TYPE OF DIABETES MELLITUS
Type 1 diabetes mellitus happens when the part of the pancreas that makes insulin is destroyed by that person’s own immune system. When a person does not make insulin, glucose – sugar – in the blood cannot get into the parts of the body that need sugar to live. In order to live, a person with Type 1 diabetes must take insulin for the rest of their life. They also need to check the amount of sugar in their blood many times each day. Type 1 diabetes happens most of the time in younger people, however it can occur in adults, although this is much less common. About 1 out of every 10 people with diabetes have Type 1 Diabetes.
Type 2 diabetes mellitus is a very different illness from Type 1 diabetes. In Type 2 diabetes, the person makes insulin, but either the insulin does not work in that person’s body as it should, or they do not make enough to process the glucose. When insulin does not work as it should, glucose (sugar) in the blood cannot get into the parts of the body that need sugar. Type 2 diabetes happens most of the time in an older person who is overweight.
Other types of diabetes
Other types of diabetes include but are not limited to:
Latent autoimmune diabetes of adults (LADA)
Maturity onset diabetes of the young (MODY)
ANATOMY AND PHYSIOLOGY:
Every cell in the human body needs energy in order to function. The body’s primary energy source is glucose, a simple sugar resulting from the digestion of foods containing carbohydrates (sugars and starches). Glucose from the digested food circulates in the blood as a ready energy source for any cells that need it. Insulin is a hormone or chemical produced by cells in the pancreas, an organ located behind the stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to open a doorway into the cell through which glucose can enter. Some of the glucose can be converted to concentrated energy sources like glycogen or fatty acids and saved for later use. When there is not enough insulin produced or when the doorway no longer recognizes the insulin key, glucose stays in the blood rather entering the cells.
PATHOPHYSIOLOGY DIABETES MELLITUS
Diabetes mellitus is a chronic condition that millions of people around the world suffer from. This article discusses the pathophysiology of diabetes mellitus.
The pathophysiology of diabetes mellitus in all forms is related to the insulin hormone. Insulin is secreted by cells in the pancreas and is responsible for regulating the level of glucose in the bloodstream. It also aids the body in breaking down the glucose to be used as energy. When someone suffers from diabetes, however, the body does not break down the glucose in the blood as a result of abnormal insulin metabolism. This results in elevated levels of glucose in the blood, which is known as hyperglycemia. When glucose levels remain high over an extended period of time, severe complications including cardiovascular disease, kidney damage, eye disorders, and nerve problems can occur. Diabetes mellitus occurs in three different forms - type 1, type 2, and gestational.
In type 1 diabetes, the pancreas does not create as much insulin as the body requires. It is suggested by the pathophysiology of type 1 diabetes mellitus that it is actually an autoimmune disease in which the sufferer's own immune system secretes substances that attack and destroy the cells in the pancreas that are supposed to produce insulin. As a result, the pancreas begins producing little or no insulin. Type 1 diabetes occurs when the pancreas produces normal amounts of the insulin hormone, but the cells in the body do not absorb it properly and do not respond to it. Like type 1 diabetes, this also causes excess glucose to build up in the bloodstream. Lastly, gestational diabetes occurs during pregnancy and is caused due to hormone fluctuations during pregnancy. This type of diabetes normally resolves itself after the baby is born.
The symptoms of all three forms of diabetes are similar and include fatigue, increased hunger and thirst, and frequent urination. It is important to begin treatment for the disease as soon as possible. When diabetes in any form is detected early, it is often possible to prevent severe complications. Because diabetes is suffered by millions of people spanning the globe, there are ongoing studies dedicated to finding cures and additional treatment options that can further help to reduce the risk of severe effects.
