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Endocrine

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Endocrine

  1. 1. <ul><li>Sex differentiation
  2. 2. Normal development
  3. 3. Ambiguous genitalia
  4. 4. Recognize the signs and symptoms of CAH
  5. 5. Females: ambiguous genitalia, usually identified at birth
  6. 6. Males: no marked effect on genitalia so might go undetected at birth
  7. 7. Salt losing form (“classic”): usually present in a crisis at about age 2 weeks (salt wasting and acute adrenal crisis)
  8. 8. Simple form: may go undetected until about 6 months of age and at that time they show signs of androgen excess like pubic and axillary hair, body odor
  9. 9. Know the lab evaluation of CAH
  10. 10. 21-OH deficient salt losers
  11. 11. elevated 17-OH progesterone
  12. 12. hypoNa, hyperK, hypoglycemia
  13. 13. elevated renin, low aldosterone
  14. 14. elevated androgens
  15. 15. 21-OH deficient non-salt losers
  16. 16. elevated 17-OH progesterone
  17. 17. elevated androgens
  18. 18. Know that CAH can be diagnosed prenatally
  19. 19. Measure the 17-OH progesterone in amniotic fluid
  20. 20. IF the couple already has a baby who had CAH or are known carriers, then mom should take oral dexamethasone for the first 10 weeks. Fetal cells then need to be sampled – either by CVS at 10-12 weeks or amnio at 14-18 weeks
  21. 21. Gender is determined, and f male then mom stops taking the dexa; if female mom keeps taking the dexa and more testing is done (the dexa is used to help prevent virilization of the females)
  22. 22. Plan the treatment for adrenal crisis in a patient with CAH
  23. 23. Need aggressive fluid therapy
  24. 24. Need to replace both glucocorticoid (hydrocortisone) and mineralocorticoid (fludricortisone); high dose hydrocortisone actually will have both a gluco and also a mineralocorticoid effect so can effectively treat
  25. 25. Stress dose of hydrocortisone os considered 100mg/m2/day
  26. 26. Might need to treat life threatening hyperK
  27. 27. Understand the value of neonatal screening for salt-losing CAH in male infants with normal genitalia
  28. 28. Since they are difficult to phenotypically identify at birth, having the neonatal test will help catch them before they come in suffering from an acute adrenal crisis around age 2 weeks
  29. 29. Tests for levels of 17-OH progesterone
  30. 30. Has a low specificity in exchange for very high sensitivity, and in fact about 98% false positive rate
  31. 31. Cases manifesting with low elevations (40-100ng/mL) can usually be repeated; if the level is higher than 100 on the initial test that needs to be urgently addressed, get serum lytes and bring peds endo on board promptly
  32. 32. Understand that maternal exposure to androgens and progestins can cause virilization in female infants
  33. 33. Timing of the exposure affect the phenotype
  34. 34. Exposure prior to 8 weeks may cause labial fusion and clitoromegaly
  35. 35. Exposure after the first trimester can lead to clitoromegaly without the midline fusion
  36. 36. Growth
  37. 37. Short stature
  38. 38. Know the most common causes of short stature
  39. 39. Kids who are on the low end (<3rd percentile) on the growth curve usully fell their sometime during the first 2 years of life and then follow their own curve afterward; they should maintain a normal growth rate.
