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The immune cell quickly recognizes that anything not in a red coat is an invader medications 2 times a day discount exelon express, and sounds the alarm to keratin treatment cheap 1.5 mg exelon with amex notify the rest of the immune system that an invader has made its way into the body symptoms xanax treats order exelon 6mg overnight delivery. Beyond distinguishing self from invader, surface proteins specifically identify cells and microbes. For example, Figure 3 shows a cartoon of the surface proteins of a measles virus and a hepatitis C virus. The circles and triangles on the outside of the viruses represent their surface proteins. The surface proteins of the measles virus and the hepatitis C virus are different. The combination of the measles surface proteins tells the immune system, "I am a measles virus. A surface protein that is recognized by the immune system and leads to antibody production is called an antigen or immunogen. Detection of foreign antigens is the primary way the immune system is alerted to the presence of invading microbes. Antibodies are substances produced by the immune system that interact with microbes to kill them. Antibodies are most effective against bacteria and viruses that live outside of cells (extracellular microbes). The immune cells that produce antibodies are special lymphocytes called activated B cells or plasma cells. Macrophage Digesting Microbe and Displaying Antigen digested microbe antigen displayed cell surface microbe macrophage 2. B Cell Digesting Microbe and Displaying Antigen digested microbe antigen displayed cell surface microbe B cell 3. When an immune cell called a T helper cell sees the same protein on the surface of a B cell and a macrophage, it sandwiches itself between the two other immune cells (see Figure 6). The formation of this bridge complex stimulates the B cell to begin dividing, making more copies of itself. Chapter 7: the Immune System And the Hepatitis C Virus - Section 1: Meet the Immune System Figure 6. T Helper Cell Activates B Cell Causing B Cell Expansion and Antibody Production macrophage T helper cell B cell activated B cells (plasma cells) antibodies against the presented antigen the antibodies produced against an invader attach to antigens on its surface. The presence of antibodies on the surface of the invader serves as a "red flag" to the rest of the immune system and marks the invader for destruction. The antibodies may cause leaks in the outer coat of the microbe; the leaky invader cannot recover and dies. More commonly, antibodies on the surface of the invader alert the killer cells of the immune system to ingest (eat) and destroy the invader. Antibodies produced in response to a specific antigen normally react only with that antigen. In certain conditions, the immune system mistakes self antigens for foreign antigens. Caring Ambassadors Hepatitis C Choices: 4th Edition More than half of all people with chronic hepatitis C have one or more autoantibodies in their blood. This is important because autoantibodies may cause additional symptoms and disease. Your doctor may test your blood for autoantibodies if you are having unexplained signs or symptoms. See Chapter 6, Laboratory Tests and Procedures for additional information about these tests. Cell-Mediated Immunity Cell-mediated immunity is another tactic the body uses to defend itself against invaders through the direct actions of specific immune cells. They kill only cells that display the antigens they are programmed to seek-and-destroy. Think of this as "the kiss of death" because once an immune system killer cell binds to an invader, that invader is doomed to die. Cell-mediated immunity defends the body against fungi, parasites, cancer cells, foreign tissue (transplanted organs), and viruses that live inside cells (intracellular viruses) such as the hepatitis C virus. Many highly skilled researchers continue to work diligently to find answers to these and other questions. This section provides an overview of some basic information scientists have discovered about the immune response to the hepatitis C virus. The rate at which a virus is able to make copies itself is called its replication rate. With the assembly line running at such a high rate of speed, the viruses produced are not perfect copies of the original. The process leading to these slight variations is called mutation, and the variant viruses produced are called quasispecies. For a thorough review of this topic including the latest research findings, see Chapter 7. However, several theories exist about the role of cell-mediated immunity in hepatitis C that have sufficient supporting evidence to warrant mentioning. A strong initial T cell response has been associated with viral clearance, while a weak initial response that builds in strength over time has been linked to chronic infection. Each of these topics and other cutting edge immunology research findings are discussed in detail in Chapter 7. However, approximately 38% of people with chronic hepatitis C also have immunologic disorders. Immune syndromes most often develop during the course of longstanding hepatitis C, and most frequently occur in people whose liver disease has progressed to cirrhosis. The location of the blocked vessels determines what symptoms a patient experiences. Chapter 7: the Immune System And the Hepatitis C Virus - Section 1: Meet the Immune System various studies conducted throughout the world. Although some people with cryoglobulinemia do not experience symptoms, others experience one or more of a range of signs and symptoms as shown in Table 1. Common Signs and Symptoms Associated with Cryoglobulinemia Symptom Weakness Kidney disease Description/notes Approximately 2/3 of people with cryoglobulinemia experience this symptom. Neuropathy is numbness, tingling, or other abnormal sensations in the hands and feet. Purpura (dark red to purple lesions on the skin) are the most common skin manifestation of cryoglobulinemia. Approximately 15% of people with cryoglobulinemia experience joint pain that may be confused with rheumatoid arthritis. Ongoing research will continue to provide insights into the interactions between hepatitis C and the immune system.
