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AIN’T LIFE GLAND...?

     VERONICA BONALES, M.D.
 CEPAMERICA EMERGENCY MEDICINE
  RMH PARAMEDIC COORDINATOR
OBJECTIVES

DISCUSS THE ANATOMY AND 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
ENDOCRINE SYSTEMS
  OR “AREN’T YOU GLAND....?”
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
FCA 1011 - Endocrine
HORMONES

CREATED IN ONE TISSUE 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
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
HORMONE CONTROL




       FEEDBACK MECHANISMS
 NEGATIVE FEEDBACK – IE: THERMOSTAT
TERMINOLOGY



HYPER – INCREASED OR OVERPRODUCTION

HYPO – DECREASED OR NO PRODUCTION

PRIMARY – DUE TO ORGAN OR GLAND FAILURE

SECONDARY – DUE TO FAILURE OF MESSENGER
PITUITARY GLAND
  THE “MASTER” GLAND!
PITUITARY GLAND
             SITS IN THE
        SELLA TURCICA AT
         THE BASE OF THE
              SKULL
          1CM IN DIAMETER
             ANTERIOR &
            POSTERIOR
             PORTIONS
PITUITARY GLAND
             SITS IN THE
        SELLA TURCICA AT
         THE BASE OF THE
              SKULL
          1CM IN DIAMETER
             ANTERIOR &
            POSTERIOR
             PORTIONS
PITUITARY GLAND
             SITS IN THE
        SELLA TURCICA AT
         THE BASE OF THE
              SKULL
          1CM IN DIAMETER
             ANTERIOR &
            POSTERIOR
             PORTIONS
PITUITARY GLAND – ANTERIOR
            LOBE
GH – GROWTH HORMONE
PRL – PROLACTIN
TSH – THYROID-STIMULATING
HORMONE
ACTH – ADRENOCORTICOTROPIC
HORMONE
GROWTH HORMONE
GROWTH HORMONE




    WARWICK
    DAVIS 3’6”
GROWTH HORMONE




    WARWICK
    DAVIS 3’6”




                 ROBERT WADLOW
                   8’11”, 490 LBS
GROWTH HORMONE




               ROBERT WADLOW
                 8’11”, 490 LBS
7’4” 540 LBS
PITUITARY GLAND – ANTERIOR
            LOBE
GH – GROWTH HORMONE
PRL – PROLACTIN
TSH – THYROID-STIMULATING HORMONE
ACTH – ADRENOCORTICOTROPIC
HORMONE
PITUITARY GLAND – ANTERIOR
            LOBE
GH – GROWTH HORMONE
PRL – PROLACTIN
TSH – THYROID-STIMULATING HORMONE
ACTH – ADRENOCORTICOTROPIC
HORMONE
FSH – FOLLICE STIMULATING HORMONE
PITUITARY GLAND – ANTERIOR
            LOBE
GH – GROWTH HORMONE
PRL – PROLACTIN
TSH – THYROID-STIMULATING HORMONE
ACTH – ADRENOCORTICOTROPIC
HORMONE
FSH – FOLLICE STIMULATING HORMONE
LH – LUTEINIZING HORMONE
A CASE STUDY



45 YEAR 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.
PROLACTINOMA
MOST COMMON PITUITARY TUMOR

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
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
ADRENAL GLAND
THE “FIGHT OR FLIGHT” GLAND!
ADRENAL GLAND
ADRENAL GLAND

CORTEX
 ALDOSTERONE
   SODIUM & POTASSIUM REGULATION

 CORTISOL
   INHIBITS PROTEIN SYNTHESIS

   PROMOTES FATTY ACID RELEASE

   GLUCONEOGENESIS

 ANDROGENS
   SEX HORMONES (ESTROGEN)

MEDULLA
 NOREPINEPHRINE
 EPINEPHRINE
FCA 1011 - Endocrine
A CASE STUDY



A 54 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.”
FCA 1011 - Endocrine
CUSHING’S SYNDROME VS. DISEASE


TOO MUCH CORTISOL      TOO MUCH ACTH
                       TUMOR OF THE
 TUMOR
                       PITUITARY GLAND
 PARANEOPLASTIC
 SYNDROME

 IATROGENIC

   PHYSICIAN-INDUCED
THYROID & PARATHYROID GLANDS
THE “BODY’S FURNACE” & THE “CALCIUM DOES A BODY GOOD
                      SUPPLIER”
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
A CASE STUDY



21 YEAR 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.”
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
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
HYPOTHYROID

MYXEDEMA COMA

BROUGHT ON BY
STRESSOR (CVA, AMI,
INFECTION, ETC.)

