Question

A 48-year-old woman is admitted to the emergency room. Her family states she has been ill for 5 days with vomiting and diarrhea and most recently has presented in a coma. The family states she has lost weight over the last month in spite of the fact she has had an increase appetite and thirst as well as urination. She has no past major medical problems. She takes no medications.

On physical examination:

BP 110/80, P 96, R 22, BMI 34

Skin: dry with decreased turgor

HEENT: oral mucous membranes are dry

Lungs: clear to auscultation

Heart: regular rhythm with no murmur

Abdomen: soft bowel sounds present, no masses

On admission, the following laboratory tests were done:

Fasting blood sugar 450

Total cholesterol 265

Triglycerides 185

High Density Lipoprotein 35

Urine

Glucose positive

Ketones positive

The physician made a diagnosis of type 1 diabetes in ketoacidosis.

1. Reviewing the above history, physical examination, and laboratory data, which of the findings support the diagnosis of type 1 diabetes? What is ketoacidosis?

3. This is a new diagnosis for the patient and the nurse in her teaching needs to describe the pathophysiology of the disease. Provide a description of the important information that should be included.

Answer 1

1.

Type 1 diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin. Insulin is a hormone needed to allow sugar (glucose) to enter cells to produce energy.Type 1 diabetes is due to the destruction of the beta cells in the pancreas by the immune system. beta cells are the ones which make insulin.

On reviewing the above history, physical examination, and laboratory data, the following signs and symptoms support the diagnosis of type1 diabetes:

• Increased thirst
• Frequent urination
• Increased appetite
• unintented weight loss
• signs of dehydration like dry skin, dry mucos membrane.
• increased blood sugar- 450mg/dl
• urine report showing positive sugar and ketones.

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate.

Diabetic ketoacidosis (DKA) is a buildup of acids in your blood. It can happen when your blood sugar is too high for too long. It could be life-threatening.

In diabetic ketoacidosis, a high concentration of ketone bodies is usually accompanied by insulin deficiency, hyperglycemia, and dehydration. Particularly in type 1 diabetics the lack of insulin in the bloodstream prevents glucose absorption, thereby inhibiting the production of oxaloacetate through reduced levels of pyruvate, and can cause unchecked ketone body production (through fatty acid metabolism) potentially leading to dangerous glucose and ketone levels in the blood. Hyperglycemia results in glucose overloading the kidneys and spilling into the urine (transport maximum for glucose is exceeded). Dehydration results following the osmotic movement of water into urine (Osmotic diuresis), exacerbating the acidosis.

3.  

Explain the patient that : Type 1 diabetes happens when your immune system destroys cells in your pancreas called beta cells. They’re the ones that make insulin.

What Does Insulin Do?

Insulin is a hormone that helps move sugar, or glucose, into your body's tissues. Cells use it as fuel.

Explain the reasons of his symptoms:

Damage to beta cells from type 1 diabetes throws the process off. Glucose doesn’t move into your cells because insulin isn’t there to do it. Instead it builds up in your blood and your cells starve. This causes high blood sugar, which can lead to:

Dehydration: When there’s extra sugar in your blood, there will be increased urination. A large amount of water goes out with that urine, causing your body to dry out.

Weight loss: The glucose that goes out when you pee takes calories with it. That’s why many people with high blood sugar lose weight. Dehydration also plays a part.

Diabetic ketoacidosis (DKA): If your body can't get enough glucose for fuel, it breaks down fat cells instead. This creates chemicals called ketones. Your liver releases the sugar it stores to help out. But your body can’t use it without insulin, so it builds up in your blood, along with the acidic ketones. This combination of extra glucose, dehydration, and acid buildup is known as "ketoacidosis" and can be life-threatening if not treated right away.

Damage to your body: Over time, high glucose levels in your blood can harm the nerves and small blood vessels in your eyes, kidneys, and heart. They can also make you more likely to get hardening of the arteries, or atherosclerosis, which can lead to heart attacks and strokes.

Type 1 DM is the culmination of lymphocytic infiltration and destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas. As beta-cell mass declines, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels. After 80-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed. Patients need exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism.

Currently, autoimmunity is considered the major factor in the pathophysiology of type 1 DM. In a genetically susceptible individual, viral infection may stimulate the production of antibodies against a viral protein that trigger an autoimmune response against antigenically similar beta cell molecules.

Approximately 85% of type 1 DM patients have circulating islet cell antibodies, and the majority also have detectable anti-insulin antibodies before receiving insulin therapy. The most commonly found islet cell antibodies are those directed against glutamic acid decarboxylase (GAD), an enzyme found within pancreatic beta cells.

The prevalence of type 1 DM is increased in patients with other autoimmune diseases, such as Graves disease, Hashimoto thyroiditis, and Addison disease.

Sensory and autonomic neuropathy in people with diabetes are caused by axonal degeneration and segmental demyelination. Many factors are involved, including the accumulation of sorbitol in peripheral sensory nerves from sustained hyperglycemia. Motor neuropathy and cranial mononeuropathy result from vascular disease in blood vessels supplying nerves.