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During acute episodes purchase ipratropium 20mcg online treatment qt prolongation, hallucinations order ipratropium 20mcg without prescription treatment in statistics, delusions and thought slippage are the most prominent symptoms discount 20 mcg ipratropium with amex medicine 5325. With treatment or natural remission these symptoms are less prominent and the loss of spontaneity, social withdrawal and personal neglect become more noticeable. Delusional disorder, in contrast, only manifests (one or more) delusions. Usually the delusion is of a paranoid type, and the patient believes he/she is being watched and is in danger from spies, organised crime, etc. The patient may be able to work and appear normal to others. As there is only one symptom and the patient may appear to function reasonably well outside the home. Suspiciousness or frank delusions result in conflict at work and the patient is usually finally placed on some form of pension. The social life is also severely impaired, the patient eventually withdrawing to live behind reinforced doors with an array of locks, in a state of constant apprehension. Last modified: November, 2015 8 Mood disorders The Oxford English Dictionary defines mood as “1, a particular sate of mind or feeling, and 2, a prevailing feeling, spirit or tone”. Thus, feelings are the central issue, and under this heading one might expect to include fear, jealousy or love. Bipolar disorder (once called manic-depressive psychosis) is the most dramatic form - characterised by mood elevated (manic) and lowered (depressed) phases. These phases may last for months or even become chronic. For a given patient, swings may predominantly occur in one direction, alternatively, about equal numbers of swings may occur in each direction. In the mood elevated phase the patient is often over confident, grandiose, irritable and disinhibited, with rapid thoughts, reduced need for sleep and abundant energy. Delusions may occur about possessing exceptional importance or skills; hallucinations (often of being spoken to by God or adoring others) less commonly occur. In depressed phases the mood and energy are low, thinking is slowed and the ability to concentrate is reduced. Sleep is disrupted, the patient often waking in the early hours and unable to return to sleep. There is loss of interest in food, sexual or any other activity, and weight loss is a frequent feature. The patient in a manic phase is clearly acting out of character, and with mood elevation as a springboard, problems arise when patients engage in risky behaviour such as unwise investments, fast driving, ill-advised sexual liaisons or audacious activities. The patient in a depressive phase may also act out of character, becoming inactive and withdrawn. However, not infrequently, the patient thinks about death and regrettably, suicide is more common among significantly depressed individuals than among the healthy population. Major depressive disorder or unipolar depression is the term applied when severe episodes of depression occur, but the individual has never experienced a manic or hypomanic episode. Cyclothymic disorder manifests both depression and elevations, but severity is insufficient for the diagnosis of bipolar disorder. Persistent depressive disorder is a chronic condition of depressed mood; this may indicate a major depressive disorder which has incompletely resolved, or a long term condition which has never reached the diagnostic criteria for major depressive disorder. Last modified: November, 2015 9 Non-psychotic disorders The non-psychotic disorders are, in general, what Freud referred to as the “neuroses”. The symptoms of the psychotic disorders such as hallucinations and delusions are largely unknown to healthy individuals. However, the symptoms of the non-psychotic disorders are known to us all, at least to some degree. These include anxiety, which is similar to worry and fear - in a mild form, this is familiar to everyone who has taken an exam or been out on a first date. Generalized anxiety disorder is characterised by continuous, unprovoked anxiety. Panic disorder is characterized by sudden attacks of extreme anxiety during which the patient may struggle to get enough air, feel the heart thumping as if to burst, and fear that he/she may collapse or die. The phobic disorders (or phobias) are characterized by episodes of anxiety which is out of proportion to the danger of a particular situation. In agoraphobia, anxiety is triggered by the thought of leaving the home, and this may worsen if the home is left. In special phobias, anxiety increases at the thought of meeting a feared, specific agent or circumstance (spiders or lifts, for example), and life may be disrupted by the steps taken to avoid those agents or circumstances. Obsessive-compulsive disorder (OCD) is a curious, disabling condition. Obsessions are repetitive thoughts which make no sense. Patients (usually) accept that these are their own thoughts, but are unable to stop them. For example, the patient may have the irrational and unwelcome thought that his/her hands are contaminated by dirt or germs, alternatively, the patient may be dogged by the irrational thought that he/she “killed God”. The patient is distressed by the loss of control and the “silliness” of his/her thought. Compulsions are repetitive actions or urges in which the patient engages. Sometimes the compulsions relate to obsessions, as when the thought is that the hands are dirty and so the hands must be washed. But the compulsion may be that the hands must be washed 10 times, when washing once would be enough. In other cases, compulsions may have no relationship with obsessions, as for example, when the patient feels anxious or uncomfortable until something is performed “correctly”; it may be that when walking into a room, night or day, the light switch must be flicked a certain number of times. The Trauma- and Stressor-Related Disorders include the well-publicised Post traumatic stress disorder (PTSD) which follows exposure to a traumatic event, particularly protracted traumatic events such as involvement in war, but sometimes following briefer, severe stress, such as rape. The Feeding and Eating Disorders is a puzzling group of conditions, the best known being anorexia nervosa and bulimia nervosa. In anorexia nervosa there is purposeful weight loss through restriction of eating, excessive exercise and sometimes purging and vomiting. In spite of emaciation and threat to life, there may be the conviction of being fat, which cannot be dispelled by the use of scales, mirrors or photographs. In bulimia nervosa there are episodes of binge eating and compensatory behaviour to prevent weight gain, such as purging and vomiting. Last modified: November, 2015 10 The Somatic Symptom and Related Disorders present with somatic symptoms associated with significant distress and impairment.

