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By N. Lisk. Westwood College Texas. 2018.

G Tonsils function to protect against pathogens and foreign substances that are inhaled or ingested 2mg ginette-35 women's health center lattimore road. True H The spleen functions in the removal of aged and defective blood cells and platelets from the blood purchase ginette-35 2mg with amex pregnancy 35 weeks. This statement doesn’t make much sense because “gastric” refers to the digestive system 2mg ginette-35 with visa menstruation 46 day cycle. J The thoracic duct originates from a triangular sac called the chyle cistern (or cisterna chyli). M Peyer’s patches are masses of lymphatic nodules found in the distal portion of the small intes- tines. You may be tempted to write “thoracic duct” here, but that’s incorrect because the duct is the largest vessel, not the largest organ. P In the center of the nodules of the lymph node are areas called germinal centers. When you read “germinal,” think of the word “germinate,” and then think of a place where lymphocytes can sprout and mature. Chapter 12 Filtering Out the Junk: The Urinary System In This Chapter Putting the kidneys on clean-up duty Tracking urinary waste out of the body f you read Chapter 9 on the digestive system, you may be chewing on the idea that undi- Igested food is the body’s primary waste product. We make more of it than we do feces — in fact, our bodies are making small amounts of urine all the time — and we release it more often throughout the day. Most important, urine captures all the leftovers from our cells’ metabolic activities and jettisons them before they can build up and become toxic. In addition, urine helps maintain homeostasis, or the proper balance of body fluids. In short, the urinary system Excretes useless and harmful material that it filters from blood plasma, including urea, uric acid, creatinine, and various salts Removes excess materials, particularly anything normally present in the blood that builds up to excessive levels Maintains proper osmotic pressure, or fluid balance, by eliminating excess water when concentration rises too high at the tissue level In this chapter, we look at how the urinary system collects, manages, and excretes the waste that the body’s cells produce as they go about busily metabolizing all day. You practice iden- tifying parts of the kidneys, ureter, urinary bladder, and urethra. Examining the Kidneys, the Body’s Filters The kidneys are nonstop filters that sift through 1. Humans have a pair of kidneys just above the waist (lumbar region) toward the back of the abdominal cavity. While sometimes the same size, the left kidney tends to be a bit larger than the right. The last two pairs of ribs surround and protect each kidney, and a layer of fat, called perirenal fat, pro- vides additional cushioning. Kidneys are retroperitoneal, which means that they’re posterior to the peritoneum. The renal capsule, or outer lining of the kidney, is a layer of collagen fibers; these fibers extend outward to anchor the organ to surrounding structures. Each kidney is dark red, about 4 ⁄12 inches long, and shaped like a bean (hence the type of legumes called kidney beans). The portion of the bean that folds in on itself, referred to as the medial border, is concave with a deep depression in it called the hilus, or hilum. The hilus opens into a fat-filled space called the renal sinus, which in turn contains the renal pelvis, renal calices, blood vessels, nerves, and fat. Immediately below the renal capsule is a granular layer called the renal cortex, and just below that is an inner layer called the medulla that folds into anywhere from 8 to 18 conical projections called the renal pyramids. Between the pyramids are renal columns that extend from the cortex inward to the renal sinus. The tips of these pyramids, the renal papillae, empty their contents into a collecting area called the minor calyx. It’s one of several sac-like structures referred to as the minor and major calyces which form the start of the urinary tract’s “plumbing” system and collect urine transmitted through the papillae from the cortex and medulla. Although the number varies between individuals, generally each of two or three major calyces branches into four or five minor calyces, with a single minor calyx surrounding the papilla of one pyra- mid. Urine passes through the minor calyx into its major calyx and then on into the ureter for the trip to the bladder. Going molecular At the microscopic level, each kidney contains hundreds of thousands of tiny tubes known as uriniferous tubules, or nephrons. At one end, each nephron is closed off and folded into a small double- cupped structure called a Bowman’s capsule, or the glomerular capsule, where the actual process of filtration occurs. This tube straightens