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ACPNP Review > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Mild Dehydration (5%)

A
  • Fatigued
  • Drinks, but may refuse
  • Normal heart rate
  • Normal to increased pulses
  • Normal breathing
  • Normal eyes
  • Tears present
  • Moist mucous membranes
  • Instant skin recoil
  • Cap refill normal
  • Warm to beginning to cool extremities
  • Mildly decreased urine output
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2
Q

Moderate Dehydration (10%)

A
  • Fatigued or restless, irritable
  • Thirsty
  • Normal to increased heart rate
  • Normal to increased pulses
  • Fast breathing
  • Slightly sunken eyes
  • Decreased tear production
  • Dry mucous membranes
  • Skin recoil < 2 sec
  • Prolonged cap refill
  • Cool extremities
  • Decreased urine output
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3
Q

Severe Dehydration (15%)

A
  • Lethargy
  • Unable to drink
  • Tachycardia
  • Weak pulses
  • Deep breathing
  • Sunken eyes, sunken fontanelles
  • Absent tears
  • Parched mucous membranes
  • Skin fold recoil prolonged
  • Prolonged cap refill
  • Cold, mottled, cyanotic extremities
  • Minimal urine output
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4
Q

Types of Dehydration

A
  1. Isonatremic
  2. Hypernatremic
  3. Hyponatremic
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5
Q

Management of Dehydration

A
  • Identify underlying problem
  • Replace electrolytes slowly
  • Correct fluid losses over 24-48 hours
  • Maintenance and replacement fluid infusion
  • Monitor intake and output
  • Monitor electrolytes
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6
Q

Fluid Dose: 0-10kg

A

100mL/kg/day

4mL/kg/hr

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7
Q

Fluid Dose: 10-20kg

A

1000mL + 50mL for each additional kg 0ver 10kg

40mL/hr + 2mL/hr for each additional kg over 10kg

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8
Q

Fluid Dose: >20kg

A

1500mL + 20mL for each additional kg over 20kg

60mL/hr + 1mL/hr for each additional kg over 20kg

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9
Q

Electrolyte abnormalities

A

Most common: Hyponatremia, hyperkalemia, hypocalcemia.

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10
Q

Hyponatremia

A

Causes:
- SIADH, adrenal insufficiency, hypervolemia, hypovolemia, excessive water intake.

Tx: Correct Na at a rate of 0.5mEq/L/hr.
- If symptomatic, NSS 20mL/kg bolus, consider hypertonic saline 3%

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11
Q

Hyperkalemia

A

Causes:

  • Excessive oral/IV intake, decreased excretion (renal failure, beta-blockers, diuretics), acidosis.
  • Make sure that potassium values were not hemolyzed.

EKG Changes: Peaked T-waves, depressed ST, wide QRS, no P-wave

Tx: Discontinue diuretics and oral/IV K+, perform EKG, obtain CMP, CPK, UA, ABG, Na bicarbonate and insulin with glucose IV, administer calcium.
- Kayexalate is sometimes used.

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12
Q

Hypocalcemia

A

Causes:
- Hypoparathyroidism, vit D deficiency, renal insufficiency.

Tx: (Hypoalbuminemia) Correct Ca+ with 0.8mg/dL for each 1g/dL, consider EKG, consider CMP, albumin.

  • Calcium replacement with calcium chloride or gluconate.
  • If given IV, administer slowly!
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13
Q

Acute Hypoglycemia

A

Glucose < 50mg/dL - ketotic vs nonketotic

Causes:
- Neonatal - diabetic mom, adrenocortical deficiency, inborn errors, SGA.

  • Childhood - Inborn errors, growth hormone deficiency, stress, hepatic dysfunction, ingestion, infection.

Tx: Glucose replacement - 0.5-1g/kg 10% or 25% glucose

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14
Q

Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH)

A

Excess of ADH with increased permeability of renal distal tubules and collecting ducts, results in increased water reabsorption and decreased urine production.

Causes: CNS injury, diseases of hypothalamus or pituitary, hepatic disease, pulmonary disease, high dose chemotherapy.

S/S:

  • Serum Sodium LOW
  • Serum Osmolarity LOW
  • Urine Sodium HIGH
  • Urine Osmolarity HIGH
  • Specific Gravity HIGH
  • Urine Output low or normal

Tx: Restrict sodium and fluid intake, monitor electrolytes and intake/output, diuretics, 0.9%NS.

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15
Q

Diabetes Insipidus (DI)

A

Central: Antidiuretic deficit.
- Genetic, congenital, acquired.

