Endocrinology Calcium An otherwise healthy 6-week infant ...

3,123 views

Published on

Published in: Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
3,123
On SlideShare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
21
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide

Endocrinology Calcium An otherwise healthy 6-week infant ...

  1. 1. Endocrinology
  2. 2. Calcium
  3. 3. <ul><li>An otherwise healthy 6-week infant presents with a generalized seizure. She is exclusively breast fed. The child is somewhat sleepy with a non focal examination. Lab data : Glucose 88 mg/dL Sodium 141 mEq/L Calcium 5.1 mg/dL Phosphorus 9.1 mg/dL Magnesium 2.1 mg/dL </li></ul><ul><li>The most likely diagnosis is: </li></ul><ul><li>Pseudohypoparathyroidism </li></ul><ul><li>Hypoparathyroidism </li></ul><ul><li>Vitamin D deficiency </li></ul><ul><li>Albright’s hereditary osteodystrophy </li></ul>
  4. 4. Actions of PTH 1. 2. Ca PO 4 NET EFFECT 25 OH Vit D 1,25 (OH) 2 Vit D 1  hydroxylase 3. Gut
  5. 5. <ul><li>An otherwise healthy 6-week infant presents with a generalized seizure. She is exclusively breast fed. The child is somewhat sleepy with a non focal examination. Lab data : Glucose 88 mg/dL Sodium 141 mEq/L Calcium 5.1 mg/dL Phosphorus 9.1 mg/dL Magnesium 2.1 mg/dL </li></ul><ul><li>The most likely diagnosis is: </li></ul><ul><li>Pseudohypoparathyroidism </li></ul><ul><li>Hypoparathyroidism </li></ul><ul><li>Vitamin D deficiency </li></ul><ul><li>Albright’s hereditary osteodystrophy </li></ul>
  6. 6. <ul><li>An otherwise healthy 6-week infant presents with a generalized seizure. She is exclusively breast fed. The child is somewhat sleepy with a non focal examination. Lab data : Glucose 88 mg/dL Sodium 141 mEq/L Calcium 5.1 mg/dL Phosphorus 9.1 mg/dL Magnesium 2.1 mg/dL </li></ul><ul><li>What is an important diagnostic consideration (i.e. what else is the child at risk for) </li></ul><ul><li>DiGeorge syndrome – thymic aplasia, congenital heart disease, immune deficiency </li></ul>
  7. 7. Biochemical changes in rickets Ca PO 4 Bone Urine Stage 1 Stage 2 N Minimal changes N Rickets Aminoaciduria Phosphaturia
  8. 8. Initial Ca: PO 4 : Alk Phos: 9.7 3.1 2514 2 ½ weeks 9.8 3.5 2185 4 months 10.5 6.5 518
  9. 9. <ul><li>Normal Normal Low </li></ul><ul><li>Low Low Low </li></ul><ul><li>Low Increased Increased </li></ul><ul><li>Low Normal Normal </li></ul><ul><li>Normal Low Increased </li></ul>CALCIUM PHOS ALK PHOS Which is consistent with vitamin D deficiency rickets?
  10. 10. Choose correct answer <ul><li>Vitamin D deficiency rickets </li></ul><ul><li>Renal osteodystrophy (renal rickets) </li></ul><ul><li>Both </li></ul><ul><li>Neither </li></ul>1. Increased phosphate level 2. Increased PTH level 3. Increased creatinine level B C B
  11. 11. THYROID
  12. 12. <ul><li>A 15 day infant has an abnormal newborn thyroid screen result: The baby was born on 5/27/07. His newborn screening tests, performed on 5/29/07 revealed: </li></ul><ul><li>  Normal range </li></ul><ul><li>TSH 37  IU/ml < 20 </li></ul><ul><li>T4 10.1  g/dl 9-19 </li></ul><ul><li>This child: </li></ul><ul><li>Has congenital hypothyroidism and should be referred to a congenital hypothyroidism treatment center </li></ul><ul><li>Will likely develop mental retardation if untreated </li></ul><ul><li>Likely does not have any thyroid abnormality </li></ul><ul><li>Has an altered hypothalamic set-point for T4 </li></ul><ul><li>Should be started on thyroxine replacement immediately </li></ul><ul><li>  </li></ul>
  13. 14. Venipuncture: (1/25/01) Normal range TSH 488  IU/ml (0.3-5.5) T4 1.2  g/dl (4.5-12.5) You are contacted by your state Neonatal Thyroid Screening Program. Baby X was born on 1/4/01. His newborn screening tests, performed on 1/6/01 revealed:   Initial filter paper Normal range TSH >200  IU/ml < 20 T4 2.1  g/dl 9-19  
