Diabetes Mellitus and Hypoglycemia
Pathophysiology: Blood glucose level is normally regulated by insulin; a hormone produced by beta cells
in the islets of Langerhans located in the pancreas. Healthy individuals secrete small amounts of insulin
continuously into the bloodstream – basal secretion. The ingestion of carbohydrates triggers the
secretion of a larger volume of insulin. Endogenous insulin – is produced internally by one’s own body.
Exogenous insulin – is obtained externally from other sources and administered to the DM patient.
DM Type 1: It is characterized by the absence of endogenous insulin. Formerly called juvenile-onset
diabetes because it most commonly occurs in juveniles and young adults. An autoimmune process,
(possibly triggered by a viral infection), destroys beta cells, the development of insulin antibodies, and
the production of islet cell antibodies (ICAs). Affected people require exogenous insulin for the rest of
their lives.
DM Type 2: It is characterized by inadequate endogenous insulin and body’s inability to properly use
insulin. Beta cells respond inadequately to hyperglycemia resulting in chronically elevated blood glucose.
Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to
the elevated glucose. It is more common in adults; but is increasingly found in children. It is controlled
by diet and exercise and may require exogenous insulin initially then maintained by oral hypoglycemic
agents.
Role of Insulin: Insulin is the hormone required for glucose metabolism.
Glucose: Insulin stimulates active transport of glucose into cells. If insulin is absent, glucose remains in
the bloodstream. Blood becomes thick, which increases its osmolality/viscosity. Increased osmolality
stimulates the thirst center, causing the patient to experience polydipsia – excessive thirst, for additional
fluids required to thin the blood. Increased fluid does not pass into body tissues; the high serum
osmolality retains fluid in the bloodstream. As blood passes through the kidneys, some glucose
eliminated. The osmotic force created by glucose draws extra fluid and electrolytes with it, causing
abnormally increased urine volume – leading to polyuria – excessive urination.
Risk Factors for DM: Obesity, Sedentary lifestyle, Family history of diabetes, Age 40 years and older,
History of gestational DM, History of delivering infant weighing more than 10 lbs./pounds, African
American (33% higher risk for type 2 DM), Latin American/Hispanic (>300% higher risk for type 2 DM),
American Indians (33% to 50% higher risk for type 2 DM), Polycystic ovary syndrome, Cardiovascular
disease and hypertension. Presence of acanthosis nigricans (dark discoloration in body folds and
creases).
Metabolic syndrome: A syndrome thought to be a precursor to diabetes, Pt’s typically have Impaired
glucose tolerance (IGT), high serum insulin, hypertension, elevated triglycerides, low HDL cholesterol,
altered size and density of LDL cholesterol, It is believed that metabolic syndrome is a chronic low-grade
inflammatory process affecting endothelial tissue(the lining of the heart, blood and lymph vessels),
Long-term effects include atherosclerosis, ischemic heart disease, left ventricular hypertrophy and type
2 DM, Research is now directed at learning how to detect this syndrome early and what interventions
might slow or arrest the progress.
, Microvascular Complications: They result from changes in blood vessels. The capillaries thicken,
impairing the exchange of nutrients, gases and wastes.
Diabetic Retinopathy: Pathological changes in the retina that are associated with DM and that are
aggravated by hypertension and smoking. DM is the leading cause of blindness among people 25 to 74
years of age. The two types of diabetic retinopathy are (1) non proliferative and (2) proliferative and can
be present at the same time. Signs and symptoms that suggest impending eye problems are the
presence of spots (“floaters”) in the field of vision, seeing “cobwebs”, or sudden visual changes. DM
patients should have an eye exam at least once per year, so that future deterioration that could lead to
blindness may be prevented, for example – better control of HTN and early treatment of macular
edema.
Know Signs and Symptoms of kidney failure: Decreased urine output, although occasionally urine output
remains normal. Fluid retention, causing swelling in your legs, ankles or feet. Shortness of breath.
Fatigue. Confusion. Nausea. Weakness. Irregular heartbeat.
