Causes of Diabetic hypoglycemia
Diabetic hypoglycemia Causes: Book Excerpts
Diabetic hypoglycemia as a symptom:
Conditions listing Diabetic hypoglycemia
as a symptom may also be potential underlying causes of Diabetic hypoglycemia.
Our database lists the following as having
Diabetic hypoglycemia as a symptom of that condition:
Medications or substances causing Diabetic hypoglycemia:
The following drugs, medications, substances or toxins are some of the possible
causes of Diabetic hypoglycemia as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
Read more about medication causes of Diabetic hypoglycemia
What causes Diabetic hypoglycemia?
Article excerpts about the
causes of Diabetic hypoglycemia:
In the DCCT, the most significant side effect of intensive treatment
was an increase in the risk for hypoglycemia (low blood sugar) episodes
severe enough to require assistance from another person. Because of this
risk, DCCT researchers do not recommend intensive therapy for children
under age 13, people with heart disease or advanced complications, older
adults, and people with a history of frequent severe hypoglycemia. (Source: excerpt from Diabetes Control and Complications Trial (DCCT): NIDDK)
What triggers Diabetic hypoglycemia?
The following conditions are listed as possible triggers
for Diabetic hypoglycemia:
Cause statistics for Diabetic hypoglycemia:
The following are statistics from various sources about the causes of Diabetic hypoglycemia:
- 4.2% of adults attending specialist diabetes services had a severe hypoglycaemic episode in Australia 2002 (Australia’s Health 2004, AIHW)
- more statistics...»
Related information on causes of Diabetic hypoglycemia:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Diabetic hypoglycemia may be found in:
Causes of Diabetic hypoglycemia: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Diabetic hypoglycemia.
Hypoglycemia:
Differential Diagnosis
(In a Page: Signs and Symptoms)
- Exogenous insulin administration is the most common cause of hypoglycemia
–Most commonly occurs in patients with known diabetes mellitus
–May occur with inadequate food ingestion or excessive exercise after an insulin injection
–May occur with delayed absorption of food (e.g., diabetic gastroparesis)
–Rarely, may occur as part of attention seeking behavior (i.e., factitious)
-
Oral hypoglycemic medications (e.g., sulfonylurea)
–This is especially common with severe liver disease, which prevents gluconeogenesis
-
Other medications (e.g., salicylates, sulfonamides, tetracyclines, warfarin, MAO inhibitors, phenothiazines)
-
Reactive hypoglycemia occurs 2–4 hours after meals, due to delayed and exaggerated insulin release (associated with a family history of type II diabetes)
-
-
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Hypothyroidism
-
-
-
Malnutrition/fasting
-
Insulinoma/islet cell hyperplasia
-
-
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Alcohol consumption
-
-
-
Sepsis
-
-
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Renal failure
-
-
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Sarcomas
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Pituitary or adrenal insufficiency
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Congenital hormone or enzyme defects
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Severe hepatic dysfunction (e.g., hepatitis, hepatic toxins, hepatic necrosis)
» READ BOOK EXCERPT ONLINE »
Source: In a Page: Signs and Symptoms, 2004
Hypoglycemia:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Normal neonates (in first 24 hours of life)
-
Ketotic hypoglycemia
-
Insulin excess
–Exogenous insulin
–Sulfonylurea ingestion
–Infant of a diabetic mother
–Perinatal stress-induced hyperinsulinism
–Congenital hyperinsulinism
–Beckwith-Wiedemann syndrome
-
Hormone deficiency
–Panhypopituitarism
–Growth hormone deficiency
–ACTH or cortisol deficiency
-
Defects of glycogenolysis
–Glycogen storage diseases
-
Defects of gluconeogenesis
–Glycogen storage disease type 1
–Fructose-1,6-diphosphatase deficiency
–Pyruvate carboxylase deficiency
–PEPCK deficiency
-
Fatty oxidation and ketogenesis defects
–Medium-chain acyl-CoA dehydrogenase deficiency (most commonly)
–Carnitine transport and metabolism
–Electron transfer
–HMG CoA synthase deficiency
–HMG CoA lyase deficiency
-
Liver disease
-
Galactosemia
-
Hereditary fructose intolerance
-
Disorders of amino acid metabolism
–Maple syrup urine disease
–Methylmalonic acidemia
–Tyrosinemia
-
Dumping syndrome
–Associated with Nissen fundoplication
-
Reye syndrome
-
Ethanol intoxication
–Impaired gluconeogensis
-
Salicylate intoxication
-
Diarrhea and malnutrition
-
Malaria
-
Jamaican vomiting sickness
-
Measurement error
–Glucometer measurements are inaccurate in low range
–Plasma glucose levels gradually fall if samples are not immediately tested
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
Hypoglycemia:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Reactive hypoglycemia may take several forms. In a diabetic patient, it may result from administration of too much insulin or, less commonly, too much oral antidiabetic medication. In a mildly diabetic patient (or one in the early stages of diabetes mellitus), reactive hypoglycemia may result from delayed and excessive insulin production after carbohydrate ingestion. Similarly, a nondiabetic patient may suffer reactive hypoglycemia from a sharp increase in insulin output after a meal. Sometimes called postprandial hypoglycemia, this type of reactive hypoglycemia usually disappears when the patient eats something sweet. In some patients, reactive hypoglycemia has no known cause (idiopathic reactive) or may result from gastric dumping syndrome and from impaired glucose tolerance.