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Motor Nerve Fibers Motor nerve fibers carry motor impulses from central nervous system to medicine look up drugs exelon 3 mg fast delivery different parts of the body medicine man aurora buy discount exelon 4.5 mg on line. Among these fibers symptoms 16 weeks pregnant order genuine exelon line, type A nerve fibers are the thickest fibers and type C nerve fibers are the thinnest fibers. Velocity of Impulse Velocity of impulse through a nerve fiber is directly proportional to the thickness of the fiber. Different types of nerve fibers along with diameter and velocity of conduction are given in Table 135. Stimulus is defined as an external agent, which produces excitability in the tissues. Different types of stimulus, qualities of stimulus and strength-duration curve are explained in Chapter 30. Response Due to Stimulation of Nerve Fiber When a nerve fiber is stimulated, based on the strength of stimulus, two types of response develop: 1. Action potential or nerve impulse Action potential develops in a nerve fiber when it is stimulated by a stimulus with adequate strength. Adequate strength of stimulus, necessary for producing the action potential in a nerve fiber is known as threshold or minimal stimulus. Electrotonic potential or local potential When the stimulus with subliminal strength is applied, only electrotonic potential develops and the action potential does not develop. Cathelectrotonic and Anelectrotonic Potentials While recording electrical potential in a nerve fiber, two electrodes, namely cathode and anode are used. The potential change that is produced at cathode is called cathelectrotonic potential. Only the cathelectrotonic potential can be transformed into electrotonic potential or action potential. If the intensity of the stimulus is increased gradually every time, there is increase in the amplitude till the firing level is reached, i. Voltage clamp technique is a modified patch clamp technique (Chapter 31) applied to nerve fibers. It is used to measure the ionic current across the membrane of nerve fiber by fixing the membrane potential at a desired voltage. Principle of Voltage Clamping Normally, the voltage-gated ion channels open and close in response to positive or negative charge within the cell. In order to understand the movement of ions across the membrane (ion flux), it would be necessary to eliminate the other variable, i. So the membrane potential is fixed (clamped) at a specific level by using voltage clamp. It allows study of the ion flux through ionic channels at specific membrane potentials. Two recording electrodes namely, the extracelluar electrode and intracellular electrode are connected to this amplifier. Extracellular electrode is placed on the outer surface of the nerve membrane and the intracellular electrode is inserted into the nerve fiber. Current generator or signal generator is used to control the resting membrane potential of the nerve fiber. The current signals generated by this instrument are passed into the nerve fiber through a current electrode. Properties of Action Potential Properties of action potential are given in Chapter 31. But, it alters the resting membrane potential and produces slight depolarization for about 7 mV. Conduction of impulse through a myelinated nerve fiber is about 50 times faster than through a nonmyelinated fiber. It is because the action potential jumps from one node to another node of Ranvier instead of travelling through the entire nerve fiber (Fig. So, the entry of sodium from extracellular fluid into nerve fiber occurs only in the node of Ranvier, where the myelin sheath is absent. Feedback amplifier receives feedback inputs from recording amplifier and current generator and accordingly modifies the current signals that are sent into the nerve fiber (Fig. Thus, by voltage clamping, it is possible to maintain the constant membrane potential at a desired voltage. Nerve Fibers Used for Voltage Clamping Earlier, the voltage clamp tests were done on the giant axon of the squid Loligo, whose size facilitates such tests. Nowadays, the tests are done on the human nerve fibers obtained from surgical procedures. Normally in the body, the action potential is transmitted through the nerve fiber in only one direction. However, in experimental conditions when, the nerve is stimulated, the action potential travels through the nerve fiber in either direction. It is because the subliminal stimuli are summed up together to become strong enough to produce the response. Absolute Refractory Period Absolute refractory period is the period during which the nerve does not show any response at all, whatever may be the strength of stimulus. Relative Refractory Period It is the period, during which the nerve fiber shows response, if the strength of stimulus is increased to maximum. Absolute refractory period corresponds to the period from the time when firing level is reached till the time when one third of repolarization is completed. Later the response decreases slowly and finally the nerve fiber does not show any response at all. Cause for Adaptation When a nerve fiber is stimulated continuously, depolarization occurs continuously. Continuous depolarization inactivates the sodium pump and increases the efflux of potassium ions. At that time, it is completely refractory and does not conduct another action potential. Axon looses the function temporarily for a short time, which is called conduction block. Useful regeneration is not possible unless the cut ends are rearranged and approximated quickly by surgery. When a peripheral nerve fiber is injured, the degenerative changes occur in the nerve cell body and the nerve fiber of same neuron and the adjoining neuron. After few days, the broken pieces appear as debris in the space occupied by axis cylinder (Fig. Macrophages invade from outside and remove the debris of axis cylinder and fat droplets of disintegrated myelin sheath.
