Is dizziness a symptom of hypoglycemia?
Hypoglycemia
Hypoglycemic symptoms can also occur when one is sleeping. Examples of symptoms during sleep can include damp bed sheets or clothes from perspiration. Having nightmares or the act of crying out can be a sign of hypoglycemia. Once the individual is awake they may feel tired, irritable, or confused and these may be signs of hypoglycemia as well.
Hyperglycemia
Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response.
Carnitine palmitoyltransferase I deficiency
Signs and symptoms of this disorder include low levels of ketones and low blood sugar (hypoglycemia). Together these signs are called hypoketotic hypoglycemia. People with this disorder typically also have an enlarged liver (hepatomegaly), muscle weakness, and elevated levels of carnitine in the blood.
Malnutrition
Hypoglycemia (low blood sugar) can result from a child not eating for 4 to 6 hours. Hypoglycemia should be considered if there is lethargy, limpness, convulsion, or loss of consciousness. If blood sugar can be measured immediately and quickly, perform a finger or heel stick.
Diabetic hypoglycemia
In North America a mild episode of diabetic hypoglycemia is sometimes termed a "low" or an "insulin reaction," and in Europe a "hypo", although all of these terms are occasionally used interchangeably in North America, Europe, Australia and New Zealand. A severe episode is sometimes also referred to as "insulin shock".
Insulin
Hypoglycemia, also known as "low blood sugar", is when blood sugar decreases to below normal levels. This may result in a variety of symptoms including clumsiness, trouble talking, confusion, loss of consciousness, seizures or death. A feeling of hunger, sweating, shakiness and weakness may also be present. Symptoms typically come on quickly.
Seale Harris
Harris' syndrome is a historical term for hyperinsulinemic hypoglycemia, such as that caused by insulin-producing tumors of the pancreas (insulinoma). The syndrome is characterized by the symptoms of low blood sugar: weakness, hunger, shakiness, increasing nervousness, mild mental confusion or even personality alterations with erratic behaviour, and the adrenergic responses of tachycardia, pallor, and sweating. The concept of the syndrome was postulated by Harris, in 1924, after he observed hypoglycemia produced during treatment of diabetic patients with the newly discovered insulin.
Diabetic hypoglycemia
Diabetic hypoglycemia is a low blood glucose level occurring in a person with diabetes mellitus. It is one of the most common types of hypoglycemia seen in emergency departments and hospitals. According to the National Electronic Injury Surveillance System-All Injury Program (NEISS-AIP), and based on a sample examined between 2004 and 2005, an estimated 55,819 cases (8.0% of total admissions) involved insulin, and severe hypoglycemia is likely the single most common event.
Idiopathic postprandial syndrome
Idiopathic postprandial syndrome, colloquially but incorrectly known by some as hypoglycemia, describes a collection of clinical signs and symptoms similar to medical hypoglycemia but without the demonstrably low blood glucose levels which characterise said condition.
Insulinoma
Patients with insulinomas usually develop neuroglycopenic symptoms. These include recurrent headache, lethargy, diplopia, and blurred vision, particularly with exercise or fasting. Severe hypoglycemia may result in seizures, coma, and permanent neurological damage. Symptoms resulting from the catecholaminergic response to hypoglycemia (i.e. tremulousness, palpitations, tachycardia, sweating, hunger, anxiety, nausea) are not as common. Sudden weight gain is sometimes seen.
Hypocalcaemia
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect (i.e. increased responsiveness) due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.
Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH levels rise, and conversely if there are high calcium levels then PTH secretion declines. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands. Hypoparathyroidism may also be due to autoimmune problem.Some causes of hypocalcaemia are as follow:
Hypoglycemia
In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed "hypoglycemia unawareness" and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.
List of causes of hypoglycemia
Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:
Hyperglycemia
Hyperglycemia (also spelled hyperglycaemia or hyperglycæmia), also known as high blood sugar, is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a blood sugar level higher than 11.1 mmol/l (200 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15–20 mmol/l (~250–300 mg/dl). A subject with a consistent range between ~5.6 and ~7 mmol/l (100–126 mg/dl) (American Diabetes Association guidelines) is considered slightly hyperglycemic, while above 7 mmol/l (126 mg/dl) is generally held to have diabetes. For diabetics, glucose levels that are considered to be too hyperglycemic can vary from person to person, mainly due to the person's renal threshold of glucose and overall glucose tolerance. On average however, chronic levels above 10–12 mmol/L (180–216 mg/dl) can produce noticeable organ damage over time.
Yorkshire Terrier
Certain genetic disorders can be found in Yorkshire Terriers, including distichiasis, hydrocephalus, hypoplasia of dens, Legg–Calvé–Perthes syndrome, luxating patella, portosystemic shunt, retinal dysplasia, tracheal collapse and bladder stones. The following are among the most common congenital defects that affect Yorkie's.Low blood sugar in puppies, or transient juvenile hypoglycaemia, is caused by fasting (too much time between meals). In rare cases hypoglycaemia may continue to be a problem in mature, usually very small, Yorkies. It is often seen in Yorkie puppies at 5 to 16 weeks of age. Very tiny Yorkie puppies are especially predisposed to hypoglycaemia because a lack of muscle mass makes it difficult to store glucose and regulate blood sugar. Factors such as stress, fatigue, a cold environment, poor nutrition, and a change in diet or feeding schedule may bring on hypoglycaemia. Low blood sugar can also be the result of a bacterial infection, parasite or portosystemic liver shunt. Hypoglycaemia causes the puppy to become drowsy, listless (glassy-eyed), shaky, uncoordinated, since the brain relies on sugar to function. During a hypoglycaemic attack, the puppy usually has very pale or grey gums. The puppy also may not eat unless force-fed. Hypoglycaemia and dehydration seem to go hand-in-hand, and force-feeding or injecting fluids may also be necessary. Additionally, a hypoglycaemic Yorkie may have a lower than normal body temperature and, in extreme cases, may have a seizure or go into a coma. A dog showing symptoms should be given sugar in the form of corn syrup or Nutri-Cal and be treated by a veterinarian immediately, as prolonged or recurring attacks of hypoglycaemia can permanently damage the dog's brain. In severe cases it can be fatal.
