Severe HYPOGLYCEMIA induced by a large dose of exogenous INSULIN resulting in a COMA or profound state of unconsciousness from which the individual cannot be aroused.
A profound state of unconsciousness associated with depressed cerebral activity from which the individual cannot be aroused. Coma generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the brain stem RETICULAR FORMATION.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE.
A scale that assesses the response to stimuli in patients with craniocerebral injuries. The parameters are eye opening, motor response, and verbal response.
A state of unconsciousness as a complication of diabetes mellitus. It occurs in cases of extreme HYPERGLYCEMIA or extreme HYPOGLYCEMIA as a complication of INSULIN therapy.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
A structurally-related group of signaling proteins that are phosphorylated by the INSULIN RECEPTOR PROTEIN-TYROSINE KINASE. The proteins share in common an N-terminal PHOSPHOLIPID-binding domain, a phosphotyrosine-binding domain that interacts with the phosphorylated INSULIN RECEPTOR, and a C-terminal TYROSINE-rich domain. Upon tyrosine phosphorylation insulin receptor substrate proteins interact with specific SH2 DOMAIN-containing proteins that are involved in insulin receptor signaling.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.

Clinical characteristics of type 1 diabetic patients with and without severe hypoglycemia. (1/17)

OBJECTIVE: To investigate the frequency of severe hypoglycemia (SH) and hypoglycemic coma and to identify clinical and behavioral risk indicators in a nonselected population of type 1 diabetic patients. RESEARCH DESIGN AND METHODS: This study involved a retrospective clinical survey of 195 consecutive patients using a questionnaire addressing the frequency of SH (i.e., help from others required) and hypoglycemic coma during the previous year, general characteristics, behavior, hypoglycemia awareness, and the Hypoglycemia Fear Survey Data regarding diabetes, treatment, long-term complications, comorbidity, and comedication were obtained from the patients' medical records. RESULTS: A total of 82% of subjects were receiving intensive insulin treatment, and mean +/- SD HbA(1c) was 7.8 +/- 1.2%. Mean duration of diabetes was 20 +/- 12 years. The occurrence of SH (including hypoglycemic coma) was 150 episodes/100 patient-years and affected 40.5% of the population. Hypoglycemic coma occurred in 19% of subjects (40 episodes/100 patient-years). SH without coma was independently related to nephropathy (odds ratio [OR] 4.8 [95% CI 1.5-15.1]), a threshold for hypoglycemic symptoms of <3 mmol/l (4.8 [1.8-12.0]), and a daily insulin dose 0.1 U/kg higher (1.3 [1.0-1.6]) (all ORs were adjusted for diabetes duration and use of comedication). Hypoglycemic coma was independently related to neuropathy (3.9 [1.5-10.4]), (nonselective) beta-blocking agents (14.9 [2.1-107.4]), and alcohol use (3.5 [1.3-9.1]) (all ORs were adjusted for diabetes duration). CONCLUSIONS: SH and hypoglycemic coma are common in a nonselected population with type 1 diabetes. The presence of long-term complications, a threshold for symptoms of <3 mmo/l, alcohol use, and (nonselective) beta-blockers were associated with SH during the previous year. If prospectively confirmed, these results may have consequences for clinical practice.  (+info)

Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma. (2/17)

In situ hybridization was used to study expression of mRNAs for members of the nerve growth factor (NGF) family in the rat brain after 2 and 10 min of forebrain ischemia and 1 and 30 min of insulin-induced hypoglycemic coma. Two hours after the ischemic insults, the level of brain-derived neurotrophic factor (BDNF) mRNA was markedly increased in the granule cells of the dentate gyrus, and at 24 h it was still significantly elevated. NGF mRNA showed a pronounced increase 4 h after 2 min of ischemia but had returned to a control level at 24 h. Both 2 and 10 min of ischemia caused a clear reduction of the level of mRNA for neurotrophin 3 (NT-3) in the dentate granule cells and in regions CA2 and medial CA1 of the hippocampus 2 and 4 h after the insults. The increase of BDNF mRNA could be partially blocked by the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist NBQX but was not influenced by the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Both NBQX and MK-801 attenuated the decrease of NT-3 mRNA after ischemia. One and 30 min of hypoglycemic coma also induced marked increases in BDNF and NGF mRNA in dentate granule cells with maximal levels at 2 h. If the changes of mRNA expression lead to alterations in the relative availability of neurotrophic factors, this could influence functional outcome and neuronal necrosis following ischemic and hypoglycemic insults.  (+info)

