How to cure cirrhosis and chronic hepatitis naturally
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
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
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
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
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.”
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