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PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
PH 131 - Endocrine Pathophysiology Report
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PH 131 - Endocrine Pathophysiology Report

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Group 5 Report on Pathophysiology

Group 5 Report on Pathophysiology

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  • 1. ENDOCRINE<br />SYSTEM<br />HORMONES * HORMONES * HORMONES<br />JANDUSAY * JAVIER * JOVEN * KAMIYA * KALAW<br />LEONG * LLAMZON * LORENZO * LUKBAN<br />
  • 2. WHAT TO EXPECT:<br />REPORT OBEJECTIVES<br />SHORT REVIEW<br />DISORDERS and DISEASES<br />REPORT SUMMARY<br />
  • 3. To provide a short review on the Endocrine System<br />To present preventive measures and cures<br />REPORT OBEJECTIVES<br />To discuss common & rare Endocrine diseases & disorders<br />To familiarize students with Endocrine processes<br />To discuss the effects on normal physiology<br />To provide a short summary on the topics discussed<br />REPORT*OBEJECTIVES<br />
  • 4. REVIEW<br />
  • 5. REVIEW<br />ENDOCRINOLOGY<br />VS.<br />neurons<br />hormones<br />
  • 6. REVIEW<br />ENDOCRINOLOGY<br />VS.<br />long-lasting<br />nervous<br />endocrine<br />fast<br />
  • 7. REVIEW<br />ENDOCRINOLOGY<br />NEGATIVE<br />FEEDBACK<br />MECHANISM<br />
  • 8. Hormone Summary<br />ENDOCRINOLOGY<br />
  • 9. DISEASES<br />AND<br />DISORDERS<br />
  • 10. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 11. PITUITARY GLAND<br />DWARFISM & GIANTISM<br />DIABETES INSIPIDUS<br />
  • 12. PITUITARY GLAND<br />DWARFISM & GIANTISM<br />DIABETES INSIPIDUS<br />
  • 13. Pituitary Gland Disorders <br />Diabetes Insipidus<br />
  • 14. Diabetes Insipidus<br />-(“diabetes”= overflow, “insipidus”= tasteless)<br />-most common abnormality associated with the dysfunction of the posterior pituitary<br />-due to defects in antidiuretic hormone receptors or inability to secrete ADH<br />-can be neurogenic (or central) or nephrogenic<br />
  • 15. Diabetes InsipidusHow does the normal physiology is disrupted?<br />
  • 16. Diabetes Insipidus<br />Symptoms:<br /> - excretion of large volumes of urine with resulting dehydration and thirst<br /> - bed-wetting<br />
  • 17. How can normal physiology be regained?<br /><ul><li>Hormone replacement, usually for life (for neurogenic DI)
  • 18. Subcutaneous injection or nasal application of ADH analogs
  • 19. Restriction of salt in the diet and diuretic drugs</li></li></ul><li>Pancreatic Islet DisorderHyperinsulinism<br />
  • 20. Pancreatic Islet Disorder<br />Hyperinsulinism<br /><ul><li>also known as hyperinsulinemia
  • 21. Usually causes Type 2 diabetes
  • 22. Occurs when there is reduced sensitivity of diabetics who undergo insulin therapy
  • 23. Can also occur when insulin is injected by non-diabetics. This is usually done by athletes who are trying to enhance their overall anaerobic performances. </li></li></ul><li>Some Causes<br />-obesity/ overweight<br />-excess glucocorticoids<br />-excess growth hormone<br />-mutations of insulin receptors<br />
  • 24. 3. Hyperinsulinism<br />
  • 25. 3. Hyperinsulinism<br />How can normal physiology be regained?<br /> - immediate intravenous administration of large quantities of glucose<br />- administration of glucagon (or, less effectively of epinephrine) can cause glycogenolysis in the liver and thereby increase blood glucose level extremely rapidly<br />**Permanent damage to the neuronal cells of the nerous system usually occurs when treatment is not given immediately.<br />
