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
