Endocrine Alterations Flashcards
Endocrine system regulates physiological processes
– Metabolic processes – Energy production – Fluid and electrolyte balance – Bone health – Stress reactions – Growth and reproduction
• Hypothalamus • Pituitary • Controlled by feedback loops – Hormone low: – Hormone high:
• Hypothalamus – Conveyed to pituitary • Pituitary – Response to hypothalamus – Increased or decreased secretion of hormone • Controlled by feedback loops – Hormone low: stimulus to release more – Hormone high: stimulus to limit production
Primary Endocrine Disorders
– Example:
Primary Endocrine Disorders
– End gland is not responsive to hormone signals of
pituitary hormone
– Example: primary hypothyroidism
• ↓T3 andT4 and FreeT4
• ↑ TSH and TRH
• End hormone and release hormones in opposite directions
Secondary Endocrine Disorders
Example:
Secondary Endocrine Disorders
– End gland is responsive to stimulating hormones but
there is problem with pituitary or hypothalamus
– Example: secondary hypothyroidism
• ↓T3 andT4 and FreeT4
• ↓ TSH and TRH
• End hormone and release hormones in same direction.
PANCREATIC DISORDERS IN THE CRITICALLY ILL PATIENT
- Stress-induced hyperglycemia
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycemic state (HHS)
- Hypoglycemia
STRESS-INDUCED HYPERGLYCEMIA
• Risk Factors
• Risk Factors – Diabetes (diagnosed or undiagnosed) – Advancing age – Administration of exogenous catecholamines – Glucocorticoid therapy – Enteral or parenteral nutrition therapy – Medications – Obesity – Pancreatitis, cirrhosis
STRESS-INDUCED HYPERGLYCEMIA
• Potential adverse consequences
• Potential adverse consequences – Immune suppression – Cerebral ischemia/stroke – Dehydration/osmotic diuresis – Impaired wound healing – Endothelial dysfunction/thrombosis – Decreased erythropoiesis – Impaired gastric motility
STRESS-INDUCED HYPERGLYCEMIA
• Clinical Management
– Establish euglycemia
• Target glucoses of 140 to 180 mg/dL
– Insulin protocol
STRESS AND CRITICAL ILLNESS
• Hyperglycemia
• Adrenal insufficiency
• Thyroid dysfunction
• Hyperglycemia – Excessive hepatic glucose production – Relative hypoinsulinemia • Adrenal insufficiency – Primary and/or secondary dysfunction • Thyroid dysfunction
HYPERGLYCEMIC CRISES
• Reduction in circulating insulin with concurrent elevation of counterregulatory hormones
• Occurrence
– DKA: Type 1 diabetes
– HHS: Type 2 diabetes
– Increasing incidence of both DKA and HHS in same patient
DIABETIC KETOACIDOSIS
• Pathophysiology
– Relative or absolute insulin deficiency
– Increase in counterregulatory hormones: glucagon, cortisol, catecholamines, and growth hormone
PHYSIOLOGICAL CHANGES IN DKA
- Hyperglycemia due to increased glucose production and decreased utilization
- Osmotic diuresis and dehydration
- Hyperlipidemia due to increased lipolysis
- Metabolic acidosis/ketosis
- Altered potassium balance
- Excess acids result in increased anion gap
- Altered consciousness related to acidosis and dehydration
DKA: ETIOLOGY
• Initial presentation of type 1 diabetes
• Infections
• Insufficient insulin relative to need
• Severe stress—trauma, surgery, acute myocardial infarction (AMI)
• Pregnancy in type 1 diabetes mellitus (DM)
• Missed or reduced insulin
– Nonadherence to insulin regimen – Insulin pump failure
– Intentional omission
• Eating disorders
• Behavioral health issues
• Medications
– Glucocorticoids
• Mismanagement of sick days
CLINICAL PRESENTATION OF DKA
• Classic signs of dehydration • Orthostasis (orthostatic hypotension) • Polyuria (excessive urination) • Polydipsia (intense thirst) • Polyphagia (Excessive eating) • Hyperventilation/Kussmaul’s respirations • Fruity odor to breath • Flushed/dry skin • Lethargy/altered consciousness • Abdominal pain/nausea/vomiting • Blood glucose greater than 250mg/dL – May be lower in pregnancy • Ketonuria/glucosuria (ketones in urine/excretion of glucose in urine) • Weight loss (may be profound) • Blood gas changes (metabolic acidosis)
