By L. Leon. Boise State University. 2018.
What kind of sound lobule buy avanafil 50mg with amex, pulmonary ligament buy avanafil 50 mg with visa, and bronchial and pneumotaxic areas related to the would be produced by a collapsed lung, or segment. Why do premature infants often require thoracic cavity with respect to the heart. Critical-Thinking Questions respiratory assistance (a mechanical Identify the various thoracic serous 1. Identify two places in the respiratory ventilator) to keep their lungs inflated? List the kinds of epithelial tissues found capillary networks are found. What is the mucus to build up and paralyzes the cilia within the respiratory system and describe function of each of these areas and why that line the respiratory tract. What protective devices of the respiratory the treatment of certain clinical system guard against pollutants, the conditions? Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Digestive System 18 Introduction to the Digestive System 635 Serous Membranes and Tunics of the Gastrointestinal Tract 636 Mouth, Pharynx, and Associated Structures 640 Esophagus and Stomach 648 Small Intestine 652 Large Intestine 656 Liver, Gallbladder, and Pancreas 660 Developmental Exposition: The Digestive System 665 CLINICAL CONSIDERATIONS 669 Clinical Case Study Answer 671 Important Clinical Terminology 672 Chapter Summary 673 Review Activities 674 Clinical Case Study A 25-year-old male construction worker was admitted to the emergency room after suffering a blow to the upper abdomen from a swinging beam. Initial assessment was significant for marked tenderness in the right upper quadrant of the abdomen and for vital signs and examination findings consistent with mild hemorrhagic shock. Intravenous fluids were administered, causing stabilization of vital signs. Peritoneal lavage (see chapter 2, Clinical Case Study) was likewise negative for blood. A CT scan demonstrated a significant hematoma (collection of blood) deep within the substance of the liver (see arrow on CT scan), as well as a notable amount of blood in the small intestine. Initial exploration revealed no trauma to the stomach or small intestine. Explain anatomically how the blood found its way into the small intestine, noting each step of its path. Given that the hepatic arterial system and hepatic venous system are possible sources of the bleeding, is there another system of blood vessels relative to the liver that could also be a source of hemorrhage? FIGURE: Positioned in the upper right quadrant of the abdominal cavity, the liver is Hint: As you study the digestive system, pay close attention to the location of each accessory the largest visceral organ. Its size and density digestive organ and note how each connects to the lumen of the gastrointestinal (GI) tract. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 18 Digestive System 635 INTRODUCTION TO THE DIGESTIVE SYSTEM The organs of the digestive system are specialized for the diges- tion and absorption of food. The digestive system consists of a tubular gastrointestinal tract and accessory digestive organs. Objective 1 Describe the activities of the digestive system and distinguish between digestion and absorption. Objective 2 Identify the major structures and regions of the digestive system. It provides the essential nutri- ents the body cannot produce for itself. The food is utilized at the cellular level, where nutrients are required for chemical reac- tions involving synthesis of enzymes, cellular division and growth, repair, and the production of heat energy. Most of the food we eat, however, is not suitable for cellular utilization until it is mechanically and chemically reduced to forms that can be absorbed through the intestinal wall and transported to the cells by the blood. Ingested food is not technically inside the body until it is absorbed; and, in fact, a large portion of this food re- mains undigested and passes through the body as waste material. The principal function of the digestive system is to prepare food for cellular utilization. This involves the following func- tional activities: • Ingestion—the taking of food into the mouth • Mastication—chewing movements to pulverize food and mix it with saliva • Deglutition—the swallowing of food to move it from the mouth to the pharynx and into the esophagus • Digestion—the mechanical and chemical breakdown of food material to prepare it for absorption • Absorption—the passage of molecules of food through the mucous membrane of the small intestine and into the FIGURE 18. It traverses the thoracic cavity and Anatomically and functionally, the digestive system can be enters the abdominal cavity at the level of the diaphragm. The GI tract, which ynx, esophagus, stomach, small intestine, and large intestine (fig. The accessory digestive organs include the teeth, tongue, salivary glands, liver, gallbladder, and pancreas. The term viscera is frequently used to refer to the abdominal organs ingestion: L. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 636 Unit 6 Maintenance of the Body TABLE 18. Specialized serous mem- with saliva (mastication); initiates digestion of branes support the GI tract and provide a structure through which carbohydrates; forms and swallows soft mass of nerves and vessels pass. The wall of the GI tract is composed of chewed food called bolus (deglutition) four tunics. Pharynx Receives bolus from oral cavity; autonomically continues deglutition of bolus to esophagus Objective 4 Describe the arrangement of the serous Esophagus Transports bolus to stomach by peristalsis; lower membranes within the abdominal cavity. These organs are supported and covered by down chyme; absorbs nutrients; transports wastes serous membranes that line the cavities of the trunk and cover through peristalsis to large intestine; prohibits the organs within these cavities. Serous membranes are com- backflow of intestinal wastes from large intestine posed of simple squamous epithelium, portions of which are rein- Large intestine Receives undigested wastes from small intestine; absorbs forced with connective tissue. Serous membranes secrete a water and electrolytes; forms, stores, and expels feces when activated by a defecation reflex lubricating serous fluid that continuously moistens the associ- ated organs. The parietal portion of the serous membrane lines the body wall, and a visceral portion covers the internal organs. As de- scribed in the previous chapter, the serous membranes associated with the lungs are called pleurae (see fig. The serous It usually takes about 24 to 48 hours for food to travel the membranes of the abdominal cavity are called peritoneal mem- length of the GI tract.
