The document discusses the functions and regulation of adrenocortical hormones produced by the adrenal glands, highlighting the roles of the adrenal cortex in secreting corticosteroids including mineralocorticoids, glucocorticoids, and androgenic hormones. It details the physiological effects of aldosterone and cortisol, their regulation, and the implications of their excess or deficiency on bodily functions. Additionally, it covers related hormones such as parathyroid hormone and gastrointestinal hormones, explaining their roles in calcium metabolism and digestive processes.

1. ADRENOCORTICAL HORMONES
TWO ADRENAL GLANDS: SUPERIOR POLES OF TWO KIDNEYS
COMPOSED: ADRENAL CORTEX AND ADRENAL MEDULLA
ADRENAL CORTEX: CORTICOSTEROIDS (MINERALOCORTICOIDS,
GLUCOCORTICOIDS, ANDROGENIC HORMONES)
ANDROGENIC HORMONES: TESTOSTERONE
MINERALOCORTICOIDS: ELECTROLYTES
GLUCOCORTICOIDS: INCREASE BLOOD GLUCOSE CONC, PROTEIN AND
FAT METABOLISM
ALDOSTERONE: MINERALOCORTICOIDS
CORTISOL: GLUCOCORTICOIDS

2. ADRENAL CORTEX
LAYERS:
 ZONA GLOMERULOSA
 ZONA FASCICULATA
 ZONA RETICULARIS
REGULATION OF SECRETION
ALDOSTERONE: ANGIOTENSIN II
CORTISOL AND ANDROGEN: ACTH

3. FUNCTIONS OF MINERALOCORTICOIDS- ALDOSTERONE
INCREASES RENAL TUBULAR REABSORPTION OF SODIUM AND SECRETION OF
POTASSIUM
CONSERVE SODIUM IN ECF AND INCREASE POTASSIUM EXCRETION IN THE
URINE
MINERALOCORTICOID DEFICIENCY CAUSES SEVERE RENAL SODIUM CHLORIDE
WASTING AND HYPERKALEMIA
WITHOUT MINERALOCORTICOID, K ION CONC IN ECF RISES AND BLOOD
VOLUME GREATLY REDUCED, DIMINISHED CARDIAC OURPUT AND SHOCK LIKE
STATE, LIFE SAVING ADRENOCORTICOID HORMONE
EXCESS ALDOSTERONE INCREASE ECF VOLUME AND ARTERIAL PRESSURE BUT
SMALL EFFECT ON PLASMA SODIUM CONC
ALDOSTERONE DECREASES SODIUM ION EXCRETION BY KIDNEY, SIMULTANEOUS
OSMOTIC ABSORPTION OF EQUIVALENT AMOUNT OF WATER

4. EXCESS ALDOSTERONE INCREASE ECF VOLUME AND ARTERIAL
PRESSURE
INCREASE IN ECF VOLUME, ALSO INCREASE ARTERIAL PRESSURE, INCREASE
WATER AND SALT EXCRETION CALLED PRESSURE DIURESIS. ELEVATED BP
RETURNS RENAL OUTPUT OF SALT AND WATER TO NORMAL AS A RESULT
OF PRESSURE DIURESIS IS CALLED ALDOSTERONE ESCAPE DESPITE EXCESS
ALDOSTERONE
CIRCULATORY SHOCK (ALDOSTERONE SECRETION ZORO): LARGE AMOUNT
OF SALT LOST AND DECREASE ECF VOLUME, LOW BLOOD VOLUME LEAD TO
CIRCULATORY SHOCK
EXCESS ALDOSTERONE CAUSES HYPOKALEMIA AND MUSCLE WEAKNESS:
EXCESS ALDOSTERONE CAUSES LOSS OF POTASSIUM FROM ECF AND
STIMULATE TRANSPORT OF POTASSIUM TO MOST OF CELL, HYPOKALEMIA
CAUSE MUSCLE WEAKNESS B/C OF ELECTRICAL EXCITABILITY OF NERVE
AND MUSCLE FIBER MEMBRANE

