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It is common for patients receiving intravenous contrast to develop a transient increase in serum creatinine cheap 135 mg colospa with amex. These agents cause renal fail- ure by inducing intrarenal vasoconstriction and reducing renal blood ﬂow purchase colospa 135 mg fast delivery, mimicking prerenal azotemia, and by directly causing tubular injury. The risk of contrast nephropa- thy may be reduced by initiating newer isoosmolar agents and minimizing the dose of contrast. When the reduction in renal blood ﬂow is severe or prolonged, tubular injury develops, causing acute renal failure. Patients with intravascular volume depletion, diabe- tes, congestive heart failure, multiple myeloma, or chronic renal failure have an increased risk of contrast nephropathy. The urine sediment is bland in mild cases, but with acute tubular necrosis, muddy brown granular casts may be seen. Saline hydration plus N-ace- tylcysteine may decrease the risk and severity of contrast nephropathy. Red cell casts indi- cate glomerular disease, and white cell casts suggest upper urinary tract infection. Urinary eosinophils are seen in allergic interstitial disease caused by many drugs. The clinical manifestations can be variable but may be characterized by fever, lumbar tenderness, leukocytosis, and hematuria. Magnetic resonance venography is the most sensitive and speciﬁc noninvasive form of imaging to make the diagnosis of renal vein thrombosis. Ultrasound with Doppler is operator-dependent and therefore may be less sensitive. Contrast venography is the gold standard for diagnosis, but it exposes the patient to a more invasive procedure and contrast load. Also known as antidiuretic hormone, vasopressin is primarily released under conditions of hyperosmolarity and volume depletion. Although sodium is the main determinant of hy- perosmolarity, sodium is not the only stimulus that affects the secretion of vasopressin. Other, less potent stimuli of vasopressin release include pregnancy, nausea, pain, stress, and hypoglycemia. This hormone acts on the principal cell in the distal convoluted tubule of the kidney to cause resorption of water. This occurs through nuclear mecha- nisms encoded by the aquaporin-2 gene that cause water channels to be inserted into the luminal membrane. The net effect is to cause the passive resorption of water along the os- motic gradient in the distal convoluted tubule. Activation of β2-adrenergic receptors in- duces cellular uptake of potassium and promotes insulin secretion by pancreatic islet β cells. Severe hy- pokalemia leads to progressive weakness, hypoventilation and eventually complete paral- ysis. The electrocardiogram ﬁndings are common but do not correlate with the degree of hypokalemia in the serum. The quantity of water required to correct a free water deﬁcit in hypernatremic patients can be estimated from the following equation: Water deﬁcit = [(plasma Na – 140)/140] × total body water Total body water is approximately 50% of lean body mass in men and 40% of lean body mass in women. In calculating the rate of water replacement, ongoing losses should be + accounted for and plasma Na should be lowered by no more than 0. More rapid administration of water and normalization of serum so- dium concentration may result in a rapid inﬂux of water into cells that have already un- dergone osmotic normalization. The main differential diagnosis is acute glomerulonephritis, but if an individual is on a culprit drug, the drug should be discontinued as an initial step. Discontinuation of the drug usually leads to complete re- versal of the renal injury, although in severe cases, prednisone may be used to improve re- covery. The clinical picture does not suggest relapse of endocarditis, worsening valvular dysfunction, or new infectious process such as a infection of the central venous catheter. Antistreptol- ysin O titers are elevated in cases of poststreptococcal glomerulonephritis due to group A streptococcus, but would not be elevated in S. The risk factors for developing hypotension during hemodialysis include ex- cessive ultraﬁltration, reduced intravascular volume before dialysis, impaired autonomic responses, osmolar shifts, food intake before dialysis, impaired cardiac function, and use of antihypertensive agents. The hypotension is usually managed with ﬂuid administration and by decreasing the ultraﬁltration rate. Anaphylactoid reac- tions to the dialyzer once were common but are also decreasing in frequency with the use of newer-generation dialysis membranes. Fever is not a usual complication of hemodialysis but suggests the presence of an infection of the dialysis access site. Symptoms of hypercalcemia depend on the severity and time course of its development. Patients may progress to complain of vague neuropsychi- atric symptoms including trouble concentrating, personality changes, and depression. Severe hypercalcemia, particularly if it develops acutely, may result in lethargy, stupor, or coma. Only after volume has been restored should loop diuretics be used to decrease se- rum calcium.