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A study by Langdon et al (2011) found olfactory hallucinations in 15% of patients with schizophrenia purchase ipratropium master card treatment x time interaction, and some patients with social anxiety and depression buy ipratropium 20mcg with amex symptoms 2 months pregnant. The authors suggested that people are more reluctant to talk about smells than voices purchase ipratropium 20mcg with amex medicine 93 2264, and that this type of hallucination may be more common than is generally accepted. Autoscopic (self see) hallucinations are the visual experience of the subject/patient seeing an image of him/herself (or parts of him/herself). This is a rare symptom which takes many forms, and is mentioned only as a curiosity – no student will fail an exam through unfamiliarity with autoscopic hallucinations. Autoscopic hallucinations occur more frequently in neurological disorders (Dening & Berrios, 1994), but can occur in psychotic disorders and stressful situations. Illusions are perceptions that are associated with an outside stimulus, but the stimulus is wrongly interpreted. For example, lapping water may be heard as laughter. Technically, illusions are not hallucinations, because they are associated with a stimulus. Illusions are frequently visual, and they are usually the result of a neurological disorder. The condition which most commonly causes illusions is delirium tremens (DTs), the disturbed state which can complicate alcohol withdrawal. Objects such as creases in bed covers may be perceived as snakes, insects or other animals. Folk law says that people in DTs see “pink elephants”. In clinical practice, however, small organisms are more commonly “seen”. Other perceptual difficulties include heightened and changed perceptions. By heightened perceptions is meant sounds seem unnaturally clear, loud or intense, colours appear more brilliant or beautiful, or details of the environment seem to stand out in a particularly interesting way. By changed perceptions is meant changes are perceived in the shape or size of people and inanimate objects in the environment. These phenomena may occur in psychotic disorders; on occasions psychotic patients may be difficult to engage in conversation because they are distracted by continuously changing perceptions. Patients may spend long periods looking in a mirror, watching their own face change. Heightened and changed perceptions may occur in other disorders, including the non-psychotic, anxiety disorders. Summary: Circumstances and disorders associated which hallucinations. Circumstances and disorders in which hallucinations may be experienced. Neuroimaging Hallucinations in schizophrenia have been studied using a range of neuroimaging techniques. Not surprisingly, both the Wernicke (left superior temporal gyrus; STG) and the Broca (left inferior frontal gyrus; IFG) speech areas have been implicated. In groups of people with schizophrenia who experience auditory hallucinations, a significant reduction in the volume of the left STG has been demonstrated (Sun et al, 2009). Also, significantly increased activity has been demonstrated in left STG, IFG, the anterior cingulate cortex, and the parahippocampal gyrus (Allen et al, 2008; Northoff & Quin, 2011). Recent theory is that the auditory hallucinations in schizophrenia are due to disruption of connections between the frontal and termporo-pariental language areas. Using diffusion tensor imaging (DTI) and magnetic transfer imaging (MTI), de Weijer et al (2011) studied the arcuate fasciculus and 3 other white matter tracts (cortical spinal tract, cingulum, and uncinate fasciculus) in people with schizophrenia and severe hallucinations. Consistent with theory, they found abnormalities in all fibre tracts, and a correlation with both DTI and MTI findings in the arcuate fasciculi and the severity of positive symptoms. The following illustrations are presented as a reminder of the anatomy of these tracts. Illustration: This diffusion tensor imaging (DTI) image (generously provided for public use by Aaron G. Filler, MD, PhD) shows the right and left arcuate fasciculus (Raf & Laf), and the right and left superior longitudinal fasciculus (Rslf & Lslf) as separate entities (they can be conceptualized as continuous). A recent meta-analysis of functional imaging studies of people with schizophrenia and auditory hallucinations (Geoffroy et al, 2014) confirmed disruptions of the white matter integrity in the left arcuate fasciculus. Using positron emission tomography (PET), they compared patients with commenting auditory hallucinations to patients without auditory hallucinations. Patients with auditory hallucinations demonstrated significantly increased metabolic rates in the left superior and middle temporal cortices, bilateral medial frontal cortex and the left caudate nucleus. In addition, there was decreased activity in the hippocampal-parahippocampal, cerebellar and parietal cortices during hallucinations. This work suggests that failure to deactivate the temporal cortex allows increased spontaneous activity, and auditory hallucinations. It is possible that decreased activity in hippocampus-parahippocampal gyrus and possibly the cerebellum allows the increased spontaneous activity of the temporal cortex. Horga et al (2011) drew attention to a possible central role for the caudate, in auditory hallucinations. Recent work (Amad et al, 2013) suggests abnormal connectivity patterns, involving the hippocampus, in people with schizophrenia and visual hallucinations. Whitford et al (2014) studied the brains of people with schizophrenia in a similar manner to de Weijer et al (2011), above. The cingulum is a bundle of white matter fibres in the cingulate gyrus, extending from the subgenual region of the anterior cingulate around the corpus callosum and on to the parahippocampal gyrus and uncus (raised cortex overlying the amygdala) of the temporal lobe. It sends off extensions and functions as a communications system between components of the (grey matter) limbic system. Whitford et al (2014) wished to substantiate that the cingulate bundle is, in fact, a series of sub-connections, and to identify which, if any are faulty in schizophrenia. They identified 5 (at least) sub-connections and one of these, which connects the rostral (front) and caudal (back) regions of the anterior cingulate gyrus was abnormally constructed (Fractional Anisotropy (FA)) in people experiencing psychosis (delusions and hallucinations). They also identified a separate sub-connection which was abnormally constructed in people experiencing negative symptoms of schizophrenia (this will be further discussed in Chapter 7). The primary auditory cortex is a bilateral region located on the upper sides of the temporal lobes (within the lateral sulcus) and extending into the lateral fissure of the temporal lobe – in old terminology, in Brodmann areas 41, 42 and 22. A recent study (Wigand et al, 2015) of this interhemispheric pathway in schizophrenia patients with verbal hallucinations concluded that this symptom was the result of microstructural changes in the interhemispheric auditory pathway. Case histories Case history: 1 Cynthia Campbell was 17 years of age and attended a local Catholic school. She lived with her parents and 15 year old sister, Melissa, in a middle class suburb of a large city. Her only other sibling, Libby, was older, in the Army, and stationed overseas.