5. TOO LITTLE ALDOSTERONE CAUSES HYPERKALEMIA AND CARDIAC TOXICITY
ALDOSTERONE DEFICIENCY IN ECF POTASSIUM CONC RISES AND CAUSE
WEAKNESS OF HEART CONTRACTION, ARRYTHMIA LEAD TO HEART FAILURE
EXCESS ALDOSTERONE INCREASE TUBULAR HYDROGEN ION SECRETION
AND CAUSES ALKALOSIS
ALDOSTERONE CAUSE SECRETION OF HYDROGEN ION IN EXCHANGE FOR
SODIUM IN THE INTERCALATED CELLS OF TUBULES, DECREASING
HYDROGEN ION IN ECF, METABOLIC ALKALOSIS
ALDOSTERONE STIMULATES SODIUM AND POTASSIUM TRANSPORT IN
SWEAT GLAND, SALIVARY GLANDS AND INTESTINAL EPITHELIAL CELLS
SECRETE LARGE AMOUNT OF SODIUMCHLORIDE, ON PASSING THROUGH
EXCRETORY DUCT REABSORBED, POTASSIUM AND HCO3IONS SECRETION
INTESTINE: ENHANCED SODIUM ABSORPTION AND PREVENT LOSS OF
SODIUM IN STOOL

6. REGULATION OF ALDOSTERONE SECRETION
• INCREASE K ION CONC IN ECF-GREATLY INCRESES ALDOSTERONE
SECRETION
• INCREASE ACTIVITY OF RENIN ANGIOTENSIN SYSTEM-GREATLY INCRESES
ALDOSTERONE SECRETION: ACTIVATION OF RENIN ANGIOTENSIN SYSTEM
IN RESPONSE TO DIMINISHED BLOOD FLOW OR SODIUM LOSS CAN
INCREASE ALDOSTERONE SECRETION ACT ON KIDNEY AND EXCRETE
POTASSIUM ION AND INCREASED BLOOD VOLUME AND ARTERIAL
PRESSURE
• INCREASE SODIUM ION CONC IN ECF-SLIGHLY DECREASE ALDOSTERONE
SECRETION
• ACTH FROM ANTERIOR PITUITARY GLAND FOR ALDOSTERONE SECRETION
BUT LITTLE EFFECT IN CONTROLLING RATE OF SECRETION

7. FUNCTIONS OF GLUCOCORTICOIDS
CORTISOL OR HYDROCORTISONE
CARBOHYDRATE METABOLISM
STIMULATE GLUCONEOGENESIS BY LIVER, INCREASE GLYCOGEN
STORAGE IN LIVER CELLS, GLYCOLYTIC HORMONES (EPINEPHRINE AND
GLUCAGON) MOBILIZE GLUCOSE IN TIMES OF NEED
DECREASE GLUCOSE UTILIZATION BY CELLS
DELAY RATE OF GLUCOSE UTILIZATION BY CELLS OF BODY
ELEVATED BLOOD GLUCOSE CONC (ADRENAL DIABETES)
INCREASE RATE OF GLUCONEOGENESIS AND REDUCTION OF GLUCOSE
UTILIZATION BY CELLS- BLOOD GLUCOSE CONC RISE

8. EFFECT OF CORTISOL ON PROTEIN METABOLISM
REDUCTION OF PROTEIN STORES IN ALL BODY CELLLS EXCEPT LIVER
CORTISOL INCREASES LIVER AND PLASMA PROTEIN
ENHANCED AMINO ACIDS TRANSPORT INTO LIVER CELL AND ENHANCE
LIVER ENZYMES FOR PROTEIN SYNTHESIS
INCREASED BLOOD AMINO ACIDS, DIMINISHED TRANSPORT OF AMINO
ACIDS INTO EXTRAHEPATIC CELLS AND ENHANCED TRANSPORT INTO
HEPATIC CELLS
CORTISOL DEPRESSES AMINO ACIDS TRANSPORT INTO MUSCLES AND
CATABOLISM OF PROTEIN RELEASE AMINO ACIDS DIFFUSE OUT OF CELLS
AND INCREASE PLASMA AMINO ACIDS CONC. CORTISOL MOBILIZE AMINO
ACIDS FROM NON-HEPATIC TISSUES AND DIMINISHES TISSUE STORE OF
PROTEIN

9. EFFECT OF CORTISOL ON FAT METABOLISM
MOBILIZE FATTY ACIDS FROM ADIPOSE TISSUES, INCREASE FREE FATTY
ACIDS IN PLASMA, ENHANCE OXIDATION OF FATTY ACIDS
CORTISOL IMPORTANT IN RESISTING STRESS AND INFLAMMATION
STRESS INCREASES ACTH SECRETION FROM ANTERIOR PITUITARY,
INCREASE CORTISOL SECRETION AND CAUSES MOBILIZATION OF
AMINO ACID AND FATS FOR ENERGY