[Treatment of type 1 diabetes mellitus revealed below 7 years of age in the Diabetes Center of Silesia, Poland]. (3/17)

INTRODUCTION: Frequency of type 1 diabetes mellitus diagnosis in young children increases. Within this group, such factors as limited cooperation, little acceptance of multiple injections and other typical patterns of behavior can strongly influence the insulin management outcome. AIM OF THE STUDY: The objective of the study was to provide information regarding metabolic control in young diabetes patients. MATERIAL AND METHODS: Charts of 58 children with T1DM, all subjects under control of our Department, that were aged at onset (1998-2003) below 7 years (mean 4.05+/-1.6) were studied retrospectively. HbA1c, total, bolus and basal daily insulin requirement (DIR), weight, height, severe hypoglycaemia and diabetic ketoacidosis (DKA) were analyzed till April 2006 in 2-year intervals. Insulin therapy model was also taken into consideration. RESULTS: Mean HbA1c was 7.2+/-1.2% for all children for the whole studied period and did not alter significantly between analyzed intervals. Most common treatment model at diabetes onset was the therapy with premixed insulin (Mix) (67%) and after 4 and 6 years - continuous subcutaneous insulin infusion (CSII) (50% and 75% respectively). A tendency for a better metabolic control was observed at multiple daily injections and CSII than at Mix. Change of the weight or height percentile channel was not revealed. Bolus and basal DIR increased in the first observation interval. Afterwards they stabilized respectively at 0.35-0.42 U/kg/24 h and 0.35-0.39 U/kg/24 h. Severe hypoglycaemia occurred 6.72/100 patient-years. CONCLUSION: Insulin therapy aimed at maintaining long-term good metabolic control is possible to achieve and is safe in young diabetic children.  (+info)

Utility values for symptomatic non-severe hypoglycaemia elicited from persons with and without diabetes in Canada and the United Kingdom. (4/17)

 (+info)

Hypoglycemia in type 1 diabetic pregnancy: role of preconception insulin aspart treatment in a randomized study. (5/17)

 (+info)

Severe hypoglycaemia in drug-treated diabetic patients needs attention: a population-based study. (6/17)

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Extracellular pH in the rat brain during hypoglycemic coma and recovery. (7/17)

It has previously been shown that hypoglycemic coma is accompanied by marked energy failure and by loss of cellular ionic homeostasis. The general proposal is that shortage of carbohydrate substrate prevents lactic acid formation and thereby acidosis during hypoglycemic coma. The objective of the present study was to explore whether rapid downhill ion fluxes, known to occur during coma, are accompanied by changes in extra- and/or intracellular pH (pHe and/or pHi), and how these relate to the de- and repolarization of cellular membranes. Cortical pHe was recorded by microelectrodes in insulin-injected rats subjected to 30 min of hypoglycemic coma, with cellular membrane depolarization. Some rats were allowed up to 180 min of recovery after glucose infusion and membrane repolarization. Arterial blood gases and physiological parameters were monitored to maintain normotension, normoxia, normocapnia, and normal plasma pH. Following depolarization during hypoglycemia, a prompt, rapidly reversible alkaline pHe shift of about 0.1 units was observed in 37/43 rats. Immediately thereafter, all rats showed an acid pH shift of about 0.2 units. This shift developed during the first minute, and pHe remained at that level until repolarization was induced. Following repolarization, there was an additional, rapid, further lowering of pHe by about 0.05 units, followed by a more prolonged decrease in pHe that was maximal at 90 min of recovery (delta pHe of approximately -0.4 units). The pHe then slowly normalized but was still decreased (-0.18 pH units) after 180 min when the experiment was terminated. The calculated pHi showed no major alterations during hypoglycemic coma or after membrane repolarization following glucose administration.(ABSTRACT TRUNCATED AT 250 WORDS)  (+info)

Cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma. (8/17)

Cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.  (+info)

An Insulin Coma is not a formal medical term, but it has been used in the past to describe a deliberate medical procedure known as Insulin Shock Therapy. This was a treatment for mental illness that involved administering large doses of insulin to induce hypoglycemia (low blood sugar), which could lead to a coma.

