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When sodium ions enter inside carrying with them large numbers of positive charges anxiety 4th hereford cattle discount tofranil 25 mg with visa, there occurs depolarization causing a local positive potential change inside the muscle fibre membrane called the end plate potential anxiety symptoms jaw spasms safe 25 mg tofranil. It is localized, nonpropagated, does not obey the all-or-none law and decays exponentially away from the plate. The action potentials are generated on either side of the end plate and are conducted away from the end plate in both the directions along the muscle fibres thus causing muscle contraction. Even at rest, small quanta of acetylcholine are released randomly from the nerve terminal. The size of the quanta of acetylcholine released in this way varies directly with the Ca2+ concentration and inversely with the Mg2+ concentration at the end plate. The miniature end plate potential similar to that seen at the myoneural junction has been observed at other cholinergic synapses as well. The acetylcholine is so potent that its stay in the synaptic space even for this short period of 1 ms is sufficient to excite the muscle fibre. It is important to note that the rapid removal of acetylcholine prevents the repeated excitation of muscle fibre. Drugs affecting and disorders of neuromuscular junction Drugs affecting neuromuscular junction Neuromuscular blockers. Neuromuscular blockers are the drugs that block transmission at the neuromuscular junction. Some of the common neuromuscular blockers, which are commonly used, in clinical practice and in research are: 1. Curare or the active principle of D-tubocurarine prevents the neuromuscular transmission by combining with acetylcholine receptors. The acetylcholine released thus cannot combine with the receptors and so the end plate potential does not develop. The curariform drugs are called receptor blockers since they block the neuromuscular transmission by acting on acetylcholine receptors. Bungarotoxin found in the venom of deadly snakes also blocks neuromuscular transmission by binding with acetylcholine receptors. Succinylcholine and carbamylcholine act like acetylcholine and cause depolarization of the postsynaptic membrane. But these are not destroyed by cholinesterase and so the muscle remains in a depolarized state for a long time. Thus, these drugs block the myoneural junction by keeping the muscle in a depolarized state. It blocks the transmission across the myoneural junction by preventing the release of acetylcholine from the terminal buttons of the nerve endings. The drugs methacholine, carbachol and nicotine act like acetylcholine and produce end plate potential exciting the muscle fibre. However, these drugs are either not destroyed or are destroyed very slowly by the enzyme acetylcholineesterase. So they cause repeated stimulation and continuous action of muscle, thereby causing a state of muscle spasm. Once this enzyme is inactivated, the acetylcholine released at the nerve terminal cannot be hydrolysed, this leads to repeated stimulation and continuous action of muscle. Myasthenia gravis is a disorder in which the myoneural junction is unable to transmit signals from the nerve fibre to muscle fibres, thereby causing paralysis of the involved muscles. In this disease, antibodies are produced against the acetylcholine-gated channels (receptors) present on the motor end plate which destroy these channels. Thus, the acetylcholine released at the nerve terminal is not able to produce adequate end plate potential to excite the muscle fibre. The main clinical feature of the disease is muscle fatigue with sustained or repeated activity. It is usually presented in following forms: · In one form, mainly extraocular, muscles are involved and in other form there is generalized weakness of skeletal muscles. Studies show that the number of receptors on motor end plates of affected muscle is reduced by 70­90%. If the disease is intense enough, the patient dies of paralysis, particularly of respiratory muscles. I n this disease, antibodies are produced against the calcium channels present on the presynaptic membrane, which destroy the channels. Consequently, Ca2+ influx into the nerve terminal is markedly decreased and thereby release of acetylcholine is also reduced. Scanty amount of acetylcholine is not able to produce adequate end plate potential to excite muscle fibres, producing muscular weakness. A similar type of syndrome can also occur after the use of aminoglycoside antibiotics which impair the functioning of Ca2+ at nerve terminals. Further, the muscle is a contractile tissue with a chemically stored energy which can be transformed into mechanical energy. There are three different types of muscles in the body: skeletal muscles, cardiac muscles and smooth muscles. Based on certain distinctive features the muscles can be grouped as: Striated versus nonstriated muscles Striated muscle cells show large number of cross striations at regular intervals when seen under a light microscope. Voluntary versus involuntary muscles Voluntary muscles can be made to contract under our will to perform the movements we desire. Skeletal muscles the skeletal muscles, as the name indicates, are attached with the bones of the body skeleton and their contraction results in the body movements. Each fasciculus is surrounded by a stronger sheath of connective tissue called perimysium. Structure of a muscle fibre Each muscle fibre is basically a long (1­4 cm), cylindrical (10­100 micron in diameter) multinucleated cell. Like any other cell, in the sarcoplasm are embedded many structures, the nuclei, Golgi apparatus, mitochondria, sarcoplasmic reticulum, ribosomes and glycogen and occasional lipid droplets.