Subjective vertigo is prosyncopal light-headedness buy cheap colospa 135 mg on-line, which may be caused by cochlear or ves- tibular ischemia buy colospa 135 mg with amex. Cholinergic antagonists reduce the excitability of labyrinthine receptors and depress con- duction from the vestibular apparatus to the vomiting center. Cholinergic antagonists are used to treat motion sickness and in preoperative situations. Cholinergic antagonists produce adverse effects that include drowsiness, dry mouth, and blurred vision. Transdermal delivery of scopolamine via a skin patch decreases the incidence of adverse effects and produces relief for 72 hours. Histamine H1-receptor antagonists include meclizine (Antivert, Bonine), cyclizine (Mare- zine), dimenhydrinate (Dramamine), and promethazine (Phenergan). These agents most likely act by inhibiting histamine pathways, and cholinergic pathways (receptor ‘‘crossover’’) of the vestibular apparatus. Histamine H1-receptor antagonists are used to treat motion sickness and true vertigo. Cyclizine and meclizine are drugs of choice for nausea and vomiting associated with pregnancy. These agents produce sedation and dry mouth and have anticholinergic side effects. These agents are contraindicated in Parkinson disease because of their extrapyramidal effects. These agents are often combined with corticosteroids such as dexamethasone (Decadron) and methylprednisolone (Solu-Medrol) to produce an enhanced antiemetic effect that is possibly due to corticosteroid inhibition of prostaglandin synthesis. Dronabinol (Marinol) is an oral preparation of D-9-tetrahydrocannabinol, the active canna- binoid in marijuana. Adverse effects include sedation, tachycardia, hypotension, and behavioral alterations simi- lar to those associated with the use of marijuana (see V X F). Diazepam is useful as atreatm entofvertigo, and it controls symptoms in Meniere disease in 60%–70% of patients. Prolonged use of some anorexigenics may lead to physical or psychologic dependence. Amphetamine, methamphetamine, dextroamphetamine, and phentermine (Adipex) act cen- trally and elevate the synaptic concentration of catecholamines and dopamine, producing a reduction in food-seeking behavior. Orlistat is a reversible lipase inhibitor used for the management of obesity and is also available over the counter. This agent is contraindicated in patients with cholestasis and malabsorption syndromes. Dronabinol (D-9-tetrahydrocannabinol) (Marinol) stimulates appetite, among its other activities. Megestrol (Megace) is a progestational agent that has a side effect increased appetite. This agent is also used as a second- or third-line therapy for breast cancer patients who have progressed on tamoxifen (see Chapter 12). Antacids are weak bases that are taken orally and that partially neutralize gastric acid, reduce pepsin activity, and stimulate prostaglandin production. Sodium bicarbonate (Alka Seltzer) (1) Sodium bicarbonate is absorbed systemically and should not be used for long-term treatment. The increase in gastric pH produced by antacids decreases the absorption of acidic drugs and increases the absorption of basic drugs. The H2-receptor antagonists, cimetidine (Tagamet), ranitidine (Zantac), famotidine (Pepcid), and nizatidine (Axid) act as competitive inhibitors of the his- tamine H2-receptor on the parietal cell. This results in a marked decrease in histamine- stimulated gastric acid secretion. Although other agents such as gastrin and acetylcholine may induce acid secretion, histamine is the predominant final mediator that stimulates parietal acid secretion. These drugs are rapidly absorbed, and effects are observed within a few minutes to hours. Therapeutic uses (1) Histamine H2-receptor antagonists are used to treat peptic ulcer disease to promote the healing of gastric and duodenal ulcers. However, when they are used as sole agents, recurrence is observed in 90% of patients. As lipophilic weak bases, these prodrugs concentrate in the acidic compartments of parietal cells where they are rapidly converted to an active thiophilic sulfonamide cation. Desired effects may take 3–4 days since not all proton pumps are inhibited with the first dose of these medications. Proton pump inhibitors are more effective for this indication than histamine H2-receptor blockers. These agents are useful in patients with Zollinger-Ellison syndrome, for reflux esophagitis, and for ulcers refractory to H2-receptor antagonists. The most common cause of peptic and duodenal ulcers is infection by the anaerobic bacteria H. The most effective treatment is ‘‘triple therapy,’’ which consists of two antibiotics (usually clari- thromycin and amoxicillin) and a proton pump inhibitor, and it may include colloidal bismuth (Pepto Bismol) (Table 8-1).