The idea behind this therapy, which was popular in the mid-20th century, was that the induced coma and subsequent recovery could have therapeutic effects on the brain and help alleviate symptoms of mental illnesses like schizophrenia. However, this treatment fell out of favor due to its significant risks and the development of more effective and safer treatments.

It's important to note that in current medical practice, inducing a coma with insulin is not a standard or recommended procedure due to the potential for severe harm, including brain damage and death.

A coma is a deep state of unconsciousness in which an individual cannot be awakened, cannot respond to stimuli, and does not exhibit any sleep-wake cycles. It is typically caused by severe brain injury, illness, or toxic exposure that impairs the function of the brainstem and cerebral cortex.

In a coma, the person may appear to be asleep, but they are not aware of their surroundings or able to communicate or respond to stimuli. Comas can last for varying lengths of time, from days to weeks or even months, and some people may emerge from a coma with varying degrees of brain function and disability.

Medical professionals use various diagnostic tools and assessments to evaluate the level of consciousness and brain function in individuals who are in a coma, including the Glasgow Coma Scale (GCS), which measures eye opening, verbal response, and motor response. Treatment for coma typically involves supportive care to maintain vital functions, manage any underlying medical conditions, and prevent further complications.

Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.

Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.

An insulin receptor is a transmembrane protein found on the surface of cells, primarily in the liver, muscle, and adipose tissue. It plays a crucial role in regulating glucose metabolism in the body. When insulin binds to its receptor, it triggers a series of intracellular signaling events that promote the uptake and utilization of glucose by cells, as well as the storage of excess glucose as glycogen or fat.

Insulin receptors are composed of two extracellular alpha subunits and two transmembrane beta subunits, which are linked together by disulfide bonds. The binding of insulin to the alpha subunits activates the tyrosine kinase activity of the beta subunits, leading to the phosphorylation of intracellular proteins and the initiation of downstream signaling pathways.

Abnormalities in insulin receptor function or number can contribute to the development of insulin resistance and type 2 diabetes.

The Glasgow Coma Scale (GCS) is a standardized tool used by healthcare professionals to assess the level of consciousness and neurological response in a person who has suffered a brain injury or illness. It evaluates three aspects of a patient's responsiveness: eye opening, verbal response, and motor response. The scores from these three categories are then added together to provide an overall GCS score, which can range from 3 (indicating deep unconsciousness) to 15 (indicating a normal level of consciousness). This scale helps medical professionals to quickly and consistently communicate the severity of a patient's condition and monitor their progress over time.

A diabetic coma is a serious and life-threatening condition that occurs when an individual with diabetes experiences severely high or low blood sugar levels, leading to unconsciousness. It is a medical emergency that requires immediate attention.

In the case of hyperglycemia (high blood sugar), the body produces excess amounts of urine to try to eliminate the glucose, leading to dehydration and a lack of essential nutrients in the body. This can result in a buildup of toxic byproducts called ketones, which can cause a condition known as diabetic ketoacidosis (DKA). DKA can lead to a diabetic coma if left untreated.

On the other hand, hypoglycemia (low blood sugar) can also cause a diabetic coma. This occurs when the brain is not receiving enough glucose to function properly, leading to confusion, seizures, and eventually unconsciousness.

If you suspect someone is experiencing a diabetic coma, it is important to seek emergency medical attention immediately. While waiting for help to arrive, try to administer glucose or sugar to the individual if they are conscious and able to swallow. If they are unconscious, do not give them anything to eat or drink, as this could cause choking or further complications.

Insulin resistance is a condition in which the body's cells become less responsive to insulin, a hormone produced by the pancreas that regulates blood sugar levels. In response to this decreased sensitivity, the pancreas produces more insulin to help glucose enter the cells. However, over time, the pancreas may not be able to keep up with the increased demand for insulin, leading to high levels of glucose in the blood and potentially resulting in type 2 diabetes, prediabetes, or other health issues such as metabolic syndrome, cardiovascular disease, and non-alcoholic fatty liver disease. Insulin resistance is often associated with obesity, physical inactivity, and genetic factors.

Insulin Receptor Substrate (IRS) proteins are a family of cytoplasmic signaling proteins that play a crucial role in the insulin signaling pathway. There are four main isoforms in humans, namely IRS-1, IRS-2, IRS-3, and IRS-4, which contain several conserved domains for interacting with various signaling molecules.