to form a structure called the descending loop of Henle and then bends back in a hairpin turn into another structure called the ascending loop of Henle. This tubule connects to a collecting tubule that it shares with the output ends of many other nephrons. The collecting tubules open into the minor calyces of the renal pelvis, which in turn open into the major calyces. Because of their role as the body’s key filters, the kidneys receive about 20 percent of all the blood pumped by the heart each minute. A large branch of the abdominal aorta, called the renal artery, carries that blood to them. After branching into smaller and smaller vessels, the blood eventually enters afferent arterioles, each of which branches into tufts of five to eight capillaries called a glomerulus (the plural is glomeruli) inside the Bowman’s capsule. After picking up waste products from the filters inside the wall of the capsule, the capillaries come back together to form efferent arterioles, which then branch to form the peritubular, or second, capillary bed surrounding the convoluted tubules, the loop of Henle, and the collecting tubule. The capillaries come together once again to form a small vein that empties blood into the renal vein to depart the kidneys. Each glomerulus and its surrounding Bowman’s capsule make up a single renal corpus- cle where basic filtration takes place. Like all capillaries, glomeruli have thin, membra- nous walls, but unlike their capillary cousins elsewhere, these vessels have unusually large pores called fenestrations or fenestrae (from the Latin word fenestra for “window”). Focusing on filtering To understand how the renal corpuscles work, think of an espresso machine: Water is forced under pressure through a sieve containing ground coffee beans, and a filtrate called brewed coffee trickles out the other end. Hydrostatic pressure forces fluids across the glomerular membranes, which capture about 125 milliliters of material per minute in the Bowman’s capsules. So despite 125 milliliters of material coming out of the blood every minute, only 1 milliliter of urine is generated each minute. This is a matter of simple subtraction: Reabsorption of about 100 milliliters per minute takes place in the proximal convoluted tubules. The distal convoluted tubules return 12 milliliters, and the collecting tubules return about 5 milliliters. That totals 124 milliliters of reabsorption per minute and explains the 1 milliliter of urine that comes out when all is said and done. While all this filtering and absorption is going on, the kidneys also sometimes secrete an enzyme called renin (also known by its more complicated chemical name of angiotensinogenase) that converts a peptide generated in the liver, called angiotensino- gen, into angiotensin I.

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Help comes from an enzyme or protein carrier that transports drug parti- cles upstream across the membrane and into the plasma cheap 2 mg ginette-35 fast delivery women's health blood in the urine. Pinocytosis Pinocytosis is the process of engulfing the drug particle and pulling it across the membrane order 2mg ginette-35 with mastercard menstruation japan. This is similar to how you eat an ice pop by engulfing a piece of it in with your mouth and swallowing it discount 2mg ginette-35 with mastercard menstrual question. How long the drug will be effective and how much drug is needed depends on the route of administration, the dose of the drug, and the dosage form (tablet, capsule, or liquid). The absorption rate of a drug is influenced by a number of factors that might increase or decrease the rate, This is similar to how more gasoline is used to drive at faster speeds. Absorption is affected by many factors that include pain, stress, hunger, fasting, food, and pH. Hot, solid, fatty foods can slow absorption such as eating a Big Mac before taking medication. During exercise, circulation to the stomach is diverted to other areas of the body and drug absorption is decreased. Circulation Blood flow to the site of administration of the drug will help increase the rate of absorption. An area that has a lot of blood vessels and good circulation will help absorb the drug quickly and circulate it to the intended site. When a patient is in shock and has a low blood pressure due to decreased circulation (blood flow) drugs may not be absorbed very quickly. Route of Administration The rate at which drug particles are absorbed is determined by the amount of blood vessels there are in the area where the drug is administered. For example, a drug is absorbed faster in the deltoid (arm) muscle than in the gluteal (butt) muscle because there are more blood vessels in the del- toid muscle. This additional step causes water- soluble drugs to be absorbed more slowly than fat-soluble drugs. If