  • 26. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 27. THYROID GLAND<br />GOITER<br />HYPERTHYROIDISM<br />HYPOTHYROIDISM<br />
  • 28. GOITER<br />WHY, YES. THIS IS A….<br />GOITER?<br />WHAT IS A GOITER?<br />ENLARGEMENT<br />OF THE<br />THYROID.<br />
  • 29. GOITER<br />SYMPTOMS<br />NORMAL PHYSIOLOGY<br />Thyroid Hormones (T3 & T4) <br />- produced by cells in thyroid gland<br />- regulated by thyroid stimulating hormone (TSH)<br />- produced through the attachment of <br />iodine atoms to ring structures of T3 and T4<br />AHEM! AHEM!<br />Breathing and swallowing difficulties<br />Coughing and hoarseness<br />
  • 30. CAUSES<br />TREATMENT<br />POSSIBLE COMPLICATIONS<br />GOITER<br />HYPERTHYROIDISM<br />Surgery- thyroidectomy <br />Lugol’s Iodine<br />Radiocative Iodine <br />HYPOTHYROIDISM<br />
  • 31. WHAT<br />OVERACTIVE<br />TISSUE IN THE<br />HYPERTHYROIDISM<br />THYROID GLAND<br />PRODUCING<br />T3<br />TOO MUCH<br />T4<br />AND<br />TRIIODOTHYRONINE<br />& THYROXINE<br />
  • 32. CAUSES<br />GRAVE’S DISEASE<br />TOXIC THYROID ADENOMA<br />NORMAL?<br />THYROIDITIS<br />WHAT<br />WHAT<br />WHAT<br />SYMPTOMS?<br />HIGH EXCITABILITY; METABOLISM<br />MILD TO EXTREME WEIGHT LOSS<br />MUSCLE WEAKNESS; TREMORS<br />
  • 33. DEVELOPMENT OF<br />PROTRUSION OF EYEBALLS<br />exophthalmos<br />EDEMATOUS<br />TISSUES &<br />DEGENERATIVE<br />MUSCLES<br />TREATMENT!<br />SURGICAL REMOVAL OF GLAND<br />LESSEN IODINE INTAKE<br />
  • 34. HYPOTHYROIDISM<br />T3<br />T4<br />TOO LITTLE<br />AND<br />
  • 35. AUTOIMMUNITY<br />AGAINST THE <br />THYROID<br />=DETERIORATION<br />AUTOIMMUNITY<br />CAUSES<br />ASSOCIATED WITH<br />THYROID GOITER<br />
  • 36. IODINE DEFICIENT<br />ENDEMIC COLLOID &<br />IDIOPATHIC NONTOXIC<br />GOITER<br />NOT IODINE DEFICIENT<br />THYROID GOITER<br />
  • 37. SYMPTOMS?<br />FATIGUE; SLEEPINESS; SLUGGISH<br />WEIGHT GAIN; CONSTIPATION<br />FAILURE OF TROPHIC FUNCTIONS<br />myxedema<br />AND<br />TREATMENT!<br />MORE IODINE<br />ORAL MEDICATON<br />
  • 38. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 39. PARATHYROID GLAND<br />HYPOPARATHYROIDISM<br />HYPERPARATHYROIDISM<br />
  • 40. FUNCTION &NORMAL PHYSIOLOGY<br />PARATHYROID GLAND<br />* control calcium within the blood. <br />* control how much calcium is in the bones, <br />and therefore, how strong and dense the bones are!<br />* As the blood filters through the parathyroid glands, <br />they detect the amount of calcium present in the blood <br /> making more or less parathyroid hormone (PTH). <br />Calcium level in the blood is too low: the parathyroid cells make more parathyroid hormone. <br />
  • 41. PARATHYROID GLAND<br />…occurs when your parathyroid glands make too much PT<br />and cause you to have too much calcium in the bloodstream. <br />CAUSES OF TOO MUCH PTH:<br />Growth on the parathyroid glands! <br />Enlargement of 2 or more of the parathyroid glands!<br /> OR medical conditions (like, lessay, kidney failure and rickets...)<br /> <br />HYPOPARATHYROIDISM<br />HYPERPARATHYROIDISM<br />
  • 42. HYPERPARATHYROIDISM<br />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.<br />PHYSIOLOGY&IMPLICATIONS<br />
  • 43. HYPERPARATHYROIDISM<br />Feeling weak or tired most of the time<br />General aches and pains<br />Frequent heartburn <br />Nausea & Vomiting; Loss of appetite<br />An increase in bone fractures or breaks<br />Confusion and memory loss<br />Kidney stones; Excessive urination<br />High blood pressure<br />THE SYMPTOMS<br />
