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Assistant Professor, Washington University School of Medicine
The transverse (T) tubular system within myocardial cells participates in this exchange of substances between capillary blood and myocardial cells (as described later medicine hat weather generic 6.5 mg nitroglycerin otc, the T tubule system also plays a key role in excitationcontraction coupling) medicine of the future cheap 2.5mg nitroglycerin amex. The T tubular system is absent or poorly developed in the atrial cells of many mammals treatment tennis elbow discount nitroglycerin 2.5 mg on line. Excitation-Contraction Coupling Results of the earliest studies on isolated hearts indicated that optimal concentrations of Na+, K+, and Ca++ in extracellular fluid are necessary for contraction of cardiac muscle. As already described, the resting membrane potential is independent of the extracellular [Na+] gradient across the membrane but very much dependent on extracellular [K+]. Decreases or increases in extracellular [K+], especially if they are large or occur quickly, can lead to arrhythmias, loss of excitability of the myocardial cells, and even cardiac arrest. Removal of Ca++ from the extracellular fluid results in decreased contractile force and eventual arrest in diastole. Conversely, an increase in extracellular [Ca++] enhances contractile force, and very high extracellular [Ca++] induces cardiac arrest in systole (rigor). The free intracellular [Ca++] is the factor principally responsible for the contractile state of the myocardium. The process by which the action potential of the cardiac myocyte leads to contraction is termed excitationcontraction coupling (see also Chapter 13). Cardiac muscle is excited when a wave of excitation spreads rapidly along the myocardial sarcolemma from cell to cell via gap junctions. Excitation also spreads into the interior of the cells via the T tubules, which invaginate the cardiac fibers at the Z lines. Electrical stimulation at the Z line or the application of Ca++ to the Z lines in a skinned cardiac fiber (whose sarcolemma is removed) elicits localized contraction of the adjacent myofibrils. During the plateau (phase 2) of the action potential, permeability of the sarcolemma by Ca++ increases. Ca++ flows down its electrochemical gradient and enters the cell through calcium channels in the sarcolemma and in the T tubules. However, the amount of Ca++ that enters the cell interior from the extracellular/ interstitial fluid is not sufficient to induce contraction of the myofibrils. Instead, it acts as a trigger (trigger Ca++) to release Ca++ from the sarcoplasmic reticulum, where the intracellular Ca++ is stored. Ca++ leaves the sarcoplasmic reticulum through Ca++ release channels, which are called ryanodine receptors because the channel protein binds ryanodine avidly. This ability of the myocardium to resist stretch at high filling pressures probably resides in the noncontractile constituents of the heart tissue (connective tissue), and it may serve as a safety factor against overloading of the heart in diastole. Usually, ventricular diastolic pressure is approximately 0 to 7 mm Hg, and the average diastolic sarcomere length is approximately 2. Thus a normal heart operates on the ascending portion of the Frank-Starling curve, as depicted in. Functional Anatomy Cardiac Muscle Cardiac muscle functions as a syncytium; that is, a stimulus applied to any part of the cardiac muscle results in contraction of the entire muscle. Gap junctions with high conductance are present in the intercalated disks between adjacent cells and facilitate conduction of the cardiac impulse from one cell to the next. Cardiac muscle must contract repetitively for a lifetime, and hence it requires a continuous supply of O2. This unblocking initiates cross-bridge cycling and hence contraction of the myofibrils. Mechanisms that raise cytosolic [Ca++] increase the force developed, and those that lower cytosolic [Ca++] decrease the force developed.