  40. 40. Linear growth rates:
  41. 41. Ist year: 25 cm/year
  42. 42. 2nd year: 12 cm/year
  43. 43. 3rd year: 8 cm/year
  44. 44. After age 3 and until puberty: 4-7cm/year
  45. 45. Familial short stature, growth hormone deficiency, hypothyroidism, chronic disease, malnutrition are among the most common causes of short stature (worldwide the leading cause is malnutrition)
  46. 46. Plan the evaluation of children whose height has decreased from the 20th to the 5th percentile
  47. 47. Important to know at what age and over what time period this happened. For example it is “normal” for a child to fall down curves prior to age three and then maintain themselves on their new, lower curve. It is NOT normal for a child to fall off curves AFTER age 3 and this always requires further evaluation
  48. 48. Assess the reliability of the measurements, calculate the growth velocity, analyze weight for height in the context of target height (need to know parental heights)
  49. 49. If no known growth velocity then need to measure a second height in 3 to 6 months
  50. 50. Check for nutritional status
  51. 51. If well nourished / obese then need to look for an endocrinopathy like GHD, hypothyroidism, glucocorticoid excess; need to check a bone age, serum IGF-1
  52. 52. If undernourished or low weight for height or an initial decline in weight followed by decreased growth velocity then need to look for primary GI, nutritional, renal or other chronic dz; especially ruling out a malabsorption problem
  53. 53. Understand that growth velocity may be decreased in children with chronic disease
  54. 54. Distinguish among constitutional short stature, genetic (familial) short stature, and growth hormone or thyroid deficiencies by growth chart evaluation
  55. 55. Constitutional short stature
  56. 56. Growth velocity slows during the first three years with both height and weight crossing growth percentiles downward
  57. 57. Normal or near normal GV, height is below but parallel to the 5th percentile during prepubertal years
  58. 58. Delayed bone age and pubertal maturation
  59. 59. Adult height usually in the normal range, but occasionally lower than expected for parental height
  60. 60. Familial short stature
  61. 61. Usually a normal weight and length at birth but then cross the linear growth percentiles downward during the first years after birth
  62. 62. They will reach their genetic appropriate linear growth percentile and stay on their own growth curve
  63. 63. Onset of puberty and its rate of progression are normal for chronologic age
  64. 64. Adult height is short, but appropriate for parental heights
  65. 65. GHD
  66. 66. Hypothyroid
  67. 67. Recognize the signs of familial short stature
  68. 68. By definition they must have no evidence of an endocrine or systemic disorder and they must have a family h/o short stature
  69. 69. Normal weight and length at birth, dropping across curves over their first three years until they get to their genetically determined curve. They follow their own curve during prepubescent years. Puberty begins at a normal age and rate of progression is normal
  70. 70. Bone age typically not delayed and is c/w chronologic age
  71. 71. Adult height is short, but in target height range based on parental heights
  72. 72. Know how to distinguish between familial short stature and other conditions
  73. 73. See above
  74. 74. Know the natural hx of familial short stature
  75. 75. See above
  76. 76. Know how to use lab tests to effectively to distinguish between constitutional growth delay and other conditions
  77. 77. Checking bone age will show a delayed bone age; plotting he height against their bone age usually “normalizes” them percentile wise
  78. 78. Know the natural h/o constitutional growth delay
  79. 79. Normal height and weight at birth, fall off growth curve at 18-24 months
  80. 80. Normal growth velocity along the 3-5%ile
  81. 81. Delayed bone and dental age
  82. 82. Onset of puberty will correlate with bone age
  83. 83. Usually have a family hx of same
  84. 84. Recognize the signs and sx of acquired and congenital growth hormone deficiency (e.g. micropenis)
  85. 85. Congenital: normal length/weight at birth
  86. 86. Microphallus due to IGF-1 deficiency
  87. 87. Direct hyperbilirubinemia
  88. 88. Hypoglycemia
  89. 89. Single central incisor
  90. 90. Acquired is often idiopathic, but can come from tumors (esp craniopharyngioma, glioma, germinoma) and also head trauma, CNS infection or radiation, surgical damage to the pituitary or hypothalamus
  91. 91. Specific clinical features vary with the cause
  92. 92. Slow growth rate is often the prominent feature
  93. 93. Tall stature
  94. 94. Differentiate among the causes of short stature
