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Pathophysiology of Hypoglycemia

Effects Of Hypoglycemia In Possible Sectors


The research is conducted to explain the aims, Pathophysiology of Hypoglycemia, causes and effects of Hypoglycemia, Somogyi effect and Dawn phenomenon. In this document there is guidance relating to low blood sugar, precautions which can be adopted to maintain blood sugar level.
The term – Hypoglycemia is derived from the Greek words in which “hypo” means low “glykys” means sweet and “haima” means blood. Hypoglycemia is a scientific word for peculiarly less quantity of sugar (glucose) in the blood (Ferry, n.d). This is the condition within which serum glucose intensity (the glucose or sugar amount in the blood) drops under 70mg/dl that recognized as Hypoglycemia, and is potentially dangerous.

It is usually caused by undue oozing of insulin by the islet cells of the pancreas. If insulin secretion is too much it results in hypoglycemia and if insulin secretion is too less it results in hyperglycemia. If no insulin is secreted, the result is diabetes (Dherbs, n.d).

Aim: The objective of the study is -

  • To study Pathophysiology of hypoglycemia.
  • To study causes and effects of hypoglycemia.
  • To provide about Somogyi effect and dawn phenomenon.
  • To study recent trends of hypoglycemia in UK.

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1.1 Normal physiological responses to hypoglycemia

The human brain exclusively uses the glucose as a fuel, but cannot synthesize or store it. As a result, for normal functioning brain requires adequate uptake of glucose from the plasma.


During normal condition insulin and glucagon regulates the extracellular supply of glucose. When the glucose level increases after a meal, glucose enters the pancreatic beta-cells. Inside the cells, phosphorylation of glucose-6-phosphate is under taken by the enzyme glucokinase. This function as the glucose sensor, which leads to series of incidences enabling the entry of calcium and release of insulin hormone.

The function of insulin is to help in restoration of normoglycemia by the following two ways:

  • Either by increasing glucose uptake by the cells of adipose tissue and skeletal muscles by translocating transporters of glucose from an intracellular pool of the cell facade
  • Or by lessening the hepatic glucose creation level by affecting both the processes of gluconeogenesis and glycogenolysis.

Such responses cause reticence of production of hepatic glucose and enhance marginal consumption of the glucose load, which is not taken up by the liver. As a consequence, level of plasma glucose generally returns to baseline values within quite a few hours (Cryer, 2011).


To protect the brain, several physiological mechanisms control the effects of hypoglycemia. In a non diabetic adult when glucose cannot be obtained from the intestinal absorption of food, the plasma glucose concentration starts declining. Glucose counter regulatory mechanisms prevent falling plasma glucose concentrations in blood. This mechanism starts before the onset of symptoms of hypoglycemia.

      • Decrease in insulin secretion.
      • Increase in glucagon secretion.
      • Increase in epinephrine secretion.
      • Cortisol and growth hormone contribute only if the hypoglycemia persists for several hours. These hormones limit glucose utilization and enhance hepatic glucose production.


Impairment of behavioral and counter regulatory responses- In diabetic patients Hypoglycemia is the effect of the interaction of relative or absolute restorative insulin excess and compromised behavioral and physiological defenses against declining glucose level of blood.

          • Insulin – Patients having beta-cell failure will not have the ability to suppress insulin release as it will not occur in them, i.e., those with long standing type 2 diabetes as well as type 1 diabetes. Hence, reticence of hepatic glucose creation carries on.
          • Glucagon - The glucagon response to hypoglycemia, although normal at the onset of diabetes, is lost in similar of insulin in type 1 diabetes and much gradually in type 2 diabetes.
          • Epinephrine – In the nonappearance of glucagon and insulin responses, patients depend upon epinephrine to defend themselves from hypoglycemia. The response of epinephrine to hypoglycemia too becomes attenuated in numerous patients. An attenuated epinephrine response grounds defective glucose contradicts regulation that is connected with a 25-fold or larger raised severe risk of hypoglycemia. An attenuated sympathoadrenal (chiefly sympathetic neural) response give effect to hypoglycemia ignorance, which is linked with a six-fold enhanced severe hazard of hypoglycemia.

