By J. Tragak. New School University. 2018.
Common causes of hyponatremia are – Pure water loss (in renal diabetes insipidus and external insensible losses via the skin and lungs) cheap zenegra 100mg overnight delivery. When volume depletion with circulatory insufficiency is predominant generic 100 mg zenegra with mastercard, vigorous treatment with isotonic saline solution is mandatory order 100mg zenegra. When the cause is diabetes insipidus zenegra 100 mg without prescription, administer 2-5 units of aqueous vasopressin, or 1-5 mcg of desmopressin (DDAVP) should be given subcutaneously or intranasally. When hypernatremia is due to excessive gain, hypotonic (0. Hyponatremia: Three types of hyponatremia are described: Hypovolemic hyponatremia: patients with low intake of sodium- containing fluids and have attempted replacement with free water may present with encephalopathy. Hypervolemic hyponatremia: usually seen in congestive heart failure or hypoalbuminemia. This condition can be treated with fluid restriction, a wise use of diuretics as well as treatment of the primary cause. Euvolemic hyponatremia: This condition is seen in syndromes of inappropriate secretion of ADH (SIADH) adrenal insufficiency, hypothyroidism, severe psychogenic polydipsia, and Medical Diseases and Metabolic Encephalopathies | 105 hypoglycemia; also in pancreatitis with hyperlipidemia and hyperproteinemia. The degree of encephalopathy produced by hyponatremia depends on the rate of fall of serum sodium rather than its value. All cases of euvolemic hyponatremia are treated with fluid restriction (800-1000 ml/d) and removal of precipitants (Young 1998). Central pontine myelinolysis (CPM): Due to rapid correction of hyponatremia by more than 10 meq/d. Clinically, patients present with quadriparesis and cranial nerve dysfunction over several days, which may be followed by encephalopathy. The maximal lesion is seen in the basis pontis, but supratentorial white matter is also affected. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH): It is a common syndrome in neurological diseases; it leads to hyponatremia and increases salt concentration in urine (>20 mmoI/L). Causes of SIADH include – Malignant neoplasms likes oat-cell carcinoma of lung, and Hodgkin disease – Non-malignant pulmonary diseases, e. Slow correction of hyponatremia by IV 3% sodium solution is recommended. IV 100 cc given over one-hour interval, until serum sodium level reach 125 mmol/l. Hypercalcemia: The encephalopathy of hypercalcemia is not different from any metabolic encephalopathy except in early anosmia. Patients start to complain at serum calcium level of 13 mg/dl, when abnormal EEG changes start to appear. Patients suffering from hyperparathyroidism may manifest seizures independent of serum calcium level due to elevated serum parathormone. Management: Hypercalcemia is corrected by saline diuresis, augmented with furosemide, followed by a choice of mithramycin steroids, phosphate or etidronate. Encephalopathy in Diabetic Patients Hypoglycemia: Clinically, patients who develop hypoglycemia are graded: – At 20 mg/dl, immediate loss of consciousness in adults and children, neonates resist hypoglycemia better, – At 45 mg/dl, confusion, irritability. Sometimes unexplained focal lesions appear with hypoglycemia. Nonketotic hyperosmolar hyperglycemia (NHH): Usually occurs in diabetic patients whose insulin production is adequate to inhibit lipolysis, but insufficient to prevent hyperglycemia, which result in a marked osmotic diuresis. In such situations, serum glucose may rise to 800-1200 mg/dl, and serum osmolarity may exceed 350 mOsm/L, which may invite development of brain edema. Management: Normal saline is infused slowly to correct hypotension and improve osmolality, in addition to insulin Medical Diseases and Metabolic Encephalopathies | 107 infusion at the rate of 10 IU/h, with regular checking of plasma glucose, since these patients are very sensitive to insulin. Glucose should be added to saline when plasma glucose is approximately 300 mg/dl (Quinn 2002). Diabetic ketoacidosis (DKA): About 80% of DKA patients have encephalopathy and 10% are comatose.