Fasting hypoglycemia usually results from an excess of insulin or insulin-like substance or from a decrease in counterregulatory hormones. It can be exogenous, resulting from such external factors as alcohol or drug ingestion, or endogenous, resulting from organic problems.
Endogenous hypoglycemia may result from tumors or liver disease. Insulinomas, small islet cell tumors in the pancreas, secrete excessive amounts of insulin, which inhibit hepatic glucose production. They’re generally benign (in 90% of patients). Extrapancreatic tumors, though uncommon, can also cause hypoglycemia by increasing glucose utilization and inhibiting glucose output. Such tumors occur primarily in the mesenchyma, liver, adrenal cortex, GI system, and lymphatic system. They may be benign or malignant. Among nonendocrine causes of fasting hypoglycemia are severe liver diseases, including hepatitis, cancer, cirrhosis, and liver congestion associated with heart failure. All of these conditions reduce the uptake and release of glycogen from the liver. Some endocrine causes include adrenocortical insufficiency, which contributes to hypoglycemia by reducing the production of cortisol and cortisone needed for gluconeogenesis; and pituitary insufficiency, which reduces corticotropin and growth hormone levels.
Hypoglycemia is at least as common in neonates and children as it is in adults and affects 1 out of 1,000 people. Usually, infants develop hypoglycemia because of an increased number of cells per unit of body weight and because of increased demands on stored liver glycogen to support respirations, thermoregulation, and muscular activity. In full-term neonates, hypoglycemia may occur 24 to 72 hours after birth and is usually transient. In neonates who are premature or small for gestational age, onset of hypoglycemia is much more rapid (it can occur as soon as 6 hours after birth) because of their small, immature livers, which produce much less glycogen. Maternal disorders that can produce hypoglycemia in neonates within 24 hours after birth include diabetes mellitus, toxemia, erythroblastosis, and glycogen storage disease.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Hypo/Hyperpigmentation:
Differential Overview
(Field Guide to Bedside Diagnosis)
Hyperpigmented Macules
❑ Nevus
❑ Seborrheic keratosis
❑ Post-inflammatory
❑ Solar purpura
❑ Solar lentigo
❑ Schamberg purpura
❑ Fixed drug eruption
❑ Melasma
❑ Atypical nevus
❑ Melanoma
❑ Cafe-au-lait
Generalized Hyperpigmentation
❑ Drugs
❑ Heavy metals
❑ Addison disease
❑ Ectopic ACTH syndrome
❑ Hemochromatosis
❑ Porphyria cutanea tarda
❑ Pellagra
❑ Whipple disease
❑ Primary biliary cirrhosis
❑ Metastatic melanoma
Hypopigmentation
❑ Tinea versicolor
❑ Vitiligo
❑ Halo nevus
❑ Postinflammatory
❑ Chemical
❑ Piebaldism
❑ Tuberous sclerosis
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
Hypoglycemia:
Causes
(Handbook of Diseases)
The two forms of hypoglycemia have different causes and occur in different types of patients.
