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ENDOCRINE SYSTEM

1.

LIST THE MAJOR ORGANS OF THE ENDOCRINE SYSTEM.

2.

DEFINE EACH OF THE FOLLOWING TERMS:

A. ENDOCRINE

B. EXOCRINE

C. ENDOCRINOLOGY

D. HORMONES

E. TARGET CELLS

F. RECEPTOR SITES

3. BE ABLE TO DEFINE THREE CHEMICAL GROUPS OF HORMONES AND GIVE AT LEAST TWO EXAMPLES FOR EACH GROUP.

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4. WRITE A SHORT EXPLANATION OF THE USE OF RECEPTOR SITES AND MESSENGERS IN THE OPERATION OF HORMONES AS THEY MOVE THROUGH THE PLASMA MEMBRANES OF CELLS.

5. DEFINE PROSTAGLANDINS. LIST A TLEAST FIVE EXAMPLES OF THEIR EFFECTS ON THE BODY AND ITS ACTIVITIES.

6. THE FOLLOWING IS A SUMMARY OF THE MATERIALS TO BE STUDIED FOR VARIOUS GLANDS OF THE ENDOCRINE SYSTEM:

I. ANTERIOR LOBE OF THE PITUITARY GLAND (ADENOHYPOPHYSIS) RECEIVES IMPULSES FROM THE HYPOTHALAMUS TO RELEASE HORMONES.

(A) GROWTH HORMONE (GH OR STH) EFFECTS= GROWTH, PROTEIN ANABOLISM, BONE AND MUSCLE DEVELOPMENT, MOBILIZES FATS AND SPARES GLUCOSE.

HYPERSECRETION= DURING GROWTH YEARS LEADS TO GIGANTISM; AFTER GROWTH YEARS LEADS TO ACROMEGALY.

HYPOSECRETION= DURING GROWTH YEARS LEADS TO DWARFISM. PAGE 3 (B) THYROID STIMULATING HORMONE (TSH) EFFECT= CONTROLS SECRETION OF HORMONES BY THE THYROID GLAND. HYPERSECRETION= GRAVES DISEASE (BULGING EYEBALLS, SWOLLEN THYROID OR GOITER, TACHYCARDIA, TREMOR OF HANDS AND FINGERS, IRRITABILITY, VOMITING AND DIARRHEA.) THE RATE IS HIGHER IN FEMALES. HYPOSECRETION= CRETINISM IN CHILDREN (CONGENITAL CONDITION). DYSTROPHY OF BONES AND SOFT PARTS, LACK OF MENTAL/PHYSICAL DEVELOPMENT, LOWERED BMR. MAY LEAD TO SEVERE MENTAL ILLNESS.

(C) ADRENOCORTICOITROPIC HORMONE (ACTH) EFFECT= ADRENAL CORTEX SECRETIONS (LIMITED)

HYPERSECRETION= CUSHINGS SYNDROME (FATIGUE, FAT GAIN, IMPOTENCE, AMENORRHEA, EDEMA, EXC ESSIVE HAIR GROWTH, DIABETES MELLITUS, OSTERPOROSIS.

HYPOSECRETION= RARE

(D) FOLLICLE STIMULATING HORMONE (FSH) EFFECT= OVA DEVELOPMENT WITHIN THE FOLLICLE AND INCREASE IN ESTROGEN LEVELS IN FEMALES. IN MALES STIMULATES TESTES TO PRODUCE SPERM.

HYPERSECRETION= NONE HYPOSECRETION= FAILURE TO DEVELOP SEXUALLY (AFFECTS OVA AND SPERM PRODUCTION)

PAGE 4 (E) PROLACTIN (LACTOGENIC HORMONE) EFFECT= WORKS WITH OTHER HORMONES TO MAINTAIN MILK SECRETION. HYPERSECRETION= STOPS MENSES IN FEMALES; IMPOTENCE IN MALES. HYPOSECRETION= POOR MILK PRODUCTION IN NURSING MOTHERS.

(F) LUTEINIZING HORMONE (LH) EFFECT= IN FEMALE OVARIES, CAUSES OVULATION AND PROGESTERONE PRODUCTION; IN MALES, PROMOTES TESTOSTERONE PRODUCTION BY TESTES.

HYPERSECRETION= NONE

HYPOSECRETION= FAILURE TO DEVELOP SEXUALLY (FAILURE TO MAINTAIN PREGNANCY.

II. POSTERIOR LOBE OF THE PITUITARY GLAND (NEUROHYPOPHYSIS) -ALSO CONTROLLED BY THE HYPOTHALAMUS AND NERVE FIBERS THAT PASS FROM THE HYPOTHALAMUS THROUGH THE INFUNDIBULUM (STALK).