  14. 15. Congenital hypothyroidism <ul><li>Thyroid dysgenesis/agenesis </li></ul><ul><li>Prevalence 1 in 4,000 [Whites 1 in 2,000; Blacks 1 in 32,000] </li></ul><ul><li>2:1 female to male ratio </li></ul><ul><li>Clinical features include: hypotonia, enlarged posterior fontanelle, umbilical hernia, indirect hyperbilirubinemia </li></ul><ul><li>Laboratory findings: Very high TSH and low T4 </li></ul><ul><li>Therapy: Thyroxine – keep TSH in normal range </li></ul>
  15. 17. 6 month female with congenital hypothyroidism ..following 4 months therapy
  16. 18. <ul><li>A baby who was born with gastroschisis has an abnormal newborn thyroid screen at 3 days which revealed a low T4 and normal TSH. Repeat venipuncture showed: T4 2.1 μ g/dL (4.5-12.5) TSH 2.3 μ IU/mL (0.3-5.0) </li></ul><ul><li>The most likely diagnosis is: </li></ul><ul><li>Hypothyroidism due to dysgenesis of the thyroid gland </li></ul><ul><li>Central hypothyroidism </li></ul><ul><li>TBG deficiency </li></ul><ul><li>Hypothyroidism from excess iodine exposure </li></ul><ul><li>Normal thyroid function (as the TSH is normal) </li></ul>
  17. 19. Central hypothyroidism - rare TBG deficiency 1:2800 vs.
  18. 20. Thyroxine (T4) <ul><li>Major product secreted by the thyroid </li></ul><ul><li>Circulates bound to thyroid binding proteins - thyroid binding globulin (TBG) </li></ul><ul><li>Only a tiny fraction (< 0.1%) is free and diffuses into tissues </li></ul><ul><li>When we measure T4, we measure the T4 that is bound to protein </li></ul><ul><li>The level of T4 is therefore largely dependent on the amount of TBG </li></ul><ul><li>Changes in T4 may reflect TBG variation rather than underlying pathology </li></ul>
  19. 21. TBG deficiency Central hypothyroidism Free T4 Low Normal TBG level Normal Low T3RU Low High
  20. 22. 17 year old female who complains of easy fatigability. Her mother developed Graves’ disease at the same age.   Thyroid function: Normal range TSH: 3.7  IU/ml 0.3-5.5 T4: 13.4  g/dl 4.5-12  
  21. 23. 17 year old female who complains of easy fatigability. Her mother developed Graves’ disease at the same age.   <ul><li>Thyroid function: Normal range </li></ul><ul><li>TSH: 3.7  IU/ml 0.3-5.5 </li></ul><ul><li>T4: 13.4  g/dl 4.5-12 </li></ul><ul><li>  </li></ul><ul><li>Which of the following medication could explain the thyroid function abnormality </li></ul><ul><li>INH </li></ul><ul><li>Ortho Tri-Cylen </li></ul><ul><li>Retinoid acid </li></ul><ul><li>Ciprofloxacin </li></ul><ul><li>Doxycycline </li></ul>
  22. 24. Conditions that cause alterations in TBG Increased TBG Decreased TBG Infancy Familial deficiency Estrogen Androgenic steroid treatment - OC Pill Glucocorticoids (large dose) - pregnancy Nephrotic syndrome Familial excess Acromegaly Hepatitis Tamoxifen treatment
  23. 25. <ul><li>A 12-yr female has diffuse enlargement of the thyroid. She is asymptomatic. Her disorder is most likely associated with which of the following pathological processes </li></ul><ul><li>Infectious </li></ul><ul><li>Inflammatory </li></ul><ul><li>Autoimmune </li></ul><ul><li>Toxic (drug) </li></ul><ul><li>Neoplastic </li></ul>
  24. 26. Normal thyroid Hashimoto thyroiditis
  25. 27. DC <ul><li>16 year 7 month </li></ul><ul><li>Growth failure x 1 1/2 years </li></ul><ul><li>Labs : TSH: 1008 µIU/ ml (0.3-5.0) T4: <1.0 µg/dl (4-12) Antithyro Ab. 232 U/ml (0-1) A-perox Ab. 592 IU/ml (<0.3) Prolactin: 29 ng/ml (2-18) </li></ul><ul><li>Cholesterol: 406 mg/dl (100-170) </li></ul>
  26. 28. DC Start of thyroxine
  27. 29. Hashimoto thyroiditis Background : Autoimmune destruction of the thyroid Family history in 30-40% Lymphocytic infiltration Clinical : Growth failure, constipation, goiter, dry skin, weight gain, slow recoil of DTR Laboratory : High TSH Anti-thyroglobulin and anti-peroxidase antibodies Therapy : Thyroxine
