Uploaded byV. Bonales, M.D.
FCA 1011 - Endocrine
This document provides an overview of the endocrine system and various endocrine glands and hormones. It discusses the anatomy and physiology of key glands like the pituitary, thyroid, parathyroid, adrenal and pancreas. It also presents several case studies relating to disorders of these glands, such as Cushing's syndrome, Graves' disease, hypothyroidism, hyperparathyroidism, and diabetes mellitus. The document aims to discuss endocrine diseases, their treatments, and associated complications.
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FCA 1011 - Endocrine
- 1. AIN’T LIFE GLAND...? VERONICA BONALES, M.D. CEPAMERICA EMERGENCY MEDICINE RMH PARAMEDIC COORDINATOR
- 2. OBJECTIVES DISCUSS THE ANATOMYAND PHYSIOLOGY OF THE ENDOCRINE SYSTEMS DISCUSS SPECIFIC DISEASE PROCESSES AS THEY RELATE TO PROBLEMS WITH ENDOCRINE GLANDS DISCUSS CASE STUDIES AS THEY RELATE TO ENDOCRINE DYSFUNCTIONS DISCUSS TREATMENT OF SPECIFIC ENDOCRINE DISORDERS
- 3. ENDOCRINE SYSTEMS OR “AREN’T YOU GLAND....?”
- 14. HORMONES CREATED IN ONETISSUE AND CARRIED VIA THE BLOOD STREAM TO ENACT AN EFFECT IN ANOTHER TISSUE PARACRINE GLANDS SECRETIONS AFFECT ONLY LOCAL TISSUES AUTOCRINE GLANDS SECRETIONS ONLY AFFECT THE SECRETING CELL TAKE SECONDS TO HOURS TO ENACT
- 15. Compound Formed from: Examples Estrogen, Steroids Cholesterol testosterone, aldosterone, cortisol Norepinephrine, Amines Amino Acids epinephrine Peptides Amino Acids ADH, oxytocin, TRH PTH, growth Proteins Amino Acids hormone, prolactin Protein & FSH, luteinizing Glycoproteins Carbohydrates hormone, TSH
- 16. HORMONE CONTROL FEEDBACK MECHANISMS NEGATIVE FEEDBACK – IE: THERMOSTAT
- 17. TERMINOLOGY HYPER – INCREASEDOR OVERPRODUCTION HYPO – DECREASED OR NO PRODUCTION PRIMARY – DUE TO ORGAN OR GLAND FAILURE SECONDARY – DUE TO FAILURE OF MESSENGER
- 18. PITUITARY GLAND THE “MASTER” GLAND!
- 19. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
- 20. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
- 21. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
- 22. PITUITARY GLAND –ANTERIOR LOBE GH – GROWTH HORMONE PRL – PROLACTIN TSH – THYROID-STIMULATING HORMONE ACTH – ADRENOCORTICOTROPIC HORMONE
- 23.
- 24. GROWTH HORMONE WARWICK DAVIS 3’6”
- 25. GROWTH HORMONE WARWICK DAVIS 3’6” ROBERT WADLOW 8’11”, 490 LBS
- 26. GROWTH HORMONE ROBERT WADLOW 8’11”, 490 LBS 7’4” 540 LBS
- 27. PITUITARY GLAND –ANTERIOR LOBE GH – GROWTH HORMONE PRL – PROLACTIN TSH – THYROID-STIMULATING HORMONE ACTH – ADRENOCORTICOTROPIC HORMONE
- 28. PITUITARY GLAND –ANTERIOR LOBE GH – GROWTH HORMONE PRL – PROLACTIN TSH – THYROID-STIMULATING HORMONE ACTH – ADRENOCORTICOTROPIC HORMONE FSH – FOLLICE STIMULATING HORMONE
- 29. PITUITARY GLAND –ANTERIOR LOBE GH – GROWTH HORMONE PRL – PROLACTIN TSH – THYROID-STIMULATING HORMONE ACTH – ADRENOCORTICOTROPIC HORMONE FSH – FOLLICE STIMULATING HORMONE LH – LUTEINIZING HORMONE
- 30. A CASE STUDY 45YEAR OLD WOMEN PRESENTS TO ED COMPLAINING OF “WHITE DRAINAGE FROM BREASTS.” THOUGHT HAD ALREADY GONE THROUGH MENOPAUSE, AND HAS NOT BEEN SEXUALLY ACTIVE. YOUNGEST CHILD IS 10 YEARS OLD.