a high concentration of the drug is given, it will tend to be absorbed more rapidly. Sometimes larger (loading or priming) doses of a drug may be given that will be more than the body can excrete. After the first large dose, small maintenance doses will help keep the therapeutic effect. Drugs can be processed when they are manufactured to add other ingredients that will help or hinder absorption. For example, hydrochloric acid in the stomach destroys some drug particles before it can pass through the membrane and into the bloodstream. The percentage of a dose that reaches the blood stream is called the bio- availability of a drug. Typically, between 20% and 40% of drugs that are admin- istered orally reach the blood stream. This is called the first pass effect and is the beginning of the metabolism of a drug that is given orally. Sometimes very lit- tle of the drug remains available for a therapeutic effect after the first pass. Only drugs administered intravenously have a 100% bioavailability because they are directly injected into the vein. Pharmaceutical manufacturers must consider bioavailability when determin- ing the dose for a drug. The percent of active ingredient in a dose is referred to as the drug concentration. These are primary loading— a large concentration that is used to achieve a fast therapeutic effect such as the first dose of an antibiotic, and maintenance dose—a typical concentration of the drug that is used to provide an ongoing therapeutic effect such as subsequent doses of an antibiotic. These are referred to as “free” drugs because they are not bound to any receptor sites. These drug–protein complexes decrease the concentration of free drug in the circulation. The drug molecule is released from the protein and it becomes free drug and can be absorbed for use. Drugs affect areas of the body with good blood supply first, such as the heart, liver, kidney, and brain and then flow to areas with less blood supply, such as muscles and fat. Drugs accumulate in an area of the body and form a reservoir by binding to tissues. These are protein binding—when a drug binds to plasma proteins, and tissue binding—fat soluble drugs are stored in adipose (fat) tissue. Inderal (propranolol) is a heart medication that is highly bound to and only about 7% of free drug is available for use at a time. In addition, some drugs, such as the antibiotic Tetracycline like to be stored in bones which can interfere with growth of fetal skeletal tissues and can discolor teeth if given to children under eight years of age. Level of Plasma Protein A low level of plasma protein and albumin might not provide enough binding sites for drug particles. This happens when there is liver or kidney disease or if the patient is mal- nourished resulting in low albumin levels (hypoalbuminemia). Healthcare professionals should monitor a patient’s plasma protein and albumin levels and the protein-binding percentage of all drugs before administering drugs to the patient. Bloodflow There must be adequate bloodflow to target areas of the body; otherwise, insuf- ficient drug particles will reach affected parts of the body. Drugs that accumulate in fat are called lipid soluble and remain for about three hours because there is low blood flow in fat tissue. Competing Drugs Two drugs administered simultaneously might compete for the same binding sites making some drug particles unable to find a binding site. Two drugs that are highly protein bound—such as Coumadin (warfarin) and Inderal (propra- nolol)—will compete for the protein sites. This can cause serious problems and can result in toxic levels of one or both of the drugs when increased amounts of free drug become available. Abscesses, exudates, body glands, and tumors hinder the distribution of drugs in the body. The placenta metabolizes some drugs making then inactive and thereby protecting the fetus from drugs given to the mother. However, steroids, nar- cotics, anesthetics, and some antibiotics can penetrate the placental barrier and cause adverse effects to the fetus. This metabolism—called biotransformation—occurs in the liver where enzymes inactivate a drug by changing it into more water-soluble compounds that can be excreted from the body. Elimination occurs mainly through the kidneys, although some drugs are also eliminated in bile, feces, lungs, sweat, and breast milk. Patients suffering from liver diseases are prone to drug toxicity because the diseased liver no longer metabolizes the drug sufficiently to allow elimination through the kidneys. The result is a buildup of the drug, which can eventually lead to a toxic effect on the body. The amount of time for half of the drug concentration to be eliminated from the body is called the drug’s half-life and is a crucial measurement used to deter- mine how often to administer a drug.