  28. 30. 15 year old female with a history of easy fatigability. Found to have an elevated pulse rate at recent MD visit   Thyroid function: Normal range TSH < 0.1  IU/ml 0.3-5.5 T4 14.8  g/dl 4.5-12 T3 580 ng/dl 90-190
  29. 31. Restlessness, poor attention span Eye changes Goiter Tachycardia, wide pulse pressure Increased GFR - polyuria Diarrhea Menstrual abnormalities Myopathy
  30. 32. Antithyroid medication (Methimazole or Propylthiouracil [PTU]) Pros : 25% remission rate every 2 years Cons: Drug induced side effects - skin rashes, agranulocytosis, lupus-like reaction Radioactive iodine ( 131 I) Pros : Easy. Essentially free of side effects Cons: Long term hypothyroidism Surgery  Blockers if markedly hyperthyroid Therapy for Graves disease :
  31. 33. Sexual differentiation
  32. 34. <ul><li>Ambiguous genitalia is found in a newborn. The baby is noted to be hyperpigmented. Ultrasound demonstrates the presence of a uterus. The most useful test to aid in the diagnosis of this medical condition is : </li></ul><ul><li>Testosterone </li></ul><ul><li>17-hydroxyprogesterone </li></ul><ul><li>Serum sodium and potassium </li></ul><ul><li>DHEAS </li></ul><ul><li>DHEAS/androstenedione ratio </li></ul>
  33. 35. Cholesterol Pregnenolone Progesterone DOCA Corticosterone ALDOSTERONE 17 (OH) pregnenolone DHEA 17 (OH) progesterone Androstenedione Compound S CORTISOL TESTOSTERONE Desmolase 3-  -HSD 3-  -HSD 3-  -HSD 17-OH 17-OH 21-OH 21-OH 11-OH 11-OH
  34. 36. <ul><li>If she has salt wasting congenital adrenal hyperplasia, which abnormalities are likely to develop. True or False for each </li></ul><ul><li>Increased serum potassium </li></ul><ul><li>Decreased serum sodium </li></ul><ul><li>Decreased bicarbonate </li></ul><ul><li>Decreased plasma cortisol </li></ul><ul><li>Increased plasma renin activity </li></ul>T T T T T
  35. 37. <ul><li>A 1-year male infant has non palpable testes. Of the following, the most appropriate next step would be </li></ul><ul><li>Schedule a re-examination in 18 months </li></ul><ul><li>Refer the patient for an exploratory laparotomy </li></ul><ul><li>Begin therapy with LHRH </li></ul><ul><li>Measure the plasma testosterone after stimulation with HCG </li></ul><ul><li>Begin therapy with testosterone enanthate, 50 mg IM monthly for 3 months. </li></ul>
  36. 38. History 9 day old male infant 1 day history of decrease feeding, vomiting and lethargy. Examination Ill appearing infant with poor respiratory effort Vital signs: T 99  F HR 100/min BP 61/40 RR 24/min Resp: Subcostal retractions but clear to auscultation Cardiac: Regular rate and rhythm. Normal S1 and S2 Abdomen: Soft, non distended. Non tender. No HSM Neuro: Lethargic. No focal deficit Genitalia: Normal male. Bilateral descended testes
  37. 39. Laboratory data: WBC 16.7 Hb 16.4 Hct 49 Plt 537 K Na 121 K 9.3 Cl 83 CO 2 6.7 Glucose 163 BUN/Creat 33/0.2 CSF: Chemistry: Protein 74 Glucose 82 Microscopy: WBC 6 RBC 100
  38. 40. Emergency therapy <ul><li>Fluid resuscitation: 20 ml/kg Normal saline </li></ul><ul><li>Glucocorticoid 2 mg/kg Solucortef IV </li></ul><ul><li>Monitor EKG </li></ul>
  39. 41. Modes of presentation <ul><li>Classical </li></ul><ul><ul><li>Simple virilizing </li></ul></ul><ul><ul><li>Virilizing with salt loss </li></ul></ul><ul><li>“ Non classical” / Late onset </li></ul>
  40. 42. Therapy and evaluation of therapy <ul><li>Glucocorticoid (Hydrocortisone) </li></ul><ul><ul><li>Monitor growth, 17-OHP, urinary pregnanetriol </li></ul></ul><ul><li>Fluorocortisol (Florinef 0.1 – 0.45 mg/day) </li></ul><ul><ul><li>Blood pressure, plasma renin activity (PRA) </li></ul></ul><ul><li>Supplemental salt </li></ul><ul><ul><li>Until introduction of infant food </li></ul></ul>
  41. 43. History 15 year female presents with primary amenorrhea Breast development began at 10 years Examination Height: 5 ft 7 in Weight 130 lb Tanner 5 breast development Scant pubic hair What is your diagnosis?