Some lawyers are fond of employing discount 100 mg avanafil otc, for big cases discount avanafil 200mg with amex, jury consultants, professional “jury experts” who read body language and pay particular attention to the responses jurors make to the voir dire questions. Other lawyers trust their own instincts when it comes to accepting or challeng- ing certain jurors; and some even feel that it doesn’t matter in the end which jurors are selected; they take any panel that meets with the judge’s approval. If your case looks like it is going to trial and you feel you have a good sense of people, your lawyer should be willing to listen to you in the jury selection process. Witnesses, Especially “Experts” All witnesses are important, especially you. A prepared witness is not a “coached” witness; a “prepared” witness is one who understands the purpose for which his or her testimony is sought, and has some understanding of the questions likely to be asked. This requires a witness to think about the best and most honest way to respond to these questions. As for adversarial witnesses, pretrial discovery will reveal who they are and what they are likely to say and not say. Knowing this information will enable you and your attorney to fashion questions that show whether a witness is credible or, if credible, why mistaken about some key fact. Who qualifies as an “expert” is defined by the law of the jurisdiction where the case is litigated. California, for example, which is typical of many jurisdictions, defines an expert as one who has “spe- cial knowledge, skill, experience, training or education” about the subject to which the testimony will relate. Federal law, for instance, makes judges the “gate-keepers” for ensuring that scientific evidence is admitted only if it is both relevant and reliable. In determining this, a court can consider whether the expert used the scientific method, whether the theory or technique relied upon has been subjected to peer review and publication, whether a particular scientific technique has a significant rate of error, and whether the methodology used is generally accepted in the relevant scientific community. Usually your attorney will want to retain a prospective expert in a given field as a “consultant” to the attorney; that way it will not be necessary to disclose your “expert’s” identity and opinion on a matter should you decide not to use him or her as an “expert. If you or your adversary decide to go ahead with certain experts at trial, however, their identities must be disclosed by a certain time in the litigation framework to give each of you an opportunity to question the expert on his or her opinion before trial. Although it used to be that the standard of care pertinent to medical negligence was a local one, the standard of care for sometime now has been a national one, which opens the door for both sides obtaining the “best” experts in the country. Moreover, because medicine is a dynamic and fast-changing profession, what was good medical practice yester- 25 Cal. Chapter 2 / Litigation 29 day may no longer be the case now; and an “expert” must be up on current medical advances and standards of care. The personal injury bar used to complain of a “conspiracy of silence,” a tacit agreement amongst or common reluctance by doctors not to testify against their colleagues in medical negligence cases. Whatever truth there may have been to this accusation, a quick glance of the copious advertisements for “forensic medical experts” in the pages of magazines published by and for the personal injury bar shows that this is no longer true. WHY IT IS CRITICALLY IMPORTANT TO “SEIZE THE TIME” WHEN SUED Time can be critical to the outcome of litigation, a fact underscored by the often used legal phrase that “time is of the essence. Usually, the period for filing an answer or other response is 30 days, a window by which, if your attor- ney acts promptly and intelligently, can give you a decided advantage