  95. 95. Most common cause = tall parents or early maturation
  96. 96. Growth hormone excess, i.e. GH secreting tumor
  97. 97. Would see other effects of GH excess like large hands and feet, soft tissue thickening, widened spaces between the teeth
  98. 98. Sotos syndrome (cerebral gigantism)
  99. 99. Not an endo problem
  100. 100. Born at >90th %ile, hit the 97th until about age 4-5 and then slow down to a normal rate
  101. 101. Beckwith Wiedemann
  102. 102. Due to excessive IGF-1
  103. 103. Fetal overgrowth: macroglossia, HSM, nephromegaly, beta cell hyperplasia
  104. 104. Often develop early hypoglycemia
  105. 105. Monitor for Wilms and nephroblastoma every 3-6 months for the first 6years of life
  106. 106. Klinefelter
  107. 107. Marfan
  108. 108. Autosomal dominant
  109. 109. Tall, increased arm span, arachnodactyly
  110. 110. Heart problem = aortic dilatation
  111. 111. Eye problem = upward lens subluxation
  112. 112. Homocysteinuria
  113. 113. Autosomal recessive
  114. 114. Inborn error of AA metabolism
  115. 115. Phenotypically similar to Marfan, BUT
  116. 116. MR
  117. 117. Eye problem = downward lens subluxation
  118. 118. Puberty
  119. 119. Normal
  120. 120. Distinguish between the variations of normal (e.g thelarche, pubarche) and precocious puberty
  121. 121. Premature thelarche
  122. 122. Isolated breast development in females age 6-7 years
  123. 123. No other signs of puberty, bone age = height age
  124. 124. Should experience normal pubertal development and normal adult height attained
  125. 125. Need to rule out estrogen excesses, either endogenous or exogenous
  126. 126. Management = thorough hx, note their growth velocity, tanner stage, skin exam to look for other signs of pubertal changes; bone age, check estrdiol and LH/FSH levels; need f/u exams q3months
  127. 127. If any of the above reveal abnorms then need to do an MRI of the head, pelvic U/C, GnRh stim test
  128. 128. Premature adrenarche
  129. 129. Development of pubic hair, axillary hair, acne, body odor in a child younger than 8 (female) or 9 (male)
  130. 130. Should have no other virilization; i.e. for boys no changes in testicular size and for girls no clitormegaly, breast development or menses
  131. 131. Can be due to CNS insults, obesity, exposure to androgens
  132. 132. Management: make sure if any of the above are present and look at the growth velocity; check a DHEAS, androstenedione, testosterone, 17OHP, bone age; follow up every 4 months
  133. 133. If initial screens as above are abnorm then need adrenal/pelvic imaging and ACTH stim test
  134. 134. Know the pathophysiology and differentiating features of normal vs abnormal gynecomastia in males
  135. 135. Normal pubertal gynecomastia occurs in up to 2/3 of boys
  136. 136. Defined as <4cm tanner 2 breast; with tanner 2, 3 or 4 pubic hair
  137. 137. Will self-resolve, usually in 12-18 months
  138. 138. Macrogynecomastia is >4cm
  139. 139. Tanner stage 3, 4 or 5 breast
  140. 140. Does not self resolve and does need referral
  141. 141. Due to increased estrogen:testosterone ratio
  142. 142. Source might be from liver, kidney or thyroid disease, adrenal tumor, testicular tumor, anabolic steroids, HCG secreting tumor, increased aromatase activity (obesity)
  143. 143. If due to decreased testo level, might be due to gonadal failure, Klinefelter
  144. 144. Understand the significance of a breast mass in an adolescent girl
  145. 145. Most are benign and represent normal physiologic changes of fibroadenomatous lesions; these can be monitored, will change with menses, wax/wane, etc
  146. 146. Mammography would rarely be indicated b/c the breast tissue of the adolescent is so dense that it will be difficult to interpret
  147. 147. Referral to a breast surgeon if the lesion is persistent, enlarging, atypical, or a source of anxiety; most masses can be monitored for at least 4-8 weeks, if it is cystlike then can follow clinically for about 3 months, if c/w a fibroadenoma then can follow for 6 months
  148. 148. Precocious puberty
  149. 149. Recognize the testosterone creams used by parents can cause virilization in male or female children
  150. 150. Recognize the si/sx of precocious puberty
  151. 151. In the female will have adrenal and gonadal changes
  152. 152. Only need gonadal changes in the male (any testicular size >3cc or 2.5 cm prior to age 9
  153. 153. Know the differential dx of precocious puberty
  154. 154. Brain tumor in 10% of the girls, 50% of the boys
  155. 155. Ectopic neural tissue (GnRH secretory hormones)
  156. 156. Know that premature thelarche occurs without other signs of puberty, is most common among those 1-4 years of age and often regresses spontaneously