  42. 44. XY Genotype Complete androgen insensitivity Testosterone Estradiol Androgen Receptor Estrogen Receptor Aromatase
  43. 45. History 15 year female presents with primary amenorrhea Breast development began at 10 years <ul><li>Examination </li></ul><ul><li>Height: 5 ft 7 in Weight 130 lb </li></ul><ul><li>Tanner 5 breast development </li></ul><ul><li>Scant pubic hair </li></ul><ul><li>Which of the following clinical features is the most likely to give you the correct diagnosis </li></ul><ul><li>Blood pressure in all 4 extremities </li></ul><ul><li>Careful fundoscopic examination </li></ul><ul><li>Rectal examination </li></ul><ul><li>Measurement of blood pressure with postural change </li></ul><ul><li>Cubitus valgus and shield shaped chest </li></ul>
  44. 46. Complete androgen insensitivity <ul><li>XY genotype </li></ul><ul><li>Non functioning androgen receptor </li></ul><ul><li>Sertoli cells – AMH </li></ul><ul><ul><li>Regression of Mullerian structures </li></ul></ul><ul><li>Leydig cells – testosterone </li></ul><ul><ul><li>No functioning receptor </li></ul></ul><ul><ul><li>Therefore Wolffian regression </li></ul></ul><ul><li>Testosterone converted to DHT </li></ul><ul><ul><li>No functioning receptor </li></ul></ul><ul><ul><li>Therefore normal female external genitalia </li></ul></ul>
  45. 47. Early Puberty
  46. 48. <ul><li>The earliest sign of puberty in a male is: </li></ul><ul><li>Enlargement of the penis </li></ul><ul><li>Enlargement of the testes </li></ul><ul><li>Growth acceleration </li></ul><ul><li>Pubic hair growth </li></ul><ul><li>Axillary hair growth </li></ul>
  47. 49. <ul><li>2 year old girl with breast development </li></ul><ul><ul><li>No growth acceleration </li></ul></ul><ul><ul><li>No bone age advancement </li></ul></ul><ul><ul><li>No detectable estradiol, LH or FSH </li></ul></ul><ul><li>The most likely diagnosis is: </li></ul><ul><li>Ingestion of her mother’s OCPs </li></ul><ul><li>Precocious puberty </li></ul><ul><li>Premature adrenarche </li></ul><ul><li>Premature thelarche </li></ul><ul><li>McCune Albright Syndrome </li></ul>
  48. 50. Benign Premature Thelarche <ul><li>Isolated breast development </li></ul><ul><ul><li>80% before age 2 </li></ul></ul><ul><ul><li>Rarely after age 4 </li></ul></ul><ul><li>Not associated with other signs of puberty (growth acceleration, advancement of bone age) </li></ul><ul><li>Children go on to normal timing of puberty and normal fertility </li></ul><ul><li>Benign process </li></ul><ul><li>Routine follow-up </li></ul>
  49. 51. 5 year female with 6 months of pubic hair growth. Very fine axillary hair as well as adult odor to sweat. No breast development No exposure to androgens Growth chart: Normal growth without growth acceleration <ul><li>Most likely diagnosis: </li></ul><ul><li>Precocious puberty </li></ul><ul><li>Benign premature adrenarche </li></ul><ul><li>Non-classical congenital adrenal hyperplasia </li></ul><ul><li>Adrenal tumor </li></ul><ul><li>Pinealoma </li></ul>
  50. 52. Benign Premature Adrenarche <ul><li>Production of adrenal androgens before true pubertal development begins </li></ul><ul><li>Presents as isolated pubic hair in mid childhood </li></ul><ul><ul><li>No growth acceleration </li></ul></ul><ul><ul><li>No testicular enlargement in boys </li></ul></ul><ul><li>If normal growth rate, routine follow-up </li></ul><ul><li>If accelerated growth and/or bone age advancement, screen for </li></ul><ul><ul><li>CAH </li></ul></ul><ul><ul><li>Virilizing tumor (adrenal/gonadal) </li></ul></ul>