The list of diagnostic tests mentioned in various sources as used in the diagnosis of Diabetes includes:
1. Physical Examination
2. Urine sugar test
3. Urine ketones test
4. Oral Glucose Tolerance Test (OGTT) - also called "glucose challenge" test.
5. Blood glucose tests
a. Fasting plasma glucose (FPG)
b. Random plasma glucose
6. C-peptide blood test
7. Insulin level blood test
8. Self-managed blood glucose testing
a. Fingerprick blood drop blood glucose tests
b. Urine glucose home testing
c. Urine ketone home testing
9. See also the various tests for complications of diabetes such as:
a. Diabetes eye tests - see also tests for diabetic retinopathy
b. Kidney tests - see also tests for diabetic nephrophathy
d. Foot tests - see also tests for diabetic peripheral neurophathy
e. Reflex tests - also for diabetic neurophathy
f. Foot reflex test
g. Knee reflex test
10. Other tests for associated conditions or other problems:
a. Cholesterol blood tests
b. Blood lipid tests
c. Liver function tests
d. Thyroid tests - see also tests for thyroid conditions
11. Type 1 diabetes antibody tests
a. Glutamic Acid Decarboxylase (GAD) antibody tests - tests for Type 1 diabetes antibodies.
b. Islet cell antibody (ICA) tests
c. Insulin antibody tests
12. Tests for conditions related to Type 1 diabetes
a. TSH blood test - tests thyroid function; see tests for thyroid conditions
b. Vitamin B12 blood test - test for pernicious anemia and other digestive problems
13. Tests for ongoing monitoring of diabetes control:
a. HbA1c blood test - an average blood sugar measure over about 3 months.
b. Fructosamine blood test - an average blood sugar measure over about 2 weeks
14. Tests to detect initially and then regularly screen for diabetes complications:
a. Lipids and cholesterol - used to test risks of heart disease from diabetes.
b. Blood pressure tests
c. Eye tests
d. Foot tests
e. Urine protein test - tests for kidney problems.
f. Microalbumin urine test - also called "microalbuminurea" test; detects early kidney problems.
Although DKA may be encountered in any setting and mild DKA may be managed at the community level, severe metabolic imbalance requires inpatient acute care on a medical unit.
- Fluid and electrolyte imbalances
- Metabolic acidosis (primary base bicarbonate deficit)
- Psychosocial aspects of care
- Patient Assessment Database
- Data depend on the severity and duration of metabolic imbalance, length/stage of diabetic process, and effects on other organ function.
- Sleep/rest disturbances
- Weakness, fatigue, difficulty walking/moving
- Muscle cramps, decreased muscle strength
- Tachycardia and tachypnea at rest or with activity
- Lethargy/disorientation, coma
- Decreased muscle strength/tone
- History of hypertension; acute myocardial infarction (MI)
- Claudication, numbness, tingling of extremities (long-term effects)
- Leg ulcers, slow healing
- Postural BP changes; hypertension
- Decreased/absent pulses
- Crackles; jugular venous distension (JVD) (if heart failure [HF] present)
- Hot, dry, flushed skin; sunken eyeballs
EGO INTEGRITYMay report:
- Stress; dependence on others
- Life stressors including financial concerns related to condition
- Anxiety, irritability
- Change in usual voiding pattern (polyuria), nocturia
- Pain/burning, difficulty voiding (infection), recent/recurrent urinary tract infection (UTI)
- Abdominal tenderness, bloating
- Pale, yellow, dilute urine; polyuria (may progress to oliguria/anuria if severe hypovolemia occurs)
- Cloudy, odorous urine (infection)
- Abdomen firm, distented
- Bowel sounds diminished or hyperactive (diarrhea)
- Loss of appetite; nausea/vomiting
- Not following diet; increased intake of glucose/carbohydrates
- Weight loss over a period of days/weeks
- Use of medications exacerbating dehydration, such as diuretics
- Dry/cracked skin, poor skin turgor
- Abdominal rigidity/distension
- Thyroid may be enlarged (increased metabolic needs with increased blood sugar)
- Halitosis/sweet, fruity odor (acetone breath)