ELECTROLYTE IMBALANCES IN DKA
• Hypokalemia (even if serum K+ is normal or high) - Will progress with addition of insulin to treatment regimen – Insulin “pushes” potassium into cells • Phosphate depletion – Enhanced by insulin administration • Mild hyponatremia • Elevated BUN/creatinine – Secondary to profound dehydration
Hyperosmolar Hyperglycemic state (HHS): PATHOPHYSIOLOGY
- Decreased use of glucose and/or increased production
- Hyperglycemia; increased extracellular osmolality
- Osmotic diuresis
- Profound dehydration
- No ketoacidosis—hyperglycemia with hyperosmolarity blocks lipolysis
HHS: ETIOLOGY
• Inadequate insulin secretion, usually with type 2 diabetes • Often in geriatric patients with decreased compensatory
mechanisms
• Stress response
HHS MEDICATIONS
• Affect blood glucose levels – Thiazides – Phenytoin – Glucocorticoids – Beta blockers – Calcium channel blockers • Enteral and parenteral nutrition
DKA AND HHS: ASSESSMENT
- Based on severity of presentation
- Dehydration and hypovolemia
- Nausea and vomiting
- Classic polyuria, polyphagia, and polydipsia
- Decreased level of consciousness (LOC)
DKA VERSUS HHS
Explain HHS
- HHS
- Blood sugar >DKA; average >1000 mg/dL
- More “normal” arterial blood gases (ABGs)
- More electrolyte imbalances and renal dysfunction
- Higher serum osmolarity than DKA
- Ketosis absent or mild
DKA AND HHS: INTERVENTIONS
• Manage airway (DKA and HHS)
• Fluid replacement (DKA and HHS)
– First use 0.9% NS, then 0.45% NS
– Dextrose added when glucose approaches 200 mg/dL
– Monitor closely for signs of fluid volume overload and cerebral edema
DKA AND HHS: INTERVENTIONS
• Insulin therapy (DKA and HHS)
– Fluid replacement initiate first; monitor K+ – Loading dose (not in children)
– Continuous infusion
– Hourly glucose monitoring
• Decrease glucose by 50 to 75 mg/dL/hr
• When glucose is less than 200 mg/dL, adjust
infusion to maintain values of 150 to 200mg/dL
DKA AND HHS: INTERVENTIONS
• Insulin therapy – transitioning to subcutaneous therapy
– Blood glucose < 200 mg/dL
– Two of the following criteria met (DKA):
• pH > 7.30
• HCO3 > 15 mEq/L
• Anion gap ≤ 12 mEq/L
– Ketosis must be resolved before transition
DKA AND HHS: INTERVENTIONS
• Insulin therapy – transitioning therapy
– Basal/bolus insulin regimen preferred
• Long-acting/short- or rapid-acting insulin
• Insulin pump
– Administer subcutaneous insulin prior to discontinuing
IV insulin with attention to insulin action profile
– Monitor at least every 6 to 8 hours
• Determined by meal schedule
• If NPO, then every 6 hours
DKA AND HHS: INTERVENTIONS
• Treatment of acidosis (DKA)
– Assess respiratory compensation and LOC
– Usually corrected by fluids and insulin
– Bicarbonate only if pH is less than 7.0
– Administered by infusion until pH is 7.1
• Electrolyte replacement (DKA and HHS)
– Potassium • Establish renal function first • Maintain between 4 and 5 mEq/L – Phosphorus – Magnesium – Monitor ECG
DKA AND HHS: INTERVENTIONS
• Survival Skill Education (Hospital)
– Insulin/medication management
– Blood glucose monitoring
• Personal targets/recordkeeping
– Sick day management
– Hypoglycemia prevention, recognition, and treatment
– Basic meal planning
– Referral to diabetes self-management education program for follow-up
- Why is the insulin drip decreased when the blood sugar reaches 250 mg/dL?
- Why is regular insulin used?
- What is the most efficient way to test blood sugar hourly?
The insulin drip is decreased when the glucose reaches 250 mg/dL in order to prevent development of cerebral edema, which can be promoted by rapid declines in glucose levels.
- regular insulin is used because Regular insulin is the preferred insulin product for IV administration and the ONLY one for IV.
- Bedside glucose monitoring using point-of-care testing procedures (bedside lab monitoring/accu-check) is most effective for frequent blood glucose testing.