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It is particularly a must for females at any age before menopause anxiety symptoms sweating 25 mg tofranil order visa, because once she is sensitized by the Rh antigen anxiety gas generic tofranil 75 mg, the anti-D antibodies are formed and she will not be able to bear an Rh +ve fetus. Blood bag/bottle should be checked for the name of recipient and blood group on the label before starting the blood transfusion. If rapid transfusion is given, citrate present in stored blood may cause chelation of calcium ions leading to decreased serum calcium level and tetany. The transfusion must be stopped if there is a rapid rise of temperature (>40°C), or any other reaction. Mismatched transfusion reaction is the most serious and potentially fatal hazard of blood transfusion. Soon, the patient complains of violent pain in the back or elsewhere and tightness of chest. The extra free haemoglobin leaks through glomerular membrane and is passed in urine producing haemoglobinuria. If urine is acidic and glomerular filtration is slow, the free haemoglobin passing through glomeruli is precipitated in the tubules as acid haematin. Acute renal shutdown usually occurs within a few minutes to few hours after transfusion of mismatched blood and continues. Circulatory overload due to hypervolaemia may occur following blood transfusion when the transfusion is rapid, especially in patients with cardiac diseases, chronic anaemia and kidney diseases. Pyrogenic reaction characterized by fever and chills may occur probably due to destruction of leucocytes and platelets by antibodies against them. Allergic reactions such as skin rashes and asthma may occur if donor blood contains substances to which patient is allergic. Hyperkalaemia may occur after excessive transfusion because K+ concentration in stored blood is high. Hypocalcaemia producing tetany may occur following massive transfusion of citrated blood. The extra citrate chelates calcium ions leading to decreased serum calcium levels and tetany. That is why, intravenous calcium gluconate is given with citrated blood transfusion. Reduced tissue oxygenation may occur in patients receiving large amounts of transfusion. Haemosiderosis due to iron overload may occur following repeated transfusions, as in thalassaemic patients. The excessive iron is deposited in liver, heart and endocrine organs and produces damage. Thrombophlebitis at the venepuncture site may develop if the needle remains in the same site for many hours. Autologous transfusion is done under following situations: · For elective surgery, a self-predonation is a common practice in some hospitals. After starting a course of iron tablets, two units of blood are collected, one 16 days and another 8 days before surgery. This practice avoids the hazards of transfusion of blood donated by some other individual. Storage of blood for transfusion Some facts about the storage of donated blood are: · One unit of blood (420 ml) can be collected from a donor at a time under all aseptic measures. Therefore, it is an ideal for patients of acute haemorrhage (> 25% of total volume loss). Apheresis is technology which is used for collection of multiple units of platelets from single donor and for preparation of various plasma derivatives such as albumin, immunoglobulin, antithrombin and coagulation factor concentrates from pooled plasma from many donors. Therefore, used in severely anaemic patients to maintain adequate oxygenation (especially hypoplastic and haemolytic anaemia). These are transfused in patients with thrombocytopenia to reduce the incidence of bleeding. Therefore, indications for fresh frozen plasma may be used as plasma for replacement therapy to expand blood volume in conditions where fluid lost from the body. Plasma derivatives: Pooled plasma from multiple donors provide specific protein derivatives: · Albumin solution is used as a plasma substitute for replacing fluid volume. Also, it acts as volume expander because it stays longer in the circulation due to its high molecular weight. The heart acts as a system of two pumps working in series and forms the driving force for blood flow. The blood vessels that take blood from the heart to various tissues are called arteries. Arterioles open into a network of capillaries, which constitute the microcirculation. Blood from capillaries (or from sinusoids) is collected by small venules which join to form veins. Thermoregulation by control of blood flow to the skin and extremities to enhance or retard heat loss, 2. The parallel arrangement of vessels supply the body organs with blood of the same arterial composition. Such a balanced output is achieved by an intrinsic property of the cardiac muscle known as Frank­Starling mechanism. The human heart weighs approximately 300 g and it consists of two halves, right and left, both structurally and functionally.