Curr Opin Otolaryngol Head Neck Surg 2003; 11: nonsyndromal) hearing impairment in a series of genes includ- 424–427 cheap 135mg colospa otc. Cystic ﬁbrosis mutation detection by hybridization to light- sensorineural hearing loss earlier purchase 135 mg colospa free shipping. Nested genetic bit analysis is freely available as full searchable text at http://www. For example, in the mammalian The auditory system seems better equipped to deal with injuries vestibular system, hair cell regeneration has been shown to occur in lower species than in mammals. The situation in the auditory inner ear will produce new sensory cells (hair cells) throughout system is less clear. There is evidence of hair cell regeneration in their life and, consequently, injured cells can be replaced contin- newborn mice given explants of cochlear duct (7) and in replac- uously. Birds lose this ability during embryonic development, but ing the damaged hair cells by converting the supporting cells (8). In contrast, mam- homologue of the drosophila gene atonal that encodes a basic malian hair cell loss has always been considered irreversible. Overexpression of The mechanism of cell death in the cochlea is produced in Atoh1 in nonsensory cells of the normal cochlea generates new two ways: through “necrotic cell death” mediated by very loud hair cells, both in vitro and in vivo. Atoh1 has been shown to act noise, or “apoptosis,” mediated by the activation of cysteine as a “prohair cell gene” and is required for the differentiation of protease family within the cells, the caspases [very loud noise can hair cells from multipotent progenitors. This ﬁnd- sic cellular pathway, respectively), but it may be assumed that ing opens new perspectives for the treatment of hearing loss and these mechanisms are more or less under statistical control in that justiﬁes the efforts to encapsulate nucleotides encoding the Math1 dependent on the characteristics of the stimulus the extent of cell gene within the nanostructures for the treatment of deafness. Each of these mechanisms provides the possibility to hearing after noise trauma has been observed in humans, implying reduce and, in some cases, to prevent cochlear cell death through that humans may also have the capacity to regain hearing function active intervention with pharmacotherapy. However, the mechanisms behind the recovery have not yet Recently, many researchers have investigated the role of been fully delineated. There is, however, substantial evidence that antioxidant agents in different models of peripheral hearing cochlear damage induced by noise can be prevented by the appli- disorders. It has been found that antioxidants protect the cation of different pharmacologically active substances (12). Thus, cochlea from noise-induced trauma, as well as cisplatin and there are grounds to expect that hearing disorders in mammals aminoglycoside exposure (2–4). The would mainly be caused by metabolic mechanisms while at outer hair cells are activated and react in a linear manner to higher levels, mechanical mechanisms would predominate. As sinusoidal sound stimulation with one impulse to one sinusoid changes in homeostasis may also occur in mechanical trauma up to 1000 Hz. At higher frequencies, other mechanisms are and the effects of metabolic stress are also likely to be expressed involved in coding the ampliﬁcation of the signal. These are as mechanical damage, it is not meaningful to make a strict sep- not known in detail. Cell tractions of the outer hair cell bodies amplify the basilar mem- death is a result of either apoptosis or necrosis. Apoptosis is a brane vibration and transduce the vibration to shear forces that strictly controlled process to eliminate dysfunctional cells with- will activate the inner hair cells. It can be viewed as a coun- enhanced basilar membrane vibration is transmitted into the terbalance to cell division, and a disturbance may, for example, central auditory system and is perceived as sound. Necrosis on the supporting cells is not clear yet but they may serve as a sup- the other hand is a more passive type of cell death, involving a porting organ to provide stability and damping of excessive rapid and disorganised breakdown of a cell, often as a conse- vibration. Damage to the cochlea may also lead to hyperacusis quence of acute trauma (toxic substances, ischaemia, etc. As and we hypothesise that this symptom may be linked to sup- the cell contents are released directly into the surrounding tis- porting cell damage (Fig. Thus, for the Obviously, noise or excessive auditory stimulation will organism, apoptosis is the preferred method when it is necessary elicit shear forces in the cochlea but at much larger amplitudes. In the auditory system, there is no conclusive There are two fundamentally different ways by which overstim- evidence that apoptosis does play a signiﬁcant role. A recent that may mechanically alter or disrupt cochlear structures caus- study on autopsy materials from subjects with no history of ing mechanical damage to cell membranes and nerve endings acoustic trauma suggests that apoptosis does not contribute sig- and disturb the blood circulation. Cellular distortion, disorgan- niﬁcantly to the regulation of the cell population in the normal isation of the stereocilia, and possible rupture of cell membranes adult inner ear (18). Nevertheless, apoptosis may be involved during noise-induced trauma, although there is to date no direct evidence in humans. Changes in cochlear blood ﬂow have generally been sug- gested as contributing to noise-induced hearing loss (19). Recent ﬁndings have clearly demonstrated noise-induced alter- ations in the cochlear microcirculation causing local ischaemia (20). The effect varies with the intensity and duration of the exposure, but when vascular insufﬁciency is manifest, the reduced oxygen and energy supply to the cochlea and the accumulation of metabolites will be accompanied by severe functional alterations. It has been shown experimentally that applying drugs blocking vasoconstriction prevents a noise- induced microcirculatory disorder and maintains normal hear- ing (21). The damage can be Chromatin condensation Chromatin destruction repaired or can be irreversible leading to cell death. With these mechanisms, the body loss by treatments increasing the antioxidant level (24).