  51. 53. Choose correct answer <ul><li>Premature theralche </li></ul><ul><li>Premature adrenarche </li></ul><ul><li>Both </li></ul><ul><li>Neither </li></ul>1. Growth acceleration 2. Normal adolescent sexual development 3. Onset of gonadal function usually in 2-3 years D C B
  52. 54. <ul><li>You suspect a 16 year female has Turner syndrome. The most definitive diagnostic test is </li></ul><ul><li>Buccal smear </li></ul><ul><li>Chromosome analysis </li></ul><ul><li>Measuring her FSH and LH </li></ul><ul><li>Determining her bone age </li></ul><ul><li>Determining her testosterone level </li></ul>
  53. 55. <ul><li>5 year old girl with pubic hair and rapid growth. She has no breast development </li></ul><ul><li>Possible sources of androgens: </li></ul><ul><li>Liver </li></ul><ul><li>Adrenal </li></ul><ul><li>Ovary </li></ul><ul><li>Pituitary </li></ul><ul><li>Pineal </li></ul>T F F F T
  54. 56. <ul><li>5 year old girl with pubic hair and rapid growth. She has no breast development </li></ul><ul><li>Which of the following should be considered </li></ul><ul><li>Answer T or F for each: </li></ul><ul><li>Central precocious puberty </li></ul><ul><li>Congenital adrenal hyperplasia </li></ul><ul><li>McCune Albright syndrome </li></ul><ul><li>Benign premature adrenarche </li></ul><ul><li>Adrenal tumor </li></ul>F T T F F
  55. 57. When does puberty occur? <ul><li>Classic teaching </li></ul><ul><ul><li>8 -13 in girls (menarche ~ 2 years after onset of puberty) </li></ul></ul><ul><ul><li>9 -14 in boys </li></ul></ul>Case : Breast development: 6 years Mother had menarche: 9.5 years
  56. 58. Why <ul><li>Reactivation of hypothalamic –pituitary –gonadal axis </li></ul>
  57. 59. Gonadatropin dependent (central) precocious puberty <ul><li>Clock turns on early </li></ul><ul><li>Idiopathic </li></ul><ul><ul><li>> 95 % girls ~ 50 % boys </li></ul></ul><ul><ul><li>Hypothalamic hamartoma (Gelastic seizures) </li></ul></ul><ul><ul><li>NF (optic glioma) </li></ul></ul><ul><ul><li>Head trauma </li></ul></ul><ul><ul><li>Neurosurgery </li></ul></ul><ul><ul><li>Anoxic injury </li></ul></ul><ul><ul><li>Hydrocephalus </li></ul></ul>
  58. 60. Treatment <ul><li>Why </li></ul><ul><ul><li>Psychosocial </li></ul></ul><ul><ul><li>Height </li></ul></ul><ul><li>What </li></ul><ul><ul><li>GnRH agonist </li></ul></ul>
  59. 61. Precocious puberty in the male Gonadotropins Prepubertal Pubertal Gonadotropin independent Central precocious precocious puberty puberty LH G Leydig cell
  60. 62. Precocious puberty in the male Gonadotropins Prepubertal Pubertal Gonadotropin independent Central precocious precocious puberty puberty LH G Leydig cell  HCG * McCune Albright syndrome G * Familial male Precocious puberty (testotoxicosis) 1. Gonadotropin independent PP 2. Polyostotic Fibrous Dysplasia 3. Café au lait macules
  61. 63. <ul><li>This child may well develop </li></ul><ul><li>Hypothyroidism </li></ul><ul><li>Acoustic neuroma </li></ul><ul><li>Precocious puberty </li></ul><ul><li>Hypocalcemia and hyperphosphatemia </li></ul><ul><li>Optic nerve hypoplasia </li></ul>
  62. 64. Growth disorders and delayed puberty
  63. 65. Delayed puberty Hypogonadism Hypergonadotropic Hypogonadism ( ↑FSH, LH) Primary gonadal failure - Chromosomal - iatrogenic (cancer therapy) - autoimmune oophoritis - galactosemia - test. biosynthetic defect Hypogonadotropic Hypogonadism (  FSH, LH) Constitutional delay Central Hypogonadism - Isolate gonad. def. - MPHD - Kallmann (anosmia) - Functional