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Though anxiety relaxation techniques cheap tofranil uk, under natural circumstances anxiety low blood pressure generic 50 mg tofranil with mastercard, the first urge to empty the bladder occurs at approximately 150 ml of urinary volume but it can be easily suppressed. Sacral micturition centre is formed by the sacral detrusor nucleus and sacral pudendal nucleus. The afferents from the stretch receptors in the bladder wall inhibit this nucleus thereby exciting the external sphincter of urethra. The postganglionic parasympathetic fibres are excitatory to the detrusor muscle and inhibitory to the internal sphincter. The cycle thus keeps on repeating itself again and again until the bladder has reached a strong degree of contraction. Once a micturition reflex has occurred but not succeeded in emptying the bladder, the nervous elements of the reflex usually remain in an inhibited state for at least a few minutes to an hour before another micturition reflex occurs. Once the micturition reflex becomes powerful enough, this causes another reflex which passes through pudendal nerves to external sphincter to cause its inhibition. If this inhibition is more potent than the voluntary constrictor signals from brain, then urination will not occur. If not so, urination will not occur unless the bladder fills still more and micturition reflex becomes more powerful. The micturition reflex is fundamentally a spinal reflex facilitated and inhibited by higher brain centres (supraspinal centres) and, like defaecation, is subjected to voxluntary facilitation and inhibition. Voluntary control is gradually acquired as a learned ability of the toilet training. Once voluntary control is acquired, the supraspinal control centres exert final control of micturition by the following means: · the higher centres keep the micturition reflex partially inhibited all the time except when it is desired to micturate. The cortical detrusor motor area is located in the medial frontal lobe (superior frontal gyrus). Role of perineal and abdominal muscles in micturition Certain muscular movements, which aid the emptying of bladder, but are not the essential component of micturition process are: · At the onset of micturition, the levator ani and perineal muscles are relaxed, thereby shortening the posturethra and decreasing the urethral resistance. Certain important facts about micturition are: · A voiding contraction, once initiated, is normally maintained until all the urine has been discharged from the urinary bladder. However, if required so, the micturition can be voluntarily stopped in between by inhibitory impulses from the higher centres. Abnormalities of micturition Effect of interference with nervous control of bladder 1. Transection of sympathetic supply Following effects are produced: · In man, the immediate effect would be relaxation of: ureteric reflexes, trigone and internal sphincter. Effect of deafferentation or atonic bladder · the destruction of sensory nerve fibres from the bladder to spinal cord prevents transmission of stretch signals from the bladder and therefore, also prevents micturition reflex contractions. In this condition: · the person loses all bladder control despite intact efferent fibres from the cord to the bladder and despite intact neurogenic connections with brain. It frequently causes constrictive fibrosis around the dorsal nerve root fibres where they enter the spinal cord and subsequently destroy these fibres. Effect of denervation When there is interruption with both afferent and efferent nerves of bladder, the following consequences are observed: · the bladder is flaccid and distended for a while, · Gradually, however, the muscle of decentralized bladder becomes active, with many contraction waves that expel dribbles of urine out of the urethra and · the bladder becomes shrunken and the bladder wall hypertrophies. The reason for the difference between the small, hypertrophic bladder seen in this condition and the distended, hypotonic bladder seen only when afferent