Fetal hemoglobin (HbF) has higher affinity for O2 than HbA medicine recall purchase nitroglycerin online pills, permitting O2 to flow from maternal circulation to fetal circulation in the placenta symptoms your dog has worms generic nitroglycerin 6.5 mg with amex. The resulting decrease in intracellular pH leads to protonation of histidine residue in 3 hemoglobin (Hb) medications qid nitroglycerin 2.5 mg line, reducing its O2 affinity and promoting O2 release. HbA2 (two a-chains and two d-chains) and HbF (two a-chains and two gchains) each contribute about 1% to 2% of total Hb. HbA1c, a glycosylated form of HbA, constitutes about 5% of the total Hb in normal adults, but the level is elevated in diabetics. Sickle cell hemoglobin (HbS) results from a mutation that replaces glutamic acid with valine at residue 6 in b-globin (b6 Glu! Deoxygenated HbS forms large linear polymers, causing normally flexible erythrocytes to become stiff and sickle shaped. Hemoglobin C (HbC) results from substitution of lysine for glutamate at position 6 in b-globin (b6 Glu! Although HbC and HbS are mutated at the same site, HbC is associated only with a mild chronic anemia in homozygotes. Hereditary methemoglobinemia results from any one of several single amino acid substitutions that stabilize heme iron in the oxidized form (HbM). Characterized by slate gray cyanosis in early infancy without pulmonary or cardiac disease b. Acquired methemoglobinemia results from exposure to nitrate and nitrite compounds, sulfonamides, and aniline dyes. Symptoms such as cyanosis (no response to O2 administration), headache, and dizziness occur. It results from deletion of one or more of the four a-globin 1 genes on chromosome 16. There are four types of a-thalassemia that range from mild to severe in their effect on the body. Hemoglobin H disease (1) In this variant, three of four a-globin chain genes are deficient. It results from mutations affecting the rate of synthesis of b-globin alleles on chromosome 11 b. Thalassemia minor or thalassemia trait (1) Mild deficiency of b-globin chains due to splicing defects (2) There are no significant health problems. Collagen is the most abundant protein in the body, and it is the major fibrous component of connective tissue. In all a-chains, much of the sequence contains glycine at every third position (boxes). Proline and hydroxyproline (or hydroxylysine) commonly occupy the other two positions in the -Gly-X-Y- repeats. B, Notice the typical staggered array of linked tropocollagen molecules in the fibrils of fibrous collagen. Tropocollagen, the basic structural unit of collagen, is a right-handed triple helix of a-chains. Ascorbic acid: hydroxylation of proline and lysine in collagen synthesis; promotes crossbridging Collagen fibrils form spontaneously from tropocollagen and are stabilized by covalent cross-links between lysine and hydroxylysine residues on adjacent chains. Proline and hydroxyproline (or hydroxylysine) are often present in the X and Y positions, respectively.
Appendicitis Obstruction of the appendiceal lumen results in distention of the appendix medications related to the female reproductive system order nitroglycerin no prescription, superimposed infection 72210 treatment discount nitroglycerin 2.5 mg online, ischemia treatment 4 water 6.5 mg nitroglycerin fast delivery, and eventually perforation. There is much debate about appropriate imaging algorithms for suspected appendicitis. Ultrasound is much more useful in girls and in patients of thin body habitus than in boys and patients who are obese. In girls, in whom ovarian causes of right lower quadrant pain (such as, hemorrhagic cyst or torsion) are not uncommon, ultrasound may be the first test of choice. Internal echoes can indicate the presence of blood, exudates, chyle, or neoplastic cells. Abscess In experienced hands and using meticulous technique, ultrasound can localize an intraabdominal abscess. A, Ultrasound scan shows a wedge-shaped hyperechoic focus (arrowhead) in the upper pole of the right kidney related to acute bacterial pyelonephritis. B, Color flow ultrasound image demonstrates diminished flow through the involved area. Technical failures are caused by the presence of severe pain, marked ascites, or obesity. In the longitudinal plane, the inflamed appendix is a fluid-filled, noncompressible, blind-ending tubular structure with a diameter of 6 mm or more. Other findings include the presence of a shadowing echogenic appendicolith, pericecal or periappendiceal fluid. Peritonitis is characterized by dilated bowel loops with thick echogenic walls and ascites, and increased blood flow in the bowel wall as demonstrated by color Doppler imaging. Ultrasound is not needed for the diagnosis, but the findings need to be recognized because they may be encountered on examinations performed for other clinical indications. However, some patients with malrotation have a normal position of the artery and Figure 25. The redundant pyloric mucosa (blue arrow) protrudes into the gastric antrum (A), forming the antral nipple sign. BiliaryTree Because of their small size, normal intrahepatic bile ducts and the cystic duct are