Macromolecular synthesis inhibi- Creatine may exert neuroprotective effects by increasing tors and NMDA antagonists blocked cell death purchase ipratropium without a prescription treatment endometriosis, suggesting phosphocreatine levels or stabilizing the MPT buy discount ipratropium line symptoms kidney disease, either of that an activity-dependent emergence of excitotoxicity con- which could mitigate excitotoxicity mediated by GluRs discount 20mcg ipratropium visa medicine dictionary. Cultured rat hippocampal Altered expression or composition of iGluR subunits neurons pretreated with BDNF exhibited increased levels may also contribute to neuronal death in HD. The editing of NR1 and NR2A, greater calcium responses to NMDA, of GluR2 mRNA is compromised in a region-specific man- and enhanced vulnerability to excitotoxic necrosis and re- ner in HD as well as in schizophrenia and AD, although duced vulnerability to apoptosis (164). Cultured cerebellar there is still a large excess of edited GluR2 in each of these granule cells, which show primarily an apoptotic death fol- disorders (171). Chen and co-workers found that coexpres- lowing KA treatment, undergo necrosis when L-type volt- sion of huntingtin containing 138 repeats with NMDA re- age-dependent calcium channels are blocked (147). Striatal spiny neurons are GLUTAMATE AND BRAIN DISORDERS selectively vulnerable in HD and ischemia, whereas large aspiny (LA) cholinergic interneurons of the striatum are Neurodegenerative Diseases spared in these pathologic conditions. Because NR1/NR2B HD is an autosomal dominant, progressive neurodegenera- is the predominant NMDA receptor expressed in medium tive disease that typically has its symptomatic onset in mid- spiny neostriatal neurons, this may contribute to the selec- life. Its manifestations include chorea, dementia, and death tive vulnerability of these neurons in HD (172). Afflicted individuals have an and associates found that membrane depolarization and in- expanded CAG repeat in the gene encoding huntingtin on ward currents produced by AMPA, KA, and NMDA were 80 Neuropsychopharmacology: The Fifth Generation of Progress much larger in spiny neurons than LA interneurons (173); ies have shown that ROS generated by A peptide inhibits moreover, concentrations of agonists producing reversible astrocyte glutamate uptake (181,182). The striatal and cortical neu- projection neurons in the hippocampus express iGluR sub- rons of R6/2 mice and mice with 94 CAG repeats displayed units from each receptor class; however, regional differences more rapid and increased swelling following NMDA treat- in immunoreactivity were apparent in AD versus normal ment than controls, whereas AMPA and KA treatments had brain. These findings suggest that NMDA GluR2(4), GluR5/6/7, and NR1 were reduced, presumably antagonists or compounds that alter sensitivity of NMDA owing to cell loss (183). In contrast, GluR2(4) immuno- receptors may be useful in the treatment of HD (174). The selective group I mGluR agonist autoradiography was also used to measure the laminar distri- 3,5-DHPG strongly enhanced membrane depolarization bution of NMDA and AMPA receptors in three areas of and intracellular calcium accumulation induced by NMDA visual cortex in control and AD postmortem human brains. Hyman and played decreased expression of AMPA- and KA- but not colleagues found no difference for the pattern of immuno- NMDA-type iGluR receptors compared to age-matched lit- staining between control and AD in either hippocampi or termate controls. These mice also had decreased expression adjacent temporal cortices for GluR1, GluR2/3, and GluR4 of mGluR1-3 that preceded the appearance of motor symp- (185); however, age-related loss of GluR2/3 immunoreac- toms; therefore, altered mGluR function may contribute to tivity prior to degeneration has been reported in nucleus subsequent pathology (176). Mac- receptors may leave these neurons vulnerable to degenera- Donald and associates examined a TAA repeat polymor- tion