Dysthymia
Dysthymia characteristics include an extended period of depressed mood combined with at least two other symptoms which may include insomnia or hypersomnia, fatigue or low energy, eating changes (more or less), low self-esteem, or feelings of hopelessness. Poor concentration or difficulty making decisions are treated as another possible symptom. Mild degrees of dysthymia may result in people withdrawing from stress and avoiding opportunities for failure. In more severe cases of dysthymia, people may even withdraw from daily activities. They will usually find little pleasure in usual activities and pastimes. Diagnosis of dysthymia can be difficult because of the subtle nature of the symptoms and patients can often hide them in social situations, making it challenging for others to detect symptoms. Additionally, dysthymia often occurs at the same time as other psychological disorders, which adds a level of complexity in determining the presence of dysthymia, particularly because there is often an overlap in the symptoms of disorders. There is a high incidence of comorbid illness in those with dysthymia. Suicidal behavior is also a particular problem with persons with dysthymia. It is vital to look for signs of major depression, panic disorder, generalised anxiety disorder, alcohol and substance misuse and personality disorder.
Squeamishness
Symptoms of squeamishness may include
dizziness,
lightheadedness,
nausea,
shaking, and
pallor
Hyperventilation syndrome
Hyperventilation syndrome is a remarkably common cause of dizziness complaints. About 25% of patients who complain about dizziness are diagnosed with HVS.
Macropsia
Endogenous hypoglycaemia can result in number of visual disturbances and sometimes macropsia. This kind of hypoglycaemia is defined as having an abnormally low blood-sugar level due to anything other than the exogenous administration of insulin. Macropsia has been observed in experimental hypoglycaemia and in patients receiving insulin therapy.
Hypoparathyroidism
The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet. Many also report a number of subjective symptoms such as fatigue, headaches, bone pain and insomnia. Crampy abdominal pain may occur. Physical examination of someone with hypocalcemia may show tetany, but it is also possible to provoke tetany of the facial muscles by tapping on the facial nerve (a phenomenon known as Chvostek's sign) or by using the cuff of a sphygmomanometer to temporarily obstruct the blood flow to the arm (a phenomenon known as Trousseau's sign of latent tetany).
Hypoglycemia
Not enough cortisol, such as in Addison's disease, not enough glucagon, or not enough epinephrine can result in low blood sugar. This is a more common cause in children.
Diabetic hypoglycemia
A commonly used "number" to define the lower limit of normal glucose is 70 mg/dl (3.9 mmol/l), though in someone with diabetes, hypoglycemic symptoms can sometimes occur at higher glucose levels, or may fail to occur at lower. Some textbooks for nursing and pre-hospital care use the range 80 mg/dl to 120 mg/dl (4.4 mmol/l to 6.7 mmol/l). This variability is further compounded by the imprecision of glucose meter measurements at low levels, or the ability of glucose levels to change rapidly.
Freediving blackout
A high level of hypocapnia is readily identifiable as it causes dizziness and tingling of the fingers. These extreme symptoms are caused by the increase of blood pH (alkalosis) following the reduction of carbon dioxide, which is required to maintain the acidity of the blood. The absence of any symptoms of hypocapnia is not an indication that the diver’s carbon dioxide is within safe limits and cannot be taken as an indication that it is therefore safe to dive. Conservative breath-hold divers who hyperventilate but stop doing so before the onset of these symptoms are likely to be already hypocapnic without knowing it.
Neuroglycopenia
Perhaps a much more common example of the same phenomenon occurs in the people with poorly controlled type 1 diabetes who develop symptoms of hypoglycemia at levels of blood glucose which are normal for most people.
Diabetic coma
Unconsciousness due to hypoglycemia can occur within 20 minutes to an hour after early symptoms and is not usually preceded by other illness or symptoms. Twitching or convulsions may occur. A person unconscious from hypoglycemia is usually pale, has a rapid heart beat, and is soaked in sweat: all signs of the adrenaline response to hypoglycemia. The individual is not usually dehydrated and breathing is normal or shallow. Their blood sugar level, measured by a glucose meter or laboratory measurement at the time of discovery, is usually low but not always severely, and in some cases may have already risen from the nadir that triggered the unconsciousness.
Hypoxia (medical)
Atmospheric pressure reduces with altitude and with it, the amount of oxygen. The reduction in the partial pressure of inspired oxygen at higher altitudes lowers the oxygen saturation of the blood, ultimately leading to hypoxia. The clinical features of altitude sickness include: sleep problems, dizziness, headache and oedema.i
Hypoesthesia
Hypoesthesia (also spelled as hypesthesia) is a common side effect of various medical conditions which manifests as a reduced sense of touch or sensation, or a partial loss of sensitivity to sensory stimuli. In everyday speech this is generally referred to as numbness.
Hypochondriasis
If a person is ill with a medical disease such as diabetes or arthritis, there will often be psychological consequences, such as depression. Some even report being suicidal. In the same way, someone with psychological issues such as depression or anxiety will sometimes experience physical manifestations of these affective fluctuations, often in the form of medically unexplained symptoms. Common symptoms include headaches; abdominal, back, joint, rectal, or urinary pain; nausea; fever and/or night sweats; itching; diarrhea; dizziness; or balance problems. Many people with hypochondriasis accompanied by medically unexplained symptoms feel they are not understood by their physicians, and are frustrated by their doctors’ repeated failure to provide symptom relief.
Ketotic hypoglycemia
The most useful diagnostic tests include measurement of insulin, growth hormone, cortisol, and lactic acid at the time of the hypoglycemia. Plasma acylcarnitine levels and urine organic acids exclude some of the important metabolic diseases. When the episodes are recurrent or severe, the definitive test is a hospitalization for a supervised diagnostic fast. This usually demonstrates "accelerated fasting"—a shorter time until the glucose begins to fall, but normal metabolic and counterregulatory responses as the glucose falls. As the glucose reaches hypoglycemic levels, the insulin is undetectable, counterregulatory hormones, fatty acids, and ketones are high, and glucagon injection elicits no rise of glucose.