When insulin binds to its receptor, the intracellular tyrosine kinase domain of the receptor becomes activated and phosphorylates specific tyrosine residues on IRS proteins. This leads to the recruitment and activation of downstream effectors, such as PI3K and Grb2/SOS, which ultimately result in metabolic responses (e.g., glucose uptake, glycogen synthesis) and mitogenic responses (e.g., cell proliferation, differentiation).

Dysregulation of the IRS-mediated insulin signaling pathway has been implicated in several pathological conditions, including insulin resistance, type 2 diabetes, and certain types of cancer.

Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.

In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.

Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.

ISBN 978-0-19-507232-7. Jones K (March 2000). "Insulin coma therapy in schizophrenia". Journal of the Royal Society of Medicine ... 76 In the early 1930s insulin coma therapy was trialed to treat schizophrenia, but faded out of use in the 1960s following the ...
Jones K (March 2000). "Insulin coma therapy in schizophrenia". Journal of the Royal Society of Medicine. 93 (3): 147-149. doi: ... Insulin shock involved injecting large doses of insulin to induce comas, which in turn produced hypoglycemia and convulsions. ...
The abuse of exogenous insulin carries with it an attendant risk of hypoglycemic coma and death when the amount used is in ... insulin and a rapid/regular insulin to provide both a basal insulin and prandial insulin. There are several challenges involved ... Medical preparations of insulin are never just insulin in water (with nothing else). Clinical insulins are mixtures of insulin ... Prandial insulin, also called mealtime or bolus insulin, is designed as a bolus dose of insulin prior to a meal to regulate the ...
A parallel development was insulin coma therapy.) A more facile form of induction of seizures, using electricity instead of ... Meduna, L. J., Gerty, F. J. and Urse, V G. Biochemical disturbances in mental disorders; anti-insulin effect of blood in cases ... Insulin Shock, Cardiozol, Sleep Treatment. (Proc. Swiss Psychiatric Association, Muensingen, Berne, 1937.) Am . J Psychiatry 94 ... Meduna, L. J. Significance of convulsive reaction during insulin and cardiozol therapy. J Nerv. Ment. Dis. 87:133-134, 19 38b. ...
Hyperglycemia (diabetic coma) and Hypoglycemia (insulin shock). Hypothermia, or Exposure, occurs when a person's core body ... the Glasgow Coma Score can be used.16 Limb movements should be inspected to evaluate potential signs of lateralization. The ...
Hervey, Cleckley (1941). "Prolonged Coma in Insulin Therapy of the Psychoses". Am J Psychiatry. 97 (4): 844-857. doi:10.1176/ ... Cleckley practiced the controversial "coma therapy", where psychiatric patients would be repeatedly put into comas over several ... weeks through overdoses of insulin, metrazol or other drugs. In the wake of sometimes fatal complications, Cleckley published ...
Deprived of her insulin, Nina fell into a diabetic coma. Sean and Brooke English's efforts helped foil the robbery and save ...
June 1974). "Treatment of diabetic coma with continuous low-dose infusion of insulin". British Medical Journal. 2 (5921): 687- ... The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given ... DKA was first described in 1886, and until the introduction of insulin therapy in the 1920s, it was almost universally fatal. ... DKA results from a shortage of insulin; in response, the body switches to burning fatty acids, which produces acidic ketone ...
In 1927 insulin coma therapy was introduced and used until 1960. Physicians deliberately put the patient into a low blood sugar ... coma because they thought that large fluctuations in insulin levels could alter the function of the brain. Risks included ... Lobotomies, Insulin shock therapy, Electro convulsive therapy, and the "neuroleptic" chlorpromazine came into use mid-century. ... prolonged coma. Electroconvulsive Therapy (ECT) was later adopted as a substitution to this treatment. DSM-IV and previous ...
The 1950s saw the introduction of insulin coma therapy and antidepressants. The Mental Health Act 1959 brought further changes ...
ISBN 978-3-319-34595-6. Doroshow, Deborah Blythe (2007). "Performing a cure for schizophrenia: insulin coma therapy on the ... 28 and other forms of psychosurgery or insulin shock therapy, and the history of racism within the profession in the United ...
She was subject to electroconvulsive therapy, sedatives, insulin coma, seclusion and confinement. Greally was transported to ...
The insulin, however, could induce a coma by lowering the blood sugar. If the blood sugar level dropped too low, it could ... Additionally, insulin was given to patients to help restore lost weight due to inactivity. ...