  157. 157. Recognize the importance of obtaining the h/o medication use, including phytoestrogens and estrogen based creams, when evaluating a child with premature breast development
  158. 158. Recognize the tumors that may produce precocious puberty (e.g. in the liver, CNS, ovary, testes, adrenal glands)
  159. 159. Hypothalamic hamartomas are non-neoplastic, congenital malformations that contain GnRH secreting cells
  160. 160. Brain, liver and mediastinum tumors can produce hCG the hCG cross-binds with LH receptors and leads to progesterone or testosterone production
  161. 161. Tumors of the adrenal cortex or gonad can produce sex steroids autonomously
  162. 162. CAH and glucocorticoid resistance can raise ACTH-induced production of adrenocortical androgens
  163. 163. Know how to use laboratory tests effectively to distinguish the adrenal etiology of precocious puberty
  164. 164. DHEA-S provides an estimate of adrenocorticoid sex steroid hormone levels
  165. 165. Values elevated beyond that expected for the pubertal stage suggesting adrenal pathology
  166. 166. Biosynthetic defects of adrenocortical steroids are identified best by high concentrations of the substrate for the enzyme that is deficient
  167. 167. i.e. high levels of 17-OH progesterone on 21-OH hydroxylase deficiency
  168. 168. Delayed Puberty
  169. 169. Recognize the signs and symptoms of delayed puberty
  170. 170. Absence of secondary sexual characterstics in a 13 year old female or a 14 year old male; or more than 5 years passing between onset of puberty and completion of puberty
  171. 171. Differiential: hypergonadotrophic hypogonadism VS hypogonadotrophic hypogonadism
  172. 172. Hyper-hypo = high FSH/LH
  173. 173. Hypo-hypo = low FSH/LH
  174. 174. Recognize the signs and symptoms of gonadal dysgenesis (Turner syndrome)
  175. 175. 45 X,0 (50%); 15% are a mosaic, 45X,0/46 XX
  176. 176. SHORT STATUE is present in 100% of cases at presentation and is due to absence of SHOX gene
  177. 177. Web neck, wide nipples, cubitus valgus, short 4th metacarpal, low posterior hairline
  178. 178. Swollen hands and feet at birth with the classic phenotype
  179. 179. At age 3-5 years will have decreased growth velocity, short stature
  180. 180. Abnormal puberty
  181. 181. Cardiac lesions: bicuspid aortic valve and coarctation of aorta are
  182. 182. Need echo every 5-10 years
  183. 183. Renal lesions: horseshoe kidney, collecting system abnormalities
  184. 184. Know the lab evaluation of gonadal dysgenesis (Turner), including karyotype, and serum concentrations of LH, FSH and estradiol
  185. 185. LH and FSH will be high due to gonadal failure
  186. 186. Estradiol can be difficult to evaluate because if the child is in early puberty it will be low, like it would be if they had Turner
  187. 187. Need a karyotype
  188. 188. Need to check thyroid because they are at a higher risk of developing chronic lymphocytic thyroiditis
  189. 189. Understand the importance of evaluating for cardiac and renal disorders in goandal dysgenesis (Turner)
  190. 190. See above
  191. 191. Understand the familial influences in the onset of puberty
  192. 192. Know the natural h/o constitutional delayed puberty
  193. 193. Know when tx for constitutional delayed puberty is indicated and understand the therapeutic options
  194. 194. Thyroid disorders
  195. 195. Hashimoto thyroiditis (aka, autoimmune/lymphocytic thyroiditis)
  196. 196. Recognize the signs and symptoms of Hashimoto thyroiditis
  197. 197. Can occasionally cause transient hyperthyroidism early in the course (hashitoxicosis)
  198. 198. Then develops sx of hypothyroid
  199. 199. Decreased growth velocity, delayed puberty, cold intolerance, constipation, myxedematous facies, dry skin, brittle hair
  200. 200. On exam can feel a firm nontender diffuse goiter with a pebbly feeling
  201. 201. Know the lab studies that distinguish Hashimoto thyroiditis, other causes of thyroid enlargement, and hypothyroidism
  202. 202. Hashimoto is confirmed with checking antibodies: antithyroperoxidase, anti thyroglobulin, antimicrosomal
  203. 203. Depending on the stage of the disease may have labwork c/w hyper. Hypo or even euthyroid
  204. 204. Know that Hashimoto thyroiditis is the most common cause of goiter in adolescents
  205. 205. Know that Hashimoto thyroiditis may be associated with other autoimmune disorders
  206. 206. Cyst, tumor, nodule
  207. 207. Recognize the si/sx of a thyroid cyst/tumor
  208. 208. A palpable mass in the thyroid
  209. 209. May have si/sx of thyrotoxicosis
  210. 210. May have local LN spread, which raises concern for malignancy
  211. 211. Understand the importance of referral in a child with a thyroid mass/nodule
  212. 212. “all children who have a discrete thyroid mass should be referred to n endocrinologist.”