nerves are interrupted is not known. The hyperactive stage in the former condition suggests the development of denervation hypersensitization even though the neurons interrupted are preganglionic rather than postganglionic. Effect of spinal cord transection During spinal shock · Voluntary micturition is completely abolished. The activity of detrusor muscle remains in abeyance for a long period, but sphincter now returns very soon. At this stage, bladder responds to filling in the same manner as the dead organ or an elastic bag. The sphincter is finally forced open by a high intravesical pressure and small quantities of urine escape at frequent intervals-a condition of retention with overflow. Cystitis may occur, and death results from the usual complications of ascending urinary infection. After spinal shock has passed, the voiding reflex returns, although there is no voluntary control. Some paraplegic patients train themselves to initiate voiding by pinching or stroking their thighs, provoking a mild mass reflex. Effects of obstruction Conditions causing obstruction to the outflow of urine from the bladder may be: · Anatomical obstacles. Effects · Retention of urine consequently tends to occur, and the intravesical pressure rises till it causes expulsion of urine. But when, finally, the bladder wall is overstretched, it becomes paralyzed and normal evacuation no longer takes place. Functional anatomy and general principles of functions of gastrointestinal system 7. Digestion and absorption Introduction To sustain life, the body needs a continual supply of water, electrolytes and nutrients. This function is served by the gastrointestinal or the so-called digestive system. Gastrointestinal system comprises alimentary canal and other associated organs such as liver, gall bladder and pancreas.

Syndromes

  • Wear light-colored clothing. Light colors are less attractive than dark colors to biting insects. It also makes it easier to spot ticks or insects that have landed.
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  • Carteolol (Cartrol)
  • Coarctation of the aorta occurs when a part of the aorta has a very narrow section, like in an hourglass timer.
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Therefore anxiety symptoms 24 7 tofranil 25 mg amex, in cardiac muscles anxiety and dizziness cheap tofranil 50 mg buy, there is only one triad per sarcomere as compared to two in skeletal muscles (page 88). Further, the tubules are much wider than in skeletal muscles and typical triads are not always present. They are often replaced by dyads having one T-tubule and one cistern of the sarcoplasmic reticulum (L-tubule). Process of excitability and contractility: An electromechanical phenomenon the cardiac muscle being an excitable tissue produces an action potential (electrical phenomenon) when stimulated and responds by contracting (mechanical phenomenon). The events which link the electrical phenomenon with mechanical phenomenon constitute the excitation­contraction coupling phenomenon. Action potential When stimulated, each cardiac muscle fibre shows an electrical activity known as propagated action potential. It is different from the electrocardiogram, which refers to extracellular recording of the summed electrical events of all the cardiac muscle fibres generated with each heart beat (see page 253). The phase 0 (upstroke) is characterized by the depolarization which proceeds rapidly, an overshoot is present, as in skeletal muscle and nerve. In this phase, amplitude of potential reaches up to +20 to +30 mV (positive interior with reference to exterior). The initial rapid depolarization and the overshoot are due to the rapid opening of voltage-gated Na+ channels and rapid influx of Na+ ions similar to that occurring in nerve and skeletal muscle. At -30- to -40-mV membrane potential, the calcium channels also open up and influx of Ca2+ ions also contributes in this phase. Rapid depolarization is followed by a very short-lived slight rapid repolarization. The initial rapid repolarization is due to closure of Na+ channels