not routinely seen at sonography. The intrahepatic ducts are considered dilated if their diameter exceeds 2 mm or is more than 40% of the diameter of the adjacent portal vein. The use of Doppler techniques allows a more confident diagnosis of intrahepatic ductal dilatation. The common bile duct extends from the junction of the cystic duct and common hepatic duct to the level of the ampulla of Vater, where it joins the main pancreatic duct in 60% to 70% of individuals. The upper limits of the common duct should not exceed 1 mm in neonates, 2 mm in infants up to 1 year old, 4 mm in children 1 to 10 years old, and 6 mm in adolescents and young adults. The distal portion of the common duct is usually larger than the proximal portion. Ductal size may increase by 1 mm or more during deep inspiration and the Valsalva maneuver. About 70% to 80% of cases of neonatal jaundice result from biliary atresia, neonatal hepatitis syndrome, and choledochal cyst. Other biliary abnormalities include bile duct paucity (Alagille syndrome), inspissated bile syndrome, and spontaneous perforation of the extrahepatic bile duct.
Alveolar pressure also rises treatment borderline personality disorder order nitroglycerin online from canada, in part because of the increase in pleural pressure (+60 cm H2O) and in part because of the elastic recoil pressure of the lung at that lung volume (which in this case is 30 cm H2O) symptoms rheumatic fever cheap nitroglycerin 6.5mg free shipping. Because alveolar pressure exceeds atmospheric pressure symptoms after embryo transfer purchase nitroglycerin 2.5mg on-line, gas begins to flow from the alveolus to the mouth when the glottis opens. As gas flows out of the alveoli, the transmural pressure across the airways decreases. This occurs for three reasons: (1) there is a resistive pressure drop caused by the frictional pressure loss associated with flow (expiratory airflow resistance); (2) as the cross-sectional area of the airways decreases toward the trachea, gas velocity increases and this acceleration of gas flow further decreases the pressure; and (3) as lung volume decreases, the elastic recoil pressure decreases. Thus as air moves out of the lung, the driving pressure for expiratory gas flow decreases. In addition, the mechanical tethering that holds the airways open at high lung volumes diminishes as lung volume decreases. There is a point between the alveoli and the mouth at which the pressure inside the airways equals the pressure that surrounds the airways. Airways toward the mouth but still inside the chest wall become compressed because the pressure outside is greater than the pressure inside (dynamic airway compression). As a consequence the transairway pressure now becomes negative [Pta = Paw - Ppl = 58 - (+60) = -2 cm H2O] just beyond the equal pressure point. No amount of effort will increase the flow further because the higher pleural pressure tends to collapse the airway at the equal pressure point, just as it also tends to increase the gradient for expiratory gas flow. It is also why airway resistance is greater during exhalation than during inspiration. In the absence of lung disease, the equal pressure point occurs in airways that contain cartilage, and thus they resist collapse. As lung volume decreases and as elastic recoil pressure decreases, the equal pressure point moves closer to the alveoli. Dynamic Compliance One additional measurement of dynamic lung mechanics should be mentioned, and this is the measurement of dynamic compliance. Infact,acuteandchronic lungdiseasescanchangetheexpiratoryflow-volume relationshipbychangesin(1)staticlungrecoilpressure,(2) airwayresistanceandthedistributionofresistancealongthe airways,(3)lossofmechanicaltetheringofintraparenchymal airways,(4)changesinthestiffnessormechanicalproperties oftheairways,and(5)differencesinseverityofthe aforementionedchangesinvariouslungregions. Dynamic compliance is always less than static compliance, and it increases during exercise. This is because during tidal volume breathing, a small change in alveolar surface area is insufficient to bring additional surfactant molecules to the surface, and thus the lung is less compliant. During exercise the opposite occurs; there are large changes in Inflation-deflation pressure-volume curve. Both of these respiratory activities are important for maintaining normal lung compliance. In contrast to the lung, the dynamic compliance of the chest wall is not significantly different from its static compliance. Changes in the mechanical properties of the lung or chest wall (or both) in the presence of disease result in an increase in the work of breathing. However, like other skeletal muscles they can fatigue, and respiratory failure may ensue. Respiratory muscle fatigue is the most common cause of respiratory failure, a process in which gas exchange is inadequate to meet the metabolic needs of the body. In restrictive lung diseases, such as pulmonary fibrosis, lung compliance is decreased and the pressure-volume curve is shifted to the right. In obstructive lung diseases, such as asthma during an exacerbation or chronic bronchitis, airway resistance is elevated.
