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**
…
What is the main difference between HHS and DKA?**
The patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur.
HHS Characteristics**
- Enough circulating insulin is present to prevent ketoacidosis.
- Fewer symptoms lead to higher glucose levels (>600 mg/dL)
- More severe neurologic manifestations because of increased serum osmolarity.
- Ketones absent or minimal in blood and urine.
HHS Treatment**
Similar to that for DKA
- IV insulin and NaCl infusions
- More fluid replacement needed
- Monitor serum potassium and replace as needed.
- Correct underlying precipitating cause
DKA/HHS Nursing Management: Monitor
- IV fluids to correct dehydration
- Insulin Therapy to reduce blood glucose and serum acetone levels
- Electrolytes
DKA and HHS Nursing Management: Assess
- Renal Status r/t hydration and electrolyte levels
- Cardiopulmonary status r/t hydration and electrolyte levels
- LOC
- V/S to determine the presence of fever, hypovolemic shock, tachycardia and kussmaul respirations.
Diabetes Insipidus **
Recognized by vast quantities of dilute urine production
Diabetes Insipidus occurs as a result of:**
- Hypothalamus producing insufficient ADH
- Posterior pituitary failing to release ADH
- Kidney nephron resistance of ADH
Diabetes Insipidus Etiology**
- Central DI (Neurogenic)
- Nephrogenic DI
- Primary
- Psychogenic DI
Diabetes Insipidus: Pathophysiology
Injury to hypothalamus or pituitary gland:
- Free water excreted in urine
- Extracellular dehydration: hypotension and hypovolemic shock
- Hypernatremia
- Decreased cerebral perfusion
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Diabetes Insipidus: Clinical Manifestations**
Urine output >300 ml/hr
Diabetes Insipidus: Lab Studies**
- Serum sodium >145 mEq/L
- Serum osmolality >295 mOsm/kg H2O
- Urine osmolality <300 mOsm/kg H2O
- Urine specific gravity <1.005
Diabetes Insipidus: Treatment**
- Volume Restoration
- Medications
Medications for Central Diabetes Insipidus**
- Vasopressin (Pitressin)
- DDAVP (Desmopressin)
Medications for Nephrogenic DI**
-Thiazide Diuretics
Diabetes Insipidus: Nursing priorities are directed toward**
- Administering fluids and medications
- Evaluating response to therapy (osmolality, Na+, BP, HR)
- Maintaining surveillance for complications
- Providing patient and family education
Syndrome of Inappropriate Secretion of ADH (SIADH) Characteristics**
- Opposite of diabetes insipidus
- Excess of ADH
- Kidneys reabsorb too much water
- Dilutional hyponatremia
SIADH Etiology**
- Head-CNS injury
- Malignant bronchogenic oat cell carcinoma
- Commonly used medications: Thiazide diuretics and Selective serotonin reuptake inhibitors (SSRI)
- PEEP with mechanical ventilation
SIADH Pathophysiology**
- ADH released by posterior pituitary gland and is responsible for regulating water and electrolyte balance
- Excessive ADH – alters sodium balance leading to:Overhydration, Low sodium (dilutional) and Concentrated urine
SIADH Clinical Manifestations**
R/t to excess fluids in the extracellular compartment and the proportionate dilution of the circulating sodium
- Lethargy
- Anorexia
- N/V
- Mental confusion
- Seizures
- Decreased LOC leading to coma
SIADH Laboratory Values**
- Serum osmolality <275 mOsm/kg H2O
- Serum sodium level below 125 mEq/L associated with severe neurological symptoms
- Urine sodium >30 mEq/L congruent with concentrated urine output of SIADH
SIADH Medical Management**
- Recognize and treat primary disease (will reduce production of ADH)
- Fluid restriction
- Sodium replacement
- Medications: stop drugs that may cause SIADH
What drugs are used to treat SIADH?**
Demeclocycline or Conivaptan
SIADH Nursing Management**
Directed toward:
- Restricting fluids
- Maintaining surveillance for complications
- Providing patient education
Thyrotoxic Crisis or Thyroid Storm**
- Though considered a life-threatening emergency, death is rare when treatment is initiated.
- Excessive amounts of hormones are released. (Hyperthyroidism)
- Results from stressors (infection, trauma, surgery) in a patient with preexisting hyperthyroidism.
Who is at an increased risk for thyrotoxic crisis?
Patients undergoing thyroidectomy are at risk because manipulation of the hyperactive thyroid glands results in an increase in hormones released.
