Group 5 Report on Pathophysiology

1. ENDOCRINE SYSTEM HORMONES * HORMONES * HORMONES JANDUSAY * JAVIER * JOVEN * KAMIYA * KALAW LEONG * LLAMZON * LORENZO * LUKBAN

2. WHAT TO EXPECT: REPORT OBEJECTIVES SHORT REVIEW DISORDERS and DISEASES REPORT SUMMARY

3. To provide a short review on the Endocrine System To present preventive measures and cures REPORT OBEJECTIVES To discuss common & rare Endocrine diseases & disorders To familiarize students with Endocrine processes To discuss the effects on normal physiology To provide a short summary on the topics discussed REPORT*OBEJECTIVES

4. REVIEW

5. REVIEW ENDOCRINOLOGY VS. neurons hormones

6. REVIEW ENDOCRINOLOGY VS. long-lasting nervous endocrine fast

7. REVIEW ENDOCRINOLOGY NEGATIVE FEEDBACK MECHANISM

8. Hormone Summary ENDOCRINOLOGY

9. DISEASES AND DISORDERS

10. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

11. PITUITARY GLAND DWARFISM & GIANTISM DIABETES INSIPIDUS

12. PITUITARY GLAND DWARFISM & GIANTISM DIABETES INSIPIDUS

13. Pituitary Gland Disorders Diabetes Insipidus

14. Diabetes Insipidus -(“diabetes”= overflow, “insipidus”= tasteless) -most common abnormality associated with the dysfunction of the posterior pituitary -due to defects in antidiuretic hormone receptors or inability to secrete ADH -can be neurogenic (or central) or nephrogenic

15. Diabetes InsipidusHow does the normal physiology is disrupted?

16. Diabetes Insipidus Symptoms: - excretion of large volumes of urine with resulting dehydration and thirst - bed-wetting

18. Subcutaneous injection or nasal application of ADH analogs

21. Usually causes Type 2 diabetes

22. Occurs when there is reduced sensitivity of diabetics who undergo insulin therapy

24. 3. Hyperinsulinism

25. 3. Hyperinsulinism How can normal physiology be regained? - immediate intravenous administration of large quantities of glucose - administration of glucagon (or, less effectively of epinephrine) can cause glycogenolysis in the liver and thereby increase blood glucose level extremely rapidly **Permanent damage to the neuronal cells of the nerous system usually occurs when treatment is not given immediately.

26. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

27. THYROID GLAND GOITER HYPERTHYROIDISM HYPOTHYROIDISM

28. GOITER WHY, YES. THIS IS A…. GOITER? WHAT IS A GOITER? ENLARGEMENT OF THE THYROID.

29. GOITER SYMPTOMS NORMAL PHYSIOLOGY Thyroid Hormones (T3 & T4) - produced by cells in thyroid gland - regulated by thyroid stimulating hormone (TSH) - produced through the attachment of iodine atoms to ring structures of T3 and T4 AHEM! AHEM! Breathing and swallowing difficulties Coughing and hoarseness

30. CAUSES TREATMENT POSSIBLE COMPLICATIONS GOITER HYPERTHYROIDISM Surgery- thyroidectomy Lugol’s Iodine Radiocative Iodine HYPOTHYROIDISM

31. WHAT OVERACTIVE TISSUE IN THE HYPERTHYROIDISM THYROID GLAND PRODUCING T3 TOO MUCH T4 AND TRIIODOTHYRONINE & THYROXINE

32. CAUSES GRAVE’S DISEASE TOXIC THYROID ADENOMA NORMAL? THYROIDITIS WHAT WHAT WHAT SYMPTOMS? HIGH EXCITABILITY; METABOLISM MILD TO EXTREME WEIGHT LOSS MUSCLE WEAKNESS; TREMORS

33. DEVELOPMENT OF PROTRUSION OF EYEBALLS exophthalmos EDEMATOUS TISSUES & DEGENERATIVE MUSCLES TREATMENT! SURGICAL REMOVAL OF GLAND LESSEN IODINE INTAKE

34. HYPOTHYROIDISM T3 T4 TOO LITTLE AND

35. AUTOIMMUNITY AGAINST THE THYROID =DETERIORATION AUTOIMMUNITY CAUSES ASSOCIATED WITH THYROID GOITER

36. IODINE DEFICIENT ENDEMIC COLLOID & IDIOPATHIC NONTOXIC GOITER NOT IODINE DEFICIENT THYROID GOITER

37. SYMPTOMS? FATIGUE; SLEEPINESS; SLUGGISH WEIGHT GAIN; CONSTIPATION FAILURE OF TROPHIC FUNCTIONS myxedema AND TREATMENT! MORE IODINE ORAL MEDICATON

38. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

39. PARATHYROID GLAND HYPOPARATHYROIDISM HYPERPARATHYROIDISM

40. FUNCTION &NORMAL PHYSIOLOGY PARATHYROID GLAND * control calcium within the blood. * control how much calcium is in the bones, and therefore, how strong and dense the bones are! * As the blood filters through the parathyroid glands, they detect the amount of calcium present in the blood  making more or less parathyroid hormone (PTH). Calcium level in the blood is too low: the parathyroid cells make more parathyroid hormone.

41. PARATHYROID GLAND …occurs when your parathyroid glands make too much PT and cause you to have too much calcium in the bloodstream. CAUSES OF TOO MUCH PTH: Growth on the parathyroid glands! Enlargement of 2 or more of the parathyroid glands! OR medical conditions (like, lessay, kidney failure and rickets...) HYPOPARATHYROIDISM HYPERPARATHYROIDISM

42. HYPERPARATHYROIDISM Normally, the amount of calcium going into your bones matches the amount of calcium passing out of your bones. This means that the amount of calcium in your bones should stay about the same all the time. If you have hyperparathyroidism, more calcium is coming out of your bones than is going back in. When this happens, your bones might hurt, ache or become weak. Weak bones break more easily and heal slower than normal bones. PHYSIOLOGY&IMPLICATIONS

43. HYPERPARATHYROIDISM Feeling weak or tired most of the time General aches and pains Frequent heartburn Nausea & Vomiting; Loss of appetite An increase in bone fractures or breaks Confusion and memory loss Kidney stones; Excessive urination High blood pressure THE SYMPTOMS

44. HYPERPARATHYROIDISM SURGERY DRINK PLENTY OF WATER LIMIT INTAKE OF CALCIUM AND VITAMIN D DO NOT SMOKE EXERCISE DAILY TREATMENT

45. HYPERPARATHYROIDISM

46. PARATHYROID GLAND HYPOPARATHYROIDISM HYPERPARATHYROIDISM

47. HYPOPARATHYROIDISM Hypoparathyroidism is a rare conditionin which your body secretes abnormally low levels of parathyroid hormone (parathormone). This hormone plays a key role in regulating and maintaining a balance of your body's levels of two minerals — calcium and phosphorus. The low production of parathyroid hormone in hypoparathyroidism leads to abnormally low ionized calcium levels in your blood and bones and to an increased amount of phosphorus. PHYSIOLOGY&IMPLICATIONS

48. HYPOPARATHYROIDISM Tingling or burning (paresthesias) Muscle aches or cramps; Twitching or spasms Fatigue or weakness Painful menstruation Patchy hair loss, such as thinning of your eyebrows Dry, coarse skin; Brittle nails Headaches; Depression, mood swings Memory problems THE SYMPTOMS

49. HYPOPARATHYROIDISM RESTORE THE CALCIUM AND MINERAL BALANCE IN THE BODY. Treatment involves calcium carbonate and vitamin D supplements, which usually must be taken for life. Blood levels are measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is recommended. TREATMENT

50. HYPOPARATHYROIDISM

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52. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

53. CUSHING’S SYNDROME CUSHING’S DISEASE ADRENAL GLAND ADDISON’S DISEASE

54. SYNDROME CUSHING’S

56. Characterized by high plasma levels of ACTH and cortisol

57. Another name hypercortisolism

58. Can occur from multiple causes including:Adenomas of the anterior pituitary that secrete large amounts of ACTH Abnormal function of the hypothalamus that causes high levels of corticotrophin-releasing hormone (CRH) “ectopic secretion” of ACTH by a tumor elsewhere in the body Adenomas of the adrenal cortex CUSHING’S

59. High blood pressure. High blood sugar. Suppressed immunity (and more infections). Insulin resistance Suppressed sex hormones and reduced libido. Suppressed thyroid hormones. - A round, red, full face, often called a "moon" face. - Muscle weakness and thin limbs. - Growth of fine hair on the face, upper back, or arms. - A lump of fat (buffalo hump) on the back of the neck. - Stretch marks over abdomen. CUSHING’S SYMPTOMS

60. CUSHING’S DISEASE

61. CUSHING’S Cushing's syndrome is treated by restoring a normal balance of hormones. This may involve surgery, radiation treatments or drugs. Tumors on the adrenal glands are removed by surgery. If there is a tumor on just one adrenal gland, the other gland usually shrinks and ceases normal productivity. TREATMENT