(A) OXYTOCIN

EFFECT= STIMULATES UTERINE CONTRACTIONS; INITIATES LABOR AND AIDS IN LACTATION. HYPERSECRETION= NONE HYPOSECRETION= NONE PAGE 5 (B) ANTIDIURETIC HORMONE (ADH) (VASOPRESSIN) EFFECT= REABSORPTION OF WATER BY THE KIDNEYS. HYPERSECRETION= NONE HYPOSECRETION= DIABETES INSIPIDUS (POLYDIPSIA, POLYURIA, URINE OUTPUT AROUND 5-10 LITERS PER 24 HOUR DAY), WEAKNESS, DRY SKIN. TREATABLE WITH VASOPRESSIN VIA INJECTION, NASAL SPRAY OR PATCH.

III. THYROID GLAND (A) THYROXINE (T4) AND TRIIODOTHYRONINE (T3) EFFECT= REGULATES METABOLISM, GROWTH, DEVELOPMENT AND NERVOUS SYSTEM ACTIVITY. HYPERSECRETION= GRAVES DISEASE (EXOPTHALMIC GOITER). IF IODINE DEFICIENCY, MAY CAUSE SIMPLE GOITER. HYPOSECRETION= CRETINISM IN CHILDREN; MYXEDEMA IN ADULTS.

(B) CALCITONIN (THYROCALCITONIN) EFFECT= LOWERS BLOOD CALCIUM LEVELS. ACCELERATES BONE ABSORPTION OF CALCIUM. [DEC. BLOOD CALCIUM AND INC. BONE DEPOSITON] ALSO INCREASES CALCIUM AND PHOPHATE RELEASE BY THE KIDNEYS INTO URINE. HYPERSECRETION= NONE

HYPOSECRETION= NONE

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IV. PARATHYROID GLANDS (A) PARATHORMONE (PARATHYROID HORMONE) (PTH) EFFECT= INCREASES BLOOD CALCIUM LEVELS AND DECREASES BLOOD PHOSPHATE LEVELS. INCREASE OF CALCIUM ABSORPTION FROM THE GASTROINTESTINAL TRACT INTO THE BLOOD. ALSO INCREASES CALCIUM ABSORPTION BY THE KIDNEYS AND PHOSPHATE EXCRETION INTO URINE. ACTIVATES VITAMIN D.

[INC. BLOOD CALCIUM AND DEC. BONE DEPOSITION]

HYPERSECRETION= HYPERPARATHYROIDISM (HIGH BLOOD CALCIUM LEVELS. LEADS TO OSTEITIS FIBROSA CYSTICA OR CAVITIES IN BONE TISSUE. EASY BONE FRACTURE, KIDNEY STONES, CALCIUM DEPOSITS IN ORGANS, MOTHBALL X-RAYS OF BONE.

HYPOSECRETION= HYPOPARATHYROIDISM (HYPOCALCEMIA, NEURON EXCITABILITY, MUSCLE SPASMS, CONVULSIONS, POSSIBLE LARYNX SPASMS, RESPITATORY PARALYSIS, TETANY AND DEATH IF UNTREATED.

PAGE 7 V. SUPRARENAL GLANDS (ADRENALS) ADRENAL CORTEX (ABOUT TWO DOZEN STEROIDS PRODUCED HERE). (A) MINERALOCORTICOIDS (PRIMARILY ALDOSTERONE MADE IN THE ZONA GLOMERULOSA) EFFECT= IN KIDNEYS, CAUSES SODIUM AND WATER RETENTION INTO BLOOD; CAUSES POTASSIUM BLOOD LEVELS TO DECREASE. BLOOD VOLUME AND BLOOD PRESSURE WILL INCREASE. HYPERSECRETION= ALDOSTERONISM (HYPERTENSION, EDEMA, POTASSIUM LOSS LEADING TO NERVE AND MUSCLE DISORDERS, TETANY, PARALYSIS, POLYURIA, POLYDIPSIA, CARDIAC IRREGULARITY. HYPOSECRETION= ADDISONS DISEASE (WEIGHT LOSS, BLACK FRECKLES ON HEAD AND NECK, DECREASED GLUCOSE AND SODIUM IN BLOOD, WATER LOSS, HYPOTENSION, SEVERE DEHYDRATION, FATIGUE, NAUSEA, VOMITING, ANOREXIA, SOMETIMES HYPOGLYCEMIA, POSSIBLE DEATH IF UNTREATED. TREATMENT IS WITH CORTICOSTEROIDS.