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Consider the ways in which you made sense of your illness and how they related to your coping strategies generic ginette-35 2 mg without prescription pregnancy kit test. The literature describing the structure of ill- ness cognitions assumes that individuals deal with their illness by processing the different forms of information order ginette-35 2 mg mastercard pregnancy on birth control. In addition discount 2mg ginette-35 overnight delivery women's health bendigo, it assumes that the resulting cognitions are clearly defined and consistent across different people. However, perhaps the information is not always processed rationally and perhaps some cognitions are made up of only some of the components (e. The literature also assumes that the structure of cognitions exists prior to questions about these cognitions. Therefore, it is assumed that the data collected are separate from the methodology used (i. However, it is possible that the structure of these cognitions is in part an artefact of the types of questions asked. In fact, Leventhal originally argued that interviews should be used to access illness cognitions as this methodology avoided ‘contaminating’ the data. This paper examines how children make sense of illnesses and discusses the possible developmental transition from a dichotomous model (ill versus healthy) to one based on a continuum. A review of conceptual and methodological issues, Psychology and Health, 12: 417–31. This paper explores the complex and ever-growing area of coping and focuses on the issues surrounding the questions ‘What is coping? This paper outlines the concept of illness cognitions and discusses the implica- tions of how people make sense of their illness for their physical and psycho- logical well-being. This is an edited collection of projects using the self-regulatory model as their theoretical framework. It describes and analyses the cognitive adaptation theory of coping with illness and emphasizes the central role of illusions in making sense of the imbalance created by the absence of health. This educational perspective explains communication in terms of the transfer of knowledge from medical expert to layperson. Such models of the transfer of expert knowledge assume that the health professionals behave according to their education and training, not their subjective beliefs. Next, the chapter focuses on the problem of variability and suggests that variability in health professionals’ behaviour is not only related to levels of knowledge but also to the processes involved in clinical decision making and the health beliefs of the health professional. This suggests that many of the health beliefs described in Chapter 2 are also relevant to health professionals. Finally, the chapter examines doctor– patient communication as an interaction and the role of agreement and shared models. Compliance has excited an enormous amount of clinical and academic interest over the past few decades and it has been calculated that 3200 articles on compliance in English were listed between 1979 and 1985 (Trostle 1988). Compliance is regarded as important primarily because following the recommendations of health professionals is considered essential to patient recovery. However, studies estimate that about half of the patients with chronic illnesses, such as diabetes and hypertension, are non-compliant with their medication regimens and that even com- pliance for a behaviour as apparently simple as using an inhaler for asthma is poor (e. Further, compliance also has financial implications as money is wasted when drugs are prescribed, prescriptions are cashed, but the drugs not taken. This claimed that compliance can be predicted by a combination of patient satisfaction with the process of the consultation, understanding of the information given and recall of this information. Several studies have been done to examine each element of the cognitive hypothesis model. Patient satisfaction Ley (1988) examined the extent of patient satisfaction with the consultation. He reviewed 21 studies of hospital patients and found that 41 per cent of patients were dissatisfied with their treatment and that 28 per cent of general practice patients were dissatisfied. Ley (1989) also reported that satisfaction is determined by the content of the consultation and that patients want to know as much information as possible, even if this is bad news. For example, in studies looking at cancer diagnosis, patients showed improved satisfaction if they were given a diagnosis of cancer rather than if they were protected from this information. Participants were asked to read some information about medica- tion and then to rate their satisfaction. Some were given personalized information such as, ‘If you take this medicine, there is a substantial chance of you getting one or more of its side effects’ whereas some were given non personalized information, ‘A substantial proportion of people who take this medication get one or more of its side effects’. The results showed that a more personalized style was related to greater satisfaction, lower ratings of the risks of side effects and lower ratings of the risk to health. The authors coded recorded consultations for their humour content and for the type of humour used. They then looked for differences between high and low satisfaction rated consultations. The results showed that high satisfaction was related to the use of more light humour, more