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These cause bursting of the vesicles by forcing the synaptic vesicles move and fuse with presynaptic membrane medicine jar best order exelon. By exocytosis symptoms 24 order exelon 6 mg online, acetylcholine diffuses through the presynaptic membrane and enters the synaptic cleft medications used for bipolar disorder buy exelon from india. It increases the permeability of postsynaptic membrane for sodium by opening the ligand-gated sodium channels. And there, sodium ions alter the resting membrane potential and develops the electrical potential called the endplate potential. Properties of Endplate Potential Endplate potential is a graded potential (Chapter 31) and it is not action potential. When more and more quanta of acetylcholine are released continuously, the miniature endplate potentials are added together and finally produce endplate potential resulting in action potential in the muscle. However, the acetylcholine is so potent, that even this short duration of 1 millisecond is sufficient to excite the muscle fiber. Rapid destruction of acetylcholine has got some important functional significance. It prevents the repeated excitation of the muscle fiber and allows the muscle to relax. Reuptake Process Reuptake is a process in neuromuscular junction, by which a degraded product of neurotransmitter reenters the presynaptic axon terminal where it is reused. Acetylcholinesterase splits (degrades) acetylcholine into inactive choline and acetate. Neuromuscular blockers used during anesthesia relax the skeletal muscles and induce paralysis so that surgery can be conducted with less complication. Following are important neuromuscular blockers, which are commonly used in clinics and research. Curare Curare prevents the neuromuscular transmission by combining with acetylcholine receptors. Since curare blocks the neuromuscular transmission by acting on the acetylcholine receptors, it is called receptor blocker. It affects the neuromuscular transmission by blocking the acetylcholine receptors. And, each quantum of this neurotransmitter produces a weak miniature endplate potential. Succinylcholine and Carbamylcholine these drugs block the neuromuscular transmission by acting like acetylcholine and keeping the muscle in a depolarized state. Botulinum Toxin Botulinum toxin is derived from the bacteria Clostridium botulinum. It prevents release of acetylcholine from axon terminal into the neuromuscular junction. For example, Laryngeal muscles: 2 to 3 muscle fibers per motor unit Pharyngeal muscles: 2 to 6 muscle fibers per motor unit Ocular muscles: 3 to 6 muscle fibers per motor unit Muscles concerned with crude or coarse movements have motor units with large number of muscle fibers. The process by which more and more motor units are put into action is called recruitment of motor unit. Thus, the graded response in the muscle is directly proportional to the number of motor units activated. Stimulation of a motor neuron causes contraction of all the muscle fibers innervated by that neuron. These muscles are present in almost all the organs in the form of sheets, bundles or sheaths around other tissues. Wall of organs like esophagus, stomach and intestine in the gastrointestinal tract 2. Mammary glands, uterus, genital ducts, prostate gland and scrotum in the reproductive system 8. Smooth muscles in the ureters propel urine from kidneys to urinary bladder through ureters. In females, these muscles accelerate the movement of sperms through genital tract after sexual act, movement of ovum into uterus through fallopian tube, expulsion of menstrual fluid and delivery of the baby. These fibers are generally very small, measuring 2 to 5 microns in diameter and 50 to 200 microns in length. Myofibrils and Sarcomere Well-defined myofibrils and sarcomere are absent in smooth muscles. Absence of dark and light bands gives the non-striated appearance to the smooth muscle. Myofilaments and Contractile Proteins Contractile proteins in smooth muscle fiber are actin, myosin and tropomyosin. However, these filaments are not arranged in orderly fashion as in skeletal muscle. These thick filaments contain more number of cross bridges than in skeletal muscle. Dense Bodies Dense bodies are the special structures of smooth muscle fibers to which the actin and tropomyosin molecules of thin filaments are attached. The dense bodies are scattered all over the sarcoplasm in the network of intermediate filaments, which is formed by the protein desmin. The anchoring of the dense bodies, intermediate filaments and thin filaments make the smooth muscle fiber shorten when sliding occurs between thick and thin filaments. Another interesting feature is that the dense bodies are not arranged in straight line. It helps to transmit the contraction from one cell to another throughout the tissue. Sarcotubular System Sarcotubular system in smooth muscle fibers is in the form of network. The gap junctions allow rapid spread of action potential throughout the tissue so that all the muscle fibers show synchronous contraction as a single unit. In this way, the visceral smooth muscle resembles cardiac muscle more than the skeletal muscle. Each muscle fiber has got an outer membrane made up of glycoprotein, which helps to insulate and separate the muscle fibers from one another 4. Distribution of Multiunit Smooth Muscle Fibers Multiunit muscle fibers are in ciliary muscles of the eye, iris of the eye, nictitating membrane (in cat), arrector pili and smooth muscles of the blood vessels and urinary bladder. It is suggested that it may be due to the rhythmic modulations in the activities of sodiumpotassium pump. The slow wave is not action potential and it cannot cause contraction of the muscle.