  64. 66. <ul><li>A 15 yr boy has short stature and delayed puberty. He is now in early puberty (Tanner 2). His parents are of average stature. His height and weight are just below 3 rd percentile. </li></ul><ul><li>All of the following are likely except: </li></ul><ul><li>A bone age of 12 ½ years </li></ul><ul><li>Growth hormone deficiency </li></ul><ul><li>Adult height in the normal range </li></ul><ul><li>Acceleration of growth and sexual maturation over the next 2 years. </li></ul><ul><li>History of normal length and weight at birth </li></ul>
  65. 67. <ul><li>A 15 yr male has delayed puberty. He also has headaches, diplopia and increased urination. His height is < 3 rd percentille </li></ul><ul><li>Which of the following is the most likely diagnosis? </li></ul><ul><li>Diabetes mellitus </li></ul><ul><li>Pinealoma </li></ul><ul><li>Cerebellar tumor </li></ul><ul><li>Craniopharyngioma </li></ul><ul><li>Pituitary adenoma </li></ul>
  66. 68. <ul><li>A 14 yr male has tender gynecomastia (3 cm in diameter bilaterally). He is in early to mid puberty. In most cases the best management for this gynecomastia is: </li></ul><ul><li>Treatment with an anti-estrogen (e.g. Tamoxifen) </li></ul><ul><li>Treatment with an aromatase inhibitor </li></ul><ul><li>Treatment with a dopamine agonist (bromocryptine) </li></ul><ul><li>Surgery </li></ul><ul><li>Reassurance </li></ul>
  67. 69. Miscellaneous
  68. 70. Hypoglycemia <ul><li>Decreased substrate </li></ul><ul><ul><li>Poor intake </li></ul></ul><ul><ul><li>Defective glycogenolysis or gluconeogenesis </li></ul></ul><ul><li>Increase utilization </li></ul><ul><ul><li>Sepsis </li></ul></ul><ul><ul><li>Hyperinsulinism </li></ul></ul><ul><li>Absent counter regulatory hormones </li></ul><ul><ul><li>GH </li></ul></ul><ul><ul><li>Cortisol </li></ul></ul>
  69. 71. Choose correct answer <ul><li>Hypoglycemia from hyperinsulinemia </li></ul><ul><li>Hypoglycemia from metabolic fuel depletion </li></ul><ul><li>Both </li></ul><ul><li>Neither </li></ul>1. Usually preceded by ketosis 2. Brisk respones to glucagon 3. Usually responds to oral glucose B A B
  70. 72. <ul><li>Side effects of corticosteroids include all of the following except </li></ul><ul><li>hypertension </li></ul><ul><li>hypoglycemia </li></ul><ul><li>decrease bone mineralization </li></ul><ul><li>myopathy </li></ul><ul><li>cataracts </li></ul>
  71. 73. <ul><li>What is the most likely diagnosis in this newborn infant? </li></ul><ul><li>Mother has SLE </li></ul><ul><li>Anasarca from cardiac failure </li></ul><ul><li>Systemic allergic reaction </li></ul><ul><li>Congenital nephrotic syndrome </li></ul><ul><li>Turner syndrome </li></ul>
  72. 74. 5 year old male with short stature <ul><li>Turner syndrome </li></ul><ul><li>VATER syndrome </li></ul><ul><li>Albright’s hereditary osteodystrophy </li></ul><ul><li>Noonan syndrome </li></ul><ul><li>Goldenhar syndrome </li></ul>
  73. 75. <ul><li>A moderately obese adolescent female has irregular periods, hirsutism and acne </li></ul><ul><li>Of the following, which is the most likely diagnosis? </li></ul><ul><li>Cushing syndrome </li></ul><ul><li>Polycystic ovarian syndrome </li></ul><ul><li>Virilizing adrenal tumor </li></ul><ul><li>Non-classical CAH </li></ul><ul><li>Hyperprolactinemia </li></ul>
  74. 76. Choose correct answer <ul><li>Diabetes mellitus </li></ul><ul><li>Diabetes insipidus </li></ul><ul><li>Both </li></ul><ul><li>Neither </li></ul>1. Osmolality of serum > 300 Osm/L 2. Osmolality of urine > 500 mOsm/L 3. Hypernatremia C A B

×