Macrovascular Complications: They are caused by accelerated atherosclerotic changes in the person
with diabetes, affecting peripheral, carotid, cerebral and coronary blood vessels. These complications
are associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and
peripheral vascular disease (PVD) – Know the signs & symptoms of PVD. Individuals with diabetes have a
2- to 4-fold increased risk for heart disease and stroke, which accounts for 68% of the deaths in people
with diabetes.
Treatment for macrovascular disease is directed toward: Weight loss – promotes insulin uptake to that
the amount of insulin circulating reduces. Exercise – sensitizes insulin receptors for uptake so that the
amount of insulin circulating reduces. Tobacco cessation –reduces vasoconstriction.
Neuropathic Complications: Neuropathy – Are pathologic changes in nerve tissue related to poor
glucose control, ischemic lesions of nerves and chemical changes in peripheral nerve cells. It can be
classified as: Mononeuropathy affects a single nerve or group of nerves resulting from inadequate blood
supply. Polyneuropathy involves both sensory and autonomic nerves. It affects both legs symmetrically.
Autonomic neuropathy affects the sympathetic and parasympathetic nervous systems. Gastroparesis –
delayed gastric emptying. Almost 30% of individuals older than age 40 with diabetes have impaired
sensation in as least one area of the foot. 60-70% of people who have DM experience neuropathies.
Acute Emergency Complications: Acute Hypoglycemia: Acute Hypoglycemia is a dangerous drop in
blood glucose in patients treated with insulin or other hypoglycemics.
Causes: Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent
pattern of exercise. Gastroparesis (stomach cannot empty itself of food in a normal way), renal
insufÏciency, and certain drugs including aspirin and beta-adrenergic blockers. Glucose levels between
50-70 mg/dl are considered moderate hypoglycemia. Please note that some patients with a glucose level
of 50 mg/dl may be asymptomatic(hypoglycemic unawareness).
Signs and symptoms may be: Adrenergic: They appear 1st and reflect the response of the nervous
system to inadequate glucose for cell function : shakiness, nervousness, irritability, tachycardia, anxiety,
lightheadedness, hunger, tingling. or numbness of the lips or tongue, and diaphoresis. Beta Blockers may
mask these symptoms causing a delay in diagnosis and treatment. Neuroglycopenic: Caused by shortage
Pathophysiology: Blood glucose level is normally regulated by insulin; a hormone produced by beta cells
in the islets of Langerhans located in the pancreas. Healthy individuals secrete small amounts of insulin
continuously into the bloodstream – basal secretion. The ingestion of carbohydrates triggers the
secretion of a larger volume of insulin. Endogenous insulin – is produced internally by one’s own body.
Exogenous insulin – is obtained externally from other sources and administered to the DM patient.
DM Type 1: It is characterized by the absence of endogenous insulin. Formerly called juvenile-onset
diabetes because it most commonly occurs in juveniles and young adults. An autoimmune process,
(possibly triggered by a viral infection), destroys beta cells, the development of insulin antibodies, and
the production of islet cell antibodies (ICAs). Affected people require exogenous insulin for the rest of
their lives.
DM Type 2: It is characterized by inadequate endogenous insulin and body’s inability to properly use
insulin. Beta cells respond inadequately to hyperglycemia resulting in chronically elevated blood glucose.
Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to
the elevated glucose. It is more common in adults; but is increasingly found in children. It is controlled
by diet and exercise and may require exogenous insulin initially then maintained by oral hypoglycemic
agents.
Role of Insulin: Insulin is the hormone required for glucose metabolism.
Glucose: Insulin stimulates active transport of glucose into cells. If insulin is absent, glucose remains in
the bloodstream. Blood becomes thick, which increases its osmolality/viscosity. Increased osmolality
stimulates the thirst center, causing the patient to experience polydipsia – excessive thirst, for additional
fluids required to thin the blood. Increased fluid does not pass into body tissues; the high serum
osmolality retains fluid in the bloodstream. As blood passes through the kidneys, some glucose
eliminated. The osmotic force created by glucose draws extra fluid and electrolytes with it, causing
abnormally increased urine volume – leading to polyuria – excessive urination.