in AD. Western blot analysis revealed average reduc- phism, which is closely linked to the GluR6 gene, in 258 tions of approximately 40% for GluR1 and GluR2/3 in the unrelated HD-affected persons and found that younger entorhinal cortex of patients with AD pathology versus age- onset age of HD was associated with linkage disequilibrium matched controls, but neither GluR1 nor GluR2/3 protein for this polymorphism (177). Rubinsztein and co-workers concentration correlated significantly with tangle density found that 13% of the variance in the age of onset of HD (188). Thus, the relationship between excitotoxicity and that was not accounted for by the CAG repeat size could neuronal loss in AD is complex and requires additional in- be attributed to GluR6 genotype variation (178). Death results from compli- acterized by a cortical neurodegeneration, particularly in the cations of the progressive paralysis. The two forms of ALS, entorhinal cortex, hippocampal CA1 region, and subicu- sporadic and familial (FALS), have similar clinical symp- lum. The etiology of AD is complex, with age, trauma, toms and neuropathology, although the latter only accounts health, and environmental and genetic factors all playing a for 10% of the cases. Mutations Cu/Zn superoxide dismutase (SOD1), and identified 11 in the presenilin-1 (PS1) gene are causally linked to many different SOD1 missense mutations in 13 different FALS cases of early-onset inherited autosomal dominant AD. Expression of high levels of a mutant form Mice transgenic for the PS1M146V gene are hypersensitive of human SOD1 for which the glycine at position 93 was to seizure-induced synaptic degeneration and necrotic neu- replaced with an alanine (G93ASOD1; a change that has ronal death in the hippocampus (180). Cultured hippocam- little effect on enzyme activity) caused a progressive motor pal neurons from PS1M146V knock in mice display in- neuron disease resulting in death by 6 months in transgenic creased vulnerability to glutamate, which is correlated with mice (191). Because the mouse gene for SOD1 is unaffected perturbed calcium homeostasis, increased oxidative stress, in the transgenic mice, the results indicate that these muta- and mitochondrial dysfunction. Glutamate toxicity is po- tions in SOD1 cause a gain-of-function that results in motor tentiated by ROS mediated inhibition of EAATs; two stud- neuron death. Chapter 6: L-Glutamic Acid in Brain Signal Transduction 81 The reason for the selective vulnerability of motor neu- inotropic non–NMDA receptors may be of value in the rons in ALS is unknown. Various molecular and neuro- treatment of motor neuron disease (198). Further research chemical features of human motor neurons may render this may allow the development of therapies that target specific cell group differentially vulnerable to such insults. Motor neurons have a very high expression of the cytosolic free radical scavenging enzyme Cu/ZnSOD1, which may render SCHIZOPHRENIA this cell group more vulnerable to genetic or posttransla- tional alterations interfering with the function of this pro- Kim and associates reported diminished concentrations of tein. The low expression of calcium binding proteins and glutamate in CSF of patients with schizophrenia and first GluR2 AMPA receptor subunit by vulnerable motor neuron proposed that hypofunction of glutamatergic systems might groups may render them unduly susceptible to calcium- cause the disorder (199). This finding has been replicated mediated toxic events following GluR activation (192). In a High levels of mRNA for GluR1, GluR3, and GluR4 are postmortem study, Tsai and associates (140) studied eight expressed in normal human spinal motor neurons; however, brain regions and found decreased concentrations of gluta- GluR2 subunit mRNA was not detectable in this cell group, mate and aspartate in the frontal cortex and decreased con- predicting that normal human spinal motor neurons express centration of glutamate in the hippocampus of patients with