Hypoglycemia
It can also be mistaken for alcohol intoxication.
Hyperinsulinemic hypoglycemia
Hyperinsulinemic hypoglycemia describes the condition and effects of low blood glucose caused by excessive insulin. Hypoglycemia due to excess insulin is the most common type of serious hypoglycemia. It can be due to endogenous or injected insulin.
Manifestations of hyperinsulinemic hypoglycemia vary by age and severity of the hypoglycemia. In general, most signs and symptoms can be attributed to (1) the effects on the brain of insufficient glucose (neuroglycopenia) or (2) to the adrenergic response of the autonomic nervous system to hypoglycemia. A few miscellaneous symptoms are harder to attribute to either of these causes. In most cases, all effects are reversed when normal glucose levels are restored.
Hypoadrenocorticism in dogs
The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.
Diabetic coma
Nonketotic hyperosmolar coma usually develops more insidiously than diabetic ketoacidosis because the principal symptom is lethargy progressing to obtundation, rather than vomiting and an obvious illness. Extremely high blood sugar levels are accompanied by dehydration due to inadequate fluid intake. Coma occurs most often in patients who have type 2 or steroid diabetes and have an impaired ability to recognize thirst and drink. It is classically a nursing home condition but can occur in all ages.
Reactive hypoglycemia
Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within four hours after a high carbohydrate meal in people both with and without diabetes. The term is not necessarily a diagnosis since it requires an evaluation to determine the cause of the hypoglycemia.
Hypoglycemia
Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.
Ketotic hypoglycemia
Ketotic hypoglycemia more commonly refers to a common but mysterious "disease" of recurrent hypoglycemic symptoms with ketosis in young children. The cause and the homogeneity of the condition remain uncertain, but a characteristic presentation, precipitating factors, diagnostic test results, treatment, and natural history can be described. It remains one of the more common causes of hypoglycemia in the age range.
Malaise
Malaise is a non-specific symptom and can be present in the slightest ailment, such as an emotion (causing fainting, a vasovagal response) or hunger (light hypoglycemia), to the most serious conditions (cancer, stroke, heart attack, internal bleeding, etc.).
Hypoglycemia
Hypoglycemia, also known as low blood sugar, is when blood sugar decreases to below normal levels. This may result in a variety of symptoms including clumsiness, trouble talking, confusion, loss of consciousness, seizures or death. A feeling of hunger, sweating, shakiness and weakness may also be present. Symptoms typically come on quickly.
The most common cause of hypoglycemia is medications used to treat diabetes mellitus such as insulin and sulfonylureas. Risk is greater in diabetics who have eaten less than usual, exercised more than usual or have drunk alcohol. Other causes of hypoglycemia include kidney failure, certain tumors, such as insulinoma, liver disease, hypothyroidism, starvation, inborn error of metabolism, severe infections, reactive hypoglycemia and a number of drugs including alcohol. Low blood sugar may occur in otherwise healthy babies who have not eaten for a few hours.
The glucose level that defines hypoglycemia is variable. In people with diabetes, levels below 3.9 mmol/L (70 mg/dL) is diagnostic. In adults without diabetes, symptoms related to low blood sugar, low blood sugar at the time of symptoms and improvement when blood sugar is restored to normal confirm the diagnosis. Otherwise, a level below 2.8 mmol/L (50 mg/dL) after not eating or following exercise may be used. In newborns, a level below 2.2 mmol/L (40 mg/dL), or less than 3.3 mmol/L (60 mg/dL) if symptoms are present, indicates hypoglycemia. Other tests that may be useful in determining the cause include insulin and C peptide levels in the blood.
Among people with diabetes, prevention is by matching the foods eaten with the amount of exercise and the medications used. When people feel their blood sugar is low, testing with a glucose monitor is recommended. Some people have few initial symptoms of low blood sugar, and frequent routine testing in this group is recommended. Treatment of hypoglycemia is by eating foods high in simple sugars or taking dextrose. If a person is not able to take food by mouth, an injection of glucagon may help. The treatment of hypoglycemia unrelated to diabetes includes treating the underlying problem as well and a healthy diet. The term "hypoglycemia" is sometimes incorrectly used to refer to idiopathic postprandial syndrome, a controversial condition with similar symptoms that occur following eating but with normal blood sugar levels.
Hypoglycemia
Determining the presence of both parts of this definition is not always straightforward, as hypoglycemic symptoms and effects are vague and can be produced by other conditions; people with recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning, and many measurement methods (especially glucose meters) are imprecise at low levels.
Diabetic hypoglycemia
Glucagon is a hormone that rapidly counters the metabolic effects of insulin in the liver, causing glycogenolysis and release of glucose into the blood. It can raise the glucose by 30–100 mg/dL within minutes in any form of hypoglycemia caused by insulin excess (including all types of diabetic hypoglycemia). It comes in a glucagon emergency rescue kit which includes tiny vials containing 1 mg, which is a standard adult dose. The glucagon in the vial is a lyophilized pellet, which must be reconstituted with 1 mL of sterile water, included in the "kit". In the widely used Lilly Emergency Kit, the water is contained in a syringe with a large needle for intramuscular injection and must be injected into the vial with the pellet of glucagon before being injected. Glucagon works if given subcutaneously, but absorption and recovery are faster if it is injected deep into a muscle (usually the middle of the outside of the thigh). It has an even more rapid effect when given intravenously but this is rarely practicable. Side effects of glucagon can include nausea and headache, but these can also occur after severe hypoglycemia even when glucagon is not used. Risks of glucagon use are far lower than risks of severe hypoglycemia, and it can usually produce a faster recovery than calling for paramedics and waiting for them to start an intravenous line to give dextrose. If someone uses this kit, they should be seen in an emergency room, as glucagon depletes glycogen stores, and can lead to a deadly rebound hypoglycemia.