- 31. PROLACTINOMA MOST COMMON PITUITARYTUMOR IN WOMEN INFERTILITY AND CHANGES IN MENSTRUATION PERIODS MAY DISAPPEAR ALTOGETHER OR PERIODS MAY BECOME IRREGULAR WOMEN WHO ARE NOT PREGNANT OR NURSING MAY BEGIN PRODUCING BREAST MILK. SOME EXPERIENCE A LOSS OF LIBIDO (INTEREST IN SEX) INTERCOURSE MAY BECOME PAINFUL BECAUSE OF VAGINAL DRYNESS (DYSPAREUNIA) IN MEN IMPOTENCE DELAY GOING TO THE DOCTOR UNTIL THEY HAVE HEADACHES OR EYE PROBLEMS CAUSED BY THE ENLARGED PITUITARY PRESSING AGAINST NEARBY EYE NERVES TX: BROMOCRIPTINE – DA AGONIST – INHIBITS SECRETION OF PROLACTIN OR SURGERY
- 32. PITUITARY GLAND – POSTERIOR LOBE ADH – ANTI-DIURETIC HORMONE LOSS LEADS TO DIURESIS SIADH (SYNDROME OF INAPPROPRIATE ADH) LEADS TO HYPONATREMIA OT – OXYTOCIN CAN BE GIVEN TO PREGNANT WOMEN TO INDUCE LABOR OR INCREASE FORCE OF CONTRACTIONS
- 33. ADRENAL GLAND THE “FIGHTOR FLIGHT” GLAND!
- 34.
- 35. ADRENAL GLAND CORTEX ALDOSTERONE SODIUM & POTASSIUM REGULATION CORTISOL INHIBITS PROTEIN SYNTHESIS PROMOTES FATTY ACID RELEASE GLUCONEOGENESIS ANDROGENS SEX HORMONES (ESTROGEN) MEDULLA NOREPINEPHRINE EPINEPHRINE
- 37. A CASE STUDY A54 YEAR OLD WOMAN PRESENTS WITH COMPLAINTS OF MULTIPLE BRUISES, WEAKNESS, AND THINKING THAT HER HAIR IS FALLING OUT. SHE THINKS THAT SHE IS GAINING WEIGHT, BUT FEELS THAT HER ARMS AND LEGS ARE “SHRINKING.”
- 39. CUSHING’S SYNDROME VS.DISEASE TOO MUCH CORTISOL TOO MUCH ACTH TUMOR OF THE TUMOR PITUITARY GLAND PARANEOPLASTIC SYNDROME IATROGENIC PHYSICIAN-INDUCED
- 40. THYROID & PARATHYROIDGLANDS THE “BODY’S FURNACE” & THE “CALCIUM DOES A BODY GOOD SUPPLIER”
- 41. THYROID GLAND THYROXINE (T4) & TRIIODOTHYRONINE (T3) ACTIONS: REGULATE METABOLISM OF CARBS, LIPIDS & PROTEINS INCREASE RATE OF ENERGY RELEASE FROM CARBS INCREASE RATE OF PROTEIN SYNTHESIS STIMULATE BREAKDOWN & MOBILIZATION OF LIPIDS REQUIRED FOR NORMAL GROWTH & DEVELOPMENT NEED IODINE SALTS FOR PRODUCTION CALCITONIN REGULATES CONCENTRATIONS OF BLOOD CALCIUM & PHOSPHATE IONS
- 42. A CASE STUDY 21YEAR OLD FEMALE CALLS 911 BECAUSE HER HEART IS “RACING.” FOUND TO BE IN SINUS TACH AT 120 BPM. HAS A MONTH LONG HISTORY OF SORE THROAT, UNEXPLAINED WEIGHT LOSS AND “FEELING HOT ALL THE TIME.”
- 43. HYPERTHYROID GRAVE’S DISEASE WOMEN > 30 AUTOIMMUNE SSX: HYPERMETABOLISM, TOXIC GOITER, EXOPHTHALMOS COMPLICATION – THYROID STORM HYPERTHERMIA, TACHYCARDIA, HEART FAILURE, DELIRIUM TX: REMOVAL, RADIOACTIVE IODINE, ANTITHYROID DRUGS
- 44. HYPOTHYROID SEVERAL DIFFERENT CAUSES(LOW IODINE, PREGNANCY, PITUITARY DISORDER) MOST COMMON: AUTOIMMUNE - HASHIMOTO’S THYROIDITIS SSX: LOW METABOLIC RATE COLD INTOLERANCE BRADYCARDIA, ENLARGED HEART LETHARGIC WEIGHT GAIN
- 45. HYPOTHYROID MYXEDEMA COMA BROUGHT ONBY STRESSOR (CVA, AMI, INFECTION, ETC.) AMS & HYPOTHERMIA Hypoglycemia, hypotension, hyponatremia, bradycardia, and hypoventilation
- 46. HYPOTHYROID CRETINISM – LITTLE ORNO THYROID HORMONE IN FETAL LIFE MENTAL RETARDATION & DWARFISM THOUGHT TO BE DUE TO INSUFFICIENT IODINE
- 47.