calcium-permeable AMPA receptors unlike most neuronal schizophrenia as compared to controls. Furthermore, the groups in the human CNS (193); however, this has not been concentration of NAAG was increased in the hippocampus borne out in studies of mouse spinal cord in the context of and the activity of GCPII was selectively reduced in the the mouse models of ALS, where GluR2 is well represented frontal cortex, temporal cortex, and hippocampus of people in spinal cord motor neurons (194). Subsequent studies with magnetic reso- sure triggers substantial mitochondrial calcium loading in nance spectroscopy have revealed significant reductions in motor neurons, but causes little mitochondrial accumula- the level of N-acetylaspartate (NAA), the product of NAAG tion in forebrain GABAergic interneurons, neurons that ex- by GCPII, in the very same regions—frontal cortex, tem- press large numbers of calcium-permeable AMPA/kainate poral cortex, and hippocampus (204). Brief exposure to Initial ligand binding studies in postmortem schizo- either AMPA or kainate caused mitochondrial depolariza- phrenic brain have revealed increases in the non–NMDA tion in motor neurons, whereas these effects were only ob- iGLURs in the prefrontal cortex (205,206) and decreases served in the GABAergic neurons after exposure to the non- in the hippocampus (207,208). Strychnine-insensitive desensitizing AMPA receptor agonist kainate. Finally, binding, which labels the glycine modulatory site on the blocking mitochondrial calcium uptake attenuated AMPA/ NMDA receptor, is increased throughout the primary sen- kainate receptor-mediated motor neuron injury. Thus, mi- sory cortex and related associational fields in schizophrenia tochondrial calcium uptake and consequent ROS genera- (209). Molecular approaches have shown a reduction in tion may be central to the injury process (195). Quantifica- mRNA encoding luR2 in the hippocampus and parahippo- tion of mRNA expression in spinal cord showed a significant campus of people with schizophrenia, and reduced editing widespread loss of NR2A from both dorsal and ventral of GluR2 in the prefrontal cortex (210,211). Although the horns with losses of 55% and 78%, respectively, in ALS as density of NMDA receptors in the prefrontal cortex of peo- compared to control. These results were substantiated by ple with schizophrenia was normal, the relative subunit analysis of spinal cord homogenates, which showed a signifi- composition differed significantly from controls with a large cant total decrease of 50% in NR2A message for ALS as increase observed for NR2D (212). A convincing link between glutamatergic dysfunction Riluzole, which attenuates the glutamate neurotransmit- and schizophrenia came from anecdotal and subsequent ter system, has been shown to prolong survival in patients controlled studies of the neuropsychologic effects of disso- with ALS (197). Riluzole affects neurons using three mecha- ciative anesthetics, which are noncompetitive antagonists of nisms: by inhibiting excitatory amino acid release, inhibit- the NMDA receptor (213). When chronically abused, PCP ing events following stimulation of iGluRs, and stabilizing produces a syndrome in normal individuals that closely re- the inactivated state of voltage-dependent sodium channels. Subanesthetic doses of keta- tor subtypes and the effect of chronic treatment with NBQX mine administered to normal subjects produces positive in the spinal cord of motor neuron disease (mnd) mice. These findings suggest that selective antagonism of characteristic of schizophrenia (214). When administered 82 Neuropsychopharmacology: The Fifth Generation of Progress to schizophrenic subjects, subanesthetic doses of ketamine nist at the glycine modulatory site with 60% efficacy and exacerbate delusion, hallucinations, and thought disorders readily crosses the blood–brain barrier (230). These effects are attenuated by ics and exhibiting prominent negative symptoms revealed the atypical antipsychotic clozapine but not haloperidol.