Acute Thyrotoxicosis: Precipitating Factors
- Unrecognized hyperthyroidism
- Infection*
- Trauma*
- Stress*
*Associated with known hyperthyroidism
Those with acute thyrotoxicosis may have a history of:
- Graves disease
- Thyroid cancer
- Iatrogenic thyroid replacement
- Excessive contrast medium
- Chronic steroid use
Acute Thyrotoxicosis: Clinical Manifestations**
- Severe tachycardia, heart failure
- Shock
- Hyperthermia
- Agitation
- Seizures
- Abdominal pain, vomiting, diarrhea
- Delirium, coma
Acute Thyrotoxicosis: Labs**
- T3, T4 elevated
- Decreased TSH
- Serum potassium and magnesium are usually low
- Serum calcium is elevated (from bone)
- Blood sugars are elevated (stress response -> cortisol which increases blood glucose)
Acute Toxicosis: Signs and Symptoms **
- Hyperpyrexia
- Tachycardia and rhythm disturbances
- Hypertension
- Hypovolemia
Acute Thyrotoxicosis: Treatment**
Necessitates aggressive treatment
- Medications to block thyroid hormone production and SNS
- Monitoring for dysrhythmias
- Ensuring adequate oxygenation
- Fluid and electrolyte replacement
Acute Thyrotoxicosis Management includes**
- Reducing circulating T3 and T4
- Decreasing temperatures
- Ensuring hemodynamics stability
Acute Thyrotoxicosis Management: Reducing circulating T3 and T4**
- Medications (PTU, sodium iodide)
- Reduce thyroid levels by plasmapheresis, dialysis or hemoperfusion adsorption)
Acute Thyrotoxicosis Management: Decrease Temperatures*
- Acetaminophen
- No ASA
Acute Thyrotoxicosis Management: Ensuring Hemodynamics Stability **
- Reduce the heart rate by giving beta-blockers like propranolol (Inderal), calcium channel blockers like diltiazem (Cardiazem), digoxin, and diuretics. Keep heart rate below 100 bpm.
- Monitor hydration status
Acute Thyrotoxicosis: Nursing Implementation
- Ensure adequate rest: calm, quiet room; cool room; light bed coverings
- Encourage and assist with exercise involving large muscle groups (tremors can interfere with small-muscle coordination) to allow the release of nervous tension and restlessness
Acute Thyrotoxicosis: Nursing Implementation if exophthalmos is present:
- Apply artificial tears to relieve eye discomfort
- Salt restriction and elevate head of bed (helps reduce periorbital edema)
- Dark glasses (prevents irritation)
- Tape eyelids closed if needed for sleep
- ROM of intraocular muscles
If exophthalmos is severe, treatment options include
- Corticosteroids
- Radiation of retroorbital tissues
- Orbital decompression
- Corrective lid or muscle surgery
If exophthalmos is present, there is a potential for
Corneal injury related to irritation and dryness.
Patient may have orbital pain.
Myxedema Coma**
- Extreme lack of thyroid hormone
- Opposite effect from hyperthyroidism
- Hypometabolic state
Myxedema Coma: Precipitating Factors
- Unknown diagnosis
- Thyroiditis
- Destruction of thyroid gland by surgery or radioactive surgery for hyperthyroidism
- Withdrawal from thyroid medication
- Tumors/malignancies
Patients myxedema coma may have a history of
- Existing thyroid condition
- Sudden exposure to cold
- Stress onset
Myxedema Coma: Lab Studies**
- Low T3/T4
- High TSH
- Sodium decreased
- Potassium increased
- Hypercapnia
- Low glucose
Myxedema Coma: Signs and Symptoms**
- Hypothermia
- Bradycardias
- Hypotension
- Myxedema coma
- Death
Myxedema Coma: Treatment**
- Support Respiratory Function: Intubation, mechanical ventilation
- Increase thyroid-containing medications: T4 preferred, T3; steroids
- IV saline and glucose
Myxedema Coma: Nursing Management
- Keep patient warm
- Assess for abdominal distention and fecal impaction
- Care of immobilized or comatose patient
- Prevent Aspiration: suction prn
Adrenal Crisis: Primary Hypoadrenalism (aka Addison’s Disease)
- Autoimmune
- Mycobacterium Tuberculosis
Adrenal Crisis: Secondary
- Abrupt withdrawal of ACTH
- Complication of therapy with cortisol
Adrenal Crisis: Precipitating Factors
- Infection, trauma, surgical procedures
- Any long-term stress in ICU can cause this to develop.
Adrenal Crisis: Labs**
- Elevated potassium
- Low sodium
- Low bicarbonate
- Low blood sugars
- Low serum cortisol levels
Adrenal Crisis: Signs and Symptoms**
- Generalized: weakness, fatigue, anorexia, nausea
- Severe dehydration secondary to sodium loss
- Weight loss
- Orthostatic hypotension
Adrenal Crisis: Treatment**
- Administer needed hormones: Hydrocortisone
- Fluid resuscitation: D5NS
- Delivery of needed electrolytes: replacement of sodium, glucose
- Monitor finger glucose measurements and calcium levels
