Ebook Oh''s intensive care manual (7/E): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Oh''s intensive care manual (7/E): Part 2
Ebook Oh''s intensive care manual (7/E): Part 2
Part EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2Insufficiency in Critical Illness 66062Acute Calcium Disorders 66658Diabetic emergenciesRichard KeaysDiabetes mellitus is due to an absolute or relative deficiency of insulin. Die sustained effect of poor glycaemic control results 111 a wide array of end-organ damage as a consequence of small- and l Ebook Oh''s intensive care manual (7/E): Part 2arge-vessel pathology. Mortality and morbidity are related to the progress ot this damage but often there are acute metabolic deteriorations that canEbook Oh''s intensive care manual (7/E): Part 2
lie hfe-threatening. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are two of the most common acute complications of diabetePart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2ed state. Coma may also result from severe hypoglycaemia due to overtreatment - usually with insulin.DIABETES MELLITUSTvpe I insulin-dependent diabetes mellitus (IDDM) has a peak incidence in the yoimg rising from 9 months to 14 years and declining thereafter. In 25% of patients the presentation is Ebook Oh''s intensive care manual (7/E): Part 2With ketoacidosis, especially 111 those under 5 years of age. Usually the fasting plasma glucose is >7.8 nunol/L and glucose and ketones may be presenEbook Oh''s intensive care manual (7/E): Part 2
t in die urine. In die asymptomatic patient with an equivocal fasting plasma glucose, an impaired glucose tolerance test may lie demonstrated.Type II Part EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2hnic variation in susceptibility. Diagnosis is often delayed and may be incidental from blood or urine sugar screening? Increasingly it is recognised that individuals can lie in a prediabetic state of impaired glucose regulation for many years, which makes them 5 to 15 times more likely to progress Ebook Oh''s intensive care manual (7/E): Part 2to diabetes. It may present with classical symptoms, as a diabetic emergency, with complications of organ damage or vascular disease.EPIDEMIOLOGYDie wEbook Oh''s intensive care manual (7/E): Part 2
orldwide prevalence of diabetes is estimated to lie 366 million people in 2011. Diabetes niellitus affects about 6% of the world's population and is sPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2ype I diabetes are such that health care costs are equivalent between tile two groups. Die annual incidence of DKA is around 14 episodes per thousand patients with diabetes and it has been estimated in the USA that about SI billion are spent each year 111 treating DKA. Hospital admissions tor DKA ha Ebook Oh''s intensive care manual (7/E): Part 2ve gone up by 30% in the last decade and tills is most likely due to the increase in ketosis-prone type II diabetics. HHS represents approximately 1%Ebook Oh''s intensive care manual (7/E): Part 2
of primary admissions to hospital with diabetes as compared with DKA. Die mortality rate in HHS remains liigli at 5-20%, whereas the mortality in DKA Part EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2al factors contribute to disease development. hl type I diabetes there is some evidence for genetic susceptibility but environmental factors play a greater part. It varies across race and regions, being highest in northern Europe and the USA and lowest in Asia and Australasia. Genetic factors UI typ Ebook Oh''s intensive care manual (7/E): Part 2e 2 diabetes are evidently crucial, with a concordance between monozygotic twins approaching 100%.PATHOGENESISNormal carbohydrate metabolism depends uEbook Oh''s intensive care manual (7/E): Part 2
pon the presence of insulin (Fig. 58.1). However, different tissues handle glucose in different ways; for example, red blood cells lack mitochondria aPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2cose disposal (Fig. 58.2). Both DKA and HHS result from a reduction in the effect of insulin with a concomitant rise in the counterregula-tory hormones such as glucagon, catecholamines, cortisol and growth hormone. Hyperglycaemia occurs as a consequence of three processes: increased gluconeogenesis, Ebook Oh''s intensive care manual (7/E): Part 2 increased glycogenolysis and reduced peripheral glucose utilisation. Die increase in glucose production occurs in both the liver and the kidneys as tEbook Oh''s intensive care manual (7/E): Part 2
