FCA 1011 - Endocrine

494 views

Published on

0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
494
On SlideShare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
2
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • \n
  • FCA 1011 - Endocrine

    1. 1. AIN’T LIFE GLAND...? VERONICA BONALES, M.D. CEPAMERICA EMERGENCY MEDICINE RMH PARAMEDIC COORDINATOR
    2. 2. OBJECTIVESDISCUSS THE ANATOMY AND PHYSIOLOGY OF THEENDOCRINE SYSTEMSDISCUSS SPECIFIC DISEASE PROCESSES AS THEYRELATE TO PROBLEMS WITH ENDOCRINE GLANDSDISCUSS CASE STUDIES AS THEY RELATE TO ENDOCRINEDYSFUNCTIONSDISCUSS TREATMENT OF SPECIFIC ENDOCRINEDISORDERS
    3. 3. ENDOCRINE SYSTEMS OR “AREN’T YOU GLAND....?”
    4. 4. HORMONESCREATED IN ONE TISSUE AND CARRIED VIATHE BLOOD STREAM TO ENACT AN EFFECTIN ANOTHER TISSUE PARACRINE GLANDS SECRETIONS AFFECT ONLY LOCAL TISSUES AUTOCRINE GLANDS SECRETIONS ONLY AFFECT THE SECRETING CELLTAKE SECONDS TO HOURS TO ENACT
    5. 5. 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, luteinizingGlycoproteins Carbohydrates hormone, TSH
    6. 6. HORMONE CONTROL FEEDBACK MECHANISMS NEGATIVE FEEDBACK – IE: THERMOSTAT
    7. 7. TERMINOLOGYHYPER – INCREASED OR OVERPRODUCTIONHYPO – DECREASED OR NO PRODUCTIONPRIMARY – DUE TO ORGAN OR GLAND FAILURESECONDARY – DUE TO FAILURE OF MESSENGER
    8. 8. PITUITARY GLAND THE “MASTER” GLAND!
    9. 9. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
    10. 10. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
    11. 11. PITUITARY GLAND SITS IN THE SELLA TURCICA AT THE BASE OF THE SKULL 1CM IN DIAMETER ANTERIOR & POSTERIOR PORTIONS
    12. 12. PITUITARY GLAND – ANTERIOR LOBEGH – GROWTH HORMONEPRL – PROLACTINTSH – THYROID-STIMULATINGHORMONEACTH – ADRENOCORTICOTROPICHORMONE
    13. 13. GROWTH HORMONE
    14. 14. GROWTH HORMONE WARWICK DAVIS 3’6”
    15. 15. GROWTH HORMONE WARWICK DAVIS 3’6” ROBERT WADLOW 8’11”, 490 LBS
    16. 16. GROWTH HORMONE ROBERT WADLOW 8’11”, 490 LBS7’4” 540 LBS
    17. 17. PITUITARY GLAND – ANTERIOR LOBEGH – GROWTH HORMONEPRL – PROLACTINTSH – THYROID-STIMULATING HORMONEACTH – ADRENOCORTICOTROPICHORMONE
    18. 18. PITUITARY GLAND – ANTERIOR LOBEGH – GROWTH HORMONEPRL – PROLACTINTSH – THYROID-STIMULATING HORMONEACTH – ADRENOCORTICOTROPICHORMONEFSH – FOLLICE STIMULATING HORMONE
    19. 19. PITUITARY GLAND – ANTERIOR LOBEGH – GROWTH HORMONEPRL – PROLACTINTSH – THYROID-STIMULATING HORMONEACTH – ADRENOCORTICOTROPICHORMONEFSH – FOLLICE STIMULATING HORMONELH – LUTEINIZING HORMONE