HYPOGLYCEMIA: ETIOLOGY
• Excess insulin/oral agents • Alcohol potentiates hypoglycemic effects • Insufficient nutrition intake • Excess exercise • Medications (e.g., beta blockers) • Renal impairment • Diabetic neuropathy – Hypoglycemia unawareness – Gastroparesis
HYPOGLYCEMIA: ASSESSMENT
• Rapid decrease in serum glucose levels • Activation of sympathetic nervous system (epinephrine release) – Tachycardia – Diaphoresis – Pallor – Dilated pupils • Hypoglycemia unawareness • Slow decrease in serum glucose levels
HYPOGLYCEMIA: ASSESSMENT
• Neuroglucopenia
– Restlessness – Difficulty thinking and speaking – Visual disturbances – Paresthesias – Change in LOC
HYPOGLYCEMIA: ASSESSMENT
• Laboratory evaluation
– Blood glucose level less than 70 mg/dL
– May vary in the following patient groups:
• Hypoglycemia unawareness
• Cognitive impairment
• Older adults at risk for falls
– If recurrent and DM long-standing, evaluate renal function
HYPOGLYCEMIA: INTERVENTIONS
• Treat hypoglycemia – 15 g carbohydrate orally – 50% dextrose (EMS, ED, ICU settings) – Glucagon – Oral glucose • Assess response: should improve rapidly • Adjust insulin regimen temporarily • Prevention and teaching
ACUTE ADRENAL INSUFFICIENCY
• Primary:
• Secondary:
- Primary: destruction of adrenal glands
- Secondary: interfere with secretion
- Deficiency of glucocorticoids (cortisol) and mineralocorticoids (aldosterone)
LACK OF CORTISOL
- Decreased production of glucose
- Decreased metabolism of protein and fat
- Decreased vascular tone
- Decreased effect of catecholamines
- Decreased intestinal motility and digestion
- Inability to respond to stress
LACK OF ALDOSTERONE
- Loss of sodium
- Loss of water
- Decreased circulating volume
- Potassium retention (hyperkalemia)
PRIMARY ACUTE ADRENAL INSUFFICIENCY
• Hypofunction – Inadequate cortisol and aldosterone – Autoimmune: Addison’s disease – Hemorrhagic destruction – Infiltration (neoplasm, amyloidosis) – Infection and sepsis – Medications – TB in countries where endemic – HIV
SECONDARY ACUTE ADRENAL INSUFFICIENCY
• Decrease ACTH secretion or suppress production of steroids
• Causes
– Withdrawal from long-term steroid use
– Pituitary and hypothalamic disorders
– Systemic inflammatory response
– Inadequate steroids in highly stressed patient who has received chronic steroid therapy
ACUTE ADRENAL INSUFFICIENCY: ASSESSMENT
• Symptoms of hypovolemia • Fluid and electrolyte imbalances – Postural hypotension – Change in LOC – Hyperkalemia • Fatigue, weakness • Gastrointestinal complaints • Decreased renal perfusion and decreased urine output
ACUTE ADRENAL INSUFFICIENCY
• Laboratory values
– Hyponatremia, hyperkalemia, and hypercalcemia – Eosinophilia – Metabolic acidosis – Hypoglycemia – Hyperuricemia • Cortisol levels • ACTH levels • Cosyntropin stimulation test
ACUTE ADRENAL INSUFFICIENCY: INTERVENTIONS
• Correct fluid and electrolyte imbalances – Normal saline and dextrose – May need 5 liters in first 24 hours • Hormonal replacement – Hydrocortisone (glucocorticoid) – Fludrocortisone (mineralocorticoid) • Patient or family education
HYPERTHYROIDISM: THYROID STORM
• Overproduction of thyroid hormones
– Affected by anterior pituitary gland and hypothalamus
– Positive and negative feedback
THYROID DYSFUNCTION IN THE CRITICALLY ILL
• Euthyroid sick syndrome (Low T3 syndrome)
– Physiological adaptation to illness
• Thyroid storm
• Myxedema coma (Loss of brain function due to low level of thyroid hormone)
HYPERTHYROIDISM: ETIOLOGY
• Toxic diffuse goiter: most common cause
– Graves’ disease (autoimmune)
• Toxic multinodular goiter
– Heart failure or severe muscle weakness
• Amiodarone therapy
• Radiation therapy
• Interferon-alpha therapy
THYROID STORM
• Inadequately controlled hyperthyroidism
• Produces a hyperdynamic and hypermetabolic state
– Affects many major body functions
• Medical emergency; death within 48 hours without treatment
THYROID STORM: ASSESSMENT
- Increased cardiac workload