- 48. PARATHYROID GLANDS PARATHYROID HORMONE AFFECTS BONES, KIDNEYS & INTESTINES INCREASES CIRCULATING LEVELS OF CALCIUM DECREASES CIRCULATING LEVELS OF PHOSPHATES
- 49. PARATHYROID DISORDERS 1O HYPOPARATHYROIDISM CONGENITAL LACK OF PARATHYROIDS HYPOCALCEMIA WEAK CARDIAC MUSCLE CONTRACTIONS TWITCHING & SPASMS – TETANY OF FACE & HANDS (CHVOSTEK SIGN)
- 50. PARATHYROID DISORDERS HYPERPARATHYROIDISM “STONES,BONES, MOANS & PSYCHIC OVERTONES” ADENOMA, HYPERPLASIA, RENAL FAILURE HYPERCALCEMIA FORCEFUL CARDIAC CONTRACTIONS OSTEOPOROSIS CALCIUM TAKEN FROM BONE KIDNEY STONES CONSTIPATION & NAUSEA
- 51.
- 52. PANCREAS ENDOCRINE PANCREAS GLUCAGON INCREASES SERUM BLOOD SUGAR LEVELS BREAKS DOWN GLYCOGEN GLUCONEOGENESIS INSULIN DECREASES SERUM BLOOD SUGAR LEVELS STIMULATES PRODUCTION OF GLYCOGEN FACILITATES DIFFUSION OF GLUCOSE ACROSS CELL MEMBRANES
- 53. A CASE STUDY JUNEIS A 43 YEAR OLD, OBESE FEMALE. SHE BEGINS TO NOTICE THAT HER PANTS FIT TIGHTER ALTHOUGH THERE HAS BEEN NO CHANGE IN HER DIET. SHE GOES TO HER M.D. WHEN SHE BEGINS GETTING UP SEVERAL TIMES A NIGHT TO URINATE (NOCTURIA). SHE ALSO NOTES THAT SHE HAS BEEN VERY THIRSTY LATELY.
- 54. DIABETES MELLITUS TYPE I– INSULIN-DEPENDENT DUE TO NON-FUNCTIONING PANCREATIC ISLET CELLS YOUNG AGE AT DIAGNOSIS LOW INSULIN LEVELS TX – REPLACE INSULIN KETOACIDOSIS
- 55. DIABETES MELLITUS TYPE II– NON-INSULIN DEPENDENT DUE TO DECREASED OR NON- FUNCTIONAL RECEPTOR CELLS OLDER AT DIAGNOSIS DECREASED OR NORMAL INSULIN LEVELS; INSULIN RECEPTORS NOT WORKING TX – DIET, EXERCISE, ORAL ANTIHYPERGLYCEMICS
- 56. KETOACIDOSIS IF NO SUGARIN CELLS CELLS USE PROTEINS & FATS KETONES ARE RESULT ACETOACETIC & BETA-HYDROXYBUTYRIC ACIDS EXCESS AMOUNTS OF KETONES CAN LEAD TO KETOACIDOSIS BIND WITH BICARBONATE LOWER PH ACIDOSIS NEEDS LOTS OF FLUIDS AND CONTROL OF HIGH BLOOD SUGARS
- 57. DIABETES FASTING BLOOD GLUCOSE > 126 MG/DL ON SEVERAL OCCASIONS HBA1C 3 MONTH ACCOUNT OF BLOOD SUGARS (< 7%) URINE KETONES SIGNAL OF POSSIBLE KETOACIDOSIS; MICROALBUMINURIA EARLY SIGN
- 58. COMPLICATIONS NEPHROPATHY NEUROPATHY RETINOPATHY VASCULOPATHY POOR WOUND HEALING& INFECTIONS HYPOGLYCEMIA DIABETIC COMA KETOACIDOSIS (TYPE I)
- 59. COMPLICATIONS NEPHROPATHY NEUROPATHY RETINOPATHY VASCULOPATHY POOR WOUND HEALING& INFECTIONS HYPOGLYCEMIA DIABETIC COMA KETOACIDOSIS (TYPE I)
- 60. COMPLICATIONS NEPHROPATHY NEUROPATHY RETINOPATHY VASCULOPATHY POOR WOUND HEALING& INFECTIONS HYPOGLYCEMIA DIABETIC COMA KETOACIDOSIS (TYPE I)
- 61. DIABETES – ANIMALRESEARCH
- 62. DIABETES – ANIMALRESEARCH
- 63. DIABETES – ANIMALRESEARCH
- 64. DIABETES – ANIMALRESEARCH
- 65. FREE THE E.COLI ? QUESTIONS ?
- 66. FREE THE E.COLI ? QUESTIONS ?
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