  213. 213. Any solitary, firm, hard, painless nodule should be further examined
  214. 214. On U/S of solid then need further workup, if solid and COLD on uptake scan then have a high likelihood of carcinoma and an excisional bx or FNA is needed
  215. 215. Note that for boards apparently the answer is FNA
  216. 216. Know the significance of previous irradiation to the head and neck in a patient with a thyroid mass/nodule
  217. 217. Increases chance of malignancy
  218. 218. Know that a solitary nodule may be a sign of thyroid cancer
  219. 219. See above
  220. 220. Other signs that raise likelihood of being cancerous:
  221. 221. More common in males
  222. 222. Fixed to underlying tissues
  223. 223. Firm and irregular in outline
  224. 224. Firm cervical LAD on the same side
  225. 225. Hypothyroidism
  226. 226. Know the consequences of untreated hypothyroidism in the neonate
  227. 227. Decreased IQ, clumsiness, decreased fine motor skills; neurosensory hearing deficit
  228. 228. Recognize the si/sx of congenital and acquired hypothyroidism
  229. 229. Congenital:
  230. 230. Early signs: large posterior fontanelle, prolonged jaundice, macroglossia, hoars cry, distended abd, hypotonia
  231. 231. Delayed signs: Feeding problems, hoarse cry, dry skin, decreased growth of nails and hair, delayed closure of fontanelles, delayed tooth eruption, protuberant abd, puffy face, large protruding tongue, hypotonia, cardiomegaly
  232. 232. Acquired – see above under Hashimoto
  233. 233. Know the various causes of congenital and acquired hypothyroidism
  234. 234. Congenital: in the US the most common cause is thyroid dysgenesis
  235. 235. Can also be caused by thyroid dyshormonogenesis, hypothalamic-pituitary hypothyroidism, transient hypothyroidism
  236. 236. Acquired: in the US the most common is Hashimoto
  237. 237. Can also be due to subacute thyroiditis, central hypothyroidism
  238. 238. Know how to manage and treat congenital and acquired hypothyroidism and the use of thyroid stimulating hormone to guide treatment
  239. 239. Both need LT4
  240. 240. Use the TSH to tell you if you need to increase (high TSH) dose or decrease (low TSH) dose; however don’t use it alone and also check a FT4 according to PREP (they say never to use TSH alone to guide thyroxine dose changes)
  241. 241. Tidbit: if you get lab on a pt being txed with thyroxine (LT4) and the TSH is high and s if the FT4, it probably means they have issues managing their meds (missed doses and then took extra to “make up” for the missed doses); they can both remain high for up to 7 days
  242. 242. Know how to recognize TBG deficiency
  243. 243. Low total T4, normal FT4, normal TSH
  244. 244. Hyperthyroidism
  245. 245. Recognize the signs and sx of hyperthyroidism
  246. 246. Thyromegaly, possibly a thyroid bruit; prominent eyes with exopthalmos or proptosis
  247. 247. Tachycardia, widened pulse pressure, systolic htn, tremor, muscle weakness, anxiety, palpitations, heat intolerance
  248. 248. Think of it in cases of persistemt htn, tachycardia, hyperdynamic circulation
  249. 249. Know how to use hx, physical exam and lab tests to effectively dx hyperthyroidism
  250. 250. Most common cause is Graves and is dxed with a positive TSI (thyroid stimulating immunoglobulin)
  251. 251. h/o weight loss despite increased appetite, heat intolerance, excessive sweating, diarrhea, emotional disturbances, poor school performance
  252. 252. exam would show findings as above
  253. 253. be aware of various modalities of tx for hyperthyroidism
  254. 254. drugs: methimazole, PTU; give propanolol for sx tx
  255. 255. safe during preg = PTU
  256. 256. surgery: thyroidectomy (might need thyroid replacement after)
  257. 257. radioactive ablation: I131 (need thyroid replacement after)
  258. 258. Recognize the si/sx of neonatal hyperthyroidism
  259. 259. IUGR, microcephaly, increased HR can be manifestations in utero
  260. 260. After delivery baby can have tachycardia, feeding probs, failure to gain weight, thyrotoxic stare, jitteriness, persistent jaundice
  261. 261. Findings might be delayed for several days after birth if baby was exposed to antithyroid meds in utero
  262. 262. The level of circulating TSI is what determines the baby’s chances of having neonatal hyperthyroidism
  263. 263. Babies who have had neonatal thyrotoxicosis might later develop a secondary hypothyroidism weeks to months after birth, they need to have their thyroid function monitored monthly for several months after delivery until the TSH normalizes and production of T4 resumes normally (TSH was shut down while in utero and takes a while to wake back up)
  264. 264. Parathyroid disorders