It has long been observed that there is a relationship between Alcohol dependence is often comorbid with other psychiat- smoking and alcoholism generic 100mg zenegra amex. More than 80% of alcoholics ric disorders quality 100mg zenegra, including drug abuse cheap zenegra 100 mg amex, major depression (MD) zenegra 100 mg with amex, smoke cigarettes and 70% are heavy smokers, compared anxiety disorders (ADs), and bulimia nervosa (BN), or anti- with 30% of the general population who smoke and 10% social personality disorder (ASPD) (17,18). In a multivariate genetic analysis currence is more common among women than men and is of the use of tobacco and alcohol in 774 MZ and 809 DZ positively associated with the persistence of alcohol depen- male and female twin pairs from the Virginia Twin Registry, dence in both men and women (18). Population comorbid- the univariate heritability of alcohol consumption was 0. Tobacco use had epidemiologic studies is their ability to detect evidence of a stronger loading on this shared genetic factor (0. However, the precise level of coexist in the same individuals, usually male. The relative the co-inheritance is less certain than the existence of co- risk of alcoholism is significantly increased in males with inheritance, and the level of genetic sharing may depend either ASPD, attention-deficit/hyperactivity disorder, or on how the phenotypes are determined. In an analysis of childhood conduct disorder, and there is evidence of co- 2,220 MZ and 2,373 DZ U. These data notwithstanding, a alcohol genetic factor accounted for 0. A study opioids are enhanced by activation of (and possibly also of 3,356 male twin pairs from the U. Registry found a substantial genetic correlation (r 0. Of the total vari- paminergic, opioid peptide, and serotoninergic neurotrans- ance in risk for alcohol dependence, 0. In contrast to opioids, which bind to specific receptors, ethanol appears to act on a variety of targets THE NEUROBIOLOGY OF ALCOHOL within the cell membrane in a less specific manner, inducing ADDICTION effects on neurotransmitter and neurohormone membrane receptors and receptor-gated and voltage-activated ion The essential features of addiction are loss of control over channels as well as modulating neurotransmitter release consumption, compulsion to obtain the next stimulus, and (34). Alterations in calcium channels may be a major com- continuation of abuse despite knowledge of negative health ponent of the changes that occur in the physical dependence and social consequences. Processes of reward and reinforcement GABA is the major inhibitory neurotransmitter in brain. It is likely that genetic variation in this neurobi- GABAA receptors are the primary site of action of benzodi- ology predisposes some individuals to a pattern of increased azepines and barbiturates, which are used in the treatment craving and loss of control. However, a path- of the glutamatergic neurotransmitter pathways, especially way that appears to be crucial to the action of all addictive at the level of the postsynaptic N-methyl-D-aspartate drugs is the mesolimbic dopamine system, which originates (NMDA) receptor, may be an important cause of its neu- in the ventral tegmental area (VTA) of the midbrain and rotoxic effects (36). Glutamate is the major excitatory brain projects to the nucleus accumbens (NAC), with projections neurotransmitter with up to 40% of all synapses being gluta- also to the limbic system and the orbitofrontal cortex (28). The mesolimbic in disinhibition of forebrain glutamatergic neurons that dopamine pathway is associated with the ability to feel plea- augment dopamine release (37). Serotoninergic neurons originating in the dorsal and receptor system may underlie intoxication and withdrawal median raphe nuclei project to mesolimbic structures, in- symptoms (38) as well as 'blackouts' (36). Homotarrine cluding the VTA and NAC, and may exert inhibitory con- (Acamprosate), a structural analogue of glutamate and an trol on mesolimbic dopamine neuron activity (29) (see NMDA-receptor antagonist, has been shown to almost dou- Chapter 95). Alcohol, psychostimulants, opiates, and nicotine (as well Some of the rewarding effects of ethanol result from acti- as tetrahydrocannabinol and phencyclidine) exert their pri- mary reinforcing or reward effects by releasing dopamine vation of opioid receptors in the VTA and/or receptors (DA) in the NAC. The acute reinforcing actions of psycho- in the NAC by the ethanol-induced release of endogenous stimulant drugs is mediated both by the blockade of DA -endorphin from terminals of the VTA and NAC as well binding to its transporter, preventing the reuptake of DA as release of enkephalins from intrinsic enkephalin neurons from the synaptic cleft (20), and by interaction with multi- in the NAC (34). The success of the opioid antagonist nal- ple DA receptors including D1, D2, and D3 (28). Cocaine trexone in modifying drinking behavior, controlling craving blocks the reuptake of serotonin (5-HT) and norepineph- and preventing relapse in alcoholics indicates that opioid rine in a similar fashion. A functional down-regulation of receptor-mediated mechanisms are activated by alcohol (34, 5-HT3 receptors in the NAC may contribute to cocaine 40). Chronic cocaine and (27) may relate to the finding that ethanol enhancement of alcohol administration also disrupts the endogenous opioid DA release in the NAC appears to require activation of system (20).