1.2 The effects of ageing on the responses to hypoglycemia

Previous investigation done in United States of America and Britain compared such responses in older plus young non-diabetic adults yielded confounded interpretation and conflict results of the data, due to several participants had co-morbidities. These results are of less value, as hypoglycemia was persuaded mostly by an intravenous bolus vaccination of insulin.
According to clamp studies on evaluating young and elderly non-diabetic people, it was determined that –

                • All through placid hypoglycemia (blood glucose 3.3 mmo1/1; 59 mg/d1) the level of epinephrine and glucagon responses was lower.
                • In both of the age groups it was analyzed that uniformity could be attained at lower blood glucose (2.8 mmo1/1; 50 mg/d1). It depicts the presentation of these responses to much profound hypoglycemia (23).
                • By increase in the age, insulin rate clearance from the transmission declines that could increase the hypoglycemia risk in elderly person.

2. Hypoglycemia Symptoms

At times the glucose level of blood goes under 60 mg/dL, hypoglycemia symptoms begins appearing. Several time individual might feel symptoms on the above of such level. Lessening of blood glucose amount below 50 mg/dL is very unsafe as brain is greatly affected.

Early symptoms – The hormone Adrenaline is the major hormones released during hypoglycemia. It causes the majority of the early symptoms.

                • Palpitations
                • Anxiety
                • Sweating
                • Trembling
                • Clammy skin
                • Hunger and irritability

Symptoms later set – When brain remnants deprived of glucose than symptoms later set follows:

                • Difficulty in thinking
                • Headache
                • Seizures and coma
                • Confusion
                • At last after loss of consciousness or coma, death could occur.

Scientifically the hypoglycemia is classified into two categories:
o Neurogenic (autonomic) – Lessening level of glucose and cause patients to identify that they are experiencing a hypoglycemia incident. Stimulated by the ANS and are arbitrated in part through sympathoadrenal discharge of catecholamines (epinephrine and nor epinephrine) from the adrenal acetylcholine and medullae from postsynaptic sympathetic nerve finishing’s.
The symptoms of Neuroglycopenic takes place as a consequence of deprivation of brain neuronal glucose. Its symptoms comprises –

          • Confusion
          • Abnormal mental, irritability
          • Headaches
          • Difficulty in speaking
          • Stupor
          • Paresthesias, ataxia
          • Ultimately (if untreated) coma, seizures, and even death.
          • The symptoms of Neuroglycopenic is fleeting focal neurological deficits (e.g. hemi paresis and diplopia)

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3. Hypoglycemia causes

3.1 Hypoglycemia causes in person without diabetes

  • Medications – Intake of wrong medication of diabetes by accident is a probable hypoglycemia cause. Incorrect medications might cause hypoglycemia, particularly in children or in person with failure of kidney for example – quinine that is utilized to treat malaria.
  • Some critical illnesses – Hepatitis, disorders of the kidney influence the level of glucose in the blood. Prolonged starvation sometimes may be due to some eating disorder like anorexia nervosa. This starvation causes decrease of elements which are very essential in the body, causing hypoglycemia.
  • Insulin overproduction – Sometimes insulin hormone is overproduced due to rare type of tumor found in the pancreas. Overproduction of insulin in the body, results in hypoglycemia. Sometimes different kinds of tumors can also cause excess production of insulin hormone. There are confirmations that tumors themselves use up extra glucose of the blood. So, the pancreas beta cells generate excess insulin resulting in hypoglycemia. There is risk for those people who've undergone gastric bypass surgery.
  • Endocrine deficiencies – Due to adrenal glands and pituitary gland disorder, it may cause few essential hormones deficiency that is very crucial for the glucose production regulation. Such kind of disorders in the small children makes them much prone to hypoglycemia than the adult’s one.
  • Hypoglycemia is caused after taking food.
  • Extreme consumption of alcohol.