Ketoacidotic diabetic coma: intravenous fluids, insulin and administration of potassium and sodium. Hyperosmolar diabetic coma ... The treatment consists of insulin and gradual rehydration with intravenous fluids. Diabetic coma was a more significant ... Diabetic coma is a life-threatening but reversible form of coma found in people with diabetes mellitus. Three different types ... insulin to reverse the ketoacidosis, and careful monitoring for complications. Nonketotic hyperosmolar coma usually develops ...
Also known as insulin shock, hypoglycemia can lead to coma or even death. In current research, the significant relationship ... The metabolism of glucose and insulin are also influenced. However, recent studies showed no significant correlation between ...
He noted that insulin-induced coma and convulsions, due to the low level of glucose attained in the blood (hypoglycemic crisis ... Insulin Coma Therapy on the Wards. Journal of the History of Medicine and Allied Sciences, Advance Access published online on ... Insulin coma therapy in schizophrenia. J. Royal Soc. Med, 93: 147-149, 2000. The History of Shock Therapy in Psychiatry TIME ... Sakel was the developer of the insulin shock therapy from 1927 while a young doctor in Vienna, starting to practice it in 1933 ...
By the late 1940s, the majority of psychiatric hospitals in the US were using insulin coma treatment. Insulin coma therapy was ... Insulin Coma Therapy Archived 15 October 2002 at the Wayback Machine by the head of the insulin coma unit at the Hillside ... sub-coma) doses of insulin. A few psychiatrists (including Sakel) claimed success rates for insulin coma therapy of over 80% in ... or on the day of the week when they didn't have insulin treatment. When they were not in a coma, insulin coma patients were ...
The grandmal seizure is the central event in electroshock (electroconvulsive therapy, ECT) and insulin coma. It was introduced ... and in the coma induced by insulin. When reserpine was studied in 1953, chlorpromazine in 1954, and imipramine in 1957, ...
Elsie Needham was the first child to return from a diabetic coma due to insulin. Boyd presented her research at the inaugural ... "Photograph of Elsie Needham , The Discovery and Early Development of Insulin". insulin.library.utoronto.ca. Retrieved July 9, ... reporting 20 cases of children with diabetes treated with insulin and concluding that "insulin will probably not cure but ... Boyd contacted Banting to get a vial of his new insulin extract in October 1922 to treat her 11-year-old patient, Elsie Needham ...
3&4, 1964.pp.325-335 3. Studies on the effects of oestradiol dipropionate in insulin coma therapy in different types of ...
He later had a leading role in the biological therapies, such as insulin coma and convulsive therapy. Throughout his career, he ...
In the 1930s, a number of medical procedures were introduced, including brain surgery, induced insulin coma, and ...
... intentionally overdosed on insulin and slipped into a coma. On September 27, 2002, Dabord died in a California hospital. In his ... and subsequently overdosed on insulin purposely instead of explaining to authorities what had happened, if that were all true. ...
While studying the dreams of insulin coma therapy patients, he became interested in the work of Swiss psychologist Carl Jung. ... the 1,000 patients were subjected to electric shock and insulin-coma therapies, and lobotomies. In 1952 during a visit to ...
After she falls into a diabetic coma, Jim leaves the warehouse to find insulin for her. Jim evades zombies and recovers insulin ...
New Zealand author Janet Frame experienced both insulin coma therapy and ECT (but without the use of anesthesia or muscle ...
In February 1924, he successfully brought a moribund patient out of a diabetic coma through the application of insulin, using ... and was one of the first Finnish physicians to use insulin to treat a diabetic coma. Von Willebrand qualified in medicine in ... and was a pioneer in the use of insulin, describing in 1922 its use in the treatment of diabetic comas. ... "Coma diabeticum- Insulinbehandling". Finska Läkaresällskapets Handlingar (in Swedish). 66: 255-273. Von Willebrand, E. A. (1926 ...
... but lapsed into a diabetic coma after overdosing on insulin. When he awoke, he tried to break it off with Rianna "for her own ...
They long advocated for a range of other 'physical' treatments, including insulin coma therapy, even well after clinical trials ...
In 1941 Hassid had a breakdown and was admitted to St Andrew's Hospital, Northampton, where he was given insulin coma therapy ...