humour that relieved tension, more self-effacing humour and more positive-function humour. Patient satisfaction is increasingly used in health care assessment as an indirect measure of health outcome based on the assump- tion that a satisfied patient will be a more healthy patient. This has resulted in the development of a multitude of patient satisfaction measures and a lack of agreement as to what patient satisfaction actually is (see Fitzpatrick 1993). However, even though there are problems with patient satisfaction, some studies suggest that aspects of patient satisfaction may correlate with compliance with the advice given during the consultation. Patient understanding Several studies have also examined the extent to which patients understand the content of the consultation. Boyle (1970) examined patients’ definitions of different illnesses and reported that when given a checklist only 85 per cent correctly defined arthritis, 77 per cent correctly defined jaundice, 52 per cent correctly defined palpitations and 80 per cent correctly defined bronchitis. Boyle further examined patients’ perceptions of the location of organs and found that only 42 per cent correctly located the heart, 20 per cent located the stomach and 49 per cent located the liver. This suggests that understanding of the content of the consultation may well be low. Further studies have examined the understanding of illness in terms of causality and seriousness. Roth (1979) asked patients what they thought peptic ulcers were caused by and found a variety of responses, such as problems with teeth and gums, food, digestive problems or excessive stomach acid. Roth also reported that 30 per cent of patients believed that hypertension could be cured by treatment. If the doctor gives advice to the patient or suggests that they follow a particular treatment programme and the patient does not understand the causes of their illness, the correct location of the relevant organ or the processes involved in the treatment, then this lack of understanding is likely to affect their compliance with this advice. This study examined the effect of an expert, directive consulting style and a sharing patient-centred consulting style on patient satisfaction. This means that it is possible to compare the effects of the two types of consulting style without the problem of identifying individual differences (these are controlled for by the design) and without the problem of an artificial experi- ment (the study took place in a natural environment). Theoretically, the study examines the prediction that the educational model of doctor–patient communication is problem- atic (i.

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Bound complement factors can: enhance the binding of microbes to phagocytozing cells; result in the activation of inflammatory cells; mediate chemotaxis; induce release of inflammatory mediators; direct bactericidal effects; and induce cell lysis (Fig 2mg ginette-35 with visa womens health nurse practitioner salary. The pro- duction of a C3 convertase order ginette-35 2mg fast delivery menstrual rash, which splits C3 into C3a and C3b discount ginette-35 2 mg on line pregnancy 32 weeks, is common to both pathways. C3b degradation products are recognized by recep- tors on B lymphocytes; they stimulate the production of antibodies as well as pathogen phagocytosis. The cleavage products C3a and C4a are chemotactic in their action, and stimulate expression of adhesion molecules. Nomenclature: the components of the alternative pathway (or cascade) are desig- nated by capital letters (B, D, H, I; P for properdin), those of the classical pathway (or cascade) plus terminal lysis are designated by “C” and an Arabic numeral (1–9). Component fragments are designated by small letters, whereby the first fragment to be split off (usually of low molecular weight) is termed “a” (e. Molecules often group to form complexes; in their designations the indi- vidual components are lined up together and are usually topped by a line. Usage subject to terms and conditions of license Immune Responses and Effector Mechanisms 87 & Solubilization of otherwise insoluble antigen-antibody complexes. Over 20 proteins of the complement system have been identified to date, and are classified as either activation or control proteins. C3 is not only present in the largest amount, but also represents a central structure for complement activation. Usage subject to terms and conditions of license 88 2 Basic Principles of Immunology Immunological Cell Death 2 Fig. During classic activation of complement, C1q must be bound by at least two antigen-antibody immune complexes, to which C4 and C2 then attach themselves. Pentameric IgM represents a particularly efficient C activator since at least two Ig Fc components in close proximity are required for C1q binding and activation. During alternative activation of complement, the splitting of C3 occurs directly via the action of products derived from microorganisms, endotoxins, polysaccharides, or aggregated IgA. C3b, which is produced in both cases, is activated by the factors B and D, then itself acts as C3 convertase. Subsequent formation of the lytic complex, C5–C9 (C5–9), is identical for both classic Kayser, Medical Microbiology © 2005 Thieme All rights reserved. Usage subject to terms and conditions of license Immune Responses and Effector Mechanisms 89 and alternative activation, but is not necessarily essential since the released chemotaxins and