Such foreign objects are irritating to the nasal mucosa and soon incite an intense inflammatory reaction with production of a thick treatment leukemia order generic nitroglycerin online, purulent symptoms of strep throat order cheap nitroglycerin online, foul-smelling discharge that helps to hide their presence medicine that makes you throw up purchase nitroglycerin 2.5mg. Because most children younger than 5 years old are unable to blow their noses and are afraid or unable to tell their parents what they have done, the object is not expelled and the problem often goes unrecognized until symptoms develop and medical attention is sought. A unilateral nasal discharge and/or a foul smell are the typical chief complaints and should lead the clinician to suspect a foreign body immediately. Even when visualization is accomplished, removal can be difficult because children are easily frightened at the prospect of instrumentation, and their struggling can result in mucosal injury during attempts at removal. To minimize problems, topical anesthetic spray and a topical vasoconstrictor can be applied, and the child can be restrained with a papoose board. If the object is anterior to the turbinates, removal can be attempted using suction; a small wire loop curette or a right-angled Day hook for spherical objects; or otologic forceps for material that can be grasped. Consultation with an otolaryngologist should be sought for removal of objects located more posteriorly or those not readily removed on initial attempts. A major concern is that in the attempted removal, a deeply situated foreign body may be dislodged into the nasopharynx, leading to aspiration or, worse, laryngeal obstruction. In such cases, the best course of action is to remove the object after the airway has been secured with an endotracheal tube in the operating room, with the patient under general anesthesia. Significant bleeding may occur during attempted removal of an intranasal foreign body, and this is another reason to strongly consider general anesthesia with an endotracheal tube to secure the airway. Small button batteries such as watch batteries in the nose can cause a great deal of caustic tissue injury from the electric current. Nasal Polyps Polyps are thought to be the end result of recurrent infection and/ or inflammation, although atopy may play a contributing role in a portion of cases. Polyps originate in the ethmoid or, less commonly, the maxillary sinuses and protrude through the sinus ostia into the nasal cavity. The phenomenon is unusual in children younger than 10 years old, with the exception of patients with cystic fibrosis, 25% of whom develop polyps, some as early as infancy. Symptoms consist of those of progressive nasal obstruction, frequently with associated discharge. Recurrent sinusitis is a common complication as a result of impaired sinus drainage. On examination, moist, glistening pedunculated growths that may have a smooth or a grapelike appearance are seen. Bilateral opacification of the ethmoid and maxillary sinuses is commonly found on radiography. Polyps must be distinguished from a nasal glioma or encephalocele, which may have a similar appearance and can produce identical symptoms. These neural mass lesions are more common in infancy but may present in older children. The consequent obstruction to normal flow of secretions then starts a vicious circle, making the child more vulnerable to recurrent infections of the ears, sinuses, and nasopharynx, which in turn further exacerbate the adenoidal and tonsillar hypertrophy. Regardless of the mode of origin, when adenoidal hypertrophy is marked, blockage of the nasal airway becomes severe and results in mouth breathing, chronic rhinorrhea, inability to blow the nose, and snoring during sleep. The child holds his or her mouth open and has little or no airflow through the nares, and his or her tonsils may also meet at the midline. A lateral neck x-ray examination reveals a large adenoidal shadow impinging on the nasal airway.
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