Risk Factors for DM: Obesity, Sedentary lifestyle, Family history of diabetes, Age 40 years and older,
History of gestational DM, History of delivering infant weighing more than 10 lbs./pounds, African
American (33% higher risk for type 2 DM), Latin American/Hispanic (>300% higher risk for type 2 DM),
American Indians (33% to 50% higher risk for type 2 DM), Polycystic ovary syndrome, Cardiovascular
disease and hypertension. Presence of acanthosis nigricans (dark discoloration in body folds and
creases).
Metabolic syndrome: A syndrome thought to be a precursor to diabetes, Pt’s typically have Impaired
glucose tolerance (IGT), high serum insulin, hypertension, elevated triglycerides, low HDL cholesterol,
altered size and density of LDL cholesterol, It is believed that metabolic syndrome is a chronic low-grade
inflammatory process affecting endothelial tissue(the lining of the heart, blood and lymph vessels),
Long-term effects include atherosclerosis, ischemic heart disease, left ventricular hypertrophy and type
2 DM, Research is now directed at learning how to detect this syndrome early and what interventions
might slow or arrest the progress.
, Microvascular Complications: They result from changes in blood vessels. The capillaries thicken,
impairing the exchange of nutrients, gases and wastes.
Diabetic Retinopathy: Pathological changes in the retina that are associated with DM and that are
aggravated by hypertension and smoking. DM is the leading cause of blindness among people 25 to 74
years of age. The two types of diabetic retinopathy are (1) non proliferative and (2) proliferative and can
be present at the same time. Signs and symptoms that suggest impending eye problems are the
presence of spots (“floaters”) in the field of vision, seeing “cobwebs”, or sudden visual changes. DM
patients should have an eye exam at least once per year, so that future deterioration that could lead to
blindness may be prevented, for example – better control of HTN and early treatment of macular
edema.
Know Signs and Symptoms of kidney failure: Decreased urine output, although occasionally urine output
remains normal. Fluid retention, causing swelling in your legs, ankles or feet. Shortness of breath.
Fatigue. Confusion. Nausea. Weakness. Irregular heartbeat.
Macrovascular Complications: They are caused by accelerated atherosclerotic changes in the person
with diabetes, affecting peripheral, carotid, cerebral and coronary blood vessels. These complications
are associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and
peripheral vascular disease (PVD) – Know the signs & symptoms of PVD. Individuals with diabetes have a
2- to 4-fold increased risk for heart disease and stroke, which accounts for 68% of the deaths in people
with diabetes.
Treatment for macrovascular disease is directed toward: Weight loss – promotes insulin uptake to that
the amount of insulin circulating reduces. Exercise – sensitizes insulin receptors for uptake so that the
amount of insulin circulating reduces. Tobacco cessation –reduces vasoconstriction.
Neuropathic Complications: Neuropathy – Are pathologic changes in nerve tissue related to poor
glucose control, ischemic lesions of nerves and chemical changes in peripheral nerve cells. It can be
classified as: Mononeuropathy affects a single nerve or group of nerves resulting from inadequate blood
supply. Polyneuropathy involves both sensory and autonomic nerves. It affects both legs symmetrically.
Autonomic neuropathy affects the sympathetic and parasympathetic nervous systems. Gastroparesis –
delayed gastric emptying. Almost 30% of individuals older than age 40 with diabetes have impaired
sensation in as least one area of the foot. 60-70% of people who have DM experience neuropathies.
Acute Emergency Complications: Acute Hypoglycemia: Acute Hypoglycemia is a dangerous drop in
blood glucose in patients treated with insulin or other hypoglycemics.
Causes: Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent
pattern of exercise. Gastroparesis (stomach cannot empty itself of food in a normal way), renal
insufÏciency, and certain drugs including aspirin and beta-adrenergic blockers. Glucose levels between
50-70 mg/dl are considered moderate hypoglycemia. Please note that some patients with a glucose level
of 50 mg/dl may be asymptomatic(hypoglycemic unawareness).
Signs and symptoms may be: Adrenergic: They appear 1st and reflect the response of the nervous
system to inadequate glucose for cell function : shakiness, nervousness, irritability, tachycardia, anxiety,
lightheadedness, hunger, tingling. or numbness of the lips or tongue, and diaphoresis. Beta Blockers may
mask these symptoms causing a delay in diagnosis and treatment. Neuroglycopenic: Caused by shortage