here is a high availability of gluconeogenic precursors such as ammo acids (protein turnover shif ts from balanced synthesis and degradation to reducePart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2ase in adipose tissue630 ;Diabetic emergenciesGlycogenTriglyceridesProtonFigure 58.1 Sources and fate of acetyl CoA. ‘pyruvate conversion by pyruvate dehydrogenase (PDH) is essentially Irreversible, therefore no net conversion of fatty acids to carbohydrates can occur. TCA=tricarboxylic acid.Figure Ebook Oh''s intensive care manual (7/E): Part 258.2 Glucose metabolism within hepatocyte: |l) glucose transport GLUT-1; (2) hexokinase phosphorylation; |3) pentose phosphate pathway (hexose monophoEbook Oh''s intensive care manual (7/E): Part 2
sphate shunt]; (4] glycolysis; |5) lactate transport out of cell; |6) pyruvate decarboxylation; (7) tricarboxylic acid cycle; |8| glycogenesis, (9] glPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2espectively. Lastly, there IS an increase in gluconeogenic enzyme activity enhanced further by stress hormones. Although hepatic gluconeogenesis is the main mechanism for producing hyperglycaemia a significant proportion can be produced by the kidneys.4 What is unclear is the temporal relationship o Ebook Oh''s intensive care manual (7/E): Part 2f these changes, although an increase in both catecholamines and the glucagon/insulin ratio are early features?Decreased insulin and increased epinephEbook Oh''s intensive care manual (7/E): Part 2
rme levels activate adipose tissue lipase causing a breakdown of triglycerides into glycerol and free fatty acids (FFAs). Once again glucagon is impliPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2ced synthesis of malonyl-CoA causes a disinlubition of acyLcarnitine synthesis and subsequent promotion of fatty acid transport into mitochondria where ketone body formation occurs. Both cortisol and growth hormone are capable of increasmg FFA andketone levels and once again the exact contribution o Ebook Oh''s intensive care manual (7/E): Part 2f insulin deficiency or stress hormone increase to ketogenesis is undetermined. As ketone bodies are comparatively strong acids, a Luge hydrogen ion lEbook Oh''s intensive care manual (7/E): Part 2
oad is produced owing to their dissociation at physiological pH. The need to buffer hydrogen ions depletes tire body's alkali reserves and ketone anioPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2gon, cortisol and growth hormone have been demonstrated in HHS relative to DKA although tills is by no means a consistent observation. However, the presence of higher levels of C-peptide in HHS (with lower levels of growth hormone) relative to DKA suggests there is just enough insulin present in HHS Ebook Oh''s intensive care manual (7/E): Part 2 to prevent lipolysis but not enough to promote peripheral glucose utilisation.'Hyperosmolarity, which is a prominent feature of HHS, is caused by theEbook Oh''s intensive care manual (7/E): Part 2
prolonged effect of an osmoticCldiuresis with impaired ability to take adequate fluids. It lias been shown that, even when well, patients who have suPart EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical I Ebook Oh''s intensive care manual (7/E): Part 2 diuresis and to variable fluid intake due to nausea and vomiting - which is often ascribed to the brainstem effects of ketones.Interestingly, hyperglycaemia with or without ketoacidosis leads to a significant increase in pro-inflammatory cytokine production, which resolves when insulin therapy is c Ebook Oh''s intensive care manual (7/E): Part 2ommenced.7 T1ŨS has led others to postulate a wider beneficial anti-inflammatory effect attributable to insulin therapy. This pro-inflammatory, pro-thEbook Oh''s intensive care manual (7/E): Part 2
rombotic state may explain the relatively high incidence of thrombotic events associated with diabetic emergencies.Part EightEndocrine Disorders58Diabetic Emergencies 62959Diabetes Insipidus and Other PolyuricSyndromes 63760Thyroid Emergencies 65261Adrenocortical IGọi ngay
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