Exam #1 Study Guide: Acute Endocrine Problems Flashcards
Diabetes Mellitus is the leading cause of
- Acute blindness
- End Stage Renal Disease
- Nontraumatic Lower Limb Amputations
Diabetes Mellitus is a major contributing factor to what?
Heart Disease and Stroke
What are classes of diabetes?
- Type I
- Type II
- Gestational
- Other specific types
- Prediabetes
Diabetes Mellitus Type I: Etiologies include*
- Autoimmune disorder
- Genetics
- Idiopathic Diabetes
- Latent autoimmune diabetes in adults
Diabetes Mellitus Type I Etiology/Pathophysiology: Autoimmune Disorder*
- Body develops autoantibodies against insulin and/or the pancreatic B cells that produce insulin.
- Autoantibodies to the islet cells cause a reduction of 80-90% of normal function before hyperglycemia and other manifestations can occur.
Diabetes Mellitus Type I: Onset of Disease*
- Autoantibodies are present for months to years before symptoms occur.
- Manifestations develop when the pancreas no longer produces insulin- then rapid onset with ketoacidosis.
- Necessitates insulin
- Patient may have temporary remission after initial treatment. (Honeymoon period)
Type II Diabetes Mellitus: Etiology/Pathophysiology*
Pancreas continues to produce some endogenous insulin but either not enough is produced OR the body does not use insulin effectively.
What is the major distinction between Type I and Type II DM?*
In type I DM, there is an absence of endogenous insulin.
Type II DM Etiology/Pathophysiology: Genetic Link *
- Insulin Resistance
- Decrease Production of Insulin by the Pancreas
- Inappropriate glucose production by the liver
- Altered production of hormones and cytokines by adipose tissue (adipokines play a role in glucose and fat metabolism and contribute to the Pathophysiology of type II diabetes)
- Research continues on role of brain, kidneys and gut in type II DM.
What increases the risk for type II DM?
Metabolic Syndrome
How does metabolic syndrome increase the risk for Type II DM?
- Elevates blood glucose levels
- Abdominal obesity
- Elevated BP
- High levels of triglycerides
- Decreased levels of HDLs
Type II DM: Onset of Disease*
- Gradual Onset
- Hyperglycemia may go many years without being detected.
- Often discovered with routine laboratory testing.
- Signs and symptoms develop when 50-80% of B cells are no longer secreting insulin.
Clinical Manifestations of Type I DM*
- 3 P’s
- Weight loss
- Weakness
- Fatigue
Clinical Manifestations of Type II DM*
- Nonspecific Symptoms
- Fatigue
- Recurrent infection
- Recurrent vaginal yeast or candida infection
- Prolonged wound healing
- Visual changes
Diabetes Mellitus Diagnostic Studies **
- Hemoglobin A1C level: 6.5% or higher
- Fasting plasma glucose level: > 126 mg/dL
- Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)
- Classic symptoms of hyperglycemia with random plasma glucose level: 200 mg/dL or higher
Hemoglobin A1C
- Reflects glucose levels over past 2-3 months
- Used to diagnose, monitor response to therapy and screen patients with prediabetes
- Goal: < 6.5% - 7%
What can influence Hgb A1C levels?
Diseases affecting RBC’s (i.e anemia)
What are other diagnostic studies for DM?*
- Fructosamine: reflects glycemia in previous 1-3 weeks; may show a change in blood glucose levels before A1C does.
- Autoantibodies (distinguish between autoimmune type I DM and diabetes d/t other causes)
Goals of Diabetes Management
- Decrease symptoms
- Promote well-being
- Prevent acute complications
- Delay onset and progression of long-term complications.
- Need to maintain blood glucose levels as near to normal as possible.
Acute Complications of DM include
- DKA
- Hyperosmolar hyperglycemic Syndrome (HHS)
- Hypoglycemia
What is DKA?**
Caused by a profound deficiency of insulin.
Most likely to occur in type I DM.
DKA is characterized by**
- Hyperglycemia
- Ketosis
- Acidosis
- Dehydration
DKA Precipitating Factors
- Illness
- Infection
- Inadequate Insulin dosage
- Undiagnosed Type I DM
- Poor self-management
- Neglect
DKA Pathophysiology**
Need to simplify this
-When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel.
-Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop.
-Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality.
-Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues.
-Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia.
-Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis.
-If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate.
Vomiting caused by the acidosis results in more fluid and electrolyte losses.
Eventually, hypovolemia will ensue and be followed by shock.
Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses.
Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable.
DKA: Clinical Manifestations**
- Dehydration: poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension
- Lethargy and weakness early
- Skin dry and loose
- Eyes soft and sunken.
- Kussmaul respirations
- Abdominal pain, anorexia, N/V
- Sweet, fruity breath odor
DKA: Laboratory Findings**
- Blood glucose level of 250 mg/dL or higher
- Blood pH lower than 7.30
- Serum bicarbonate level < 16 mEq/L
- Moderate to high ketone levels in urine or serum
DKA: Hospitalization/Outpatient
- Less severe form may be treated on outpatient basis
- Hospitalize for severe fluid and electrolyte imbalance, fever, N/V, diarrhea and altered mental state.
- Also if communication with HCP is lacking.
DKA: Treatment**
- Ensure patent airway; administer O2
- Establish IV access; begin fluid resuscitation (d/t fluid and electrolyte imbalance)
- Continuous regular insulin drip 0.1 u/kg/hr (*Must check serum K+ levels before starting insulin)
- Potassium replacement as needed.
DKA: Fluid Resuscitation
- NaCl 0.45% or 0.9%
- Add 5% to 10% dextrose when blood glucose level approaches 250 mg/dL (prevents hypoglycemia as well as a sudden drop in glucose that can be associated with cerebral edema)
Why must you check potassium levels before administering insulin?
Insulin administration will further decrease potassium levels because it allows water and potassium to enter the cell along with glucose.
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Hyperosmolar Hyperglycemic Syndrome**
- Life-threatening, medical emergency
- High mortality rate
- Occurs with Type II DM
- Diabetic who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis and ECF depletion.
HHS Precipitating Factors
- UTIs, pneumonia, sepsis
- Acute illness
- Newly diagnosed type 2 diabetes
- Impaired thirst sensation and/or inability to replace fluids
HHS Pathophysiology**
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