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. Endocrinology 76 Question Comprehensive Exam (Members Only)

  2. Endocrine System Flashcards (Members Only)

    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
  3. 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
    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%