The abuse of exogenous insulin carries with it an attendant risk of hypoglycemic coma and death when the amount used is in ... insulin and a rapid/regular insulin to provide both a basal insulin and prandial insulin. There are several challenges involved ... Medical preparations of insulin are never just insulin in water (with nothing else). Clinical insulins are mixtures of insulin ... Prandial insulin, also called mealtime or bolus insulin, is designed as a bolus dose of insulin prior to a meal to regulate the ...
Categories: Insulin Coma Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 36 ...
He also had short-lived iatrogenic coma because of hypoglycemia secondary to insulin administration. These events triggered a ...
Use glucagon to treat insulin coma or insulin reaction resulting from severe hypoglycemia (low blood sugar). Symptoms of severe ... Careful adjustment of the insulin program so that the type (or types) of insulin, dose, and time (or times) of administration ... They can practice giving a shot by giving you your normal insulin shots. It is important that they practice. A person who has ... WARNING: THE PATIENT MAY BE IN A COMA FROM SEVERE HYPERGLYCEMIA (HIGH BLOOD GLUCOSE) RATHER THAN HYPOGLYCEMIA. IN SUCH A CASE, ...
Insulin Lispro Injection: learn about side effects, dosage, special precautions, and more on MedlinePlus ... Insulin lispro injection products should not be mixed with insulin preparations other than NPH insulin. Insulin lispro ... Do not dilute insulin lispro or mix it with any other type of insulin when using it with an external insulin pump. When using ... Insulin lispro injection products are a short-acting, manmade version of human insulin. Insulin lispro injection products work ...
What is Diabetes? Diabetes Definition: Diabetes is a disorder in which either the pancreas does not secrete enough insulin to ... Difference between Diabetes and Hypoglycemia Diabetes is a disorder related to insulin in which blood sugar levels are too high ... In addition, some diabetics can develop ketoacidosis which can lead to coma. This happens because they are not metabolizing ... or enough insulin is produced but the cells in the body become resistant to the insulin. ...
Ive just come out of an insulin shock coma, and the guilt is eating away at me. I slowly try to sit up in bed, the five ... A1c Levels AskNadia Blood Glucose Reading Diabetes High Blood Sugar Insulin Medication Type1 Type2 ... willing him to feel how sorry I am for putting him through another insulin shock and another sleepless night. He is rigid at ...
E15.) Nondiabetic hypoglycaemic coma ** Drug-induced insulin coma in nondiabetic * Hyperinsulinism with hypoglycaemic coma ... E10-E16) Pancreas / Insulin, glucagon (E10-E14) Diabetes mellitus * Note: the following conditions are subtypes of each code ... Diabetes mellitus (type 1, type 2, coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy) - Hypoglycemia - ... 1.2 (E10-E16) Pancreas / Insulin, glucagon *1.2.1 (E10-E14) Diabetes mellitus ...
I had never heard of insulin coma treatments or electroconvulsive therapy. My introduction to the proposed insulin treatment ... A few things were not explained to my mother or me about this new treatment-for example, what would 40 insulin-induced comas do ... What about the side effects, the potential brain damage, the memory loss and the risk of death? Was the insulin treatment ...
Hypoglycemic coma secondary to big insulin-like growth factor II secretion by a giant phyllodes tumor of the breast.. Aguiar ... 3. A case of a giant phyllodes tumor of the breast with hypoglycemia caused by high-molecular-weight insulin-like growth factor ... 8. Residents case series: Insulin-secreting cystosarcoma phyllodes of the breast: a case report and literature review.. Herr M ... 7. A Hypoglycemia-inducing Giant Borderline Phyllodes Tumor Secreting High-molecular-weight Insulin-Like Growth Factor II: ...
Optimal insulin delivery in diabetic ketoacidosis and hyperglycemic, hyperosmolar nonketotic coma. Diabetes Care. 1982;5(suppl ... Human insulin should generally be used. Patients with insulin-treated diabetes require an individualized insulin regimen based ... Dont stop taking insulin even if you cant eat. Your health care provider may change your insulin dose or may tell you to ... Insulin therapy. Patients treated with oral hypoglycemic agents should be switched to insulin before they become pregnant. ...
It was not until the 1930s that Manfred Sakel in Vienna introduced hypoglycaemic coma, produced by injections of insulin, as a ...
... diabetic coma after therapy with insulin, and excess treatment with sodium salts. ...
Insulin-coma therapy was introduced by Manfred Sakel in the 1930s in Vienna and was soon being used in many countries to treat ... An insulin injection was administered six days a week for several weeks, producing a state of light coma lasting about an hour ... Friday essay: black bile, malaria therapy and insulin comas - a brief history of mental illness. ... showed conclusively that the coma itself was of no therapeutic value. Any positive change was probably due to the staffs ...