Nephrogenic: Adequate levels of ADH, results in decreased water reabsorption, increased urine output, hypernatremia, and dehydration.
- Congenital or acquired as a result of renal disease, metabolic conditions or medication related.

Causes: CNS injury or infection, disorders of the hypothalamus, pituitary or panhypopituitarism after tumor resection, primary and secondary renal defects.

S/S:

  • Serum Sodium HIGH
  • Serum Osmolarity HIGH
  • Urine Sodium LOW
  • Urine Osmolarity LOW
  • Specific Gravity LOW or NORMAL
  • Urine Output HIGH, > 4mL/kg/hr

Tx: Vasopressin or DDAVP, fluid replacement, monitoring of fluids and electrolytes.

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16
Q

Cerebral Salt Wasting (CSW)

A

Atrial natriuretic hormone excess, results in Na excretion into urine and diuresis.
- Hyponatremia, euvolemia or hypovolemia.

Causes: CNS injury or infection, endocrine disturbances including DKA, chronic lung disease or BPD, cardiac disease.

S/S:

  • Serum Sodium LOW
  • Serum Osmolarity LOW
  • Urine Sodium HIGH
  • Urine Osmolarity HIGH
  • Specific Gravity HIGH or normal
  • Urine Output HIGH, 2-3mL/kg/hr

Tx: Treat underlying problem, replace sodium slowly, maintain fluid intake, monitoring of fluids and electrolytes.

17
Q

Type 1 Diabetes

A

Condition in which the pancreas no longer produces enough insulin or cells stop responding to the insulin that is produced, so that glucose levels are elevated and other metabolic problems persist.

S/S: Polyuria, polydipsia, polyphagia, fatigue, and weight loss. Complications of poorly managed diabetes may include cardiovascular disease, diabetic neuropathy, diabetic retinopathy.

Tx: Subcutaneous insulin, short and long-acting.
- Short: 0.5-1 unit/kg/day

18
Q

Diabetic Ketoacidosis (DKA)

A

State of insulin deficiency in which a starvation state triggers a cascade of metabolic responses, including hyperglycemia and ketone body formation with lactic acidosis from decreased tissue perfusion resulting in metabolic acidosis.

  • Can present with initial diagnosis or throughout lifetime of patient with IDDM.
  • pH < 7.3 and HCO3 < 15

S/S: Abdominal pain, vomiting, puolyuria, hyperglycemia, ketonuria, lethargy, and other mental status changes, tachycardia, signs of dehydration, and Kussmaul respirations.

Dx: Glucose, electrolytes, UA, VBG, serum ketones, CBC, LFTs, amylase, lipase.

  • Typical findings include increased glucose, low pH, HCO3 < 15, + ketonuria, + serum ketones.
  • For newly diagnosed diabetics and children in DKA, a HgbA1c should be obtained, labs should include insulin autoantibodies, insulin level, thyroid function tests, islet cell antibodies, C-peptide levels.

Tx: NS bolus 20mL/kg, begin insulin drip at 0.1 units/kg/hr, add glucose when serum glucose is about 250-300 or if glucose levels are dropping faster than 100/hr, replace potassium, consider buffered fluids such as potassium acetate, replace phosphorus.

  • Frequent labs, glucose q1hr, VBG. VS with neuro checks every 1-2 hours, cardiac monitor.
  • Convert to subcutaneous insulin when lab values (pH and HCO3) are normalized.

Complications: Cerebral edema - headache, irritability, confusion, seizures, altered LOC, Cushing triad.

19
Q

Adrenal Insufficiency

A

Dysfunction of the adrenal gland.

Primary: Congenital Adrenal Hyperplasia (CAH), sepsis, surgical removal, Addison disease, adrenal hemorrhage.

Secondary: Destroyed or inactive adrenal gland, ACTH deficiency.

Tertiary: Suppression from steroids, rapid taper of steroids.

Relative: Critical illness, shock.

20
Q

Adrenal Crisis

A

Rapid, overwhelming, potentially fatal situation.
- Occurs with chronic adrenal insufficiency, acute damage, abrupt withdrawal of steroids.

S/S: Hypotension, fatigue, vomiting, muscle pain, anorexia, weight loss.
- With cortisol deficiency - hypotension, hypoglycemia, weakness, anorexia, nausea, vomiting.

Dx: Obtain CMP, glucose, ACTH, am cortisol level and aldosterone concentration.