Diabetic hypoglycemia
For people with insulin-requiring diabetes, hypoglycemia is one of the recurrent hazards of treatment. It limits the achievability of normal glucoses with current treatment methods. Hypoglycemia is a true medical emergency, which requires prompt recognition and treatment to prevent organ and brain damage.
Idiopathic hypoglycemia
Idiopathic hypoglycemia is a medical condition in which the glucose level in the blood (blood glucose) is abnormally low due to an undeterminable cause. This is considered an incomplete and unsatisfactory diagnosis by physicians and is rarely used by endocrinologists, as it implies an unfinished diagnostic evaluation. In general, the more severe the hypoglycemia and the more clearly it is proven, the less likely it is to remain "idiopathic".
Adrenal insufficiency
Signs and symptoms include: hypoglycemia, dehydration, weight loss, and disorientation. Additional signs and symptoms include weakness, tiredness, dizziness, low blood pressure that falls further when standing (orthostatic hypotension), cardiovascular collapse, muscle aches, nausea, vomiting, and diarrhea. These problems may develop gradually and insidiously. Addison's disease can present with tanning of the skin that may be patchy or even all over the body. Characteristic sites of tanning are skin creases (e.g. of the hands) and the inside of the cheek (buccal mucosa). Goitre and vitiligo may also be present. Eosinophilia may also occur.
Complications of diabetes mellitus
Furthermore, reduced sympathoadrenal responses can cause hypoglycemia unawareness. The concept of hypoglycemia-associated autonomic failure (HAAF) in diabetes posits that recent incidents of hypoglycemia causes both defective glucose counterregulation and hypoglycemia unawareness. By shifting glycemic thresholds for the sympathoadrenal (including epinephrine) and the resulting neurogenic responses to lower plasma glucose concentrations, antecedent hypoglycemia leads to a vicious cycle of recurrent hypoglycemia and further impairment of glucose counterregulation. In many cases (but not all), short-term avoidance of hypoglycemia reverses hypoglycemia unawareness in affected patients, although this is easier in theory than in clinical experience.
Hyperinsulinemic hypoglycemia
When the cause of hypoglycemia is not obvious, the most valuable diagnostic information is obtained from a blood sample (a "critical specimen") drawn during the hypoglycemia. Detectable amounts of insulin are abnormal and indicate that hyperinsulinism is likely to be the cause. Other aspects of the person's metabolic state, especially low levels of free fatty acids, beta-hydroxybutyrate and ketones, and either high or low levels of C-peptide and proinsulin can provide confirmation.
Causes of seizures
Hypoglycemic seizures are usually a complication of treatment of diabetes mellitus with insulin or oral medications. Less commonly, it can be the result of excessive insulin produced by the body (hyperinsulinemia) or other causes.
Diabetes in dogs
Hypoglycemia, or low blood glucose, can happen even with care, since insulin requirements can change without warning. Some common reasons for hypoglycemia include increased or unplanned exercise, illness, or medication interactions, where another medication potentiates the effects of the insulin. Vomiting and diarrhea episodes can bring on a hypoglycemia reaction, due to dehydration or simply a case of too much insulin and not enough properly digested food. Symptoms of hypoglycemia need to be taken seriously and addressed promptly. Since serious hypoglycemia can be fatal, it is better to treat a suspected incident than to fail to respond quickly to the signs of actual hypoglycemia. Dr. Audrey Cook addressed the issue in her 2007 article on diabetes mellitus: "Hypoglycemia is deadly; hyperglycemia is not. Owners must clearly understand that too much insulin can kill, and that they should call a veterinarian or halve the dose if they have any concerns about a pet's well-being or appetite. Tell owners to offer food immediately if the pet is weak or is behaving strangely."
Oxyhyperglycemia
Oxyhyperglycemia is a special type of impaired glucose tolerance characterized by a rapid and transient hyperglycemia (i.e. rise in blood glucose) spike after an oral intake of glucose, the peak of this spike being high enough to cause transient, symptom free glycosuria (i.e. detectable glucose in urine), but this hyperglycemia reverses rapidly and may even go to hypoglycemia in the later phase. This sharp downstroke overshooting towards hypoglycemia distinguishes this pathologic phenomenon from the artificial hyperglycemia inducible by an intravenous bolus dose of a large amount of glucose solution. Early dumping syndrome patients usually have oxyhyperglycemia associated with any meal or OGTT.
Glycerol kinase deficiency
Glycerol Kinase Deficiency causes the condition known as hyperglycerolemia, an accumulation of glycerol in the blood and urine. This excess of glycerol in bodily fluids can lead to many more potentially dangerous symptoms. Common symptoms include vomiting and lethargy. These tend to be the only symptoms, if any, present in adult GKD which has been found to present with fewer symptoms than infant or juvenile GKD. When GKD is accompanied by Duchenne Muscular Dystrophy and Adrenal Hypoplasia Congenita, also caused by mutations on the Xp21 chromosome, the symptoms can become much more severe. Symptoms visible at or shortly after birth include:
Some other symptoms that become more noticeable with time would be:
Many of the physically visible symptoms, such as cryptorchidism, strabismus, learning disabilities, and myopathy, tend to have an added psychological effect on the subject due to the fact that they can set him or her apart from those without GKD. Cryptorchidism, the failure of one or both of the testes to descend to the scrotum, has been known to lead to sexual identity confusion amongst young boys because it is such a major physiological anomaly. Strabismus is the misalignment of one's eyes. Typically, one is focused but the other is “lazy” and is directed inward or out ward (up and down is less common but does occur).
