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Basic Pediatric endocrinology

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Show Notes

Slide 1 :

Basic Endocrinology Omar Ali MD

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A bit of history Early 19th century: Secretions from glands are carried by ducts and act at specific sites. Late 19th century: several investigators discovered that some glands seem to secrete chemicals directly into the blood (“ductless glands”) and these act far from where they are secreted.

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Arnold A Berthold (1803-1861) In one of the first endocrine experiments ever recorded, Professor Arnold A. Berthold of Gottingen did a series of tests on roosters in 1849 while he was curator of the local zoo.

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Ablation and replacement Berthold found that a rooster's comb is an androgen-dependent structure. Following castration, the comb atrophies, aggressive male behavior disappears, and interest in the hens is lost. Importantly, Berthold also found that these castration-induced changes could be reversed by administration of a crude testicular extract (or prevented by transplantation of the testes).

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Claude Bernard (1813-1878) Claude Bernard stated that the endocrine system regulates the internal milieu of an animal. The “internal secretions” were liberated by one part of the body, traveled via the bloodstream to distant targets cells. Circa 1854

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Endocrine system maintains homeostasis The concept that hormones acting on distant target cells to maintain the stability of the internal milieu was a major advance in physiological understanding. The secretion of the hormone was evoked by a change in the milieu and the resulting action on the target cell restored the milieu to normal.The desired return to the status quo results in the maintenance of homeostasis

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Two control systems Nervous system. Endocrine system

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Nervous system The nervous system exerts point-to-point control through nerves, similar to sending messages by conventional telephone. Nervous control is electrical in nature and fast.

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Hormones travel via the bloodstream to target cells The endocrine system broadcasts its hormonal messages to essentially all cells by secretion into blood and extracellular fluid. Like a radio broadcast, it requires a receiver to get the message - in the case of endocrine messages, cells must bear a receptor for the hormone being broadcast in order to respond.

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A cell is a target because it has a specific receptor for the hormone Most hormones circulate in blood, coming into contact with essentially all cells. However, a given hormone usually affects only a limited number of cells, which are called target cells. A target cell responds to a hormone because it bears receptors for the hormone.

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Response vs. distance traveled Endocrine action: the hormone is distributed in blood and binds to distant target cells.Paracrine action: the hormone acts locally by diffusing from its source to target cells in the neighborhood.Autocrine action: the hormone acts on the same cell that produced it.

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Control of Endocrine Activity The physiologic effects of hormones depend largely on their concentration in blood and extracellular fluid. Almost inevitably, disease results when hormone concentrations are either too high or too low, and precise control over circulating concentrations of hormones is therefore crucial.

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Feedback Control of Hormone Production Feedback loops are used extensively to regulate secretion of hormones in the hypothalamic-pituitary axis. An important example of a negative feedback loop is seen in control of thyroid hormone secretion

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Feedback control Negative feedback is most common: for example, LH from pituitary stimulates the testis to produce testosterone which in turn feeds back and inhibits LH secretion

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Figure 18.1 The Endocrine System

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Importance of the hypothalamus in homeostasis Regulates body temperature, sense of hunger, water balance Also controls the pituitary gland Pituitary helps regulate other glands Negative feedback keeps things stable

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The Hypophyseal Portal System Figure 18.7

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Contains axons of hypothalamic nerves. These release hormones that are synthesized in the hypothalamus and transported down to the post. pituitary neurons of the supraoptic nucleus manufacture antidiuretic hormone (ADH) Decreases the amount of water lost at the kidneys. Makes the urine more concentrated. At higher doses: Elevates blood pressure The posterior lobe of the pituitary gland

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Neurons of the paraventricular nucleus manufacture oxytocin Stimulates contractile cells in mammary glands Stimulates smooth muscle cells in uterus The posterior lobe of the pituitary gland (neurohypophysis)

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Thyroid stimulating hormone (TSH) Thyrotropin releasing hormone promotes the release of TSH TSH stimulates synthesis and release of thyroid hormones Adrenocorticotropic hormone (ACTH) Corticotrophin releasing hormone causes the secretion of ACTH ACTH stimulates the release of glucocorticoids from the adrenal gland

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Gonadotropin releasing hormone (GNRH) promotes the secretion of FSH and LH Follicle stimulating hormone (FSH) Stimulates follicle development and estrogen secretion in females and sperm production in males Leutinizing hormone (LH) Causes ovulation and progestin production in females and Testosterone production in males

Slide 23 :

Prolactin (PH) Stimulates the development of mammary glands and milk production. Not essential? Growth hormone (GH or somatotropin) Stimulates cell growth and replication through release of somatomedins or IGFs by the liver Also stimulates the production of IGF binding protein 3 and ALS.