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In hereditary or acquired AM E cheap ipratropium amex symptoms influenza, 11 -H SD is defective or is inactiveted (by licorice or carbenoxalone) generic ipratropium 20 mcg visa symptoms for bronchitis. Cortisol best ipratropium 20mcg adhd medications 6 year old, which is present at concentrations approxim ately 1000-fold that of aldosterone, becom es a m ineralocorticoid. The hyperm ineralo- corticoid state results in increased transcription of subunits of the sodium channel and the N a+-K+-ATPase pum p. The favorable elec- trochem ical gradient then favors potassium secretion [7,15]. These enzymes have identical intron-extron structures and are closely linked on chromosome 8. The chimeric gene is now under the contol of ACTH, and aldosterone secretion is enhanced, thus causing hypokalemia and hypertension. By inhibiting pituitary release of ACTH, glucocorticoid administration leads to a fall in aldosterone levels and correction of the clinical and biochemical abnormalities of GRA. The presence of Aldo S activity in the FIGURE 3-17 zona fasciculata gives rise to characteristic ele- Genetics of glucocorticoid-remediable aldosteronism (GRA): schematic representation of vations in 18-oxidation products of cortisol unequal crossover in GRA. The genes for aldosterone synthase (Aldo S) and 11 -hydroxylase (18-hydroxycortisol and 18-oxocortisol), (11 -OHase) are normally expressed in separate zones of the adrenal cortex. Hypokalemia: Clinical M anifestations CLINICAL M ANIFESTATIONS OF HYPOKALEM IA Cardiovascular Renal/electrolyte Abnormal electrocardiogram Functional alterations Predisposition for digitalis toxicity Decreased glomerular filtration rate Atrial ventricular arrhythmias Decreased renal blood flow Hypertension Renal concentrating defect Neuromuscular Increased renal ammonia production Smooth muscle Chloride wasting Constipation/ileus Metabolic alkalosis Bladder dysfunction Hypercalciuria Skeletal muscle Phosphaturia W eakness/cramps Structural alterations Tetany Dilation and vacuolization of Paralysis proximal tubules Myalgias/rhabdomyolysis Medullary cyst formation Interstitial nephritis Endocrine/metabolic Decreased insulin secretion Carbohydrate intolerance Increased renin FIGURE 3-19 Decreased aldosterone Electrocardiographic changes associated with hypokalemia. A, The Altered prostaglandin synthesis U wave may be a normal finding and is not specific for hypokalemia. Growth retardation B, W hen the amplitude of the U wave exceeds that of the T wave, hypokalemia may be present. The QT interval may appear to be prolonged; however, this is often due to mistaking the QU interval for the QT interval, as the latter does not change in duration with FIGURE 3-18 hypokalemia. C, Sagging of the ST segment, flattening of the T wave, and a prominent U wave are seen with progressive hypokalemia. D, The QRS complex may widen slightly, and the PR interval is often prolonged with severe hypokalemia. Hypokalemia promotes the appearance of supraventricular and ventricular ectopic rhythms, especially in patients taking digitalis. The predom inant pathologic finding accom pa- nying potassium depletion in hum ans is vacuolization of the epithelium of the proxim al convoluted tubules. The vacoules are large and coarse, and staining for lipids is usually negative. The tubular vacuolation is reversible with sustained correction of the hypokalem ia; however, in patients with long-standing hypokalem ia, lym phocytic infiltra- tion, interstitial scarring, and tubule atrophy have been described. Increased renal am m o- nia production m ay prom ote com plem ent activation via the alternate pathway and can contribute to the interstitial nephritis [17,18]. Hypokalemia: Treatment FIGURE 3-21 Treatment of hypokalemia: estimation of potassium deficit. In the absence of stimuli that alter intracellular-extracellular potassium dis- tribution, a decrease in the serum potassium concentration from 3. Factors such as the rapidity of the fall in serum potassium and the presence or absence of symptoms dictate the aggressiveness of replacement therapy. In general, hypokalemia due to intracellular shifts can be managed