Glutamate dehydrogenase 1
Familial hyperinsulinism, linked to mutations in GLUD1, is characterized by hypoglycemia that ranges from severe neonatal-onset, difficult-to-manage disease to childhood-onset disease with mild symptoms and difficult-to-diagnose hypoglycemia. Neonatal-onset disease manifests within hours to two days after birth. Childhood-onset disease manifests during the first months or years of life. In the newborn period, presenting symptoms may be nonspecific, including seizures, hypotonia, poor feeding, and apnea. In severe cases, serum glucose concentrations are typically extremely low and thus easily recognized, whereas in milder cases, variable and mild hypoglycemia may make the diagnosis more difficult. Even within the same family, disease manifestations can range from mild to severe. Individuals with autosomal recessive familial hyperinsulinism, caused by mutations in either ABCC8 or KCNJ11 (FHI-KATP), tend to be large for gestational age and usually present with severe refractory hypoglycemia in the first 48 hours of life; affected infants usually respond only partially to diet or medical management (i.e., diazoxide therapy) and thus may require pancreatic resection. Individuals with autosomal dominant FHI-KATP tend to be appropriate for gestational age at birth, to present at approximately age one year (range: 2 days - 30 years), and to respond to diet and diazoxide therapy. Exceptions to both of these generalities have been reported. FHI-GCK, caused by mutations in GCK, may be much milder than FHI-KATP; however, some persons have severe, diazoxide-unresponsive hypoglycemia. FHI-HADH, caused by mutations in HADH, tends to be relatively mild, although severe cases have been reported. Individuals with FHI-HNF4A, caused by mutations in HNF4A, are typically born large for gestational age and have mild features that respond to diazoxide treatment. FHI-UCP2, caused by mutations in UCP2, is a rare cause of diazoxide-responsive FH1. Hyperammonemia/hyperinsulinism (HA/HI) is associated with mild-to-moderate hyperammonemia and with relatively mild, late-onset hypoglycemia; most but not all affected individuals have mutations in GLUD1.
Diabetic hypoglycemia
Although one expects hypoglycemic episodes to be accompanied by the typical symptoms (e.g., tremor, sweating, palpitations, etc.), this is not always the case. When hypoglycemia occurs in the absence of such symptoms it is called "hypoglycemic unawareness". Especially in people with long-standing type 1 diabetes and those who attempt to maintain glucose levels which are closer to normal, hypoglycemic unawareness is common.
Diabetic hypoglycemia
The most common treatment for this condition is to liberalize the patient's target glucose levels, in an attempt to decrease the frequency of hypoglycemic episodes. Hypoglycemic unawareness will sometimes disappear when the frequency of hypoglycemic episodes has declined, but this is not always the case.
Glucagon rescue
At the first signs of hypoglycemia, an insulin user should treat it immediately by consuming carbohydrate to restore blood glucose to safe levels (thereby preventing progression to severe hypoglycemia). However, not all insulin users can feel and recognize the early signs, particularly when sleeping. This can quickly lead to an emergency resulting in unconsciousness, inability to swallow, seizures, and in extreme cases death. In the past, treatment consisted of intravenous delivery of dextrose (glucose) usually in a hospital emergency department; however, the delay in treatment due to emergency response and transport to a medical facility is life-threatening.
Vertiginous epilepsy
In the late 19th century and early 20th century, Hughlings Jackson and W.R. Gowers recognized that episodes of dizziness were a symptom of epilepsy. During this time, when epileptic symptoms were brought to the forefront of study, there was no distinction between dizziness and vertigo. Sir George Frederick (1868–1941), known for his work in pediatric rheumatoid arthritis referred to as Still’s disease, was the first to publish a description of episodic vertigo in children within the broad category of ‘headaches in children’ in 1924. Until recently, it was not widely recognized that episodes of suspected dizziness might be caused by epilepsy.
Diabetes management
Relying on their own perceptions of symptoms of hyperglycemia or hypoglycemia is usually unsatisfactory as mild to moderate hyperglycemia causes no obvious symptoms in nearly all patients. Other considerations include the fact that, while food takes several hours to be digested and absorbed, insulin administration can have glucose lowering effects for as little as 2 hours or 24 hours or more (depending on the nature of the insulin preparation used and individual patient reaction). In addition, the onset and duration of the effects of oral hypoglycemic agents vary from type to type and from patient to patient.
Hypothermia
Symptoms of mild hypothermia may be vague, with sympathetic nervous system excitation (shivering, high blood pressure, fast heart rate, fast respiratory rate, and contraction of blood vessels). These are all physiological responses to preserve heat. Increased urine production due to cold, mental confusion, and liver dysfunction may also be present. Hyperglycemia may be present, as glucose consumption by cells and insulin secretion both decrease, and tissue sensitivity to insulin may be blunted. Sympathetic activation also releases glucose from the liver. In many cases, however, especially in people with alcoholic, hypoglycemia appears to be a more common. Hypoglycemia is also found in many people with hypothermia, as hypothermia may be a result of hypoglycemia.
Hypoglycemia
The word "hypoglycemia" is also spelled "hypoglycaemia" or "hypoglycæmia". The term means low blood sugar in Greek. "ὑπογλυκαιμία", from "hypo-", "glykys", "haima".
Hypovolemia
Hypovolemia can be recognized by tachycardia, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.
Hyperglycemia
Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.
Dumping syndrome
Late dumping syndrome occurs 2 to 3 hours after a meal. It results from excessive movement of sugar into the intestine, which raises the body's blood glucose level and causes the pancreas to increase its release of the hormone insulin. The increased release of insulin causes a rapid drop in blood glucose levels, a condition known as alimentary hypoglycemia, or low blood sugar.
Hypoglycemia
Brief or mild hypoglycemia produces no lasting effects on the brain, though it can temporarily alter brain responses to additional hypoglycemia. Prolonged, severe hypoglycemia can produce lasting damage of a wide range. This can include impairment of cognitive function, motor control, or even consciousness. The likelihood of permanent brain damage from any given instance of severe hypoglycemia is difficult to estimate and depends on a multitude of factors such as age, recent blood and brain glucose experience, concurrent problems such as hypoxia, and availability of alternative fuels. Prior hypoglycemia also blunts the counterregulatory response to future hypoglycemia . While the mechanism leading to blunted counterregulation is unknown several have been proposed.