Drug choice is related to the mechanism of drug action in one of the following general categories: a order colospa 135 mg line. Host determinants include history of drug reactions; site of infection; renal buy colospa 135 mg, hepatic, and immune status; age; pregnancy and lactation; metabolic abnormalities; pharmacokinetic factors; preexisting organ dysfunction; and genetic factors. Bacterial determinants include intrinsic resistance, escape from antibiotic effect, and acquired resistance, which can occur as a result of the following: 1. Spontaneous, random chromosomal mutations, which occur at a frequency of 10–12 to 10–5. These mutations are commonly due to a change in either a structural protein receptor for an antibiotic or a protein involved in drug transport. Conjugation is the passage of genes from bacteria to bacteria via direct contact through a sex pilus or bridge. Conjugation occurs primarily in gram-negative bacilli, and it is the prin- cipal mechanism of acquired resistance among enterobacteria. Structure and mechanism of action (1) Penicillins are analogues of alanine dipeptide (Fig. Modifications of the R-group side- chain (attached to the b-lactam ring) alter the pharmacologic properties and resistance to b-lactamase. Gram-positive bacteria with thick external cell walls are particularly susceptible. The genes for b-lactamases can be transmitted during conjugation or as small plasmids (minus conjugation genes) via transduction. Common organisms capable of producing penicillinase include Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Neisseria gonorrhoeae, and Bacillus, Proteus, and Bacteroides species. Selected drugs and their therapeutic uses (Table 11-1) (1) Penicillin G and penicillin V are mainly used to treat infections with the following organisms (resistant strains of bacteria are being isolated more frequently): (a) Gram-positive cocci (aerobic): Pneumococci, streptococci (except S. This group represents the most common pathogens for which first-generation penicillins are used today. Pro- benicid, a uricosuric agent that blocks renal secretion of penicillin, is used rarely for this purpose. Chapter 11 Drugs Used in Treatment of Infectious Diseases 255 (3) Penicillinase-resistant penicillins (oxacillin, dicloxacillin, and nafcillin) are used pre- dominantly for penicillinase-producing staphylococcal infections. Ampicillin is useful for infections caused by Haemophilus influenzae, Streptococcus pneumonia, Streptococcus pyrogenes, Neisseria meningitides, Pro- teus mirabilis, and Enterococcus faecalis. Amox- icillin is commonly used for endocarditis prophylaxis before major procedures. Piperacillin/tazobactam is effective against most gram-negative organisms, including Pseudomonas spp. Adverse effects (1) Penicillins cause hypersensitivity reactions in nearly 10% of patients. All types of reac- tions, from a simple rash to anaphylaxis, can be observed within 2 minutes or up to 3 days following administration. Endocarditis prophylaxis (1) Endocarditis prophylaxis is indicated for patients with prosthetic heart valves; those who have previously been diagnosed with endocarditis; patients born with cyanotic heart disease; and patients with surgically constructed systemic pulmonary shunts. Patients with intermediate risk for endocarditis are those who were born with other con- genital cardiac abnormalities; those with acquired valvular dysfunction; and patients with hypertrophic cardiomyopathy. Structure and mechanism of action (1) Cephalosporins consist of a 7-aminocephalosporanic acid nucleus and a b-lactam ring linked to a dihydrothiazine ring (see Fig. Third-generation cephalosporins are sensitive to another class of b-lactamase, the cephalosporinases (genes are generally located on chromosomes as opposed to plasmids). They are used in treatment of streptococcal infections as well as infections Chapter 11 Drugs Used in Treatment of Infectious Diseases 257 caused by E. Ceftriaxone is used for sexually trans- mitted infections caused by gonorrhea, as well as in empiric therapy for commu- nity-acquired meningitis. Adverse effects and drug interactions (1) Cephalosporins most commonly cause hypersensitivity reactions (2%–5%); 5%–10% of penicillin-sensitive persons are also hypersensitive to cephalosporins. Aztreonam (Azactam) (1) Aztreonam is a naturally occurring monobactam lacking the thiazolidine ring that is highly resistant to b-lactamases. Vancomycin (Vancocin, Vancoled) (1) Vancomycin is a tricyclic glycopeptide that binds to the terminal end of growing pepti- doglycan to prevent further elongation and cross-linking; this results in decreased cell membrane activity and increased cell lysis. Rapid infusion may cause anaphylactoid reactions and ‘‘red neck’’ syndrome (flushing caused by release of histamine). Bacitracin (1) Bacitracin inhibits dephosphorylation and reuse of the phospholipid required for accep- tance of N-acetylmuramic acid pentapeptide, the building block of the peptidoglycan complex. Cycloserine (Seromycin) (1) Cycloserine is an amino acid analogue that inhibits alanine racemase and the incorpo- ration of alanine into the peptidoglycan pentapeptide.
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