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In addition to symptoms week by week order exelon in united states online pulse oximetry medicine 0829085 buy generic exelon 3mg online, frequent arterial blood gas analysis can reveal evolving acid-base disturbances and assess the adequacy of ventilation medications with codeine purchase 1.5 mg exelon overnight delivery. Intra-arterial pressure monitoring is frequently performed to follow blood pressure and to provide arterial blood gases and other blood samples. Pulmonary artery (Swan-Ganz) catheters can provide pulmonary artery pressure, cardiac output, and systemic vascular resistance measurements. However, no morbidity or mortality benefit from pulmonary artery catheter use has been demonstrated, and rare but significant complications from placement of central venous access. Thus, routine pulmonary artery catheterization in critically ill pts is not recommended. For intubated pts receiving volume-controlled modes of mechanical ventilation, respiratory mechanics can be followed easily. The peak airway pressure is regularly measured by mechanical ventilators, and the plateau pressure can be assessed by including an end-inspiratory pause. The inspiratory airway resistance is calculated as the difference between the peak and plateau airway pressures (with adjustment for flow rate). Increased airway resistance can result from bronchospasm, respiratory secretions, or a kinked endotracheal tube. Lowdose dopamine treatment does not protect against the development of acute renal failure. Less common but important neurologic complications include anoxic brain injury, stroke, and status epilepticus. Management depends on determining its cause, alleviating triggering and potentiating factors, and providing rapid relief whenever possible. Pain may be of somatic (skin, joints, muscles), visceral, or neuropathic (injury to nerves, spinal cord pathways, or thalamus) origin. Neuropathic Pain Definitions: neuralgia: pain in the distribution of a single nerve, as in trigeminal neuralgia; dysesthesia: spontaneous, unpleasant, abnormal sensations; hyperalgesia and hyperesthesia: exaggerated responses to nociceptive or touch stimulus, respectively; allodynia: perception of light mechanical stimuli as painful, as when vibration evokes painful sensation. Causalgia is continuous severe burning pain with indistinct boundaries and accompanying sympathetic nervous system dysfunction (sweating; vascular, skin, and hair changes-sympathetic dystrophy) that occurs after injury to a peripheral nerve. Sensitization refers to a lowered threshold for activating primary nociceptors following repeated stimulation in damaged or inflamed tissues; inflammatory mediators play a role. Sensitization contributes to tenderness, soreness, and hyperalgesia (as in sunburn). Referred pain results from the convergence of sensory inputs from skin and viscera on single spinal neurons that transmit pain signals to the brain. Because of this convergence, input from deep structures is mislocalized to a region of skin innervated by the same spinal segment. Several factors can cause, perpetuate, or exacerbate chronic pain: (1) painful disease for which there is no cure. These second-order neurons form crossed ascending pathways that reach the thalamus and are projected to somatosensory cortex. Parallel ascending neurons connect with brainstem nuclei and ventrocaudal and medial thalamic nuclei. These parallel pathways project to the limbic system and underlie the emotional aspect of pain. Noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. Inputs from frontal cortex and hypothalamus activate cells in the midbrain that control spinal pain-transmission cells via cells in the medulla. Anticonvulsants (gabapentin, carbamazepine) may be effective for aberrant pain sensations arising from peripheral nerve injury. Narcotic analgesics are usually required for relief of severe pain; the dose should be titrated to produce effective analgesia. Psychological evaluation is key; behaviorally based treatment paradigms are frequently helpful. Some pts may require referral to a pain clinic; for others, pharmacologic management alone can provide significant help. The tricyclic antidepressants are useful in management of chronic pain from many causes, including headache, diabetic neuropathy, postherpetic neuralgia, atypical facial pain, chronic low back pain, and post-stroke pain. Anticonvulsants or antiarrhythmics benefit pts with neuropathic pain and little or no evidence of sympathetic dysfunction. The combination of the anticonvulsant gabapentin and an antidepressant such as nortriptyline may be effective for chronic neuropathic pain. The long-term use of opioids is accepted for pain due to malignant disease but is controversial for chronic pain of nonmalignant origin. When other approaches fail, long-acting opioid compounds such as levorphanol, methadone, sustained-release morphine, or transdermal fentanyl may be considered for these pts (Table 6-2). The average energy intake is about 2800 kcal/d for men and about 1800 kcal/d for women, though these estimates vary with age, body size, and activity level. Fat should comprise 30% of calories, and saturated fat should be <10% of calories. Two forms of severe malnutrition can be seen: marasmus, which refers to generalized starvation that occurs in the setting of chronically decreased energy intake, and kwashiorkor, which refers to selective protein malnutrition due to decreased protein intake and catabolism in the setting of acute, life-threatening illnesses or chronic inflammatory disorders. Aggressive nutritional support is indicated in kwashiorkor to prevent infectious complications and poor wound healing. Etiology the major etiologies of malnutrition are starvation, stress from surgery or severe illness, and mixed mechanisms. B12, pyridoxine, folate), diminished taste (zinc), inflamed and bleeding gums (vit. For a more detailed discussion, see Dwyer J: Nutritional Requirements and Dietary Assessment, Chap. Enteral therapy refers to feeding via the gut, using oral supplements or infusion of formulas via various feeding tubes (nasogastric, nasoduodenal, gastrostomy, jejunostomy, or combined gastrojejunostomy). Parenteral nutrition is often indicated in severe pancreatitis, necrotizing enterocolitis, prolonged ileus, and distal bowel obstruction.
