Endocrinology 6% Flashcards
Hyperparathyroidism, primary
↑ PTH usually caused by a PTH secreting parathyroid ADENOMA
Hyperparathyroidism, secondary
↑ PTH by a physiologic response to hypocalcemia or vitamin D deficiency.
Chronic kidney disease is the most common cause of secondary hyperparathyroidism.
Hyperparathyroidism, presentation:
“stones, bones, abdominal groans, psych moans, fatigue overtones”:
Nephrolithiasis, DI, bone pain, arthralgia, PUD, constipation, depression, fatigue.
Hyperparathyroidism, labs
Hypercalcemia ↑ CA+, ↓ phosphorus, elevated ↑ PTH, and moderately elevated urinary calcium.
Hyperparathyroidism, treatment
Acute - Saline, calcitonin, bisphosphonates.
Definitive - Surgical correction. Remove overactive parathyroid gland. If all 4, remove 3.5 glands.
Hypoparathyroidism, presentation
Tingling, Tetany, cataracts.
Hypoparathyroidism, signs
Chvostek’s sign: tap facial nerve illicit cheek twitch.
Trousseau’s sign: BP cuff inflation illicit carpal spasm.
Hypoparathyroidism, labs
Hypocalcemia ↓ CA+, low ↓ PTH, hyperphosphatemia, low urinary calcium.
Hypoparathyroidism, etiology
Two most common etiologies are postsurgical (damage from neck or thyroid surgery) or autoimmune.
Hypoparathyroidism, treatment
Vitamin D and Calcium
Tetany- secure airway, IV calcium gluconate
Hyperthyroidism, etiology
Grave’s disease (autoimmune). Toxic adenoma, thyroiditis, pregnancy, amiodarone.
Hyperthyroidism symptoms
Heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia.
Hyperthyroidism, Grave’s signs
Diffuse goiter with a bruit, exophthalmos, pretibial myxedema.
Hyperthyroidism, Thyroid storm
Fever, tachycardia, delirium.
Hyperthyroidism, diagnosis
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.
Grave’s - Thyrotropin receptor antibodies (TRAb, also called TSI, TBII, or TBI).
Hyperthyroidism, treatment
Beta-blockers (symptomatic), methimazole/propylthiouracil, radioactive iodine, thyroidectomy.
Hypothyroidism, etiology
Hashimoto’s (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital.
Hypothyroidism, symptoms; signs
Cold intolerance, fatigue, constipation, depression, weight gain, bradycardia.
Congenital: round face, large tongue, hernia, delayed milestones, poor feeding.
Hypothyroidism, diagnosis
TSH is elevated in primary disease. Low T4 (↑ TSH and ↓ Free T4).
Hashimoto’s: Antithyroid peroxidase (TPO), antithyroglobulin antibodies (Tg).
Hypothyroidism, treatment
Levothyroxine. Follow up with serial TSH monitoring.
Thyroid neoplastic disease, findings
Hoarse voice; cold nodule on thyroid uptake scan.
Most often papillary carcinoma (80%).
Thyroid neoplastic disease, diagnosis
Usually normal thyroid function.
Ultrasound is the best initial screen followed by a thyroid uptake scan.
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).
Thyroid neoplastic disease, treatment
Surgical resection with chemotherapy and external beam radiation reserved for anaplastic thyroid cancer.
Thyroiditis
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.
Corticoadrenal insufficiency (Addison’s Disease)
Typically autoimmune. May be due to Tuberculosis in endemic areas.
Destruction of the Adrenal cortex resulting in loss of cortisol production (↓ cortisol).
Corticoadrenal insufficiency (Addison’s Disease), symptoms
Nonspecific symptoms: Hyperpigmentation, hypotension, fatigue, myalgias, GI complaints, weight loss.
Corticoadrenal insufficiency (Addison’s Disease), diagnosis
↓ 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.
Corticoadrenal insufficiency (Addison’s Disease), treatment
Hydrocortisone/prednisone PO daily.
Cushing’s syndrome/disease
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.
Cushing’s syndrome symptoms; signs
Fat redistribution (buffalo hump, moon facies) pigmented striae, obesity, skin atrophy, weight gain, easy bruising, elevated glucose, infections, cataracts, hirsutism.
Cushing’s syndrome, diagnosis
↑ Cortisol, ↓ potassium, ↑ BP .
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.
Cushing’s syndrome, treatment
Resection of tumor/adenoma.