(B) GLUCOCORTICOIDS (MAINLY CORTISOL PRODUCED BY THE ZONA FASCICULATA) LIVER CONVERTS SOME CORTISOL INTO CORTISONE. EFFECT= GLUCONEOGENESIS, HYPERGLYCEMIA, FAT MOBILIZATION, PROTEIN CATABOLISM. HELPS BODY TO RESIST STRESS, DEPRESSED IMMUNE AND INFLAMMATORY RESPONSES.

HYPERSECRETION= CUSHINGS SYNDROME

HYPOSECRETION= ADDISONS DISEASE

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(C) GONADOCORTICOIDS (MAINLY ANDROGENS AND ESTROGENS

PRODUCED IN THE ZONA RETICULARIS).

AMOUNTS NORMALLY SO LOW THEY MAY HAVE LITTLE EFFECT. EFFECT= GENERALLY NO EFFECT ON ADULTS; HOWEVER, MAY INFLUENCE FEMALE LIBIDO AND BE ESTROGEN AFTER MENOPAUSE.

SOURCE

HYPERSECRETION= ANDROGENS (1) ANDROGENITAL SYNDROME IN YOUNG PREPUBERTY MALES. IT CAUSES MASCULINIZATION, SECONDARY SEX CHARACTERISTICS, ORGAN MATURITY, SEXUAL DESIRE. ALL OF THESE MAY OCCUR AT AN EARLIER AGE THAN , NORMAL. (2) IN YOUNG PREPUBERTY FEMALES, THIS MAY CAUSE BEARD GROWTH, BODY HAIR, DEEP VOICE, MUSCLE DEVELOPMENT, CLITORIS GROWS TO SMALL PENIS. MASCULINIZATION OF FEMALE.

HYPERSECRETION= ESTROGENS AS FEMINIZING HORMONES (1) IN YOUNG FEMALE, MAY LEAD TO EARLY DEVELOPMENT OF SECONDARY SEX CHARACTERISTICS.
(2) IN YOUNG MALE, MAY LEAD TO GYNECOMASTIA (EXCESSIVE

BREAST DEVELOPMENT).

PAGE 9 ADRENAL MEDULLA (A) EPINEPHRINE (80%) AND NOREPINEPHRINE (20%) -COLLECTIVELY CALLED CATACHOLAMINES. -SIMILAR IN ACTION EXCEPT EPINEPHRINE IS MORE POTENT ON HEART AND METABOLISM WHILE NOREPINEPHRINE IS MORE ACTIVE ON BLOOD PRESSURE AND VASOCONSTRICTION. EFFECT= STIMULATES ORGANS VIA SYMPATHETIC DIVISION. INCREASES HEART RATE, BLOOD PRESSURE , CAUSES VASOCONSTRICTION, DILATION OF BRONCHI AND BRONCHIOLES, RELIEVES ASTHMA. HYPERSECRETION= HYPERTENSION, TACHYCARDIA, HYPERGLYCEMIA, INCREASED BMR, NERVOUSNESS AND PERSPIRATION. HYPOSECRETION= NONE

VI. PANCREAS (ISLETS OF LANGERHANS) (A) GLUCAGON - PRODUCED BY ALPHA CELLS OF THE ISLETS. - 1 MOLECULE CAN RELEASE 100 MILLION MOLECULES OF GLUCOSE INTO BLOODSTREAM. EFFECT= INCREASES BLOOD SUGAR LEVEL, INCREASES GLYCOGENOLYSIS,

INCREASES GLUCONEOGENESIS. HYPERSECRETION= NONE HYPOSECRETION= NONE PAGE 10 (B) INSULIN (PRODUCED BY BETA CELLS OF THE ISLETS). EFFECTS= LOWERS BLOOD SUGAR LEVEL, INCREASES GLYCOGENESIS, DECREASES GLYCOGENOLYSIS AND GLUCONEOGENESIS, INCREASES LIPOGENESIS AND PROTEIN SYNTHESIS. HYPERSECRETION= HYPERINSULINISM (HYPOGLYCEMIA, TREMORS, DIPLOPIA, HUNGER, WEAKNESS, DISORIENTATION, CONVULSIONS, STAGGERING, UNCONSCIOUSNESS, POSSIBLE DEATH (ASSOCIATED WITH INSULIN SHOCK IF INDUCED BY INJECTION).