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Bundles of neurofibrils form an anastomosing network around the nucleus and extend into the dendrites and axon medications safe while breastfeeding order exelon 6 mg. Ultrastructurally symptoms valley fever generic 6 mg exelon with amex, neurofibrils consist of aggregates of slender neurofilaments treatment xdr tb guidelines purchase exelon with mastercard, 10 nm in diameter, and microtubules that, although called neurotubules, appear to be identical to microtubules found in other cells. Neurofilaments act as an internal scaffold for the perikaryon and its processes and function to maintain the shape of neurons. The perikarya of most neurons contain characteristic chromophilic (Nissl) substance, which, when stained with dyes such as cresyl violet or toluidine blue, appears as basophilic masses within the cytoplasm of the perikaryon and dendrites. It is absent from the axon and axon hillock, the region of the perikaryon from which the axon originates. In electron micrographs, Nissl substance is seen to consist of several parallel cisternae of granular endoplasmic reticulum. Small slender or oval mitochondria are scattered throughout the cytoplasm of neurons and contain lamellar and tubular cristae. Although centrioles are seen occasionally, neurons in the adult usually do not divide. Dark brown granules of melanin pigment occur in neurons from specific regions of the brain, such as the substantia nigra, locus ceruleus, and dorsal motor nucleus of the vagus nerve, and in spinal and sympathetic ganglia. More common inclusions are lipofuscin granules, which increase with age and are the by-products of normal lysosomal activity. Lysosomes are abundant in most neurons due to the high turnover of plasmalemma and other cellular components. The lipid droplets seen in many neurons represent storage material or may occur as the result of pathologic metabolism. Each neuron usually has several dendrites that extend from the perikaryon, dividing repeatedly to form branchlike extensions. Although tremendously diverse in the number, size, and shape of dendrites, each variety of neuron has a similar branching pattern. The dendritic cytoplasm contains elongate mitochondria, Nissl substance, scattered neurofilaments, and parallel-running microtubules. The cell membrane of most dendrites forms numerous minute projections called dendritic spines or gemmules that serve as areas for synaptic contact between neurons; an important function of dendrites is to receive impulses from other neurons. Dendrites provide most of the surface area for receptive synaptic contact between neurons, although in some neurons the perikaryon and initial segment of the axon also may act as receptor areas. The number of synaptic points on the dendritic tree varies with the type of neuron but may be in the hundreds of thousands. A neuron has only one axon, which conducts impulses away from the parent neuron to other functionally related neurons or effector organs. The axon arises from the axon hillock, an elevation on the surface of the perikaryon that lacks Nissl substance. Axons usually are much longer and more slender than dendrites and may or may not give rise to side branches called collaterals, which, unlike dendritic branches, usually leave the parent axon at right angles. Axons also differ in that the diameter is constant throughout most of the length and the external surface generally is smooth. Axons end in several branches called telodendria, which vary in number and shape and may form a network or basket-like arrangement around postsynaptic neurons. The cytoplasm of the axon, the axoplasm, contains numerous neurofilaments, neurotubules, elongate profiles of smooth endoplasmic reticulum, and long, slender mitochondria. Since axoplasm does not contain Nissl substance, protein synthesis does not occur in the axon. Protein metabolized by the axon during nerve transmission is replaced by that synthesized in cisternae of granular endoplasmic reticulum in the Nissl substance of the perikaryon. Neurotubules function to transport the new protein as well as other materials within the axon. Antegrade transport involves movement of material from the perikaryon to axon terminals and may be slow or fast. Fast transport (410 mm/day) involves transfer of membranous organelles, neurosecretory vesicles, calcium, sugars, amino acids, and nucleotides: Slow transport (1-6 mm/day) includes movement of proteins, metabolic enzymes, and elements of the cytoskeleton. The remaining end undergoes cyclic interaction with the microtubule wall, resulting in movement toward the axon terminal. Retrograde transport is the transfer of exhausted organelles, proteins, small molecules, and recycled membrane from the axonal endings to the perikaryon and provides a route by which some toxins (tetanus) and viruses (herpes, polio, rabies) can invade the central nervous system. Axons transmit responses as electrical impulses called action potentials, which begin in the region of the axon hillock and the initial segment of the axon. Only when the threshold of activity is reached is the action potential transmitted along the axon to its terminations, which synapse with adjacent neurons or end on effector cells. An axon always induces a positive activity - for example, causing muscle cells to contract or stimulating epithelial cells to secrete. Gray matter contains the perikarya of neurons and their closely related processes, whereas white matter is composed chiefly of bundles or masses of axons and their surrounding sheaths. In the spinal cord, gray matter has a central location surrounded by white matter; in the cerebral and cerebellar cortices, gray matter is at the periphery and covers the white matter. Aggregates of perikarya occur within the gray matter of the central nervous system and act as distinct functional units called nuclei. Similar aggregates or individual neurons located outside the central nervous system are called ganglia. Some neurons have numerous, welldeveloped dendrites and very long axons that leave the gray matter to enter the white matter of the central nervous system and ascend or descend in the major fiber tracts of the brain or spinal cord or leave the central nervous system and contribute to the formation of peripheral nerves. Neurons of this type conduct impulses over long distances and are called Golgi type I neurons. These are especially numerous in the cerebellar and cerebral cortices and retina of the eye. Bipolar neurons have a single dendrite and an axon, usually located at opposite poles of the perikaryon. They are found in the retina, olfactory epithelium, and cochlear and vestibular ganglia. Neurons of all craniospinal ganglia originate as bipolar neurons in the embryo, but during development, the dendrite and axon migrate to a common site in the cell body, where they unite to form a single process. The combined process, often called a dendraxon, may run for a short distance and then divide into two processes, one of which serves as a dendrite and receives stimuli from peripheral regions of the body and the other acts as an axon and enters the gray matter of the central nervous system to synapse with other neurons. Although the process directed toward the periphery acts as a dendrite, it is unusual because, morphologically, it resembles an axon. This functional dendrite is smooth and unbranched and usually receives nervous input from a receptor organ. They vary considerably in size and shape and are characterized by multiple dendrites. Macroscopically, cranial and spinal ganglia appear as globular swellings on the sensory roots of their respective nerves. Each ganglion is enveloped by a connective tissue capsule and may contain perikarya of only a few neurons or as many as 55,000. A delicate network of collagenous and reticular fibers, accompanied by small blood vessels, extends between individual neurons and together with bundles of nerve processes often separates the perikarya into groups. The outer capsule lies immediately outside the basal lamina of the satellite cells and consists of a delicate vascular connective tissue.