    20. 20. A CASE STUDY45 YEAR OLD WOMEN PRESENTS TO ED COMPLAINING OF“WHITE DRAINAGE FROM BREASTS.”THOUGHT HAD ALREADY GONE THROUGH MENOPAUSE,AND HAS NOT BEEN SEXUALLY ACTIVE. YOUNGESTCHILD IS 10 YEARS OLD.
    21. 21. PROLACTINOMAMOST COMMON PITUITARY TUMORIN 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 NERVESTX: BROMOCRIPTINE – DA AGONIST – INHIBITSSECRETION OF PROLACTIN OR SURGERY
    22. 22. PITUITARY GLAND – POSTERIOR LOBEADH – ANTI-DIURETIC HORMONE LOSS LEADS TO DIURESIS SIADH (SYNDROME OF INAPPROPRIATE ADH) LEADS TO HYPONATREMIAOT – OXYTOCIN CAN BE GIVEN TO PREGNANT WOMEN TO INDUCE LABOR OR INCREASE FORCE OF CONTRACTIONS
    23. 23. ADRENAL GLANDTHE “FIGHT OR FLIGHT” GLAND!
    24. 24. ADRENAL GLAND
    25. 25. ADRENAL GLANDCORTEX ALDOSTERONE SODIUM & POTASSIUM REGULATION CORTISOL INHIBITS PROTEIN SYNTHESIS PROMOTES FATTY ACID RELEASE GLUCONEOGENESIS ANDROGENS SEX HORMONES (ESTROGEN)MEDULLA NOREPINEPHRINE EPINEPHRINE
    26. 26. A CASE STUDYA 54 YEAR OLD WOMAN PRESENTS WITH COMPLAINTSOF MULTIPLE BRUISES, WEAKNESS, AND THINKING THATHER HAIR IS FALLING OUT.SHE THINKS THAT SHE IS GAINING WEIGHT, BUT FEELSTHAT HER ARMS AND LEGS ARE “SHRINKING.”
    27. 27. CUSHING’S SYNDROME VS. DISEASETOO MUCH CORTISOL TOO MUCH ACTH TUMOR OF THE TUMOR PITUITARY GLAND PARANEOPLASTIC SYNDROME IATROGENIC PHYSICIAN-INDUCED
    28. 28. THYROID & PARATHYROID GLANDSTHE “BODY’S FURNACE” & THE “CALCIUM DOES A BODY GOOD SUPPLIER”
    29. 29. THYROID GLAND THYROXINE (T4) & TRIIODOTHYRONINE (T3) ACTIONS:REGULATE METABOLISM OF CARBS, LIPIDS & PROTEINSINCREASE RATE OF ENERGY RELEASE FROM CARBS INCREASE RATE OF PROTEIN SYNTHESISSTIMULATE BREAKDOWN & MOBILIZATION OF LIPIDS REQUIRED FOR NORMAL GROWTH & DEVELOPMENTNEED IODINE SALTS FOR PRODUCTION CALCITONIN REGULATES CONCENTRATIONS OFBLOOD CALCIUM & PHOSPHATE IONS
    30. 30. A CASE STUDY21 YEAR OLD FEMALE CALLS 911 BECAUSE HER HEART IS“RACING.”FOUND TO BE IN SINUS TACH AT 120 BPM. HAS A MONTHLONG HISTORY OF SORE THROAT, UNEXPLAINED WEIGHTLOSS AND “FEELING HOT ALL THE TIME.”
    31. 31. 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
    32. 32. HYPOTHYROIDSEVERAL DIFFERENT CAUSES (LOW IODINE,PREGNANCY, PITUITARY DISORDER) MOST COMMON: AUTOIMMUNE - HASHIMOTO’S THYROIDITISSSX: LOW METABOLIC RATE COLD INTOLERANCE BRADYCARDIA, ENLARGED HEART LETHARGIC WEIGHT GAIN
    33. 33. HYPOTHYROIDMYXEDEMA COMABROUGHT ON BYSTRESSOR (CVA, AMI,INFECTION, ETC.) AMS & HYPOTHERMIA Hypoglycemia, hypotension, hyponatremia, bradycardia, and hypoventilation