  • 44. HYPERPARATHYROIDISM<br />SURGERY<br />DRINK PLENTY OF WATER<br />LIMIT INTAKE OF CALCIUM AND VITAMIN D<br />DO NOT SMOKE<br />EXERCISE DAILY<br />TREATMENT<br />
  • 45. HYPERPARATHYROIDISM<br />
  • 46. PARATHYROID GLAND<br />HYPOPARATHYROIDISM<br />HYPERPARATHYROIDISM<br />
  • 47. HYPOPARATHYROIDISM<br />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.<br />The low production of parathyroid hormone in hypoparathyroidism leads to abnormally <br />low ionized calcium levels in your blood and bones <br />and to an increased amount of phosphorus.<br />PHYSIOLOGY&IMPLICATIONS<br />
  • 48. HYPOPARATHYROIDISM<br />Tingling or burning (paresthesias) <br />Muscle aches or cramps; Twitching or spasms <br />Fatigue or weakness<br />Painful menstruation<br />Patchy hair loss, such as thinning of your eyebrows<br />Dry, coarse skin; Brittle nails<br />Headaches; Depression, mood swings<br />Memory problems<br />THE SYMPTOMS<br />
  • 49. HYPOPARATHYROIDISM<br />RESTORE THE CALCIUM <br />AND MINERAL BALANCE IN THE BODY.<br />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.<br />TREATMENT<br />
  • 50. HYPOPARATHYROIDISM<br />
  • 51. HEP!<br />HEP!<br />HEP!<br />HAVE YOO BEEN LISTENING? <br />Test your knowledge and try your luck…<br />With our game!<br />
  • 52. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 53. CUSHING’S SYNDROME<br />CUSHING’S DISEASE<br />ADRENAL GLAND<br />ADDISON’S DISEASE<br />
  • 54. SYNDROME<br />CUSHING’S<br />
  • 55. <ul><li>Occurs when your body is exposed to high levels of the hormone cortisol
  • 56. Characterized by high plasma levels of ACTH and cortisol
  • 57. Another name hypercortisolism
  • 58. Can occur from multiple causes including:</li></ul>Adenomas of the anterior pituitary that secrete large amounts of ACTH<br />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<br />Adenomas of the adrenal cortex<br />CUSHING’S<br />
  • 59. High blood pressure.<br />High blood sugar.<br />Suppressed immunity (and more infections).<br />Insulin resistance <br />Suppressed sex hormones and reduced libido.<br />Suppressed thyroid hormones.<br />  - 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.<br />CUSHING’S<br />SYMPTOMS<br />
  • 60. CUSHING’S<br />DISEASE<br />
  • 61. CUSHING’S<br />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.<br />TREATMENT<br />
  • 62. ADDISON’S<br />DISEASE<br />
  • 63. Addison's disease results from damage to the adrenal cortex.<br /> This damage may be caused by the following:<br />The immune system mistakenly attacking the gland (autoimmune disease)<br />Infections such as tuberculosis, HIV, or fungal infections<br />Hemorrhage, blood loss<br />Tumors<br />Use of blood-thinning drugs (anticoagulants) <br />A disorder that occurs when your body produces insufficient amounts of certain hormones produced by your adrenal glands. <br />It may be due to :<br />a disorder of the adrenal glands themselves (primary adrenal insufficiency) or <br /> inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency)<br />ADDISON’S<br />
  • 64. ADDISON’S<br /><ul><li>Changes in blood pressure or heart rate
  • 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 movement</li></ul>SYMPTOMS<br />
  • 73. ADDISON’S<br />Taking hormones to replace the insufficient amounts being made by your adrenal glands (glucocorticoids (cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone))<br />TREATMENT<br />
  • 74. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 75. DIABETES MELLITUS<br />PANCREATIC ISLET<br />
  • 76.