Adrenal neoplastic disease (pheochromocytoma)
Adrenal neoplasm - catecholamine secreting adrenal tumor - secretes norepinephrine and epinephrine autonomously and intermittently.
Adrenal neoplastic disease (pheochromocytoma), symptoms
Recurrent headaches, HTN, sweating, palpitations.
Adrenal neoplastic disease (pheochromocytoma), diagnosis
24-hour catecholamines including metabolites - metanephrine and vanillylmandelic acid (VMA)
MRI or CT of abdomen to visualize tumor.
Adrenal neoplastic disease (pheochromocytoma); treatment
Resect tumor - complete adrenalectomy.
Acromegaly/gigantism, etiology
Usually caused by a pituitary adenoma that secretes excessive amounts of Growth Hormone.
Rarely, they are caused by non-pituitary tumors that secrete GHRH.
Acromegaly/gigantism (Growth Hormone) presentation
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.
Acromegaly/gigantism (Growth Hormone), diagnosis; treatment
Growth hormone (↑GH) test 2 hours after glucose load.
Increased ↑IGF-1.
MRI/CT shows pituitary tumor.
Pituitary tumor removal.
Diabetes insipidus
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.
Diabetes insipidus, diagnosis
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.
Diabetes insipidus, treatment
Central: desmopressin.
Nephrogenic: indomethacin +/- HCTZ, desmopressin.
Pituitary dwarfism (GH deficiency)
Pituitary gland does not make enough Growth hormone.
Congenital - achondroplasia (mutation in FGFR3).
Pituitary dwarfism (GH deficiency), signs
Short stature/limbs, prominent brow, midfacial hypoplasia.
Pituitary dwarfism (GH deficiency), diagnosis
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_
Pituitary dwarfism (GH deficiency), treatment
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.
Pituitary adenoma and neoplasm
Most common tumors are microadenomas (<10 mm) that are functional (hypersecretion of pituitary hormones), nonfunctional or compressive.
Pituitary adenoma and neoplasm, diagnosis
MRI is the study of choice to look for sellar lesions/tumors.
Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH.
Prolactinoma (50%)
↑ Prolactin.
Secretes prolactin: Galactorrhea, infertility, amenorrhea.
Nonsecreting Adenoma (34%)
Null Cell - No secretion
Somatotroph Adenoma (10%)
↑ Growth Hormone/Prolactin.
Secretes GH - Presentation: Acromegaly.
Corticotroph Adenoma (5%)
↑ ACTH.
Secretes ACTH - Cushing syndrome.
Thyrotroph Adenoma (1%)
↑ TSH.
Secretes TSH - Hyperthyroidism.
Diabetes mellitus type 1, diagnosis criteria
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%.
Diabetes mellitus type 1, presentation
Children, polyuria, polydipsia, polyphagia, fatigue, and weight loss. Diabetic ketoacidosis (DKA) is commonly the initial presentation: Fruity breath, nausea, vomiting, dehydration.
Diabetes mellitus type 1, 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.
Diabetes mellitus type 1, Somogyi effect
Nocturnal hypoglycemia followed by rebound hyperglycemia due to surge in growth hormone.
Treat with decreased nighttime insulin dose or give bedtime snack.
Diabetes mellitus type 1, Insulin waning
Progressive rise in glucose from bed to morning.
Treat with change of insulin dose to bedtime.
Diabetes mellitus type 1, Hemoglobin A1c
Represents mean glucose level from previous 8-12 weeks (approx lifespan of an RBC).
Treatment goal of A1c < 7.0%.
Diabetes mellitus type 1, “finger-stick” blood glucose monitoring
Treatment goals: < 130 mg/dL fasting and < 180 mg/dL peak postprandial.
Diabetes mellitus type 1, comorbidities
Blood pressure should be maintained at < 130/80.
Statins for 40-50 y/o with LDL-C 70-189.
Diabetes Mellitus Type 2, diagnosis criteria
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%.
Diabetes Mellitus Type 2, prediabetes, diagnostic criteria
A1C 5.7-6.4;
Fasting glucose 100-125;
2-hour oral glucose tolerance test 140-199.
Diabetes Mellitus Type 2, Medications
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.
Diabetes Mellitus Type 2, 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.
Diabetes Mellitus Type 2, complications
Neuropathy (most common), retinopathy (leading cause of blindness), nephropathy.
Hypercholesterolemia, 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%.