10. ANTI-INFLAMMATORY EFFECTS OF CORTISOL
LARGE AMOUNT OF CORTISOL BLOCK INFLAMMATION, RAPID
RESOLUTION OF INFLAMMATION AND RAPID HEALING
CORTISOL STABILIZE LYSOSOMAL MEMBRANE
CORTISOL DECREASE PERMEABILITY OF CAPILLARIES
DECREASE MIGRATION OF WBC INTO INFLAMMED AREA
CORTISOL SUPPRESSES IMMUNE SYSTEM
CORTISOL ATTENUATES FEVER
REGULATION OF CORTISOL SECRETION
CRF (PEPTIDE SECRETED BY HYPOTHALAMUS)-ACTH-CORTISOL
STRESS STIMULI
NEGATIVE FEEDBACK INHIBITION
CIRCADIAN RHYTHM OF GLUCOCORTICOID SECRETION

11. ADRENOGENITAL SYNDROME
EXCESS ADRENAL ANDROGENS SECRETION, INTENSE MASCULINIZING
EFFECTS, CAUSE: ADRENOCORTICAL TUMOR
SYMPTOMS: IN FEMALE, MUSCULINE HAIR DISTRIBUTION, DEEPER
VOICE, INCREASE MUSCLE PROTEIN, IN MALE, RAPID DEVELOPMENT
OF MALE SECONDARY SEXUAL CHARACTERISTICS
CUSHING DISEASE
EXCESS CORTISOL SECRETION DUE TO ANTERIOR PITUITARY GLAND
TUMOR SECRETE EXCESS ACTH
SYMPTOMS: DISTURBANCES IN METABOLISM, EDEMATOUS
APPEARANCE OF FACE, ACNE, HIRSUTISM, HYPERTENSION

12. ACTIONS OF EPINEPHRINE AND NOREPINEPHRINE
ADRENAL MEDULLA FUNCTIONALLY
RELATED TO SYMPATHETIC NERVOUS
SYSTEM, SYNTHESIS: TERMINAL NERVE
ENDING OF ADRENERGIC FIBERS
EYES: CONTRACT FIBERS OF IRIS, DIALATE
PUPIL
GLANDS: VASOCONSTRICTION OF BLOOD
VESSELS CAUSE REDUCTION RATE OF
SECRETION
GIT: INHIBIT PERISTALSIS, INCREASE
TONE OF SPHINCTER
BLOOD VESSELS: CONSTRICTED
ARTERIAL PRESSURE: INCREASE

13. HEART: SYMPATHETIC STIMULATION INCREASE OVERALL ACTIVITY OF
HEART, INCREASE RATE ANF FORCE OF HEART CONTRACTION
METABOLIC EFFECT: SYMPATHETIC STIMULATION CAUSES RELEASE OF
GLUCOSE FROM LIVER, INCREASE BLOOD GLUCOSE CONC, INCREASE
GLYCOGENOLYSIS IN LIVER AND MUSCLES STRENGTH,INCREASE BASAL
METABOLIC RATE AND INCREASE MENTAL ACTIVITY
PHEOCHROMOCYTOMA
TUMOR OF ADRENAL MEDULLA (OR SYMPATHETIC GANGLIA) SECRETED
EXCESS CATECHOLAMINES
SYMPTOMS: HEADACHE, DIZZINESS, ANXIETY, TACHYCARDIA,
PALPITATION, HYPERTENSION, INCREASE RATE AND DEPTH OF
RESPIRATION, NAUSEA, VOMITING, INCREASE SWEATING

14. PARATHYROID HORMONE
LOCATED: FOUR PARATHYROID
BEHIND UPPER AND LOWER POLE OF
THYROID GLAND
FUNCTION
MEHANISM FOR CONTROLLING
EXTRACELLULAR CALCIUM AND
PHOSPHATE CONC
EXCESS ACTIVITY OF PTH RAPID
ABSORPTION OF CALCIUM FROM
BONES AND HYPERCALCEMIA
LACK OF PTH ACTIVITY
HYPOCALCEMIA WITH TETANY

15. EFFECT OF PTH ON CALCIUM AND PHOSPHATE CONC IN BLOOD
AFTER INFUSION OF PTH CALCIUM ION CONC RISES AND PHOSPHATE
CON FALLS RAPIDLY, PTHINCREASE CALCIUM AND PHOSPHATE
ABSORPTION FROM BONES. PTH DECREASE EXCRETION OF CALCIUM BY
KIDNEY BUT INCREASE RENAL EXCRETION OF PHOSPHATE WHICH
OVERRIDE ABSORPTION FROM BONES
PTH INCREASES INTESTINAL ABSORPTION OF CALCIUM AND
PHOSPHATE: INCREASE FORMATION OF I, 25 DIHYDRO
CHOLECALCIFEROL FROM VIT D IN THE KIDNEYS
CACITONIN
SECRETED THYROID GLAND, DECREASE PLASMA CALCIUM CONC
STIMULI: INCREASE PLASMA CALCIUM ION CONC