Diabetic hypoglycemia
Since epinephrine release is a function of the autonomic nervous system, the presence of autonomic neuropathy (i.e., a damaged autonomic nervous system) will cause the epinephrine release in response to hypoglycemia to be lost or blunted. Unfortunately, damage to the autonomic nervous system in the form of autonomic neuropathy is a common complication of long-standing diabetes (especially type 1 diabetes), so the presence of hypoglycemic unawareness may be a sign of autonomic neuropathy, although the autonomic response to hypoglycemia is already impaired in patients with type 1 diabetes mellitus even in the absence of autonomic neuropathy.
Hyperosmolar hyperglycemic state
Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing.
Diabetes in dogs
Successful home treatment of a hypoglycemia event depends on being able to recognize the symptoms early and responding quickly with treatment. Trying to make a seizing or unconsicous animal swallow can cause choking on the food or liquid. There is also a chance that the materials could be aspirated (enter the lungs instead of being swallowed). Seizures or loss of consciousness because of low blood glucose levels are medical emergencies.
Hypoglycemia
In cases of recurrent hypoglycemia with severe symptoms, the best method of excluding dangerous conditions is often a "diagnostic fast". This is usually conducted in the hospital, and the duration depends on the age of the patient and response to the fast. A healthy adult can usually maintain a glucose level above 50 mg/dL (2.8 mM) for 72 hours, a child for 36 hours, and an infant for 24 hours. The purpose of the fast is to determine whether the person can maintain his or her blood glucose as long as normal, and can respond to fasting with the appropriate metabolic changes. At the end of the fast the insulin should be nearly undetectable and ketosis should be fully established. The patient's blood glucose levels are monitored and a critical specimen is obtained if the glucose falls. Despite its unpleasantness and expense, a diagnostic fast may be the only effective way to confirm or refute a number of serious forms of hypoglycemia, especially those involving excessive insulin.
D-Glyceric acidemia
Symptoms of the disease (in its most severe form) include progressive neurological impairment, mental/motor retardation, hypotonia, seizures, failure to thrive and metabolic acidosis.
Reactive hypoglycemia
The condition is related to homeostatic systems utilised by the body to control the blood sugar level. It is described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be lessened if a lot of physical activity is undertaken in the first few hours after food consumption.
Hyperinsulinemia
There are often no visible symptoms of hyperinsulinemia unless hypoglycaemia (low blood sugar) is present.
Oxyhyperglycemia
In early dumping syndrome, pancreatic glucagon is augmented in the early postprandial period, probably through stimulation the catecholamines involved in the generalized autonomic surge induced by the osmotic load, but at 120 min, when most of the hypoglycemias are encountered, pancreatic glucagon is no longer detectable, likely through inhibition by GLP-1. Incretins including GLP1 and GIP also bring in the late dumping effects including the insulin rise and the reactive hypoglycemia.
Reactive hypoglycemia
A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:
Freediving blackout
A high level of hypocapnia is readily recognized as it causes dizziness and tingling of the fingers. These extreme symptoms are caused by the increase of blood pH (alkalosis) following the reduction of CO, which is required to maintain the acidity of the blood. The absence of any symptoms of hypocapnia is not an indication that the diver’s carbon dioxide level is within safe limits and cannot be taken as an indication that it is therefore safe to dive. Conservative breath-hold divers who hyperventilate but stop doing so before the onset of these symptoms are likely to be hypocapnic already without knowing it.
Optic nerve hypoplasia
Absence of GH may often be indicated by short stature, although this is not always the case. Other indicators of GH deficiency may include hypoglycemic events (including seizures), prolonged jaundice, micropenis in boys, and delayed dentition. Testing for GH may involve blood tests (IGF-1 and IGFBP-3), growth hormone stimulation test, or bone age x-ray of the hand or wrist (or body for children younger than 2 years).
Reactive hypoglycemia
The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.
Chvostek sign
The Chvostek sign () is a clinical sign of existing nerve hyperexcitability (tetany) seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped in front of tragus the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia (i.e. from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of nerves. Though classically described in hypocalcemia, this sign may also be encountered in respiratory alkalosis, such as that seen in hyperventilation, which causes decreased serum Ca with a normal calcium level due to a shift of Ca from the blood to albumin which has become more negative in the alkalotic state.
Hyperinsulinism
Hyperinsulinism refers to an above normal level of insulin in the blood of a person or animal. Normal insulin secretion and blood levels are closely related to the level of glucose in the blood, so that a given level of insulin can be normal for one blood glucose level but low or high for another. Hyperinsulinism can be associated with several types of medical problems, which can be roughly divided into two broad and largely non-overlapping categories: those tending toward reduced sensitivity to insulin and high blood glucose levels (hyperglycemia), and those tending toward excessive insulin secretion and low glucose levels (hypoglycemia).
Hyperinsulinism due to reduced insulin sensitivity is usually asymptomatic. In contrast, hyperinsulinemic hypoglycemia can produce any of the entire range of hypoglycemic symptoms, from shakiness and weakness, to seizures or coma.
Glucose meter
In contrast, people who do not have diabetes may periodically have hypoglycemic symptoms but may also have a much higher rate of false positives to true, and a meter is not accurate enough to base a diagnosis of hypoglycemia upon. A meter can occasionally be useful in the monitoring of severe types of hypoglycemia (e.g., congenital hyperinsulinism) to ensure that the average glucose when fasting remains above 70 mg/dl (3.9 mmol/l).
Dizziness
Dizziness is an impairment in spatial perception and stability. The term "dizziness" is imprecise: it can refer to vertigo, presyncope, disequilibrium, or a non-specific feeling such as giddiness or foolishness.
Hypoadrenocorticism in dogs
Symptoms of hypoadrenocorticism can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters. Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning hypoadrenocorticism the nicknames of "the Great Mimic" and "the Great Imitator". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.
Diabetic hypoglycemia
Because the autonomic response is, in effect, the body's backup system for responding to hypoglycemia, patients with type 1 diabetes are forced to rely almost exclusively on a backup system for protection, which can unfortunately, deteriorate over time. The reduced autonomic response (including the sympathetic neural norepinephrine and acetylcholine as well as the adrenomedullary epinephrine response) causes the clinical syndrome of hypoglycemia unawareness — loss of the largely neurogenic warning symptoms of developing hypoglycemia.