  • 77. PANCREAS<br />retroperitoneal<br />Exocrine gland<br />Endocrine gland<br />-98% of the secreting cells in the pancreas make digestive enzymes <br />-2% of the cells make hormones that are secreted into the portal vein<br />
  • 78. Pancreatic Hormones<br />
  • 79. Normal Physiology<br /> Circulating glucose is derived from three sources:<br />1. intestinal absorption during the fed state<br /> 2. glycogenolysis -breakdown of glycogen<br /> 3. gluconeogenesis -formation of glucose primarily from lactate and amino acids during the fasting state<br />insulin is the key regulatory hormone of glucose disappearance (hypoglycemic hormone), and glucagon is a major regulator of glucose appearance (extremely potent hyperglycemic agent)<br />
  • 80.
  • 81. Disruptions on Physiology<br />
  • 82. Insulin and glucagon <br />antagonistic interaction<br />humoral stimuli   <br />potent regulators <br />of glucose metabolism<br />bi-hormonal <br />definition of diabetes:<br />diabetic state = insulin deficiency <br />+ glucagon excess<br />
  • 83. Diabetes [Mellitus] Pathophysiology<br />
  • 84.
  • 85.
  • 86. NOTE:<br />TYPE1 – noticeable early <br />symptoms<br />TYPE2 – may occur without <br />or gradual development of symptoms<br />
  • 87. Diabetes Complications (VASCULAR)<br />
  • 88. Diabetes Complications (NEURAL)<br />
  • 89. Treatment and Prevention<br />
  • 90. DISEASES&DISORDERS<br />PITUITARY GLAND<br />THYROID GLAND<br />PARATHYROID GLAND<br />ADRENAL GLAND<br />PANCREATIC ISLET<br />SEX HORMONES<br />
  • 91. KLINEFELTER’S DISEASE<br />POLYCYSTIC OVARIES<br />SEX HORMONES<br />
  • 92. PCOS<br />polycystic ovary syndrome<br />
  • 93. PCOS<br />Management<br /><ul><li>Lifestyle modification: health control; exercise
  • 94. Birth control pills
  • 95. Diabetes medications
  • 96. Fertility medications
  • 97. Surgery - laparascopic ovarian drilling</li></ul>Symptoms<br /><ul><li> irregular or non-existent periods
  • 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
  • 103. overweight</li></ul>What causes PCOS?<br /><ul><li>Resistance to the hormone insulin diabetes
  • 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 resistance</li></ul>polycystic ovary syndrome<br />
  • 109. <ul><li>a condition in which human males have an extra X chromosome instead of the normal XY
  • 110. also known as XXY Syndrome or 47, XXY
  • 111. low testosterone level</li></ul> <br />What causes XXY Syndrome?<br /><ul><li>X and Y chromosome fail to pair and fail to exchange genetic material  production of an additional X chromosome</li></ul>KLINEFELTER’SDISEASE<br />
  • 112. KLINEFELTER’SDISEASE<br />Symptoms<br /><ul><li>Small, firm testes
  • 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 problems</li></ul>Management and Treatment<br />Educational guidance<br />Therapeutic Options <br />Medical Options <br />e.g. Testosterone Replacement Therapy (TRT)<br />
  • 120. HEP!<br />HEP!<br />HEP!<br />HAVE YOO BEEN LISTENING? <br />Test your knowledge and try your luck…<br />By giving me a hand with these case studies!<br />
  • 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.<br />What can she be suffering from?<br />
  • 122. What can she be suffering from?<br />
  • 123. References:<br />Elaine N. Marieb, KatjaHoehn. Human Anatomy & Physiology 7th edition<br />Aronoff, S. et al. Glucose Metabolism and Regulation: Beyond Insulin and Glucagon. Retrieved from http://spectrum.diabetesjournals.org/content/17/3/183.full<br />http://www.hormone.org/Diabetes/diabetes.cfm<br />Photos from Google images<br />
  • 124. References:<br />Guyton, A. & Hall, J. Textbook of Medical Physiology. 11th Edition<br />Tortora, G. & Derrickson, B. Principles of Anatomy and Physiology. 11th Edition<br />http://emedicine.medscape.com/article/117648-overview<br />

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