over your adversary. If you waste or allow any of this time to pass in the belief (indisputably true) that you don’t have to respond until the end of that 30 days, or that your attorney can probably get an extension of time by which to respond (almost always true), you could lose valu- able opportunities to seize important advantages. The Importance of Time in the Discovery Process To illustrate the importance of time in litigation, consider the proce- dural device of discovery, the means by which parties are to find out from each other what evidence is known to that party or others in support or derogation of the lawsuit. One of these discovery mechanisms is the right to compel a party to appear and answer relevant questions under oath from your lawyer. The answers given to these questions often reveal facts that will determine whether the plaintiff has a viable claim against you or whether you have a defense against liability. Absent a showing to the court of “good cause,” a plain- tiff must normally wait 20 days after serving summons before noticing the defendant’s deposition; however, the defendant need not wait any period of time after being served to notice the plaintiff’s deposition. Hence, it is possible for a defendant to get the jump on the plaintiff and smoke out his or her case early regarding the extent of damage suffered and why the plaintiff believes the defendant is responsible for it. The longer you wait to take the plaintiff’s deposition, the greater the likelihood that “facts” will be revealed or become “known” to the plain- tiff that strengthen his or her case. For this reason, some defense lawyers prefer to wait to take the plaintiff’s deposition until later in the lawsuit, especially because you usually only get one opportunity to take the plaintiff’s deposition, unless there are unusual circumstances involved. However, if you have reason to believe the plaintiff has not put together a case by the time you are served, then it may be possible to get rid of the case early by showing that it is missing one or more elements critical to the liability equation. Time and Summary Judgment or Summary Adjudication Another procedural mechanism that can be combined with the prompt taking of the plaintiff’s deposition is a motion for summary judgment or partial summary adjudication. This motion is a way for the court to look behind the pleadings and determine if the opposing party’s pleadings lack evidentiary support that warrants limiting or terminating the lawsuit. A defendant who does not pay close attention to the passage of time could, through inadvertence, lose the right to invoke summary judgment and end up having to go to trial (perhaps unnecessarily). Chapter 2 / Litigation 31 Therefore, when served with summons, you should immediately notify your medical liability insurer and get a copy of the summons and complaint to the appropriate representative. While doing this, you should also request your insurer to inform you right away of the lawyer who will be defending you. Once you know the identity of your counsel, contact him or her and ask to meet and confer about your case, preferably in person; however, if that cannot be done right away, then make contact by telephone. WHY YOU SHOULD MEET WITH YOUR LAWYER RIGHT AWAY AND WHAT YOU SHOULD SEEK TO ACCOMPLISH The Importance of a Litigation Strategy and Discovery Plan To ensure that the meeting with your lawyer is as productive as possible, you should first read the complaint and try to discern from it what you are accused of having done or not done that supposedly makes you liable. If the complaint is what is known as a form com- plaint, this generally will be more difficult than if it is written by the plaintiff’s counsel and sets forth some specific facts. However, in read- ing the complaint, you will at least be able to learn the identity of the plaintiff and when the event that allegedly resulted in injury occurred, even if it is a general form.