Hypoglycemia
The glucose level that defines hypoglycemia is variable. In diabetics a level below 3.9 mmol/L (70 mg/dL) is diagnostic. In adults without diabetes, symptoms related to low blood sugar, low blood sugar at the time of symptoms, and improvement when blood sugar is restored to normal confirm the diagnosis. This is known as the Whipple's triad. Otherwise a level below 2.8 mmol/L (50 mg/dL) after not eating or following exercise may be used. In newborns a level below 2.2 mmol/L (40 mg/dL) or less than 3.3 mmol/L (60 mg/dL) if symptoms are present indicates hypoglycemia. Other tests that may be useful in determining the cause include insulin and C peptide levels in the blood. Hyperglycemia, a high blood sugar, is the opposite condition.
Hyperglycerolemia
The Human Phenotype Ontology provided the following list of symptoms and signs for hyperglycerolemia: Abnormality of metabolism/homeostasis, Cognitive Deficit, EMG abnormality, Muscular Hypotonia, Myopathy, Neurological speech impairment, Primary adrenal insufficiency, Short stature, Cryptorchidism, EEG abnormality, Lumbar Hyperlordosis, Reduced bone mineral density, Scoliosis, Seizures, Abnormal facial shape, and Adrenal insufficiency. Adrenal insufficiency is associated with the genetic disease X-linked adrenal hypoplasia congenita. If the glycerol kinase gene is deleted then the NROB1 gene is also often deleted, which causes X-linked adrenal hypoplasia congenita.
Glycerol and glycerol kinase activity analyses are usually not offered by routine general medical laboratories. To diagnose hyperglycerolemia, blood and urine can be tested for the amounts of glycerol present.
There are three clinical forms of GKD: infantile, juvenile, and adult. The infantile form is associated with severe developmental delay and results in a syndrome with Xp21 gene deletion with congenital adrenal hypoplasia and/or Duchenne muscular dystrophy. The infantile diagnosis is made by measuring plasma glycerol and is characterized by glycerol levels between 1.8 and 8.0 mmol/L and glyceroluria more than 360 mmol/24h. To confirm the diagnosis, genetic testing of the Xp21 gene is definitive. Children with GKD have severe hypoglycemic episodes and profound metabolic acidosis, or are completely symptom free. Individuals who are unable to form glucose from the glycerol released during triglyceride catabolism also the hypoglycemic episodes often disappear during adolescence. Patients with the juvenile and adult forms often have no symptoms and are diagnosed fortuitously when a medical professional tests for another medical condition. The juvenile form is an uncommon form characterized by Reye syndrome-like clinical manifestations including episodic vomiting, acidemia, and disorders of consciousness.
Neuroglycopenia
Neuroglycopenia is a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. Glycopenia affects the function of neurons, and alters brain function and behavior. Prolonged or recurrent neuroglycopenia can result in loss of consciousness, damage to the brain, and eventual death.
Neuroglycopenia
In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia.
Hyperglycemia
Ketoacidosis is a life-threatening condition which requires immediate treatment. Symptoms include: shortness of breath, breath that smells fruity (such as pear drops), nausea and vomiting, and very dry mouth.
Chronic hyperglycemia (high blood sugar) injures the heart in patients without a history of heart disease or diabetes and is strongly associated with heart attacks and death in subjects with no coronary heart disease or history of heart failure.
3-hydroxyacyl-coenzyme A dehydrogenase deficiency
Typically, initial signs and symptoms of this disorder occur during infancy or early childhood and can include poor appetite, vomiting, diarrhea, lethargy, hypoglycemia, hypotonia, liver problems, and hyperinsulinism (high levels of insulin). Insulin controls the amount of sugar that moves from the blood into cells for conversion to energy. Individuals with 3-hydroxyacyl-coenzyme A dehydrogenase deficiency are also at risk for complications such as seizures, life-threatening heart and breathing problems, coma, and sudden unexpected death.
Ketotic hypoglycemia
The presence or absence of ketosis is therefore an important clue to the cause of hypoglycemia in an individual patient. Absence of ketosis ("nonketotic hypoglycemia") most often indicates excessive insulin as the cause of the hypoglycemia. Less commonly, it may indicate a fatty acid oxidation disorder.
3-Hydroxy-3-methylglutaryl-CoA lyase deficiency
This disorder usually appears within the first year of life. The signs and symptoms of HMG-CoA lyase deficiency include vomiting, dehydration, lethargy, convulsions, and coma. When episodes occur in an infant or child, blood sugar becomes extremely low (hypoglycemia), and harmful compounds can build up and cause the blood to become too acidic (metabolic acidosis). These episodes are often triggered by an infection, fasting, strenuous exercise, or sometimes other types of stress.
Reactive hypoglycemia
Acute low blood sugar symptoms are best treated by consuming small amounts of sweet foods, so as to regain balance in the body's carbohydrate metabolism. Suggestions include sugary foods that are quickly digested, such as:If there is no hypoglycemia at the time of the symptoms, this condition is called "postprandial syndrome." It might be an "adrenergic postprandial syndrome" — blood glucose levels are normal, but the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient. This is often seen in dysautonomic disorders as well. Dietary recommendations for reactive hypoglycemia can help to relieve symptoms of postprandial syndrome.
Glutamate dehydrogenase 1
FHI is characterized by hypoglycemia that ranges from severe neonatal-onset, difficult-to-manage disease to childhood-onset disease with mild symptoms and difficult-to-diagnose hypoglycemia. Neonatal-onset disease manifests within hours to two days after birth. Childhood-onset disease manifests during the first months or years of life. In the newborn period, presenting symptoms may be nonspecific, including seizures, hypotonia, poor feeding, and apnea. In severe cases, serum glucose concentrations are typically extremely low and thus easily recognized, whereas in milder cases, variable and mild hypoglycemia may make the diagnosis more difficult. Even within the same family, disease manifestations can range from mild to severe.