Pascual J purchase 100 mg zenegra with visa, Liaño F 100 mg zenegra with amex, the M adrid ARF Study Group: Causes and prog- 20:5–78 purchase zenegra 100 mg free shipping. Gerrard JM buy zenegra 100 mg with visa, Catto GRD, Jones M C: Acute renal failure: An iceberg 46:1–5. Kleinknecht D: Epidem iology of acute renal failure in France today. Acute Renal Failure Conference, In Acute Renal Failure in the Intensive Therapy Unit. Chugh S, Sakhuja V, M alhotra H S, Pereira BJG: Changing trends in of acute renal failure in Kuwait: A 2-year prospective study. J Trop acute renal failure in Third-W orld countries— Chandigarh study. Seedat YK, N athoo BC: Acute renal failure in blacks and Indians in prospective study on incidence and outcom e (Abstract). N ephron 1993, Congress of EDTA-ERA, Paris, 1992, p 54. Sanchez Rodrìguez L, M artÌn Escobar E, Lozano L, et al. Feest TG, Round A, H am ad S: Incidence of severe acute renal failure 17. Br M ed J 1993, com e of hospital-acquired acute renal failure. Lauzurica R, Caralps A: Insuficiencia renal aguda producida en el 29. M ed ClÌn organ failure assessm ent) score to describe organ dysfunction/failure. Liaño F, Solez K, Kleinknecht D: Scoring the patient with ARF. Liaño F, Pascual J: Acute renal failure, critical illness and the artificial Critical Care N ephrology. Doum a CE, Redekop W K, Van der M eulen JH P, et al. Kierdorf H , Sieberth H G: Continuous treatm ent m odalities in acute m ortality in intensive care patients with acute renal failure treated renal failure. Knaus W A, Draper EA, W agner DP, Zim m erm an JE: APACH E II: A 32. Viviand X, Gouvernet J, Granthil C, Francois G: Sim plification of the severity of disease classification system. Crit Care M ed 1985, SAPS by selecting independent variables. Bion JF, Aitchison TC, Edlin SA, Ledingham IM : Sickness scoring and system: Risk prediction of hospital mortality for critically ill hospitalized response to treatm ent as predictors of outcom e from critical illness. Chew SL, Lins RL, Daelem ans R, De Broe M E: O utcom e in acute score for ICU patients. Liaño F: Severity of acute renal failure: The need of m easurem ent. Le Gall, Lem eshow S, Saulnier F: A new Sim plified Acute Phisiology N ephrol D ial Transplant 1994, 9(Suppl. Score (SAPS II) based on a European/N orth Am erican m ulticenter study. Bonom ini V, Stefoni S, Vangelista A: Long-term patient and renal prognosis in acute renal failure. Turney JH : W hy is m ortality persistently high in acute renal failure? Knaus W A, Draper EA, W agner DP, Zim m erm an JE: Prognosis in APACH E II en el fracaso renal agudo de las unidades de cuidados acute organ-system failure.
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