    34. 34. HYPOTHYROIDCRETINISM – LITTLEOR NO THYROIDHORMONE IN FETALLIFEMENTALRETARDATION &DWARFISMTHOUGHT TO BE DUETO INSUFFICIENTIODINE
    35. 35. PARATHYROID GLANDS
    36. 36. PARATHYROID GLANDS PARATHYROID HORMONE AFFECTS BONES, KIDNEYS & INTESTINES INCREASES CIRCULATING LEVELS OF CALCIUM DECREASES CIRCULATING LEVELS OF PHOSPHATES
    37. 37. PARATHYROID DISORDERS1O HYPOPARATHYROIDISM CONGENITAL LACK OF PARATHYROIDS HYPOCALCEMIA WEAK CARDIAC MUSCLE CONTRACTIONS TWITCHING & SPASMS – TETANY OF FACE & HANDS (CHVOSTEK SIGN)
    38. 38. PARATHYROID DISORDERSHYPERPARATHYROIDISM “STONES, BONES, MOANS & PSYCHIC OVERTONES” ADENOMA, HYPERPLASIA, RENAL FAILURE HYPERCALCEMIA FORCEFUL CARDIAC CONTRACTIONS OSTEOPOROSIS CALCIUM TAKEN FROM BONE KIDNEY STONES CONSTIPATION & NAUSEA
    39. 39. PANCREASTHE “SHUGA” GLAND
    40. 40. PANCREASENDOCRINE 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
    41. 41. A CASE STUDYJUNE IS A 43 YEAR OLD, OBESE FEMALE. SHE BEGINS TONOTICE THAT HER PANTS FIT TIGHTER ALTHOUGH THERE HASBEEN NO CHANGE IN HER DIET.SHE GOES TO HER M.D. WHEN SHE BEGINS GETTING UPSEVERAL TIMES A NIGHT TO URINATE (NOCTURIA). SHE ALSONOTES THAT SHE HAS BEEN VERY THIRSTY LATELY.
    42. 42. DIABETES MELLITUSTYPE I – INSULIN-DEPENDENT DUE TO NON-FUNCTIONING PANCREATIC ISLET CELLS YOUNG AGE AT DIAGNOSIS LOW INSULIN LEVELS TX – REPLACE INSULIN KETOACIDOSIS
    43. 43. DIABETES MELLITUSTYPE 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
    44. 44. KETOACIDOSISIF NO SUGAR IN 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
    45. 45. DIABETESFASTING BLOOD GLUCOSE > 126 MG/DL ON SEVERAL OCCASIONSHBA1C 3 MONTH ACCOUNT OF BLOOD SUGARS (< 7%)URINE KETONES SIGNAL OF POSSIBLE KETOACIDOSIS;MICROALBUMINURIA EARLY SIGN
    46. 46. COMPLICATIONSNEPHROPATHYNEUROPATHYRETINOPATHYVASCULOPATHYPOOR WOUND HEALING & INFECTIONSHYPOGLYCEMIADIABETIC COMAKETOACIDOSIS (TYPE I)
    47. 47. COMPLICATIONSNEPHROPATHYNEUROPATHYRETINOPATHYVASCULOPATHYPOOR WOUND HEALING & INFECTIONSHYPOGLYCEMIADIABETIC COMAKETOACIDOSIS (TYPE I)
    48. 48. COMPLICATIONSNEPHROPATHYNEUROPATHYRETINOPATHYVASCULOPATHYPOOR WOUND HEALING & INFECTIONSHYPOGLYCEMIADIABETIC COMAKETOACIDOSIS (TYPE I)
    49. 49. DIABETES – ANIMAL RESEARCH
    50. 50. DIABETES – ANIMAL RESEARCH
    51. 51. DIABETES – ANIMAL RESEARCH
    52. 52. DIABETES – ANIMAL RESEARCH
    53. 53. FREE THE E. COLI? QUESTIONS ?
    54. 54. FREE THE E. COLI? QUESTIONS ?

    ×