  265. 265. Recognize the typical lab findings associated with hypoparathyroidism
  266. 266. True hypoparathyroidism will have low PTH and low Ca with high PO4
  267. 267. Pseudohypoparathyroidism will have normal to high PTH levels but still the low ca and high PTH
  268. 268. Know that DiGeorge syndomre (22q-) can be a cause of hypoparathyroidism
  269. 269. noted
  270. 270. Adrenal gland disorders
  271. 271. General
  272. 272. Be aware of adrenoleukodystrophy
  273. 273. It is a syndrome of adrenal cortex deficiency with demyelination of the CNS
  274. 274. Vey high levels of very long chain fatty acids on body tissues and fluids
  275. 275. Degenerative neurologic d/o with onset in childhood or adolescence, confirm the dx with checking a VLCFA level
  276. 276. Can have milder forms, bit classic form leads to ongoing dterioration of CNS and then death
  277. 277. Addision Dz
  278. 278. Recognize the si/sx of Addision dz
  279. 279. Hyperpigmentation, salt craving, postural hypotension, fasting hypoglycemia, anorexia, weakness, episodes of shock during severe illness
  280. 280. Know how to use tests effectively for the dx of Addison dz
  281. 281. Baseline and ACTH-stimulated cortisol levels are subnormal which confirms the dx
  282. 282. Hyponatremia, hyperK and elevated plasma rennin activity indicate a mineralocorticoid deficiency
  283. 283. Recognize that Addision dz is usually an automiinue d/o
  284. 284. noted
  285. 285. Recognize the si/sx of adrenal insufficiency after d/c of exogenous corticosteroid tx
  286. 286. Basically the same as for Addison dz
  287. 287. Cushing syndrome
  288. 288. Recognize the si/sx of Cushing syndrome
  289. 289. Progressive or central obesity, failure to grow taller, hirsutism, weakness, buffalo hump, acne, striae, and hyperpigemntation (if increased ACTH)
  290. 290. Pituitary gland disorders
  291. 291. Diabetes
  292. 292. General most of these should be second nature ; a couple were not really clear so there is more info below
  293. 293. Recognize the si/sx of DM1
  294. 294. Know how to treat DM1 effectively to achieve good control: insulin, diet, exercise and psychologic acceptance of the disease
  295. 295. Know the value of A1C in managing DM1
  296. 296. Know the natural h/o DM1 (ie. “honeymoon” period)
  297. 297. Know how to manage sick days in diabetic patients
  298. 298. By “sick days” they mean days when a patient diabetes is actually ill
  299. 299. Need to monitor their sugars more closely – they might need more insulin due to the stress, etc and subsequent increase in blood glucose; they might need less of they have poop o intake
  300. 300. Also important for them to check urine ketones about every 3-4 hours to prevent DKA from occurring when already ill
  301. 301. Should be in close contact with their DM team
  302. 302. Know long term complications of DM1
  303. 303. Know the importance of blood glucose control in prevention of long-term side complications of DM1
  304. 304. Recognize the association between DM1 and other autoimmune d/os including celiac dz
  305. 305. DKA
  306. 306. Know the complications of DM1, particularly DKA and its pathophysiology, tx, complications
  307. 307. Recognize cerebral edema as a complication of the tx of DKA
  308. 308. Understand the risks of using bicarb in DKA
  309. 309. Know that non-compliance is a major cause of recurrent DKA
  310. 310. DM2
  311. 311. Understand the difference between type 1 and type 2 DM
  312. 312. Boards wants you to use autoantibodies to distinguish DM1 and DM2
  313. 313. Know that acanthosis is a marker for insulin resistance
  314. 314. Formulate the treatment approaches to DM2
  315. 315. plan the appropriate screening tests for DM2
  316. 316. Metabolic syndrome
  317. 317. Plan the appropriate screening tests for metabolic syndrome
  318. 318. Identify risk factors that necessitate tests for metabolic syndrome
  319. 319. Plan the appropriate initial management of a patient with Metabolic syndrome, including lfiestyle modification with diet and physical activity
  320. 320. Recognize the adverse conditions associated with metabolic syndrome
  321. 321. Disorders of PTH, calcium. And phosphate metabolism
  322. 322. Hypocalcemia
  323. 323. Know the causes of hypoCa in a neonate
  324. 324. Know that hypoCa with HypoPhos suggests vit D deficiency
  325. 325. HyperCa
  326. 326. Recognize the si/sx of hyperca
  327. 327. Recognize the possibility of hyperca and its complications following prolonged immobilization
  328. 328. Hypophosphatemia
  329. 329. Recognize the typical clinical and lab findings associated with familial hypophosphatemic rickets
  330. 330. Plan the treatment of a child with hypophos rickets

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