  AMS & HYPOTHERMIA

  Hypoglycemia,
  hypotension,
  hyponatremia,
  bradycardia, and
  hypoventilation
HYPOTHYROID


CRETINISM – LITTLE
OR NO THYROID
HORMONE IN FETAL
LIFE
MENTAL
RETARDATION &
DWARFISM
THOUGHT TO BE DUE
TO INSUFFICIENT
IODINE
PARATHYROID GLANDS
PARATHYROID GLANDS


      PARATHYROID HORMONE

       AFFECTS BONES, KIDNEYS &
       INTESTINES

        INCREASES CIRCULATING
        LEVELS OF CALCIUM

        DECREASES CIRCULATING
        LEVELS OF PHOSPHATES
PARATHYROID DISORDERS


1O HYPOPARATHYROIDISM
 CONGENITAL LACK OF PARATHYROIDS
 HYPOCALCEMIA
  WEAK CARDIAC MUSCLE CONTRACTIONS

  TWITCHING & SPASMS – TETANY OF FACE &
  HANDS (CHVOSTEK SIGN)
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
PANCREAS
THE “SHUGA” GLAND
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
A CASE STUDY



JUNE IS 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.
DIABETES MELLITUS

TYPE I – INSULIN-DEPENDENT
 DUE TO NON-FUNCTIONING PANCREATIC
 ISLET CELLS
 YOUNG AGE AT DIAGNOSIS
 LOW INSULIN LEVELS
 TX – REPLACE INSULIN
 KETOACIDOSIS
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
KETOACIDOSIS

IF 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
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
COMPLICATIONS

NEPHROPATHY
NEUROPATHY
RETINOPATHY
VASCULOPATHY
POOR WOUND HEALING & INFECTIONS
HYPOGLYCEMIA
DIABETIC COMA
KETOACIDOSIS (TYPE I)
COMPLICATIONS

NEPHROPATHY
NEUROPATHY
RETINOPATHY
VASCULOPATHY
POOR WOUND HEALING & INFECTIONS
HYPOGLYCEMIA
DIABETIC COMA
KETOACIDOSIS (TYPE I)
COMPLICATIONS

NEPHROPATHY
NEUROPATHY
RETINOPATHY
VASCULOPATHY
POOR WOUND HEALING & INFECTIONS
HYPOGLYCEMIA
DIABETIC COMA
KETOACIDOSIS (TYPE I)
DIABETES – ANIMAL RESEARCH
DIABETES – ANIMAL RESEARCH
DIABETES – ANIMAL RESEARCH
DIABETES – ANIMAL RESEARCH
FREE THE E. COLI




? QUESTIONS ?
FREE THE E. COLI



? QUESTIONS ?

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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 ANATOMY AND 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 ONE TISSUE 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 – INCREASED OR 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
  • 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 45 YEAR 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 PITUITARY TUMOR 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 “FIGHT OR FLIGHT” GLAND!
  • 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 A 54 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 & PARATHYROID GLANDS 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 21 YEAR 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 ON BY STRESSOR (CVA, AMI, INFECTION, ETC.) AMS & HYPOTHERMIA Hypoglycemia, hypotension, hyponatremia, bradycardia, and hypoventilation
  • 46. HYPOTHYROID CRETINISM – LITTLE OR NO THYROID HORMONE IN FETAL LIFE MENTAL RETARDATION & DWARFISM THOUGHT TO BE DUE TO INSUFFICIENT IODINE
  • 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
  • 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 JUNE IS 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 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
  • 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)
  • 65. FREE THE E. COLI ? QUESTIONS ?
  • 66. FREE THE E. COLI ? QUESTIONS ?

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