16. CALCIUM METABOLISM
CALCIUM AND PHOSPHATE METABOLISM, FORMATION OF BONES
AND TEETH, REGULATION OF VIT D, PTH AND CALCITONIN ARE
CLOSELY CONNECTED
IMPORTANT ASPECT OF CALCIUM METABOLISM IS THE REGULATION
OF CALCIUM IONS IN THE BLOOD PLASMA WITHIN NARROW LIMITS.
 BONE TISSUE ACTS AS A CALCIUM STORAGE CENTER FOR DEPOSITS
AND WITHDRAWALS AS NEEDED BY THE BLOOD
THYROID GLAND, AND THE PARATHYROID GLANDS CONSTANTLY
SENSING THE CONCENTRATION OF CALCIUM IONS IN THE BLOOD
FLOWING THROUGH THEM.

17. WHEN THE PLASMA CALCIUM CONCENTRATION RISES
THYROID GLAND INCREASE SECRETION OF CALCITONIN, REDUCE RATE OF
PARATHYROID HORMONE SECRETION INTO THE BLOOD
CALCITONIN STIMULATE THE SKELETON TO REMOVE CALCIUM FROM THE
BLOOD PLASMA AND DEPOSITED
THE REDUCED LEVELS OF PTH INHIBIT REMOVAL OF CALCIUM FROM THE
SKELETON, INCREASE THE LOSS OF CALCIUM IN THE URINE,INHIBIT THE LOSS
OF PHOSPHATE IONS, FORM INSOLUBLE SALTS WITH CALCIUM IONS,
REMOVING THEM FROM THE BLOOD
LOW LEVELS OF PTH ALSO INHIBIT THE FORMATION OF CALCITRIOL BY
THE KIDNEYS, INHIBITING ABSORBTION OF CALCIUM FROM THE INTESTINE

18. WHEN THE PLASMA CALCIUM CONCENTRATION FALL
CALCITONIN SECRETION IS INHIBITED AND PTH SECRETION IS
STIMULATED, CALCIUM BEING REMOVED FROM BONE TO RAPIDLY
CORRECT THE PLASMA CALCIUM LEVEL.
THE HIGH PLASMA PTH LEVELS INHIBIT CALCIUM LOSS IN THE URINE
WHILE STIMULATING THE EXCRETION OF PHOSPHATE IONS
THEY STIMULATE THE KIDNEYS TO MANUFACTURE CALCITRIOL,
ENHANCES THE ABILITY OF THE GUT TO ABSORB CALCIUM FROM THE
INTESTINE
THE PTH STIMULATED PRODUCTION OF CALCITRIOL ALSO CAUSES
CALCIUM TO BE RELEASED FROM BONE INTO THE BLOOD

19. GASTROINTESTINAL HORMONES
GASTRIN
SECRETED: “G” CELLS OF ANTRUM OF STOMACH
STIMULI: MEAL, DISTENTION OF STOMACH, PROTEINS AND GASTRIN
RELEASING PEPTIDE
ACTIONS: GASTRIC ACID SECRETION, GROWTH OF GASTRIC MUCOSA
CHOLECYSTIKININ
SECRETED: “I” CELLS IN THE MUCOSA OF THE DUODENUM AND
JEJUNUM
STIMULI: FAT, FATTYACIDS AND MONOGLYCERIDES
ACTIONS: BILE, INHIBIT STOMACH CONTRACTION AND APPETITE

20. SECRETIN
SECRETED: “S”CELLS IN THE MUCOSA OF THE DUODENUM, STIMULI: ACIDIC
GASTRIC JUICE
ACTIONS: PANCREATIC SECRETION OF BICARBONATE, NEUTRALIZE ACID IN
SMALL INTESTINE
GASTRIC INHIBITORY PEPTIDE
SECRETED: MUCOSA OF UPPER SMALL INTESTINE, STIMULI: FATTY ACIDS,
AMINO ACIDS, LESSER EXTENT TO CARBOHYDRATES
ACTIONS: DECREASE STOMACH MOTILITY, INSULIN SECRETION
MOTILIN
SECRETED: STOMACH AND UPPER DUODENUM, STIMULI: FASTING
ACTIONS: INCREASE GASTROINTESTINAL MOTILITY, WAVES OF
GASTROINTESTINAL MOTILITY (90 MIN)