- Increased oxygen demands and alterations in respirations
- Severe fever
- Fear, delirium, overt psychosis, convulsions, stupor, or coma
- Fatigue
- Nausea, vomiting, diarrhea, and cramps
THYROID STORM: DIAGNOSIS
• Elevated T3 and T4 • Elevated T3 resin intake • Lowered thyroid-stimulating hormone – Due to negative feedback • Electrolyte imbalances
THYROID STORM: INTERVENTIONS
• Goals of treatment
– Inhibit thyroid hormone biosynthesis – Block thyroid hormone release – Antagonize peripheral effects of thyroid hormone – Provide supportive care – Treat precipitating cause – Educate
THYROID STORM: INTERVENTIONS
• Administer medications
• Administer medications
– Inhibit thyroid hormone production and CV effects
– Propylthiouracil (PTU) and methimazole (Tapazole) inhibit thyroid synthesis
– Iodide agents retard release of hormones
– Medication to block effects: beta blockers, steroids
THYROID STORM: INTERVENTIONS (7)
- Monitor cardiovascular status
- Monitor and treat hyperthermia
- Promote oxygenation
- Fluid replacement
- Adequate nutrition
- Prevent injury
- Patient and family education
MYXEDEMA COMA
• Pathophysiology
– Hypofunction of thyroid
– Hypometabolism and hypodynamic state
MYXEDEMA COMA: ETIOLOGY
• Primary disease
– Hashimoto’s thyroiditis
– Surgical or radioactive treatment for Graves’ disease with inadequate follow-up treatment
• Insufficient thyroid stimulation due to hypothalamus or pituitary disease
• Exacerbation of hypothyroid state
MYXEDEMA COMA: ASSESSMENT
• Cognitive changes • Activity intolerance, decreased reflexes, and slow movements • Cardiovascular – Bradycardia, hypotension – Cardiomegaly – Decreased cardiac output – Electrocardiogram (ECG) changes – Edema • Pulmonary disturbances – Hypoventilation – CO2 retention – Pleural effusion – Upper airway and tongue edema • Hypothermia
MYXEDEMA COMA: DIAGNOSIS
• Primary myxedema
• Secondary myxedema
• Primary myxedema – ↓ T3 and T4; ↓ T3 resin update – ↑ TSH • Secondary myxedema – ↓ T3 and T4; ↓ T3 resin update – ↓ TSH • Hypoglycemia • Hyponatremia – Secondary to fluid retention
MYXEDEMA: INTERVENTIONS
• Treat with replacement thyroid hormone • Fluid and electrolyte replacement; thyroid replacement usually corrects sodium • Monitor gas exchange and respiratory status • Monitor cardiovascular status • Manage hypothermia • Protect from injury and infection • Educate patient and family
Explain why narcotics are avoided or used cautiously in the patient with myxedema coma.
Patients with myxedema coma may experience hypoventilation and resultant carbon dioxide retention due to weakness of respiratory muscles. Narcotics and sedatives would further decrease respiratory drive and further reduce the patient’s mental status.
DIABETES INSIPIDUS (DI) • Pathophysiology
– Deficiency in synthesis or release of antidiuretic hormone (ADH)
– Excessive water loss
– Types
• Neurogenic (central): ADH deficiency
• Nephrogenic: kidneys insensitive to ADH
ANTIDIURETIC HORMONE DISORDERS
• Diabetes insipidus
• Syndrome of inappropriate secretion of antidiuretic
hormone
• Cerebral salt wasting
DI: NEUROGENIC ETIOLOGY • Genetically predisposed • Head trauma • Neurological abnormalities – Increased intracranial pressure (ICP) • Pituitary surgery
DI: NEUROGENIC ETIOLOGY • Genetically predisposed • Head trauma • Neurological abnormalities – Increased intracranial pressure (ICP) • Pituitary surgery
DI: NEUROGENIC ETIOLOGY
• Genetically predisposed • Head trauma • Neurological abnormalities – Increased intracranial pressure (ICP) • Pituitary surgery • Chronic renal disease • Multisystem disorders affecting kidney – Multiple myeloma, sickle cell disease, and cystic fibrosis
DI: NEPHROGENIC ETIOLOGY
• Drugs
– Ethanol – Phenytoin (Dilantin) – Lithium carbonate – Demeclocycline – Amphotericin – Methoxyflurane (inhaled anesthetic)
DI: ASSESSMENT