- Fainting spells/dizziness
- Tingling, numbness, weakness in muscles
- Visual disturbances
- Confusion/disorientation; drowsiness, lethargy, stupor/coma (later stages)
- Memory impairment (recent, remote)
- Deep tendon reflexes (DTRs) decreased (coma)
- Seizure activity (late stages of DKA or hypoglycemia)
- Abdominal bloating/pain (mild/severe)
- Facial grimacing with palpation; guarding
- Air hunger (late stages of DKA)
- Cough, with/without purulent sputum (infection)
- Increased respiratory rate (tachypnea); deep, rapid (Kussmaul’s) respirations (metabolic acidosis)
- Rhonchi, wheezes
- Yellow or green sputum (infection)
- Dry, itching skin; skin ulcerations
- Paresthesia (diabetic neuropathy)
- Fever, diaphoresis
- Skin breakdown, lesions/ulcerations
- Decreased general strength/ROM
- Weakness/paralysis of muscles, including respiratory musculature (if potassium levels are markedly decreased)
- Vaginal discharge (prone to infection)
- Problems with impotence (men); orgasmic difficulty (women)
- Familial risk factors: diabetes mellitus (DM), heart disease, strokes, hypertension
- Slow/delayed healing
- Use of drugs, e.g., steroids, thiazide diuretics, phenytoin (Dilantin), and phenobarbital (can increase glucose levels)
- May/may not be taking diabetic medications as ordered
- Discharge plan considerations:
- DRG projected mean length of inpatient stay: 5.9 days
- May need assistance with dietary regimen, medication administration/supplies, self-care, glucose monitoring
- Refer to section at end of plan for postdischarge considerations.
- Serum glucose: Increased 200–1000 mg/dL or more.
- Serum acetone (ketones): Strongly positive.
- Fatty acids: Lipids, triglycerides, and cholesterol level elevated.
- Serum osmolality: Elevated but usually less than 330 mOsm/L.
- Glucagon: Elevated level is associated with conditions that produce (1) actual hypoglycemia, (2) relative lack of glucose (e.g., trauma, infection), or (3) lack of insulin. Therefore, glucagon may be elevated with severe DKA despite hyperglycemia.
- Glycosylated hemoglobin (HbA1C): Evaluates glucose control during past 8–12 wk with the previous 2 wk most heavily weighted. Useful in differentiating inadequate control versus incident-related DKA (e.g., current upper respiratory infection [URI]). A result greater than 8% represents an average blood glucose of 200 mg/dL and signals a need for changes in treatment.
- Serum insulin: May be decreased/absent (type 1) or normal to high (type 2), indicating insulin insufficiency/improper utilization (endogenous/exogenous). Insulin resistance may develop secondary to formation of antibodies.
- Sodium: May be normal, elevated, or decreased.
- Potassium: Normal or falsely elevated (cellular shifts), then markedly decreased.
- Phosphorus: Frequently decreased.
- Arterial blood gases (ABGs): Usually reflects low pH and decreased HCO3 (metabolic acidosis) with compensatory respiratory alkalosis.
- CBC: Hct may be elevated (dehydration); leukocytosis suggest hemoconcentration, response to stress or infection.
- BUN: May be normal or elevated (dehydration/decreased renal perfusion).
- Serum amylase: May be elevated, indicating acute pancreatitis as cause of DKA.
- Thyroid function tests: Increased thyroid activity can increase blood glucose and insulin needs.
- Urine: Positive for glucose and ketones; specific gravity and osmolality may be elevated.
- Cultures and sensitivities: Possible UTI, respiratory or wound infections.
- Restore fluid/electrolyte and acid-base balance.
- Correct/reverse metabolic abnormalities.
- Identify/assist with management of underlying cause/disease process.
- Prevent complications.
- Provide information about disease process/prognosis, self-care, and treatment needs.
- Homeostasis achieved.
- Causative/precipitating factors corrected/controlled.
- Complications prevented/minimized.
- Disease process/prognosis, self-care needs, and therapeutic regimen understood.
- Plan in place to meet needs after discharge.