by treating the underlying condition (hyperinsulinemia, theophylline intoxica- tion). Hypokalemic periodic paralysis and hypokalemia associated with myocardial infarction (secondary to endogenous -adrenergic agonist release) are best managed by potassium supplementation. Hyperkalemia: Diagnostic Approach either leukocytes or platelets results in leak- age of potassium from these cells. Fam ilial pseudohyperkalem ia is a rare condition of increased potassium efflux from red blood cells in vitro. Ischem ia due to tight or prolonged tourniquet application or fist clenching increases serum potassium con- centrations by as m uch as 1. H yperkalem ia can also result from decreases in K m ovem ent into cells or increases in potassium m ovem ent from cells. H yper- chlorem ic m etabolic acidosis (in contrast to organic acid, anion-gap m etabolic acidosis) causes potassium ions to flow out of cells. H ypertonic states induced by m annitol, hypertonic saline, or poor blood sugar con- trol prom ote m ovem ent of water and potas- sium out of cells. Depolarizing m uscle relax- ants such as succinylcholine increase perm e- ability of m uscle cells and should be avoided by hyperkalem ic patients. The m echanism of hyperkalem ia with -adrenergic blockade FIGURE 3-23 is illustrated in Figure 3-3. Digitalis im pairs Approach to hyperkalem ia: hyperkalem ia without total body potassium excess. Spurious function of the N a+-K+-ATPase pum ps and hyperkalem ia is suggested by the absence of electrocardiographic (ECG) findings in patients blocks entry of potassium into cells. The m ost com m on cause of spurious hyperkalem ia is fluoride intoxication can be treated with hem olysis, which m ay be apparent on visual inspection of serum. For patients with extrem e cation-exchange resins or dialysis, as leukocytosis or throm bocytosis, potassium levels should be m easured in plasm a sam ples attem pts at shifting potassium back into that have been prom ptly separated from the cellular com ponents since extrem e elevations in cells m ay not be successful. N orm okalem ia can be m aintained in patients who consum e norm al quantities of potassium until GFR decreases to less than 10 m L/m in; however, dim inished GFR predisposes patients to hyperkalem ia from excessive exogenous or endogenous potassi- um loads. H idden sources of endogenous and exogenous potassium — and drugs that pre- dispose to hyperkalem ia— are listed. FIGURE 3-25 Approach to hyperkalemia: hyporeninemic hypoaldosteronism. Hyporeninemic hypoal- dosteronism accounts for the majority of cases of unexplained hyperkalemia in patients with reduced glomerular filtration rate (GFR) whose level of renal insufficiency is not what would be expected to cause hyperkalemia. Interstitial renal disease is a feature of most of the diseases listed. Although the transtubular potassium gradient should be low in both disorders, exogenous mineralocorticoid would normal- ize transtubular potassium gradient in hyporeninemic hypoaldosteronism. Secretion of potassium in the cortical collecting duct and outer medullary collecting duct accounts for the vast majority of potassium excreted in the urine. Potassium secretion in these segments is influenced mainly by aldosterone, plasma potassi- um concentrations, and the anion composition of the fluid in the lumen. Use of the TTKG assumes that negligible amounts of potassi- um are secreted or reabsorbed distal to these sites. The final urinary potassium concentration then depends on water reabsorption in the medullary collecting ducts, which results in a rise in the final urinary potassium concentration without addition of significant amounts of potassium to the urine. The TTKG is calculated as follows: TTKG = ([K+]urine/(U/P)osm )/[K+]plasm a The ratio of (U/P)osm allows for “correction” of the final urinary potassium concentration for the am ount of water reabsorbed in the medullary collecting duct. In effect, the TTKG is an index of the gradient of potassium achieved at potassium secretory sites, indepen- dent of urine flow rate. The urine must at least be iso-osmolal with respect to serum if the TTKG is to be meaningful.

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