into maintain the differences in ion concentrations. They ion releases potential energy when it moves down an elec- pump protons from the cytosol into these organelles, keep- trochemical gradient, just as a body releases energy when ing the inside of the organelles more acidic (at a lower pH) falling to a lower level. Cells have developed several carrier mechanisms to ATPases because they were first discovered in intracellular transport one solute against its concentration gradient by vacuolar structures, have now been detected in plasma using the energy stored in the favorable gradient of an- membranes. In mammals, most of these mechanisms use plasma membrane of kidney cells is characterized as a V- sodium as the driver solute and use the energy of the type ATPase. By secreting protons, it plays an important sodium gradient to carry out the “uphill” transport of an- role in acidifying the tubular urine. A solute is moved against its con- expose the binding sites to the cytosol, where Na readily dissoci- centration gradient by coupling it to Na moving down a favor- ates because of the low intracellular Na concentration. Binding of extracellular Na to the carrier protein lease of Na decreases the affinity of the carrier for solute and may increase the affinity of binding sites for solute, so that solute forces the release of the solute inside the cell, where solute con- also can bind to the carrier, even though its extracellular concen- centration is already high. CHAPTER 2 The Plasma Membrane, Membrane Transport, and the Resting Membrane Potential 29 dient is maintained by the action of the sodium-potassium in the human intestine has been cloned and sequenced. It is pump, the function of these transport systems also de- called sodium-dependent glucose transporter (SGLT).
Under no circumstances should the patient be left with unanswered questions or concerns as these only drive attempts to get explanations from an attorney proven depakote 250mg medications given during dialysis. Complications of induction of labor discount 500mg depakote medications herpes, although not very common, do occur and have associated risks to mother and, more commonly, baby. Informed consent should be obtained according to ACOG Practice Bulletin regarding induction of labor (7). Elements of the consent include the indication for the induction, the agents and methods of labor stimulation, the risks attendant to the use of these agents, meth- ods and alternatives (typically expectant management or Cesarean section [C-section]), and the associated risk for mother and baby. It is noteworthy that the bulletin states, “A physician capable of perform- ing a Cesarean delivery should be readily available. It is rec- ommended that all patients undergoing labor induction have electronic fetal heart rhythm and uterine contraction monitoring although its utility is problematic except in the high-risk pregnancy. Electronic fetal heart rate (FHR) monitoring is a classic example of a procedure becoming codified as the standard of care without proof of effectiveness. In fact, the prevalence of cerebral palsy has not been altered by this modality (8). The physician must be certain that he or she and the nurses are using the same terminology in describing the FHR tracing. For example, quantification of variability is subjective, and there is no such terminology as late variables—indeed variable decelerations are so named in part because the timing of the decelera- tion to the uterine contraction varies in its onset, including occurring late. Just as important, the physician should review the nurses’ notes with special attention to the terminology used, contact times, informa- tion given to the physician, and the physician’s responses. Particular emphasis should be placed on the review of the initial, admission FHR tracing to ascertain whether or not the tracing should be characterized as reassuring. The previously damaged fetus, now Chapter 11 / Obstetrics and Gynecology 145 with recovered acid–base status, may demonstrate a reassuring trac- ing. A nonreassuring tracing, particularly with little or no baseline variability, does highly correlate with a neurologically injured fetus. The umbilical cord gases correlate well with neurological injury in the newborn, but they must be assessed immediately after birth. Follow- ing neonatal resuscitation, respiratory gas values typically show a more severe metabolic acidosis than is evident at the time of birth. Accordingly, umbilical cord gases should be obtained in all depressed or resuscitation-requiring newborns. Hypoxic-ischemic encephalopathy (HIE) injury pattern in the new- born must be placed in perspective with all the known pertinent clini- cal information. After dealing with the emergent situation, all actions taken or not taken should be clearly documented in the medical record along with explanations provided to the parents. Communication with the baby’s physician is very important not only to clarify the timing of the baby’s neurological injury but also to facilitate the obstetrician’s trans- lation of the baby’s status to the mother and family. The associations with maternal factors are weak except for an expulsive resolution to the second stage of labor and fetal macrosomia often seen in cases of maternal diabetes. Even making the diagnosis of macrosomia is difficult, and late pregnancy sonography is no better than clinical guesstimate. Elective induction of labor or elective C-section delivery for women suspected of carrying a macrosomic fetus is generally not recommended. On the other hand, the case has been made for elective C-section when the estimated fetal weight exceeds 4500 g in women with diabetes. It is essential to review the nurses’ notes to ascertain their concor- dance with your own notes on clinical events. For example, it is not uncommon for the nurse’s notes to reflect the use of fundal pressure rather than suprapubic pressure. Although there are no data to support the use of one maneuver over another, the McRobert’s patient posi- tioning is simple and resolves about 50% of the cases of anterior shoul- der impaction. Fundal pressure prior to the diagnosis of shoulder dystocia is not a standard-of-care issue. Cervical plexus injury has been reported without documented shoulder dystocia at the time of vaginal birth (9) as well as at the time of planned C-section (10). There is no scientific basis that all or even most brachial plexus injuries result from inappropriate maneuvers at deliv- ery (11).