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Bone formation: Development and mineralization of new matrix (osteoblastic activity) medicine used to treat chlamydia purchase 1.5 mg exelon. The osteoclast present in this compartment attaches itself to treatment hypothyroidism purchase exelon 4.5mg with amex the periosteal or endosteal surface of bone through villi-like membranous extensions medicine 027 order 3 mg exelon mastercard. Resorption of that particular compartment occurs by some substances released from membranous extensions of osteoclasts such as: 1. Osteoblasts synthesize and release collagen into the shallow cavity formed after resorption in the bone resorbing compartment. The collagen fibers arrange themselves in regular units and form the organic matrix called osteoid. Mineralization Mineralization is the process by which the minerals are deposited on bone matrix. Afterwards, the hydroxide and bicarbonate ions are gradually added causing the formation of hydroxyapatite crystals. The process of mineralization is accelerated by the enzyme alkaline phosphatase, secreted by osteoblast. Now, the synthetic activity of osteoblast is reduced slowly and the cell is converted into osteocytes. Later, the bone is arranged in concentric lamellae on the inner surface of the cavity. At the end of the formation of new bone, the cavity is reduced to form Haversian canal. Regulation of Bone Remodeling Bone remodeling occurs continuously throughout the life. However, in persons like athletes, soldiers and others, in whom the bone stress is more, the bone becomes heavy and strong. It is because of the stimulation of osteoblastic activity and mineralization of bone by repeated physical stress. Apart from the physical stress, a variety of hormonal substances and growth factors are involved in regulation of bone resorption and bone formation (Table 68. Formation of hematoma between the broken ends of bone and surrounding soft tissues. Hematoma meansswellingormassofbloodclotconfinedtoa tissue or space due to rupture of blood vessel 2. Reshaping of new bone by osteoclasts, which remove excess callus and formation of canal in the new bone. Osteoporosis Osteoporosis is the bone disease characterized by the loss of bone matrix and minerals. Calcitonin Inhibiting Factors Bone formation Cortisol Mineralization Cortisol Bone resorption Testosterone Causes of osteoporosis Osteoporosis occurs due to excessive bone resorption and decreased bone formation. Manifestations of osteoporosis Loss of bone matrix and minerals leads to loss of bone strength, associated with architectural deterioration of bone tissue. Rickets Rickets is the bone disease in children, characterized by inadequate mineralization of bone matrix. Endocrine disorders like hypothyroidism, Cushing syndrome, acromegaly and hypogonadism. DeficiencyofvitaminDaffectsthereabsorptionof calcium and phosphorus from renal tubules, resulting in calcium deficiency. This deformity of the chest with projecting sternum is called pigeon chest or chicken chest or pectus carinatum. It is because of the development of nodules at sternal end of ribs, which forms the rachitic rosary iii. Kyphosis: Extreme forward curvature of the upper back bone (thoracic spine) with convexity backward (forward bending). Lordosis: Extreme forward curvature of back bone in lumbar region: also called hollow back or saddle back v. Tetany: In advanced stages, the patient may die because of tetany, involving the respiratory muscles. Proinsulin is converted into insulin and C peptide through a series of peptic cleavages. Insulin is degradedinliverandkidneybyacellularenzymecalled insulin protease or insulin-degrading enzyme. Insulin reduces the blood glucose level by its following actions on carbohydrate metabolism: i. Increases transport and uptake of glucose by the cells Insulin facilitates the transport of glucose from blood intothecellsbyincreasingthepermeabilityofcellmembranetoglucose. Glucose transporters:Usually,glucoseistransportedinto the cells by sodium-glucose symport pump. Promotes peripheral utilization of glucose Insulin promotes the peripheral utilization of glucose. In liver, when glycogencontentincreasesbeyondits storingcapacity, insulin causes conversion of glucose into fatty acids. Increasing the storage of glucose by converting it into glycogen in liver and muscle iv. On Protein Metabolism Insulin facilitates the synthesis and storage of proteins and inhibits the cellular utilization of proteins by the followingactions: i. Facilitating the transport of amino acids into the cellfromblood,byincreasingthepermeabilityof cell membrane for amino acids ii. Preventing protein catabolism by decreasing the activity of cellular enzymes which act on proteins iv. Thus, insulin is responsible for the conservation and storage of proteins in the body. Synthesis of fatty acids and triglycerides Insulin promotes the transport of excess glucose into cells,particularlythelivercells. Insulin promotes the synthesis of lipids by activating the enzymeswhichconvert: a. Transport of fatty acids into adipose tissue Insulin facilitates the transport of fatty acids into the adipose tissue. Storage of fat Insulin promotes the storage of fat in adipose tissue by inhibitingtheenzymeswhichdegradethetriglycerides. On Growth Alongwithgrowthhormone,insulinpromotesgrowthof body by its anabolic action on proteins. It enhances the Chapter 69 t Endocrine Functions of Pancreas 417 transport of amino acids into the cell and synthesis of proteins in the cells. Houssay Animal the importance of insulin and growth hormone in the growthofthebodyisdemonstratedbyHoussayanimal. Administration of either insulinorgrowthhormonealonedoesnotinducegrowth in this animal.
