PANCE Blueprint Endocrinology (6%)

PANCE Blueprint Endocrinology (6%)

PANCE Blueprint Endocrinology (6%)

Follow Along with the NCCPA™ PANCE and PANCE Endocrine System Content Blueprint

  • 24 PANCE and PANRE Endocrinology Content Blueprint Lessons (FREE)
  • 76 Question Endocrinology Comprehensive Exam (available to smartypance members)
  • Endocrinology Pearls Flashcards (available to smartypance members)
  • 5 Endocrinology high yield summary tables (FREE)
  • ReelDX™ integrated video content (available to paid ReelDx+ members)

Lessons

    1. Hyperparathyroidism has two cause: primary and secondary 
      • Primary: ↑ PTH usually caused by a PTH secreting parathyroid ADENOMA
      • Secondary: ↑ PTH by a physiologic response to hypocalcemia or vitamin D deficiency. Chronic kidney disease is the most common cause of secondary hyperparathyroidism.
      • Presentation: “stones, bones, abdominal groans, psych moans, fatigue overtones”
        • Nephrolithiasis, DI, bone pain, arthralgia, PUD, constipation, depression, fatigue
      • Labs: Hypercalcemia ↑ CA+, ↓ phosphoruselevated ↑ PTH and moderately elevated urinary calcium
      • Treatment:
        • Acute- Saline, calcitonin, bisphosphonates
        • Definitive- Surgical correction. Remove overactive parathyroid gland. If all 4, remove 3.5 glands.
    2. Two most common etiologies are postsurgical (damage from neck or thyroid surgery) or autoimmune
      • Presentation: Tingling, Tetany, cataracts
      • Labs: Hypocalcemia ↓ CA+, low ↓ PTH, hyperphosphatemia, low urinary calcium
      • Treatment: Vitamin D and Calcium
        • Tetany- secure airway, IV calcium gluconate
    3. Grave’s disease (autoimmune). Toxic adenoma, thyroiditis, pregnancy, amiodarone
      • Heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia
      • Graves- Diffuse goiter with a bruit, exophthalmos, pretibial myxedema
      • Thyroid storm- Fever, tachycardia, delirium
      • TSH (best test): Decreased in primary disease (↓ TSH  and ↑ Free T4), elevated in secondary disease (↑ TSH  and ↑ Free T4)
      • Thyroid radioactive iodine uptake:
        • Graves: Diffusely high uptake
        • Toxic multinodular: Discrete areas of high uptake
      • Graves: Thyrotropin receptor antibodies (TRAb, also called TSI, TBII, or TBI)
      • Beta-blockers (symptomatic)methimazole/propylthiouracil, radioactive iodine, thyroidectomy
    4. Etiology: Hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital
      • Cold intolerance, fatigue, constipation, depression, weight gain, bradycardia
      • Congenital: round face, large tongue, hernia, delayed milestones, poor feeding
      • TSH is elevated in primary disease. Low T4 (↑ TSH and ↓ Free T4)
        • Hashimoto’s: Antithyroid peroxidase (TPO), antithyroglobulin antibodies (Tg)
      • Levothyroxine. Follow up with serial TSH monitoring
    5. Hoarse voice, cold nodule on thyroid uptake scan
      • Most often papillary carcinoma (80%)
      • Ultrasound is the best initial screen followed by a thyroid uptake scan. Usually normal thyroid function.
      • Microcalcifications, hypoechogenicity, a solid cold nodule, irregular nodule margins, chaotic intranodular vasculature, and a nodule that is more tall than wide.
      • Fine needle biopsy for definitive diagnosis (all lesions >1 cm should be biopsied)
      • Surgical resection with chemotherapy and external beam radiation reserved for anaplastic thyroid cancer
    6. Painful vs. Painless may be hypo or hyperthyroid
      • Hashimoto’s thyroiditis:
        • Diffusely enlarged, painless, nodular goiter
      • Subacute thyroiditis:
        • Young women, after a viral infection
        • Painful enlarged thyroid with dysphagia, mild fever
        • Aspirin
      • Postpartum thyroiditis:
        • 1-2 months of hyperthyroidism after delivery
        • Completely resolves, give propranolol for cardiac symptoms
      • Suppurative thyroiditis:
        • Fever, pain, redness, fluctuant mass. ↑ WBC
        • Antibiotic/surgical drainage
  1. Diseases of the Adrenal Glands (PEARLS)