Tx: Glucocorticoids, monitoring of function.

21
Q

Congenital Adrenal Hyperplasia (CAH)

A

Hyperkalemia, hyponatremia, dehydration.

Dx: Serum electrolytes, ACTH stimulating test, cortisol levels.

Tx: Manage fluid and electrolytes, glucocorticoids, hydrocortisone.

22
Q

Thyroid Storm

A

Life-threatening condition due to untreated hyperthyroidism.

S/S: HTN, fever, ALOC, tachycardia, sweating.

Complications: CHF and pulmonary edema can develop rapidly and lead to death.

23
Q

Hyperthyroidism

A

S/S: Nervousness, irritability, emotional lability, tremor, excessive appetite, weight loss, smooth and moist skin, increased perspiration, heat intolerance, goitre, exophthalmos, tachycardia, widened pulse pressure.

24
Q

Thyroiditis

A

Inflammation of the thyroid leading to hyperthyroidism.

Dx: Thyroid function tests - elevated T4, decreased TSH.

Tx: Varies, sometimes no therapy is warranted.

25
Q

Hypothyroidism

A

S/S: Growth retardation, diminished physical activity, impaired tissue perfusion, constipation, thick tongue, poor muscle tone, hoarseness, anemia, intellectual retardation.

Dx: Thyroid function tests - low T4 and T3, elevated TSH.

Tx: Replace thyroid hormone as levothyroxine.

26
Q

Metabolic Disorders

A

Inborn Errors of Metabolism

  • Amino Acid Disorders
  • Glycogen Storage Diseases
  • Lysosomal Storage Diseases
  • Mitochondrial Diseases
  • Organic Acidemias
  • Peroxisomal Disorders
  • Phenylketonuria
  • Urea-Cycle Diseases

Concern when infant presents with seizures, lethargy or coma, recurrent unexplained illness, hepatosplenomegaly, hypotonia, signs of sepsis, developmental delay, loss of milestones, poor feeding, vomiting, eye/hair/skin abnormalities.
- KEY FINDINGS: hypoglycemia, hyperammonemia, ketosis, metabolic acidosis.

27
Q

Amino Acid Disorders

A

Disorder of protein metabolism.

  • Most common disorders, caused by defect in the metabolic pathway of amino acids resulting in abnormal accumulation of amino acids in plasma.
  • Often present acutely in newborn, will result in coma, encephalopathy or death if not identified.
28
Q

Organic Acid Disorders

A

Disorder of protein metabolism.

  • Enzyme deficiency or abnormal step in pathways of amino acid degradation, accumulation of abnormal organic acid metabolites and increased excretion of organic acids in the urine.
  • Presents in newborn period with poor feeding, lethargy, acidosis and ketosis, high ammonia levels.
29
Q

Urea Cycle Disorders

A

Disorder of protein metabolism.

  • Deficiency of enzyme or cofactor that transforms nitrogen to urea for excretion.
  • Presents few days after birth with poor feeding, vomiting, tachypnea, and AMS after a few days of protein intake.
30
Q

Glycogen Storage Disease

A

Disorder of glucose metabolism.

  • Carbohydrate disorders such as galactosemia.
  • Deficiency of galactose-1-phosphate uridyl transferase (GALT), disorders of glycogen breakdown.
  • Present as seizures, poor growth, hypotonia, metabolic acidosis and hyperbilirubinemia.
31
Q

Fatty Acid Oxidation Disorder

A

Disorder of fat metabolism.

  • Involves single-enzyme defects either in one of the beta-oxidation steps for fatty acids or in the pathway that transfers electrons from FADH2 to the electron-transport.
  • Previously healthy child presents with vomiting, lethargy/coma, occasionally seizures, +/- hepatomegaly triggered by acute illness.
32
Q

Lysosomal Storage Disorder

A

Disorder of organelles.

  • Mucopolysaccharidosis.
  • Deficiency of lysosomal enzymes leading to excessive tissue storage of lipid material or incomplete degradation and storage of mucopolysaccharides.

S/S: Developmental delay, mental retardation, hepatomegaly, splenomegaly, neurologic regression, short stature, coarsening of facial features, limitation of small and large joints, cardiac disease.

33
Q

Key Points

A
  • An infant with acidosis or who presents with symptoms of sepsis should have an ammonia level sent.
  • Sodium less than 130 will predispose a child to seizures.
  • High potassium levels can cause severe arrhythmias.
  • The most concerning complication of DKA is cerebral edema!

ACPNP Review (14 decks)

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