Malnutrition
Hypoglycemia, whether known or suspected, can be treated with a mixture of sugar and water. If the child is conscious, the initial dose of sugar and water can be given by mouth. If the child is unconscious, give glucose by intravenous or nasogastric tube. If seizures occur after despite glucose, rectal diazepam is recommended. Blood sugar levels should be re-checked on two hour intervals.
Balance disorder
Pre-syncope is a feeling of lightheadedness or simply feeling faint. Syncope, by contrast, is actually fainting. A circulatory system deficiency, such as low blood pressure, can contribute to a feeling of dizziness when one suddenly stands up.
Hypercalcaemia
Other symptoms include cardiac arrhythmias (especially in those taking digoxin), fatigue, nausea, vomiting (emesis), anorexia, abdominal pain, constipation, & paralytic ileus. If renal impairment occurs as a result, manifestations can include polyuria, nocturia, and polydipsia. Psychiatric manifestation can include emotional instability, confusion, delirium, psychosis, & stupor. Limbus sign seen in eye due to hypercalcemia.
Anorexia nervosa
Abnormalities in conduction and repolarization of the heart that can result from anorexia nervosa include QT prolongation, increased QT dispersion, conduction delays, and junctional escape rhythms. Electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, can cause anomalies in the electrical activity of the heart, and result in life-threatening arrhythmias. Hypokalemia most commonly results in anorexic patients when restricting is accompanied by purging (induced vomiting or laxative use). Hypotension (low blood pressure) is common, and symptoms include fatigue and weakness. Orthostatic hypotension, a marked decrease in blood pressure when standing from a supine position, may also occur. Symptoms include lightheadedness upon standing, weakness, and cognitive impairment, and may result in fainting or near-fainting. Orthostasis in anorexia nervosa indicates worsening cardiac function and may indicate a need for hospitalization. Hypotension and orthostasis generally resolve upon recovery to a normal weight. The weight loss in anorexia nervosa also causes atrophy of cardiac muscle. This leads to decreased ability to pump blood, a reduction in the ability to sustain exercise, a diminished ability to increase blood pressure in response to exercise, and a subjective feeling of fatigue.
Paresthesia
In older individuals, paresthesia is often the result of poor circulation in the limbs (such as in peripheral vascular disease), most often caused by atherosclerosis, the build up of plaque within artery walls, over decades, with eventual plaque ruptures, internal clots over the ruptures and subsequent clot healing but leaving behind narrowing of the artery openings or closure, both locally and in downstream smaller branches. Without a proper supply of blood and nutrients, nerve cells can no longer adequately send signals to the brain. Because of this, paresthesia can also be a symptom of vitamin deficiency and malnutrition, as well as metabolic disorders like diabetes, hypothyroidism, and hypoparathyroidism. It can also be a symptom of mercury poisoning.
Beta blocker
Hypoglycemia can occur with beta blockade because β2-adrenoceptors normally stimulate glycogen breakdown (glycogenolysis) in the liver and pancreatic release of the hormone glucagon, which work together to increase plasma glucose. Therefore, blocking β2-adrenoceptors lowers plasma glucose. β1-blockers have fewer metabolic side effects in diabetic patients; however, the fast heart rate that serves as a warning sign for insulin-induced low blood sugar may be masked, resulting in hypoglycemia unawareness. This is termed beta blocker induced hypoglycemia unawareness. Therefore, beta blockers are to be used cautiously in diabetics.
Reactive hypoglycemia
The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an "insulin spike"), which in turn initiates rapid glucose uptake by tissues, either storing it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash". Another cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.
Dopamine beta hydroxylase deficiency
Another commonly experienced symptom is hypoglycemia, which is thought to be caused by adrenomedullary failure. In looking at the cardiovascular system, a loss of noradrenergic control is seen as T-wave abnormalities on electrocardiogram. Prolactin is frequently suppressed by excessive dopamine found in the patient's central nervous system. Excess dopamine can also affect digestion, producing vomiting and inhibiting motor signaling to the GI tract.
Neonatal hypoglycemia
Some observed symptoms are (these symptoms may be transient but reoccurring):Screening for hypoglycemia is done on every neonate on admission. One way of screening includes a heal stick to test the blood glucose level at the bedside. Diagnosing hypoglycemia in neonates requires two consecutive blood glucose readings of less than 40 mg/dl to properly diagnose hypoglycemia. Bedside glucose monitoring is only effective if the equipment is accurate, rapid, and reliable. This form of testing is often faster and more cost effective. Laboratory serum glucose testing is the most accurate way of testing blood glucose levels. These specimens are either taken from the heel, arterial, or venous punctures and must be store immediately on ice in order to prevent glycolysis, further altering the results. The hypoglycemic neonate should have a glucose test every 2-4 hours for the first 24 hours of life.
Reactive hypoglycemia
The NIH states: "The causes of most cases of reactive hypoglycemia are still open to debate. Some researchers suggest that certain people may be more sensitive to the body’s normal release of the hormone epinephrine, which causes many of the symptoms of hypoglycemia. Others believe deficiencies in glucagon secretion might lead to reactive hypoglycemia.
Diabetes mellitus
Low blood sugar (hypoglycemia) is common in people with type 1 and type 2 DM. Most cases are mild and are not considered medical emergencies. Effects can range from feelings of unease, sweating, trembling, and increased appetite in mild cases to more serious effects such as confusion, changes in behavior such as aggressiveness, seizures, unconsciousness, and (rarely) permanent brain damage or death in severe cases. Moderately low blood sugar may easily be mistaken for drunkenness; rapid breathing and sweating, cold, pale skin are characteristic of low blood sugar but not definitive. Mild to moderate cases are self-treated by eating or drinking something high in sugar. Severe cases can lead to unconsciousness and must be treated with intravenous glucose or injections with glucagon.
Neuroglycopenia
Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms. Specific manifestations vary by age and by the severity of the hypoglycemia. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person do tend to be similar from episode to episode.