In this case discount 50mg avanafil, the local stimulus is the inward cause the internal axoplasmic resistance purchase 100 mg avanafil otc, Ra, decreases, al- sodium current that accompanies the action potential. The lowing the current to spread farther down the inside of the larger the space constant, the farther along the membrane axon before leaking back across the membrane. Affected individuals generally have no neurons and muscle cells and in synaptic transmission. The defect in membrane repolar- nel properties derived from biophysical studies of isolated ization could be a result of a prolonged inward sodium cells or their membranes. The advent of molecular ap- current or a reduced outward potassium current. In fact, proaches resulted in the cloning of the genes for a variety mutations in potassium channels account for two differ- of channels and the subsequent expression of these genes ent LQT syndromes, and a third derives from a sodium in a large cell, such as the Xenopus oocyte, for further char- channel mutation. Myotonia is a condition characterized by a delayed re- This approach also allowed experimental manipulation laxation of muscle following contraction. There are several of the channels by expressing genes that were altered in types of myotonias, all related to abnormalities in muscle known ways. Some myotonias are associated with a skele- which parts of channel molecules were responsible for tal muscle sodium channel, and others are associated with particular properties, including voltage sensitivity, ion a skeletal muscle chloride channel. This genetic understand- and spinocerebellar ataxias, some forms of epilepsy, and ing of the control of channel properties led to the realiza- familial hemiplegic migraine. Ataxias are a disruption in tion that many unexplained diseases may be caused by al- gait mediated by abnormalities in the cerebellum and terations in the genes for ion channels. One specific ataxia associated with altered ion channel function are now collectively called an abnormal potassium channel is episodic ataxia with channelopathies. In this disease, which is autosomal-dominant, muscle, cardiac muscle, and even nonexcitable cells, such cerebellar neurons have abnormal excitability and motor as kidney tubular cells. This hyperex- One of the best-known sets of channelopathies is a citability causes indiscriminant firing of motor neurons, group of channel mutations that lead to the Long Q-T observed as the twitching of small groups of muscle fibers, (LQT) syndrome in the heart. The QT interval on the elec- akin to worms crawling under the skin (myokymia). It is trocardiogram is the time between the beginning of ven- likely that many other neuronal (and muscle) disorders of tricular depolarization and the end of ventricular repolar- currently unknown pathology will be identified as chan- ization. This in- axon, more of the adjacent region that is depolarized by crease in Rm increases the space constant. The layers of the inward current accompanying the action potential myelin also decrease the effective capacitance of the axonal reaches the threshold for action potential generation. The membrane because the distance between the extracellular result is that the speed at which action potentials are con- and intracellular conducting fluid compartments is in- ducted, or conduction velocity, increases as a function of creased. Because the capacitance is decreased, the time increasing axon diameter and concomitant increase in the constant is decreased, increasing the conduction velocity. While the effect of myelin on Rm and capacitance are Several factors act to increase significantly the conduc- important for increasing conduction velocity, there is an tion velocity of action potentials in myelinated axons. In myelinated axons, voltage-gated Na CNS wrap themselves around axons to form myelin, layers channels are highly concentrated in the nodes of Ranvier, of lipid membrane that insulate the axon and prevent the where the myelin sheath is absent, and are in low density passage of ions through the axonal membrane (Fig. When an action potential Between the myelinated segments of the axon are the nodes is initiated at the axon hillock, the influx of Na ions of Ranvier, where action potentials are generated. This, in turn, causes axons apparently derives from the axon, and its potency is depolarization of the next node of Ranvier and the even- a function of axon size. In general, axons larger than ap- tual initiation of an action potential. Action potentials are proximately 1 m in diameter are myelinated, and the successively generated at neighboring nodes of Ranvier; thickness of the myelin increases as a function of axon di- therefore, the action potential in a myelinated axon ap- ameter. Since the smallest myelinated axon is bigger than pears to jump from one node to the next, a process called the largest unmyelinated axon, conduction velocity is faster saltatory conduction (Fig. In addition, the faster conduction velocity for myelinated than unmyeli- myelin acts to increase the effective resistance of the axonal nated axons. The conduction velocity in mammals ranges membrane, Rm, since ions that flow across the axonal mem- from 3 to 120 m/sec for myelinated axons and 0. CHAPTER 3 The Action Potential, Synaptic Transmission, and Maintenance of Nerve Function 45 Peak of action ated no matter how much the membrane is depolarized. The absolute re- 1 Inward current fractory period also prevents action potentials from travel- ing in the wrong direction along the axon. Since these channels have returned to their initial resting state, they Axon can now respond to depolarizations of the membrane. Con- Depolarized region sequently, when the membrane is depolarized, many of the channels open their activation gates and permit the influx of Direction of propagation Na ions. However, because only a portion of the Na chan- nels have returned to the resting state, depolarization of the A membrane to the original threshold level activates an insuffi- cient number of channels to initiate an action potential. With greater levels of depolarization, more channels are activated, until eventually an action potential is generated. The K channels are maintained in the open state during the relative refractory period, leading to membrane hyperpolarization. By these two mechanisms, the action potential threshold is in- Axon creased during the relative refractory period. At electrical synapses, passageways known as gap junctions connect the cytoplasm of adjacent neurons (see Fig. Elec- Glial cell potential node Axon trical synapses are uncommon in the adult mammalian here here nervous system. Typically, they are found at dendroden- dritic sites of contact; they are thought to synchronize the activity of neuronal populations.
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