HYPOSECRETION= DIABETES MELLITUS

TYPE 1 (10%)= JUVENILE ONSET OR INSULIN-DEPENDENT DIABETES. OCCURS ABRUPTLY, USUALLY BEFORE AGE 15, REQUIRES INSULIN INJECTIONS. TRIGGERED BY VIRAL INFECTIONS AND AUTOIMMUNE RESPONSE PROBLEMS. (1) FATS BREAKDOWN RAPIDLY = KETOSIS (A FORM OF ACIDOSIS). (2) HYPERGLYCEMIA OCCURS (NEED INSULIN).
(3) MAY LEAD TO HEART ATTACKS, GANGRENE, STROKES,

ATHEROSCLEROSIS, BLINDNESS, IMPOTENCE, LOSS OF BLADDER CONTROL. TYPE 2 (90%)= MATURITY ONSET OR NON-INSULIN DEPENDENT. USUALLY OCCURS AFTER AGE 40, HEREDITARY, PATIENTS ARE USUALLY OVERWEIGHT.* SYMPTOMS CAN USUALLY BE CONTROLLED BY DIET AND EXERCISE. PATIENT MUST WATCH WEIGHT AS OBESITY MAKES

INSULIN SENSITIVE TO INSULIN.

RECEPTORS BECOME LESS

*SOMETIMES SUDDEN, SEVERE WEIGHT LOSS AND EXTREME FATIGUE MAY ALSO SIGNAL THIS PROBLEM. PAGE 11 VII. OVARIES (A) ESTROGENS EFFECT= FEMALE SECONDARY SEX CHARACTERISTICS, REGULATE MENSTRUAL CYCLE, HELP TO MAINTAIN PREGNANCY. HYPERSECRETION= NONE HYPOSECRETION= LACK OF FEMALE SECONDARY SEX CHARACTERISTICS. (B) PROGESTERONE EFFECT= HELPS TO MAINTAIN PREGNANCY. HYPERSECRETION= NONE HYPOSECRETION= INABILITY TO MAINTAIN PREGNANCY (ASSOCIATED WITH OTHER HORMONAL AND PHYSICAL PROBLEMS).

VIII. TESTES (A) TESTOSTERONE EFFECT= MALE SECONDARY SEX CHARACTERISTICS HYPERSECRETION= NONE HYPOSECRETION= LACK OF MALE SECONDARY SEX CHARACTERISTICS.

(B) INHIBIN

EFFECT= INHIBITS SECRETION OF FSH TO CONTROL SPERM PRODUCTION. HYPERSECRETION= NONE HYPOSECRETION= NONE PAGE 12 IX. PINEAL GLAND (A) MELATONIN EFFECT= POSSIBLE CONTROL OF DAY/NIGHT CYCLES AND INHIBITING TOO EARLY SEXUAL MATURATION. MAY AFFECT APPETITE, BODY TEMPERATURE, MOOD, AND MAY HAVE A SEDATIVE EFFECT.

NO HYPERSECRETION OR HYPOSECRETION KNOWN.

X. THYMUS (A) THYMOIN, ETC. EFFECT= AIDS IN THE DEVELOPMENT OF IMMUNE SYSTEM (DEVELOPMENT OF T-CELLS AIN EARLY LIFE).

NO HYPERSECRETION OR HYPOSECRETION KNOWN.

XI. PLACENTA (A) HUMAN CHORIONIC GONADOTROPHIN (HCG)

EFFECT= MAINTAINS PREGNANCY BY PROMOTING GROWTH OF CORPUS LUTEUM DURING PREGNANCY. GENERALLY

DECLINES IN IMPORTANCE AFTER FOURTH MONTH.

NO HYPERSECRETION OR HYPOSECRETION KNOWN.

PAGE 13 DIGESTIVE HORMONES

(1) GASTRIN PROMOTES GASTRIC JUICE SECRETION.

(2) ENTEROGASTERONE INHIBITS GASTRIC JUICE SECRETION.

(3) SECRETIN EXCITED FLOW OF PEPSINOGEN AND PANCREATIC BICARBONATE (FLUID); INHIBITS HCl SECRETION.

(4) PANCREOZYMIN STIMULATES SECRETION OF PANCREATIC ENZYMES.

(5) CHOLECYSTOKININ STIMULATES CONTRACTION OF THE GALLBLADDER TO RELEASE BILE.

ADDITIONAL CHEMICALS

(1) ANGIOTENSIN ELEVATES PERIPHERAL BLOOD PRESSURE, STIMULATES ADRENAL CORTEX TO SECRETE ALDOSTERONE.

(2) HISTAMINES VASODILATION, HELP PROMOTE INFLAMMATORY RESPONSE.

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WRITE A SHORT FLOW CHART DESCRIBING THE ACTION OF RENIN. USE THE TERMS ANGIOTENSINOGEN, ANGIOTENSIN I, ANGIOTENSIN II, AND ANGIOTENSIN CONVERTING ENZYMES (ACES). ALSO EXPLAIN WHICH STAGE OF THIS PROCESS IS BLOCKED BY THE ACTION OF ACE INHIBITORS.