62. ADDISON’S DISEASE

63. Addison's disease results from damage to the adrenal cortex. This damage may be caused by the following: The immune system mistakenly attacking the gland (autoimmune disease) Infections such as tuberculosis, HIV, or fungal infections Hemorrhage, blood loss Tumors Use of blood-thinning drugs (anticoagulants) A disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands. It may be due to : a disorder of the adrenal glands themselves (primary adrenal insufficiency) or inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency) ADDISON’S

65. Chronic diarrhea

66. Darkening of the skin ; Paleness

67. Extreme Weakness

68. Unintentional weight loss

69. Mouth lesions on the inside of a cheek

70. Nausea and vomiting

71. Salt craving

72. Slow, sluggish movementSYMPTOMS

73. ADDISON’S Taking hormones to replace the insufficient amounts being made by your adrenal glands (glucocorticoids (cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone)) TREATMENT

74. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

75. DIABETES MELLITUS PANCREATIC ISLET

77. PANCREAS retroperitoneal Exocrine gland Endocrine gland -98% of the secreting cells in the pancreas make digestive enzymes -2% of the cells make hormones that are secreted into the portal vein

78. Pancreatic Hormones

79. Normal Physiology Circulating glucose is derived from three sources: 1. intestinal absorption during the fed state 2. glycogenolysis -breakdown of glycogen 3. gluconeogenesis -formation of glucose primarily from lactate and amino acids during the fasting state insulin is the key regulatory hormone of glucose disappearance (hypoglycemic hormone), and glucagon is a major regulator of glucose appearance (extremely potent hyperglycemic agent)

81. Disruptions on Physiology

82. Insulin and glucagon antagonistic interaction humoral stimuli potent regulators of glucose metabolism bi-hormonal definition of diabetes: diabetic state = insulin deficiency + glucagon excess

83. Diabetes [Mellitus] Pathophysiology

86. NOTE: TYPE1 – noticeable early symptoms TYPE2 – may occur without or gradual development of symptoms

87. Diabetes Complications (VASCULAR)

88. Diabetes Complications (NEURAL)

89. Treatment and Prevention

90. DISEASES&DISORDERS PITUITARY GLAND THYROID GLAND PARATHYROID GLAND ADRENAL GLAND PANCREATIC ISLET SEX HORMONES

91. KLINEFELTER’S DISEASE POLYCYSTIC OVARIES SEX HORMONES

92. PCOS polycystic ovary syndrome

94. Birth control pills

95. Diabetes medications

96. Fertility medications

98. very light or very heavy bleeding during your period

99. mild to moderate abdominal discomfort

100. excessive hair growth on your face, chest and lower abdomen

101. acne

102. Infertile

104. Too much production of LH compared to FSH  follicles on the ovaries produce more of the male hormone testosterone than the female hormone estrogen adrenal glands start to produce increased amounts of testosterone

105. Too much testosterone  prevents ovulation

106. Estrogenis still produced  deficiency in progesterone

107. one of the most common female endocrine disorders

108. a health problem caused by hormonal system imbalance: increase in ovarian production and insulin resistancepolycystic ovary syndrome

110. also known as XXY Syndrome or 47, XXY

113. Osteoporosis (in young or middle-age men)

114. Motor delay or dysfunction

115. Speech and language difficulties

116. Attention deficits

117. Learning disabilities

118. Dyslexia or reading dysfunction

119. Psychosocial or behavioural problemsManagement and Treatment Educational guidance Therapeutic Options Medical Options e.g. Testosterone Replacement Therapy (TRT)

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121. She had puffiness around her nose and eyes. Her menses gegan at age 16 and were irregular with scant flow. She had no interest in the opposite sex. There was an absence of pubic hair. She was constipated, gained weight easily, had dry skin and hair, had anemia, and she tired easily. What can she be suffering from?

122. What can she be suffering from?

123. References: Elaine N. Marieb, KatjaHoehn. Human Anatomy & Physiology 7th edition Aronoff, S. et al. Glucose Metabolism and Regulation: Beyond Insulin and Glucagon. Retrieved from http://spectrum.diabetesjournals.org/content/17/3/183.full http://www.hormone.org/Diabetes/diabetes.cfm Photos from Google images

124. References: Guyton, A. & Hall, J. Textbook of Medical Physiology. 11th Edition Tortora, G. & Derrickson, B. Principles of Anatomy and Physiology. 11th Edition http://emedicine.medscape.com/article/117648-overview