    1. Typically autoimmune. May be due to Tuberculosis in endemic areas
      • Destruction of the Adrenal cortex resulting in loss of cortisol production (↓ cortisol)
      • Nonspecific symptoms: Hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss
      • sodium, 8 AM cortisol, ↑ ACTH (primary), ACTH (secondary), potassium (primary), DHEA
      • High Dose Cosyntropin (synthetic ACTH) Stimulation Test: Blood or urine cortisol are measured after an IM injection of cosyntropin (synthetic ACTH)
        • Normal response is a rise in blood and urine cortisol levels after synthetic ACTH is given
        • Adrenal insufficiency results in little or no increase in cortisol levels (< 20 mcg/dL) after ACTH is given
      • Hydrocortisone/prednisone PO daily
    2. Cushing's syndrome

      • Cushing's Syndrome: primary ↑ cortisol secretion from an adrenal tumor or excess glucocorticoids
      • Cushing's Disease: secondary ↑ cortisol caused by a pituitary adenoma resulting in ↑ ACTH secretion - ACTH causes adrenals to secrete cortisol
      • ↑ Cortisol, ↓ potassium, ↑ BP 
      • Fat redistribution (buffalo hump, moon facies) pigmented striae, obesity, skin atrophy, weight gain, easy bruising, elevated glucose, infections, cataracts, hirsutism
      • 24-hour urinary free cortisol is the most reliable index of cortisol secretion: Urine cortisol excretion of > 125 mg/dL in 24 hrs
      • Low dose dexamethasone suppression test → give a steroid (dexamethasone) failure of steroid to decrease cortisol levels is diagnostic, proceed next to high dose dexamethasone suppression test - no suppression = Cushing's Syndrome
      • Resection of tumor/adenoma
    3. Pheochromocytoma: Adrenal neoplasm - catecholamine secreting adrenal tumor - secretes norepinephrine and epinephrine autonomously and intermittently
      • Recurrent headaches, HTN, sweating, palpitations.
      • 24-hour catecholamines including metabolites - metanephrine and vanillylmandelic acid (VMA)
      • MRI or CT of abdomen to visualize tumor
      • Resect tumor - complete adrenalectomy
    1. Gigantism and acromegaly are usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormone; rarely, they are caused by non-pituitary tumors that secrete GHRH
      • Gigantism occurs if growth hormone (GH) hypersecretion begins in childhood, before closure of the epiphyses
      • Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop
      • Large hands, feet, nose, lips, ears, jaw, tongue
      • Presents as gigantism (excessive height) if occurs before epiphyseal closure
      • Growth hormone (↑GH) test 2 hours after glucose load
      • Increased ↑IGF-1
      • MRI/CT shows pituitary tumor
      • Pituitary tumor removal
    2. Diabetes insipidus (DI) is caused by a deficiency of or resistance to vasopressin (ADH), which decreases the kidneys' ability to reabsorb water, resulting in massive polyuria
      • Central diabetes insipidus - Deficiency of ADH from posterior pituitary/hypothalamus
        • No ADH production most common type: idiopathic, autoimmune destruction of posterior pituitary from head trauma, brain tumor, infection, or sarcoidosis
      • Nephrogenic diabetes insipidus - Lack of reaction to ADH
        • Partial or complete insensitivity to ADH: caused by drugs (Lithium, Amphoterrible), hypercalcemia and hypokalemia affect the kidney's ability to concentrate urine, acute tubular necrosis
      • 24 hr urine: ↓ urine specific gravity < 1.010 and ↓ urine osmolarity < 200
      • Desmopressin (ADH) stimulation test: differentiates nephrogenic from central DI Give ADH
        • Central DI - reduction in urine output indicating response to ADH
        • Nephrogenic DI - continued production of dilute urine (no response to ADH) because kidneys can't respond
      • Central – desmopressin. Nephrogenic— indomethacin +/- HCTZ, desmopressin
    3. Pituitary gland does not make enough Growth hormone
      • Congenital - achondroplasia (mutation in FGFR3)
      • Short stature/limbs, prominent brow, midfacial hypoplasia
      • Labs: ↓ GH, ↓ IGF1
      • BONE AGE: X-ray the child's hand to determine the child's bone age by comparing this to the child's actual chronological age.
      • Growth hormone - If dwarfism is due to decreased human growth hormone
      • Surgery may be necessary to remove a pituitary adenoma if that is the cause of the dwarfism.
    4. Most common tumors are microadenomas (<10 mm) that are functional (hypersecretion of pituitary hormones), nonfunctional or compressive