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Cholagogue Action Cholagogue is an agent which causes contraction of gallbladder and release of bile into the intestine treatment 7 february purchase 1.5 mg exelon overnight delivery. Bile salts act as cholagogues indirectly by stimulating the secretion of hormone cholecystokinin medications during childbirth buy exelon 6mg cheap. Bile salts act as laxatives by stimulating peristaltic movements of the intestine treatment yeast infection nipples breastfeeding 1.5mg exelon. PreventionofGallstoneFormation Bile salts prevent the formation of gallstone by keeping the cholesterol and lecithin in solution. In the absence of bile salts, cholesterol precipitates along with lecithin and forms gallstone. Bilirubin and biliverdin are the two bile pigments and bilirubin is the major bile pigment in human beings. Senile erythrocytes are destroyed in reticuloen dothelial system and hemoglobin is released from them 2. Bilirubin circulating in the blood is called free bilirubin or unconjugated bilirubin 8. Within few hours after entering the circulation, the free bilirubin is taken up by the liver cells 9. In the liver, it is conjugated with glucuronic acid to form conjugated bilirubin 10. In intestine, 50% of the conjugated bilirubin is converted into urobilinogen by intestinal bacteria. First the conjugated bilirubin is deconjugated into free bilirubin, which is later reduced into urobilinogen. Remaining 50% of conjugated bilirubin from intestine is absorbed into blood and enters the liver through portal vein (enterohepatic circulation). Most of the urobilinogen from intestine enters liver via enterohepatic circulation. In urine, due to exposure to air, the urobilinogen is converted into urobilin by oxidation 5. It performs many vital metabolic and homeostatic functions, which are summarized below. It synthe sizes all the plasma proteins and other proteins (except immunoglobulins) such as clotting factors, complement factors and hormonebinding proteins. Bile helps to carry away waste products and breakdown fats, which are excreted through feces or urine. It stores vitamin B12 necessary for erythropoiesis and iron necessary for synthesis 256 Section 4 t Digestive System of hemoglobin. The fatsoluble drugs are converted into water soluble substances, which are excreted through bile or urine. Foreign bodies such as bacteria or antigens are swallowed and digested by reticuloendothelial cells of liver by means of phagocytosis. Reticuloendothelial cells of liver also produce substances like interleukins and tumor necrosis factors, which activate the immune system of the body (Chapter 17). Liver cells are involved in the removal of toxic property of various harmful substances. Conversion of toxic substances into non toxic materials by means of conjugation with glucuronic acid or sulfates. But it is released into intestine only intermittently and most of the bile is stored in gallbladder till it is required. The mucosa of gallbladder rapidly reabsorbs water and electrolytes, except calcium and potassium. When bile is released into the intestine, mucin acts as a lubricant for movement of chyme in the intestine. MaintenanceofPressureinBiliarySystem Due to the concentrating capacity, gallbladder maintains a pressure of about 7 cm H2O in biliary system. This pressure in the biliary system is essential for the release of bile into the intestine. While taking food or when chyme enters the intestine, gallbladder contracts along with relaxation of sphincter of Oddi. Because of the increase in pressure, the bile from gallbladder enters the intestine. Gallbladder is not essential for life and it is removed (cholecystectomy) in patients suffering from gallbladder dysfunction. NeuralFactor Stimulation of parasympathetic nerve (vagus) causes contraction of gallbladder by releasing acetylcholine. The vagal stimulation occurs during the cephalic phase and gastric phase of gastric secretion. HormonalFactor When a fatty chyme enters the intestine from stomach, the intestine secretes the cholecystokinin, which causes contraction of the gallbladder. Choleretics Substances which increase the secretion of bile from liver are known as choleretics. Cholagogues Cholagogue is an agent which increases the release of bile into the intestine by contracting gallbladder. Secretion of bile from liver and release of bile from the gallbladder are influenced by some chemical factors, which are categorized into three groups: 258 Section 4 t Digestive System Common cholagogues are: i. Inorganic acids All these substances stimulate the secretion of cholecystokinin, which in turn causes contraction of gallbladder and flow of bile into intestine. Hydrocholeretic Agents Hydrocholeretic agent is a substance which causes the secretion of bile from liver, with large amount of water and less amount of solids. Hepatic or Hepatocellular or CholestaticJaundice Hepatic jaundice is the type of jaundice that occurs due to the damage of hepatic cells. Because of the damage, the conjugated bilirubin from liver cannot be excreted and it returns to blood. Infection (infective jaundice) by virus, resulting in hepatitis (viral hepatitis) ii. Posthepatic or Obstructive or ExtrahepaticJaundice Posthepatic type of jaundice occurs because of the obstruction of bile flow at any level of the biliary system. Formation of urobilinogen also increases resulting in the excretion of more amount of urobilinogen in urine. Excess administration of drugs like paracetamol Poisons like carbon tetrachloride and aflatoxin Wilson disease (Chapter 151) Circulatory insufficiency Inheritance from mother during parturition. Stomach pain Paleness of skin Darkcolored urine and pale stool Jaundice Personality changes. Hepatitis caused by hepatitis B virus is more common and considered more serious because it may lead to cirrhosis and cancer of liver. Fever, nausea and vomiting Jaundice Increased heart rate and cardiac output Portal hypertension Muscular weakness and wasting of muscles Drowsiness Lack of concentration and confused state of mind Coma in advanced stages.