• High urine output • Thirst and polydipsia • Hypotension • Decreased skin turgor • Dry mucous membranes • Tachycardia • Weight loss • Low right atrial pressure/central venous pressure (RAP/CVP) and pulmonary artery (PA) pressure • Neurological changes – Hypernatremia and hypovolemia
DI: DIAGNOSIS
- Dilute urine with low specific gravity
- Increased serum osmolality
- Increased blood urea nitrogen (BUN) and creatinine
- Hypokalemia or hypercalcemia
- Water deprivation test
- Vasopressin test (to differentiate)
DI: INTERVENTIONS
• Volume replacement – Monitor for fluid overload and water intoxication once therapy has been initiated • Hormone replacement – Vasopressin (desmopressin) • Thiazide diuretics (nephrogenic)
DI: INTERVENTIONS
• Patient education
– Pathogenesis of DI
– Dose, side effects, and rationale for prescribed medications
– Parameters for notifying the physician
– Importance of adherence to medication regimen
– Importance of recording daily weight measurements to identify weight gain
– Importance of wearing a Medic-Alert identification bracelet
– Importance of drinking according to thirst and avoiding
excess drinking
SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE (SIADH)
• Pathophysiology
– Excess ADH
– Plasma hypotonicity
SIADH: ETIOLOGY
• Central nervous system disease – Trauma – Tumor • Malignancy – Small-cell lung carcinoma – Hodgkin’s lymphoma – Pancreatic and duodenal carcinoma • Pulmonary disorders – TB, lung abscess, pneumonia, COPD • Medications – Many medications can result in SIADH
SIADH: ASSESSMENT • Central nervous system • Pulmonary system • Cardiovascular • GI system
• Central nervous system
– Confusion, headache, seizures, and weakness
• Pulmonary system
– Increased respiration, dyspnea, and adventitious lung
sounds
• Cardiovascular
– Hypertension and elevated CVP and PA pressures, edema
• GI system
– Anorexia, nausea, vomiting, muscle cramps, and decreased bowel sounds
SIADH: DIAGNOSIS
SIADH: DIAGNOSIS • Hyponatremia (due to water retention so it dilutes NA+) • Decreased serum osmolality • High urine sodium • Concentrated urine (water retention) • Decreased BUN and creatinine • Decreased albumin
LABORATORY INDICATORS OF SIADH
1) Sodium (serum)
2) Osmolality (serum)
3) Osmolality (urine)
4) Sodium (urine)
1) Sodium (serum)
- <135 mEq/L
- Free water retention due to oversecretion of ADH dilutes sodium
2) Osmolality (serum)
- <280 mOsm/kg H2O
- Free water retention due to oversecretion of ADH decreases osmolality
3) Osmolality (urine)
- >100 mOsm/kg H2O
- Lack of water excretion increases urine osmolality
4) Sodium (urine)
- >200 mEq/L
- Sodium excretion in an attempt to excrete excess water
SIADH: INTERVENTIONS
- Fluid restriction (800-1000 mL/day), including fluids high in sodium content
- If needed, hypertonic saline and diuretics
- Intake and output, serum sodium, urine and serum specific gravity, and daily weights
- Loop diuretics
- Mouth and skin care
- Patient and family education
CEREBRAL SALT WASTING (CSW)
• Result of serious brain injury • Disorder of sodium or fluid balance • Similar to SIADH • Pathophysiology not understood – Defect in sodium transport
CSW: ASSESSMENT
- Tachycardia
- Weight loss
- Hypotension
- Dry mucous membranes; poor skin turgor
- Lethargy and weakness
- Mental status changes
- Seizures and coma
LABORATORY INDICATORS OF CSW
1) Sodium (serum)
2) Osmolality (serum)
3) Osmolality (urine)
4) Sodium (urine)
1) Sodium (serum)
- <135 mEq/L
- Inability of kidneys to conserve sodium
2) Osmolality (serum)
- >295 mOsm/kg
- Inability of kidneys to conserve water
3) Osmolality (urine)
- <100 mOsm/kg H2O
- Free water loss into urine decreases urine osmolality
4) Sodium (urine)
- >200 mEq/L
- Sodium wasting through renal tubules
CSW: INTERVENTIONS
• Restore sodium and fluid volume – Isotonic saline
– Hypertonic saline
• Oral or IV fludrocortisone
CSW: INTERVENTIONS
• Restore sodium and fluid volume – Isotonic saline
– Hypertonic saline
• Oral or IV fludrocortisone
CSW: INTERVENTIONS
• Restore sodium and fluid volume
– Isotonic saline
– Hypertonic saline
• Oral or IV fludrocortisone