      • MRI is the study of choice to look for sellar lesions/tumors
      • Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH
      • Prolactinoma (Galactorrhea) ↑ Prolactin (50%)
        • Secretes prolactin - Galactorrhea, infertility, amenorrhea
      • Nonsecreting Adenoma (34%)
        • Null Cell - No secretion
      • Somatotroph Adenoma (Acromegaly) ↑ Growth Hormone/Prolactin (10%)
      • Corticotroph Adenoma (Cushing's Syndrome) ↑ ACTH (5%)
      • Thyrotroph Adenoma (Hyperthyroidism) ↑ TSH (1%)
      • Random blood glucose level of > 200 mg/dL AND diabetic symptoms
      • 2 separate fasting (8 hours) glucose levels of > 126 mg/dL
      • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
      • Hemoglobin A1c of > 6.5%
      Children, polyuria, polydipsia, polyphagia, fatigue, and weight loss
      • Diabetic ketoacidosis (DKA) is commonly the initial presentation - Fruity breath, nausea, vomiting, dehydration
      • Dawn Phenomenon: Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and nightly surge of counter-regulatory hormones during nighttime fasting
        • Treat with bedtime injection of insulin to blunt morning hyperglycemia, avoiding carbohydrate snack late at night
      • Somogyi effect: Nocturnal hypoglycemia followed by rebound hyperglycemia due to surge in growth hormone
        • Treat with decreased nighttime insulin dose or give bedtime snack
      • Insulin waning: progressive rise in glucose from bed to morning
        • Treat with change of insulin dose to bedtime
      • Hemoglobin A1c
        • represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC)
        • Treatment goal of A1c < 7.0%
      • "finger-stick" blood glucose monitoring
        • Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial 
      • Blood pressure should be maintained at < 130/80
      • Statins for 40-50 y/o with LDL-C 70-189
      • Random blood glucose level of > 200 mg/dL AND diabetic symptoms
      • 2 separate fasting (8 hours) glucose levels of > 126 mg/dL
      • 2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)
      • Hemoglobin A1c of > 6.5%
      • Diagnostic criteria for prediabetes: A1C 5.7-6.4, Fasting glucose 100-125, 2-hour oral glucose tolerance test 140-199
      Medications for Type II
      • Metformin - decreases hepatic glucose production and peripheral glucose utilization, decreases intestinal glucose absorption (these are reasons it leads to weight loss)
        • Side effects: Lactic acidosis, GI side effects
      • Sulfonylureas - stimulates pancreatic beta cell insulin release (insulin secretagogue)
        • Glyburide, glipizide, glimepiride
        • Side effects: Hypoglycemia
      • Thiazolidinediones - increases insulin sensitivity in peripheral receptor site adipose and muscle. Has no effect on pancreatic beta cells.
        • Pioglitazone
        • Contraindications: CHF, liver disease
      • Alpha-glucosidase inhibitors - Delays intestinal glucose absorption
        • Acarbose, miglitol
        • GI side effects
      • Incretins - Dipeptidyl peptidase inhibition - inhibits degradation of GLP-1 so more circulating GLP-1
        • DDP4- sitagliptin, Incretin mimetics-Exenatide
        • Side effects: Hypoglycemia, severe allergy
      • Insulin – add if HbA1C >9
      Glucose goals and basic management
      • A1C < 7.0 % check every 3 months if not controlled and 2x per year if controlled
      • Preprandial glucose 80-110 (60-90 if pregnant)
      • Postprandial blood glucose goal is < 140
      • Annual dilated eye exams, ACEI if microalbuminuria, annual foot examination
      • Blood pressure should be maintained at < 130/80
      • New statin guidelines: recommend statins in persons with diabetes mellitus who are 40 to 75 years of age with LDL-C levels of 70 to 189 mg per dL but without clinical ASCVD (see guidelines)
      • Annual- ophthalmologist visit, urine microalbumin
      • Complications –neuropathy (most common), retinopathy (leading cause of blindness), nephropathy
  2. Endocrinology 76 Question Comprehensive Exam (Members Only)

  3. Endocrine System Flashcards (Members Only)

    1. Four groups most likely to benefit from statin therapy are identified:
      • Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)
      • Patients with primary LDL-C levels of 190 mg per dL or greater.
      • Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL.
      • Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%