and opening of K+ channels resulting in transient outward current. This plateau in action potential explains the 5­15 times longer contraction time of the cardiac muscle as compared to the skeletal muscle. Very slow repolarization during the plateau phase is due to: · Slow influx of Ca2+ ions resulting from opening of sarcolemmal L-type Ca2+ channels, and · Closure of a distinct set of K+ channels called the inward-rectifying K+ channels. During this phase, complete repolarization occurs and the membrane potential falls to the approximate resting value of -80 mV. The slow repolarization results from closing of Ca2+ channels and opening of following two types of K+ channels. The duration of action potential (primarily repolarization is about 250 ms) at a heart rate of 75 beats/min. The duration of action potential decreases with increased heart rate (150 ms at a heart rate of 200 beats/min). As discussed in functional anatomy, the cardiac muscle acts as a physiological syncytium due to the presence of gap junctions amongst the cardiac muscle fibres. Because of this, the action potential spreads through the cardiac muscles very rapidly. Further, as there are two syncytia (the atrial and the ventricular) in the heart, the action potential is transmitted from atria to ventricles only through the fibres of specialized conductive system. Excitation­contraction coupling phenomenon in cardiac muscles Excitation­contraction coupling refers to the sequence of events by which an excited plasma membrane of a muscle fibre leads to cross-bridge activity by increasing sarcoplasmic calcium concentration. The sequence of events during excitation­contraction coupling in the cardiac muscles is similar to those observed in a skeletal muscle (see page 89), with the following exception: In cardiac muscles (as against that in skeletal muscles), extra calcium ions diffuse into the sarcoplasm from T-tubules without which the contraction strength would be considerably reduced. The T-tubules of cardiac muscle contain mucopolysaccharides which are negatively charged and bind an abundant store of calcium ions. T-tubules open directly to the exterior and therefore, Ca2+ ions in them directly come from extracellular fluid. A, in resting state; B, calciuminduced calcium release during excitation and contraction state; C, during relaxation state. Process of cardiac muscle contraction the molecular mechanism of cardiac muscle contraction by cross-bridge cycling and sliding of filaments is primarily similar to that of skeletal muscles (page 89) and smooth muscles (page 117). Relaxation of cardiac muscle Relaxation of cardiac muscle (diastole) occurs when levels of Ca2+ ions fall in the cardiac muscle fibres. Properties of cardiac muscle the basic properties of cardiac muscle include: · Automaticity, · Rhythmicity (chronotropism), · Conductivity (dromotropism), · Excitability (bathmotropism) and · Contractility (inotropism). Some of the properties of cardiac muscle, viz automaticity, rhythmicity and conductivity are discussed in Chapter 4. Excitability Excitability (bathmotropism) is the property by which tissues respond to stimuli. One of the characteristics of cardiac muscle excitability which needs a special emphasis is its refractory period. Refractory period Refractory period refers to the period following action potential during which the cardiac muscle does not respond to a stimulus. Cardiac muscle has a long refractory period (250­300 ms in ventricles and about 150 ms in atria). During this period the muscle shows response if the strength of stimulus is increased to maximum. Since the heart has to function as a pump, it must relax, get filled up with blood and then contract to pump out the blood. Experimental demonstration of refractory period in heart can be done both in a beating heart as well as in a quiescent heart. Refractory period in a beating heart of a pithed frog can be demonstrated during recording of a cardiogram. The total duration of the extra systole and the compensatory pause is equivalent to the duration of two cardiac cycles.

