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The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Hypoglycaemia is a biochemical diagnosis based on a blood glucose of less than 4mmol/L (JBDS 2018). It may be caused by insulin overdosage, a delayed meal following administration of insulin or increased metabolic rate due to exercise or acute febrile illness. The patient who is hypo-glycaemic will exhibit autonomic symptoms such as sweating, warmth sensation, anxiety, nausea and palpitations as a result of sympathetic nervous system stimulation. Other symptoms (e.g., tiredness, poor coordination, visual disturbances, drowsiness, confusion, seizures) are due to the effects of low glucose levels upon the nervous system (neuroglycopenia). Prolonged low blood glucose levels may starve the brain of glucose, resulting in coma and possibly death. The autonomic symptoms usually occur first, with neuroglycopenia more evident with a blood glucose of less than 2.5mmol/L.
Medicine
Published in Andrew Schofield, Paul Schofield, The Complete SAQ Study Guide, 2019
Andrew Schofield, Paul Schofield
A teenage boy is rushed into A&E, with his parents looking very concerned. They were unable to fully rouse him from bed this morning; he is unresponsive. He is a known diabetic. What would be your first bedside test? (1)Give two ways of raising the glucose level in this patient. (2)What do you think is the likely cause of the hypoglycaemia? (1)Name two symptoms of neuroglycopenia other than coma. (2)What can repeated episodes of hypoglycaemia lead to? (1)What advice would you give to the patient and his family regarding prevention of future episodes? (2)Name a cause of hypoglycaemia in non-diabetic patients. (1)
Hypoglycemia in diabetic pregnancy
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Graziano Di Cianni, Cristina Lencioni, Emilia Lacaria, Laura Russo
The insufficient contribution of glucose to the brain (neuroglycopenia) with an associated cerebral reduction of oxygen causes neuroglycopenic symptoms. The cognitive function becomes impaired when plasma glucose concentration falls below 50–55 mg/dL (2.7–3 mmol/L).7 These symptoms include abnormal mentation, irritability, difficult speaking, ataxia, paresthesia, headache, stupor, and eventually (if untreated) seizure, coma, and even death. Neuroglycopenic symptoms also include transient focal neurological deficits (e.g., diplopia, hemiparesis). These symptoms usually represent the alarm signal of a more serious hypoglycemic attack, and they usually precede the alterations of the cortical function. In this phase, the person is completely vigilant, but he/she can completely prevent the attack from occurring by consuming foods rich in fast-absorbing carbohydrates.
Current challenges in the pathophysiology, diagnosis, and treatment of paroxysmal movement disorders
Published in Expert Review of Neurotherapeutics, 2021
Cécile Delorme, Camille Giron, David Bendetowicz, Aurélie Méneret, Louise-Laure Mariani, Emmanuel Roze
Diagnosis of PMD secondary to an insulinoma is often challenging with a median delay reported to be as long as 2 to 3 years [130,131]. The wide phenotypic expression of neuroglycopenia and its potential variability in a single subject (as also observed in GLUT1-deficiency syndrome) may largely account for this delay. Characteristics of the paroxysmal episodes may provide good clues to the diagnosis i) episodes sometimes occur during the second part of the night or early morning or are triggered by prolonged exercise ii) paroxysmal symptoms tend to increase and decrease within an episode in a gradual manner iii) mixed hyperkinetic movements could vary from one day to another, lasting minutes to hours iv) motor manifestations are combined with behavioral disturbances, such as aggressiveness/disinhibition or psychomotor slowing v) drowsiness/dreaminess are frequently observed vi) neurovegetative features can also be present, such as sweating. One diagnosis pitfall is that hyperkinetic abnormal movements may sometimes combine genuine movement disorders and awkward pseudo-voluntary movements accompanying the behavioral problems [132–134]. The key diagnostic investigation is the measurement of ictal glycemia, which is very low (0.2 to 0.4 g/L in reported cases) [132–134]. Frequent misdiagnosis occurs for psychiatric conditions, epilepsy, or functional movement disorder [132,133]. Ictal glycemia should thus be largely assessed in patients with PMD without a definite diagnosis. Treatment mostly consists in the resection of the insulinoma.
Management of hypoglycemia in older adults with type 2 diabetes
Published in Postgraduate Medicine, 2019
The counter-regulatory mechanism in response to hypoglycemia in healthy individuals is shown in Figure 1 [28]. When blood glucose levels fall, insulin release is suppressed, and counter-regulatory hormones, such as glucagon and epinephrine, are activated to stimulate hepatic glucose production and inhibit peripheral glucose uptake until euglycemia is restored. In adults with diabetes this counter-regulation is defective: there is a loss of ability to decrease insulin production and to increase glucagon release, combined with an attenuated increase in epinephrine [12]. The response by older adults to a drop in glucose appears to depend on how frequently they experience hypoglycemia [12]. Recurrent hypoglycemia reduces the glucose level at which the counter-regulatory response occurs; consequently, patients with frequent hypoglycemia experience the symptoms from the adrenergic response to a decrease in blood glucose at lower and lower glucose levels. In some instances the glucose level that triggers the counter-regulatory response is below the glucose level associated with neuroglycopenia, also called hypoglycemia unawareness, and results from attenuated increases in sympathoadrenal activity. The combination of a defective counter-regulation with hypoglycemia unawareness is called hypoglycemia-associated autonomic failure, and is caused most often by prior hypoglycemic episodes [12].
Doege-Potter syndrome in a patient with a giant abdominal solitary fibrous tumor: a case report and review of the literature
Published in Acta Clinica Belgica, 2023
Joris Rötgens, Bruno Lapauw, Guy T’Sjoen
In about half of the patients with Doege-Potter syndrome, development of hypoglycemia leads to the diagnosis of the tumor. In other cases, hypoglycemia occurs after the tumor has already been diagnosed, mainly because of symptoms due to the tumor mass itself. Because small tumors are generally asymptomatic, SFTs may attain large sizes before presentation, with intra-abdominal SFTs being typical more than 20 cm at the time of diagnosis. When hypoglycemia develops, both neuroglycopenic and autonomic symptoms may occur. Neuroglycopenic symptoms can range from mild to severe (confusion, amnesia, psychosis, seizures and coma). Due to repeated hypoglycemic events and insidious progression, autonomic symptoms (sweating, anxiety and tremor) are frequently blunted or absent [10]. Interestingly, there are a few cases in which there was a spectacular improvement in metabolic control in pre-existing diabetes. Acromegalic features (due to increased activation of the IGF-I receptor by big IGF-II) are a rare manifestation and disappear after surgery. Our patient presented with multiple skin tags, which could be a manifestation of increased activation of IGF-R, as reported in earlier cases. Hypokalemia has also been described (due to insulin-like activity of big IGF-II) [6,11]. In addition to Doege-Potter syndrome, SFTs can also give rise to another paraneoplastic manifestation, namely Pierre-Marie-Bamberger syndrome (characterized by clubbing of the fingers, long bone periostitis and arthritis due to hypertrophic osteoarthropathy). This occurs in up to 35% of cases with SFT and is thus more prevalent than Doege-Potter syndrome. Cases have been described were patients exhibit both paraneoplastic features [12].