In the early days of IPT, a person had to be put into an insulin coma in order for IPT to be effective. This is no longer the ... Insulin Potentiation Therapy. For example, in the 1940s it was said that cancer can be treated with insulin. Insulin is said to ... This led to the development of Insulin Potentiation Therapy (IPT).. *"Beyond these metabolic effects of insulin here, what is ... It is thought that this effect exists on account of the insulin receptors on the cancer cell membranes and that these ...
Taking too much insulin can put you in a coma or kill you. Dont risk messing with insulin injections if you dont have to, and ... The pros use insulin. Similar to reason #9, but insulin in the most dangerous. Ive written before about how to manipulate your ... Pro bodybuilders inject insulin, even when they are not diabetic, to make the most of their meals and training.Problem is, you ... if you want to look like a pro bodybuilder, unless you are a true genetic mutant, you will probably have to use insulin. ...
The treatments available today would not have been possible without the discovery of insulin. Read on to learn more about the ... history of insulin and the controversy surrounding its development. ... Diabetes is a disorder centering around a deficiency or lack of insulin. ... diabetic coma. *death from ketosis. The first physiologist to suggest that the pancreatic islets, or the islets of Langerhans, ...
Both natural and recombinant forms of insulin are used therapeutically to treat type 1 diabetes. While insulin itself is not ... high doses including overdoses of insulin and glucose can result in hepatic glycogenosis and serum aminotransferase elevations. ... Insulin is a pancreatic hormone that plays an essential role in regulation of blood glucose as well as lipid and carbohydrate ... 48 year old woman who injected 2000 IU of insulin in a suicide attempt and was admitted to a hospital in coma, developed ...
Similarly, a diabetic who without insulin would lapse into a coma would be substantially limited because the individual cannot ... a pharmacist with diabetes who controlled his condition with insulin injections and a controlled diet;7 ... assistant with diabetes who controlled her condition to some degree by daily blood sugar tests and daily injections of insulin; ... Eighth Circuit found that the employee was not substantially limited in any major life activities when the effects of insulin ...
Insulin-induced coma, lobotomy, and electroshock were still accepted treatments for schizophrenia, and Thorazine was initially ... led to brain-damaging therapies-insulin coma, metrazol-induced seizure, electroshock, and prefrontal lobotomy-that were applied ...
... or by using high doses of insulin causing hypoglycemic coma and finally death." ...
For overdoses with insulin, relatively high rates of serious symptoms and deaths were observed. ... Physicians should take into account that long-acting insulin formulations and concomitant substances were frequently used. ... The etiology of overdoses with insulin was mainly deliberate self-poisoning. ... Objective: Overdoses with insulin are common, and cases of hypoglycemic coma can be fatal and cause cerebral defects. However, ...
Without insulin, the victim slipped into a diabetic coma from which she would never recover. ... The victim died a painful and unnecessary death when she was deprived of insulin and denied medical care during her three days ... allowing her to slip into a diabetic coma. ... been rushed to the hospital in an irreversible diabetic coma. ...
In the 1930s and 40s, so-called miracle cures emerged, such as insulin coma therapy, electroconvulsive therapy (also known as ...
Treatment is IV saline solution and insulin. Complications include coma, seizures, and death. ... Occasional patients with insulin-resistant type 2 diabetes with hyperosmolar hyperglycemic state require larger insulin doses. ... Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia ... Insulin Інсулін General treatment of diabetes mellitus for all patients involves lifestyle changes, including diet and exercise ...
... insulin coma therapies, and other harsh somatic treatments? Or better than they were in the early 1800s, when Quakers created ... "like insulin for diabetes." Yet, now that I had asked to see the evidence for that claim, I was informed that "like insulin for ... I understood that they fixed chemical imbalances in the brain, and thus were like insulin for diabetes. I also understood that ...
Insulin-induced factitious hypoglycemic coma. Gen Hosp Psychiatry 1986;8:291-293. ...

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