opsonins are often alone enough to mediate the functions of microbe neutralization and elimination. Some viruses can activate the complement system without the intervention of antibodies by virtue of their ability to directly bind C1q. Importantly, without a stringent control mechanism complement would be activated in an uncontrolled manner, resulting in the lysis of the hosts own cells (for instance erythrocytes). Complement Control Proteins The following regulatory proteins of the complement system have been character- ized to date: C1 inhibitor, prevents classic complement activation. This protein is lacking in patients suffering from paroxysmal nocturnal hemoglobinuria. This is a glycolipid anchored within the cell surface which prevents C9 from binding to the C5b-8 complex, thus protecting the cell from lysis. Those complement components with the most important biological effects include: & C3b, results in the opsonization of microorganisms and other antigens, either directly or in the form of immune complexes. C5a initi- ates the chemotactic recruitment of granulocytes and monocytes, promotes their aggregation, stimulates the oxidative processes, and promotes the re- lease of the thrombocyte activating factor. Immunological Tolerance & T-cell tolerance, as defined by a lack of immune reactivity can be due to a number of processes: Firstly, Negative selection in the thymus (referred to as deletion); secondly a simple lack of reactivity to antigen (self or nonself) as a result of the antigen having not been present in the secondary lymphoid organs in a sufficient quantity or for a sufficient amount of time; and thirdly an excessive stimulation of T-cells resulting from the ubiquitous presence of sufficient antigen resulting in T cell exhaustion. Finally, it may also be possible that Tcells can become temporarily “anergized” by partial or incom- plete antigen stimulation. As a general rule, self-reactive (autoimmune) B cells are not generally deleted by negative selection and can therefore be present in the periphery. Exceptions to this rule include B cells specific for membrane-bound self-determinants, some of which are deleted or aner- gized. B cells react promptly to antigens, even self-antigens, which are ar- ranged repetitively. However, they only react to soluble monomeric antigens if they additionally receive T cell help. Thus, B-cell non-reactivity largely results from a lack of patterned antigen presentation structures or as a result of T-cell tolerance. Tolerance is acquired, and can be measured as the selective absence of immunological reactivity against specified antigens. T-Cell Tolerance A distinction can be made between central tolerance, which develops in the thymus and is based on the negative selection (deletion) of Tcells recognizing self antigens present in the thymus, and peripheral tolerance. Peripheral tolerance results in the same outcome as central tolerance, however, this Kayser, Medical Microbiology © 2005 Thieme All rights reserved. Usage subject to terms and conditions of license Immunological Tolerance 91 formoftoleranceinvolvesantigenrecognitionbyantigen-reactiveperipheralT cells, followed by a process of clonal cell proliferation, end differentiation and death. The following mechanisms have been postulated, and in some cases confirmed, to account for a lack of peripheral T-cell responsiveness (Table 2. Most self-antigens, not present in the serum or in lymphohema- topoietic cells, belong to this category and are ignored despite the fact that they are potentially immunogenic. Certain viruses, and their antigens, actu- ally take advantage of this system of ignorance. For instance, the immune system ignores the rabies virus when it is restricted to axons, and papilloma viruses as long as the antigens are restricted to keratinocytes (warts). The main reason why many self antigens, and some foreign antigens, are ignored by T cells is that immune responses can only be induced within the spleen or in lymph nodes, and non-activated (or naive) T cells do not migrate into the periphery. It has also been postulated that those naive T and B cells which do encounter antigens in the periphery will become anergized, or inactivated, due to a lack of the so-called costimulatory or secondary signals at these sites. Experiments seeking to understand the “indifference” of T cells are summarized in the box on p. In all probability, a great many self-antigens (as well as periph- eral tumors) are ignored by the immune system in this way. During such a scenario the responding T cells differentiate into short- lived effector cells which only survive for two to four days. This induction phase may actually correspond to the postulated phenomenon of anergy (see Table 2. Should this be the case, anergy—defined as the inability of T cells to react to antigen stimulation in vitro—may in fact be explained by the responding cells having already entered a pathway of cell death (apoptosis) (see Fig. Once all the terminally differentiated effector T cells have died, immune reactivity against the stimulating antigen ends. Tolerance is hereafter maintained, as should the responsible antigen have entered into the thymus those newly maturing thymocytes will be subjected to the process of negative selection (e. Moreover, those newly matured T cells which may have escaped negative selection and emigrated into the per- Kayser, Medical Microbiology © 2005 Thieme All rights reserved.

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