Reactive hypoglycemia
Several forms of reactive hypoglycemia occur. In a diabetic patient, it may result from administration of too much insulin or, less commonly, too much oral antidiabetic medication. In a mildly diabetic patient (or one in the early stages of diabetes mellitus), reactive hypoglycemia may result from delayed and excessive insulin production after carbohydrate ingestion.
Similarly, a nondiabetic patient may suffer reactive hypoglycemia from a sharp increase in insulin output after a meal. Sometimes called postprandial hypoglycemia, this type of reactive hypoglycemia usually disappears when the patient eats something sweet.
In some patients, reactive hypoglycemia may have no known cause (idiopathic reactive) or may result from total parenteral nutrition due to gastric dumping syndrome or from impaired glucose tolerance.
Fasting hypoglycemia
Fasting hypoglycemia usually results from an excess of insulin or insulin-like substance or from a decrease in counterregulatory hormones. It can be exogenous, resulting from such external factors as alcohol or drug ingestion, or endogenous, resulting from organic problems.
Endogenous hypoglycemia may result from tumors or liver disease. Insulinomas, small islet cell tumors in the pancreas, secrete excessive amounts of insulin, which inhibits hepatic glucose production. They’re generally benign (in 90% of patients).
Extrapancreatic tumors, although uncommon, can also cause hypoglycemia by increasing glucose utilization and inhibiting glucose output. Such tumors occur primarily in the mesenchyma, liver, adrenal cortex, GI system, and lymphatic system. They may be benign or malignant.
Among nonendocrine causes of fasting hypoglycemia are severe liver diseases, including hepatitis, cancer, cirrhosis, and liver congestion associated with heart failure. All these conditions reduce the uptake and release of glycogen from the liver.
Some endocrine causes include destruction of pancreatic islet cells; adrenocortical insufficiency, which contributes to hypoglycemia by reducing the production of cortisol and cortisone needed for gluconeogenesis; and pituitary insufficiency, which reduces corticotropin and growth hormone levels.
Causes in infants and children
Hypoglycemia is at least as common in neonates and children as it’s in adults. Usually, infants develop hypoglycemia because of an increased number of cells per unit of body weight and because of increased demands on stored liver glycogen to support respirations, thermoregulation, and muscle activity.
In full-term neonates, hypoglycemia may occur 24 to 72 hours after birth and is usually transient. In neonates who are premature or small for gestational age, onset of hypoglycemia is much more rapid — it can occur as soon as 6 hours after birth — due to their small, immature livers, which produce much less glycogen. A rare cause of hypoglycemia in infants is nesidioblastosis, a benign condition of the insulin-producing islet cells. The treatment is surgical.
Maternal disorders that can produce hypoglycemia in infants within 24 hours after birth include diabetes mellitus, pregnancy-induced hypertension, erythroblastosis, and glycogen storage disease.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Hyperinsulinism/Hypoglycemia:
Hyperinsulinism/Hypoglycemia - pathophysiology
(The 5-Minute Pediatric Consult)
- These mutations result in uncoupling of insulin secretion from the glucose-sensing machinery of the pancreatic beta cell, and inappropriate insulin secretion even in the face of low blood glucose.
- The most common and severe forms of HI arise from mutations in the KATP channel, which can manifest in focal or diffuse disease
- In hyperinsulinism/hyperammonemia syndrome, protein inappropriately stimulates insulin secretion and causes persistently elevated ammonia level. This is due to mutations in glutamate dehydrogenase.
Hyperinsulinism/Hypoglycemia - etiology
- Mutations in 5 genes have been associated with congenital HI: Genes coding for either of the 2 subunits of the beta cell KATP channel [SUR1, sulfonylurea receptor (ABCC8); Kir6.2, inwardly rectifying potassium channel (KCNJ11)], glucokinase (GCK), glutamate dehydrogenase (GLUD-1), and SCHAD (HADHSC).
- A transient form of HI has been associated with perinatal stress (small for gestational age [SGA] birth weight, maternal hypertension, precipitous delivery, or hypoxia), but the mechanism has not been elucidated.
» READ BOOK EXCERPT ONLINE »
Source: The 5-Minute Pediatric Consult, 2008
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