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Growth Fat and short is the most worrying combination Not an emergency, so refer. Accurate growth charts and parent heights are very important. Rule out obvious causes of malnutrition/chronic illness

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Normal Variant Short Stature =3rd percentile =97th percentile 100 150 4 6 8 10 12 14 16 18 -4 SD +2 SD mean -2 SD Height (cm) Age (years) Males 3-18 years

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27 Diagnostic Workup Complete blood cell count (CBC) Erythrocyte sedimentation rate (ESR) Electrolytes Chemistry panel Urinalysis T4/TSH IGF-1 (somatomedin C) and IGFBP-3 Dietary evaluation

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BONE AGE Most common standards for bone ages are those of Gruelich and Pyle Left hand and wrist film

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Rules of Growth Evaluation 6. A rock will grow if given enough growth hormone. 7. Growth hormone deficiency is the toughest disease to diagnose but the easiest to treat. 8. If your height and weight curves meet, you are in trouble. 9. If your weight is on the height curve, you are obese. 10. If your height is in the weight curve, you are short. TOP TEN

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Thyroxine (T4) and T3. T4 is converted to T3 peripherally, which is the active form Exert a calorigenic effect Increase metabolic rate So: increased heart rate, body temperature, energy use, appetite, growth etc etc. Thyroid hormones

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Hypothyroidism Thyroid hormone deficiency causing a decrease in the basal metabolic rate Person is “slowed down” Causes of Primary Hypothyroidism: Congenital thyroid aplasia Radioactive iodine ablation Hashimoto’s thyroiditis - autoimmune destruction Non-compliance with levothyroxine

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Hypothyroidism Confusion, drowsiness, coma Cold intolerance Hypotension, Bradycardia Muscle weakness Decreased respirations Weight gain, Constipation Non-pitting peripheral edema Depression Facial edema, loss of hair Dry, coarse skin Earliest sign is SLOWING GROWTH Appearance of Myxedema

Slide 33 :

Hyperthyroidism Excessive levels of thyroid levels cause hypermetabolic state Person is “sped up”. Causes of Hyperthyroidism Grave’s Disease Overmedication with levothyroxine (Synthroid®) Adenoma

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Hyperthyroidism Nervousness, irritable, tremors, paranoid Warm, flushed skin Heat intolerance Tachycardia - High output CHF Hypertension Tachypnea Diarrhea Weight loss with increased appetite Exophthalmos Goiter

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Exophthalmos

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C cells produce calcitonin Helps regulate calcium concentration in body fluids. Decreases calcium levels. Not as important as PTH C-Cells of the thyroid gland

Slide 37 :

Thyroid disorders Screen for hypothyroidism by measuring Free thyroxine by dialysis and TSH. If hyperthyroidism is suspected, also test for free T3 Anti-thyroglobulin and anti-thyroperoxidase antibodies Thyroid stimulating antibody for Grave’s disease.

Slide 38 :

The Parathyroid Glands Figure 18.14

Slide 39 :

PTH Secreted in response to low serum calcium Reduces urinary calcium excretion and increases phosphate excretion Increased calcium mobilization from bone Stimulates activation of Vitamin D, which increases calcium and phosphorous absorption in the gut. Net effect is to increase serum Ca.

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Manufactures steroid hormones (corticosteroids) Cortex divided into three layers Zona glomerulosa (produces mineralocorticoids)…salty Zona fasciculate (produces glucocorticoids)..sweet Zona reticularis (produces androgens)..sexy Adrenal cortex

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Adrenal disorders Primary: disorder in the adrenal gland itself (adenoma->XS production, infiltrative disease or infarction ->deficiency) Secondary: disorder in the hypothalamus or pituitary gland causing abnormal ACTH release (excessive ->hyperadrenalism, deficient -> hypoadrenalism or adrenal insufficiency)

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Abnormal Adrenal Function Hyperadrenalism Hyperaldosteronism (Conn’s syndrome) Cushing’s Syndrome & Disease Hyperandrogenism (virilization) Pheochromocytoma Hypoadrenalism (adrenal insufficiency) Inadequate activity of the adrenal gland Addison’s disease

Slide 43 :

Hyperadrenalism Cushing’s Syndrome Results from increased adrenocortical secretion of cortisol Causes include: ACTH-secreting tumor of the pituitary (Cushing’s disease) excess secretion of cortisol by a neoplasm within the adrenal cortex excess secretion of ACTH by a malignant growth outside the adrenal gland (esp small cell lung ca) = ectopic ACTH pdtn excessive or prolonged administration of steroids

Slide 44 :

Hyperadrenalism Cushing’s Syndrome Characterized by: truncal obesity moon face buffalo hump acne, hirsutism abdominal striae hypertension psychiatric disturbances osteoporosis Amenorrhea Growth failure

Slide 45 :

Hyperadrenalism Adrenogenital syndrome “Bearded Lady” Group of disorders caused by adrenocortical hyperplasia or malignant tumors Excessive secretion of adrenocortical steroids especially those with androgenic effects Characterized by masculinization of women premature sexual development of children

Slide 46 :

Adrenal enzyme pathways

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Slide 48 :

CAH, 46,XX

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CAH, simple-virilizing (21-OHase deficiency)

Slide 50 :

Adrenal Crisis When to suspect: Patient is sicker than expected. Hypotensive, hypothermic, hypoglycemic Critically ill patient Neonate with ambigous genitalia Neonate with unexplained sudden illness associated with dehydration and collapse.