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Effect on the metabolic rate in general As described in the mechanism of action anxiety relief games cheap tofranil 25 mg with mastercard, the thyroid hormone in general stimulates the metabolic activities and increases the basal rate of oxygen consumption and heat production in most tissues of the body except the brain anxiety and depression association of america order line tofranil, retina, gonads, lungs and spleen. Resting oxygen use in humans ranges from about 150 ml/min in hypothyroid state to about 400 ml/min in the hyperthyroid state (normal 225­ 250 ml/min). The magnitude of calorigenic action of thyroxine partly depends on the level of circulating catecholamines. Increased metabolic rate is associated with increased utilization of many hormones, vitamins and certain drugs. On the other hand, patients with hypothyroidism may show toxic effects at usual doses of certain drugs. Effects on metabolism the increased O2 consumption and metabolic rate ultimately depends on an increased supply of necessary substrate for oxidation. Thyroid hormones stimulate the provision of these substrates by their effect on carbohydrate, fat and protein metabolism. T4 and T3 lead on to overall increase in enzymes, causing: · Increased glucose absorption from gastrointestinal tract and · Acceleration in almost all aspects of glucose metabolism, i. Thyroid hormones cause: · Mobilization of fat from adipose tissue, · Increase in the levels of fatty acids and enhanced oxidation of free fatty acids by cells and · Decrease in the quantity of cholesterol, phospholipids and triglycerides in plasma and plasma cholesterol level is lowered due to increased excretion in bile. Hypothyroidism is associated with elevated plasma cholesterol levels, which can be reversed by thyroid hormone administration. In high concentrations, thyroid hormones have a catabolic effect leading to negative nitrogen balance. Therefore, muscle weakness and creatininuria are characteristic features of a hyperthyroid patient. T4 and T3 potentiate the respective stimulatory effects of epinephrine, norepinephrine, glucagon, cortisol and growth hormone on gluconeogenesis, lipolysis, ketogenesis and proteolysis of the labile protein pool. Therefore, thyroid hormones cause increased need for vitamins leading to relative vitamin deficiency in hyperthyroidism. In hypothyroidism, this reaction is very slow and carotene accumulation in the blood and tissues (carotenaemia) gives a yellow colour to the skin. Carotenaemia can be clinically differentiated from jaundice by the fact that sclera of the eyeballs are not affected in the former condition. This fact is clear from the observation that impairment of the thyroid function is associated with retention of water and electrolytes, which can be reversed by hormonal administration. The overall metabolic effect of thyroid has been aptly described as accelerating the response to starvation. Respiratory effects Thyroid hormones cannot stimulate O2 utilization for long without also enhancing oxygen supply, which is accomplished by the following effects of T4 and T3. Increase in the resting respiratory rate, minute ventilation and ventilatory responses to hypercapnia and hypoxia. Increase in oxygen-carrying capacity of blood by slightly increasing the red blood cell mass. This increase in red blood cell mass results from stimulation of erythropoietin production, which arises directly by alteration of its gene expression and indirectly by way of the renal tissue hypoxia that results from increased O2 use. Cardiovascular effects Thyroid hormone increases cardiac output, ensuring sufficient oxygen delivery in the tissues. In general, the thyroid hormones have the following effects on cardiovascular system: i. Vasodilatation and increased blood flow to tissues occurs by two mechanisms: · Indirect mechanism. These effects cause vasodilatation and increase in blood flow in most of the tissues especially skin, muscle and heart. Cutaneous vasodilatation is particularly a prominent feature, which helps in dissipation of excessive heat produced. Thyroid hormones directly decrease systemic vascular resistance by dilating arterioles in the peripheral circulation. Blood volume in circulation is increased because of: · the effect of vasodilatation produced, as described above and also · By activating the renin­angiotensin­aldosterone axis and thereby increasing renal tubular sodium reabsorption. Thyroid hormone produces tachycardia by directly increasing the excitability of the heart and indirectly via adrenergic stimulation. Force of cardiac contraction is increased by moderate increase in thyroid hormone. The cardiac inotropic effects are partly indirect, via adrenergic stimulation and partly by direct effect of hormones on cardiac muscle. Myocardial calcium uptake and adenylyl cyclase activity are increased and enhance contractile force. Cardiac output is increased as a result of increased blood volume, increased heart rate and increased force of contraction which occurs due to both direct and indirect effects of the hormone, as described above. Systolic blood pressure is increased due to increased strength and rate of heart beat; whereas, diastolic blood pressure is decreased due to peripheral vasodilatation. This results into increased pulse pressure, but the mean arterial pressure is usually unchanged. I mportant N ote It is important to note that the cardiac effects of thyroid hormone are particularly important when ageing individuals develop hypothyroidism. The only clinical manifestation may be the development of rapid atrial arrhythmias, such as flutter or fibrillation.

References

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