Dr. Saad Kleman Abd Diabetes Mellitus - · Web viewType I and type II diabetes mellitus are two separate and distinct pathophysiological cases. In persons genetically susceptible to

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Dr. Saad Kleman Abd Diabetes Mellitus

Diabetes is a Greek word that means to siphon or to pass thru. Mellitus is Latin and refers to something sweet or honey. It’s a metabolic disorder characterized by hyperglycemia resulting from lack of insulin, lack of insulin effect, or both. Our pancreas is supposed to produce and secrete insulin. Insulin is required to move glucose out of the vascular space and into the cell. If glucose is not pulled from the vascular space, it will build up in the blood. The cells need the glucose (sugar) for energy. Without insulin, the body enters a state of catabolism. Catabolism means to tear down and anabolism means to build up. The cells need energy, so they begin to break down fats and proteins. Fat breakdown (not protein breakdown) leads to ketone formation. Ketones are acids, this increase in ketones in the blood leads to metabolic acidosis.

Three general classifications are recognized for diabetes: type I diabetes —absolute insulin insufficiency type II diabetes —insulin resistance with varying degrees of insulin

secretory defects

gestational diabetes —manifested during pregnancy.

WHAT’S THE DIFFERENCE BETWEEN TYPE I AND TYPE II DIABETES?Type I:_ Begins in childhood or adolescence, usually around the age of 14._ Also called juvenile diabetes mellitus or insulin-dependent diabetes mellitus._ The pancreas does not function properly and does not produce insulin at all._ Even if these patients take a medication to stimulate insulin

production, the pancreas still will not produce insulin._Oral antidiabetic agents do not work in type I diabetics. Patient

must take insulin hormone replacement therapy.

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_ Sudden onset: the patient typically does not even know he has a glucose problem until waking in the emergency department where he recovers from diabetic ketoacidosis.

Type II:_ Far more common than type I, and accounts for 90% of all diabetes._ Trend in the United States related to obesity. Childhood

diabetes is related to childhood obesity._ Usually occurs after age 30 and is most commonly seen

between the ages of 50 and 60.Also known as adult-onset diabetes.

_ Nonketotic form of diabetes because there is sufficient insulin production to prevent breakdown of fats leading to ketosis.

_ Exact cause is unknown._ These patients do not have enough insulin, or the insulin they

have does not work properly at the cellular level (insulin resistance).

_ Insulin resistance; can also be defined as fasting hyperglycemia despite having available endogenous insulin.

_ Genetic tendency to type II diabetes._ Other risk factors may include obesity, dietary intake, and

environmental factors._ Special diet and an exercise plan are used in an attempt to

control the blood glucose._ Oral agents, and then if these do not work, insulin injections may be used._ As many as 20% to 30% of patients with type II diabetes

require treatment with insulin._ It is important to understand that type II diabetics may finally

end up with (type I diabetes) due to complete failure of the pancreas to produce insulin.

_Type II diabetes is a major cardiovascular risk factor._Type II diabetes is usually found by accident, (a wound that won’t heal, repeated infections (especially vaginal infections).

_ Bacteria love a high-glucose environment, compromised vascular system could impair blood flow to wounds.

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What causes it and why

Environment

(infection, toxins) Stress, diet, lack of exercise in genetically susceptible persons

Pregnancy

PathophysiologyType I and type II diabetes mellitus are two separate and distinct pathophysiological cases. In persons genetically susceptible to type I diabetes, a triggering event, possibly a viral infection, causes production of autoantibodies which kill the beta cells of the pancreas. This leads to a decline in and an ultimate lack of insulin secretion. Insulin deficiency, when more than 90% of the beta cells have been destroyed, leads to hyperglycemia, enhanced lipolysis, and protein catabolism.Signs and symptoms

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Diagnostic test resultsIn men and nonpregnant women

Two of the following criteria obtained more than 24 hours apart, using the same test twice or any combination are indicators of the disease:

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o fasting plasma glucose level of 126 mg/dl or more on at least two occasions

o typical symptoms of uncontrolled diabetes and random blood glucose level of 200 mg/dl or more

o blood glucose level of 200 mg/dl or more 2 hours after ingesting 75g of oral dextrose.

Other criteria include:

o diabetes retinopathy on ophthalmologic examination

o other diagnostic and monitoring tests, including urinalysis for acetone and glycosylated hemoglobin (reflects glycemic control over the past 2 to 3 months).

In pregnant women Positive glucose tolerance test reveals high peak blood sugar levels after

ingestion of glucose (1g/kg body weight) and delayed return to fasting levels.