Slide 51 :

Labs Critical sample. One red top and one green top tube, store on ice/in freezer. ACTH Cortisol 17 hydroxy progesterone in the neonate

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Treatment Volume expanders (normal saline, lactated Ringers) Glucose Emergency Hydrocortisone. 25 mg IV in neonates 50 mg in young children 100 mg in adolescents. Then 30 -40 mg per meter square per day

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Produces epinephrine (~75 - 80%) Produces norepinephrine (~25-30%) Adrenal medulla

Slide 54 :

Pheochromocytoma Catecholamine secreting tumor of adrenal medulla Presentation Anxiety Pallor, diaphoresis Hypertension Tachycardia, Palpitations Dyspnea Hyperglycemia

Slide 55 :

Clusters of endocrine cells within the pancreas called Islets of Langerhans or pancreatic islets Alpha cells secrete glucagons Beta cells secrete insulin Delta cells secrete somatostatin F cells secrete pancreatic polypeptide The pancreatic islets

Slide 56 :

Insulin lowers blood glucose by increasing the rate of glucose uptake and utilization Glucagon raises blood glucose by increasing the rates of glycogen breakdown and glucose manufacture by the liver Insulin and glucagon

Slide 57 :

Interstitial (Leydig) cells of the testes produce testosterone Most important sex hormone in males In females, oocytes develop in follicles Follicle cells produce estrogens After ovulation, the follicle cells form a corpus luteum that releases a mixture of estrogens and progesterone The gonads

Slide 58 :

Early Puberty More likely to be benign in girls, more likely to be pathological in boys. Isolated thelarche and premature adrenarche are generally benign. Growth chart is very important. Refer girls less than 8 and boys less than 9 years of age.

Slide 59 :

TANNERSTAGE

Slide 60 :

TANNERSTAGE

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Delayed puberty More likely to be pathological in girls than boys. Refer girls if no pubertal changes by 13 and boys if no changes by 14. First finding is thelarche in girls and testicular enlargement in boys. No periods by 16 or within 5 years of thelarche = referral.

Slide 62 :

Leptin, a feedback control for appetite Resistin, which reduces insulin sensitivity Adipose tissues secrete

Slide 63 :

Obesity Rarely endocrine Tall and fat is almost always nutritional. Short and fat deserves a workup Thyroid Cushings Genetic disorders, e.g. PWS

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ACANTHOSIS NIGRICANS = HYPERINSULINEMIA=T2DM Risk Direct action of insulin on keratin layers. Can occur anywhere on the body. More common in flexor and extensor folds. Goes away with treatment of insulin resistance. Severe cases can progress to skin tags, usually requiring dermatologic treatment. Katz et al: Dermatology Online Journal, vol 6, 2000 (dermatology.cdlib.org)

Slide 66 :

A Practical CHO-Limited Diet Avoid ALL Simple Sugars No regular sodas, sweetened juices. Limit unsweetened juices. No foods with >5g sugar/serving. Limit Complex Carbohydrates Bread, Potato, Rice, Pasta, Tortilla 1-3 Servings 3 times a day only

Slide 67 :

Avoid Fried/Fatty Foods These foods may increase cholesterol levels and cardiovascular risk Eat More Lean Proteins Pork, Beef<15% fat, skinless poultry most fish and shellfish Use Low or Non- Carbohydrate Snacks Exercise Goal: 30 min sustained, strenuous exercise 3-5 X/wk

Slide 68 :

A Practical CHO-Limited Diet:METFORMIN trade name: Glucophage (Bristol Meyers Squibb) classified as an “oral anti-hyperglycemic” agent, NOT an “oral hypoglycemic” primary mechanism of action unknown actions include: decreased hepatic gluconeogenesis, decreased intestinal glucose transport and increased insulin sensitivity works best with a CHO-limited diet primary side effect: lactic acidosis (~3/100K pt-years); contraindicated in renal insufficiency Monitor: clinical status, LFTs, RFTs

Slide 69 :

Figure 18.1 The Endocrine System

Slide 70 :

History Growth charts/growth pattern/weight loss and gain. Chronic illness/concurrent illnesses/past illness Medications Previous treatment for cancer Head trauma

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Family history Thyroid disease Diabetes Growth pattern Hormone issues Hormones at home Ethnic background

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Physical examination Growth parameters Dysmorphic features/midline defects/proportions Goiter Skin pigmentation Birthmarks striae Genitalia/Tanner stage

Slide 73 :

Screening at birth Hypothyroidism. 1/5000 babies Usually screen by checking TSH California standard >25 May miss some babies. Repeat and treat if really high. Repeat if borderline

Slide 74 :

Screening at birth CAH Controversial Many false positives. Due to start in California sometime soon Repeat and refer. Monitor electrolytes

Slide 75 :

Thank You

	oali@mcw.edu 1 Years ago. Category: Pediatrics

Tags:	Pediatrics

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