3.2 Reasons of Hypoglycemia in individuals without diabetes

In a diabetic patient the insulin effects is drastically eliminated. It is due to doesn’t enough produce of pancreas (type 1 diabetes) or because cells are not as much of responsive to it (type 2 diabetes). In order to deal with such situation patient generally depends on insulin or several other drugs premeditated to lower levels sugar of blood.
If an individual takes so many insulin relative to the level of glucose in your streams of blood than it gives result in blood sugar lessening concentration i.e. hypoglycemia. After the diabetes medication patient should take adequate amount of food, in absence of this i.e. after diabetes medication if patient do not take meal or exercise more than the normal, hypoglycemia may be caused.
It is not always the case that the hypoglycemia occurs before meals but sometimes it may also be caused after meals. It may be due to more production of insulin in the body than actually required. This type of hypoglycemia is referred as postprandial or postprandial hypoglycemia. It is observed in the patients who have undergone gastric bypass surgery as well as in other people who haven't had surgery (Mayo Clinic Staff, 2012).

4. Effects of Hypoglycemia

Hypoglycemia has following effects:

4.1 Adrenal Type Anxiety Induced Hypoglycemia

The stress hormones adrenaline is produced by the Adrenal gland in response to the message given by the body at the times when level of insulin is much high as well as sugar level of blood is low. On adrenaline secretion, insulin is “turned off” as well as it continues to sustain balance via adaptation. The experiences of hypoglycemic person are panic, fear and terror. This is due to fuel (glucose) deficient of brain and concurrently it is flooded with stress hormones-adrenaline, as a result of emotions symptoms (like nightmare, palpitation, panic attacks, nervousness, rage, violence, phobias and even fits) occur.

4.2 Hypoglycemia long term effects (if untreated)

“Over time steady attacks and stress of over secretion hormones deplete the body resistance and might also degrade organs of the body, resulting in adrenal fatigue as well as finally loss of pancreas causing diabetes. Thus, anxiety in hypoglycemia person is a consequence of over emission of stress hormones and immediate concentration of low blood sugar.

4.3 GABA effects

According to research, it was identified that there is an association among low levels of GABA and more levels of insulin. GABA acts as neurotransmitters and supports in inhibition of calming the body and stress signals. Benzodiapienes and Valium work by raising level of GABA (During and et. al., 1995).

4.4 Other Effects

Several times hypoglycemia could cause other illness, such as arthritis, ulcers, mental disorders, impotence, allergies, epilepsy and asthma. Functional hypoglycemia has been removed in person with such disorders as hyperactivity, delinquency and obesity, drug addiction, alcoholism, juvenile delinquency, schizophrenia (Hypoglycemia, n.d).


  • Brown, C.A. and Anderson, C.M., 2007. Study Guide to Accompany Pathophysiology: Functional Alterations in Human Health. Lippincott Williams & Wilkins.
  • Choudhary, P., 2011. Hypoglycaemia: current management and controversies. Postgrad Med J.
  • Cryer, P.E. 2011. Physiologic response to hypoglycemia in normal subjects and patients with diabetes mellitus. [Online]. Available at: <>. [Accessed on 2nd November 2012].
  • Desouza, C.V., Bolli, G.B. and Fonseca, V., 2010. Hypoglycemia, Diabetes, and Cardiovascular Events. Diabetes Care. 33(6). pp.1389-1391.
  • Dherbs. n.d Hypoglycemia. [Online]. Available at: <>. [Accessed on 2nd November 2012].
  • Diedrich, L., Sandoval, D. and Davis, S.N., 2002. Hypoglycemia associated autonomic failure. Clinical Autonomic Research. 12(5). pp. 358-365.
  • During, M.J. Leone, P. And et. al., 1995. Glucose modulates rat substantia nigra GABA release in vivo via ATP-sensitive potassium channels. Molecular Pharmacology and Neurogenetics Laboratory. 95(5). pp.2403-8.
  • Ferry, R. Jr. n.d. Hypoglycemia. [Online]. Available at: <>. [Accessed on 2nd November 2012].
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