What can harm the patient?_ Diabetic ketoacidosis._ Coma._ Myocardial infarction._ Retinopathy (vision problems and blindness)._ Amputations related to complications from infected and poor healing wounds._ Kidney failure._ Smoking (causes more vasoconstriction, leading to compromised tissue perfusion to heart, kidneys, legs, feet, etc.).CHRONIC COMPLICATIONS OF DIABETESChronic complications of diabetes are characterized as macrovascular (large vessel) or microvascular (small vessel).Macrovascular:_ Coronary artery disease, peripheral vascular disease, and cerebrovascular

disease are common in poorly managed diabetics and increase mortality (death) rates for this population.

_ Related to associated problems like hypertension, inactive lifestyle, lipid abnormalities, hyperglycemia.

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_ Remember, a large majority (80% or greater) of clients with type II diabetes are obese.

Microvascular:_ Nephropathy (kidney damage), neuropathy (an example is erectile dysfunction

or burning of the feet), and retinopathy (damage to the retina) occur in patients with diabetes.

_ Evidence supports the theory that these microvascular complications occur less when glucose is better controlled.

_ Hyperglycemia not only damages vessels but nerves as well._ Neuropathies are nerve dysfunctions related to progressive deterioration of

nerves leading to decreased nerve function._ Damage to sensory nerve fibers lead to pain and loss of sensation. The

etiology is not completely understood._ Increased levels of sorbitol and fructose in the nerves act as “poisons,”

causing damage to cells, resulting in pain, paresthesias, or numbness._ Paresthesia refers to burning, prickling, or stinging sensation. Sugar kills

nerves.Whether macrovascular or microvascular, these complications are a result of changes to the vessel lining due to hyperglycemia. These vessels thicken and narrow, decreasing blood flow to the area, resulting in ischemia and/or necrosis. Smaller blood vessels leak or are destroyed, thereby decreasing the delivery of nutrients and oxygen to tissues.chronic complications of diabetes

Diabetic ketoacidosis (DKA);

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DKA is an acute complication of diabetes. Occurs in 2% to 5% of type I diabetics. Infection is most often the cause. The 3 Ps; polyuria, polydipsia, and polyphagia, usually precede complete DKA.

Pathway to DKA:1. Lack of insulin.2. Glucose cannot enter cells.3. Cells are starved.4. Body breaks down fat for energy.5. Fat = ketones.6. Ketones = acids.7. Metabolic acidosis = DKA.

Signs and symptoms and whyThe signs and symptoms of DKA are the same as seen with diabetes mellitus. The most severe symptoms;1. Decreased level of consciousness due to metabolic acidosis and shock.2. Severe hypovolemia due to shock.

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3. Electrolyte imbalances, especially potassium problems.In addition, the patient will have polyuria initially to excrete excess sugar particles. When the sugar is excreted by the kidneys, fluid is excreted along with it. As a result, the patient becomes hypovolemic.When hypovolemia occurs, polyuria progresses to oliguria and, maybe, anuria—the kidneys are either trying to hold on to what little fluid the body has left, or they might not be adequately perfused. Remember, you must monitor intake and output closely to prevent as much kidney damage as possible.Tests:_ Urinalysis: glycosuria, ketonuria._ Blood gases: low pH indicating ketoacidosis (metabolic acidosis)._ Blood chemistry: high serum potassium._ Blood test for kidney function BUN and creatinine.

Hyperglycemic hyperosmolar nonketotic (HHNK) syndrome:This complication presents in a similar way as DKA but without acidosis and usually with higher blood sugar levels. Again, the body is making just enough insulin to prevent breakdown of body fat. If there is no breakdown of body fat, then no ketones are formed. No ketones = no acidosis. This patient will not experience Kussmaul respirations because they are not acidotic.

Tests:_ Serum glucose: severe elevation of glucose, ranging from 600 to 2400 mg/dL._ Serum blood chemistry: hyponatremia related to mild dehydration.Serum sodium can increase as dehydration progresses. Ketosis and acidosis are usually absent or mild.

Hypoglycemia:What is it?Hypoglycemia occurs when the blood sugar is too low, less than 70 mg/dL.It is uncommon in those who do not have diabetes. The brain is very sensitive to low levels of blood glucose, so hypoglycemia must be dealt with quickly. If

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blood sugar falls below normal range, the brain triggers the adrenal glands to release epinephrine. Other responses of the body include glucagon release by the pancreas and growth hormone release from the pituitary gland. All of theses responses contribute to the release of sugar into the blood by the liver.What causes it and why

Signs and symptoms and why

Tests:_ Low capillary glucose via finger-stick is usually followed by serum glucose to confirm the decreased glucose value.

What can harm my client?_ Brain damage due to prolonged hypoglycemia._ Permanent organ damage._ Death.

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Dr. Saad Kleman Abd Diabetes Mellitus - · Web viewType I and type II diabetes mellitus are two separate and distinct pathophysiological cases. In persons genetically susceptible to