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Endolymph Scala media is filled with endolymph symptoms intestinal blockage 1.5mg exelon with visa, which contains high concentration of potassium and low concentration of sodium medications zanx purchase exelon 6 mg mastercard. It is due to treatment genital warts buy 1.5 mg exelon with mastercard continuous secretion of potassium ions by stria vascularis into scala media. Electrical Potential Difference in potassium concentration is responsible for the development of an electrical potential difference between endolymph and perilymph. Significance of Endocochlear Potential Lower portion of the hair cells is bathed by perilymph. Head portion of hair cells penetrates the lamina reticularis and it is bathed by endolymph (Fig. High potential difference sensitizes the hair cells so that, the excitability of hair cells increases. Action potential to a click sound with moderate intensity level consists of three successive spike potentials called N1 N2 N3 representing synchronous repetitive firing in many fibers. At high frequency, the synchronization of action potential disappears and single spike occurs. There the receiver instrument converts the electrical impulses back into sound waves. Similarly, cochlea just converts the sound waves into electrical impulses of same frequency. Impulses are transmitted by auditory nerve fibers to cerebral cortex, where perception and analysis of sound occur. It is believed that, the nerve fibers can transmit maximum of 1,000 impulses per second. Thus, the telephone theory fails to explain the transmission of sound waves with frequency above 1,000 cycles per second. According to this theory, the impulses of sound waves with frequency above 1,000 cycles per second are transmitted by different groups of nerve fibers. Resonance Theory of Helmholtz Resonance theory was the first theory of hearing to emerge in 1863. Helmholtz named these basilar fibers resonators and compared them with the resonators of piano. Similarly, when the sound with a particular frequency is applied, the basilar fibers in a particular portion of basilar membrane are stimulated. Resonance theory was not accepted because the individual resonators could not be identified in cochlea. Gradually, this theory was modified into another theory called the place theory, which is more widely accepted. Place Theory According to this theory, nerve fibers from different portions (places) of organ of Corti on basilar membrane give response to sounds of different frequency. Accordingly, corresponding nerve fiber from organ of Corti gives information to the brain regarding the portion of organ of Corti that is stimulated. Frequency of sound audible to human ear lies between 20 and 20,000 Hz or cycles/second. The range of greatest sensitivity lies between 2,000 and 3,000 Hz (cycles/second). According to the first group, the analysis of sound frequency is the function of cerebral cortex and the cochlea merely transmits the sound. According to the second group of theories, the frequency analysis is done by cochlea, which later sends the information to cerebral cortex. Telephone Theory of Rutherford Telephone theory was postulated by Rutherford in 1880. According to this Chapter 174 t Mechanism of Hearing 1021 Experimental evidences supporting place theory i. If a person is exposed to a loud noise of a particular frequency for a long period, he becomes deaf for that frequency. In experimental animals, destruction of a portion of organ of Corti occurs by exposing the animal to loud noise of a particular frequency iii. In human high-tone deafness, there is degeneration of organ of Corti near the base of cochlea or degeneration of nerve supplying the cochlea near the base iv. During exposure to high-frequency sound, cochlear microphonic potentials show greater voltage in hair cells near base of the cochlea. Also, during the exposure to low-frequency sound, cochlear microphonic potentials show greater voltage in hair cells near apex of the cochlea. Traveling Wave Theory From place theory, emerged yet another theory called the traveling wave theory. Development, generation, movement and disappearance of traveling wave are already described earlier in this chapter. When loudness of sound increases, it produces large vibrations, which spread over longer area of basilar membrane. This activates large number of hair cells and recruits more number of auditory nerve fibers. It is important for survival and it helps to protect us from moving objects such as vehicles. Cerebral cortex and medial geniculate body are responsible for localization of sound. Otosclerosis (fixation of footplate of stapes against oval window) due to ankylosis. Degeneration of hair cells due to some antibiotics like streptomycin and gentamicin ii. However, some simple tests called bedside tests are usually carried before doing conventional types of hearing tests. Chapter 175 t Auditory Defects 1023 Whispering Test the examiner stands about 60 cm away from the subject at his side and whispers some words. If the subject is not able to hear the whisper, then hearing deficit is suspected. Tickling of Watch Test Wrist watch with tickling sound is kept near the ear of the subject. The subject suffering from hearing defects cannot hear the tickling sound of watch. When the subject does not hear the sound any more, the tuning fork is held in air in front of the ear of same side. Normal person hears vibration in air even after the bone conduction ceases because, in normal conditions, air conduction via ossicles is better than bone conduction. But in conduction deafness, the vibrations in air are not heard after cessation of bone conduction. In nerve deafness, both air conduction and bone conduction are diminished or lost.