HORMONES OF THE ENDOCRINE SYSTEM

HORMONES OF THE ENDOCRINE SYSTEM

HORMONES OF THE PITUITARY
NEUROHYPOPHYSIS--POSTERIOR PITUITARY ADENOHYPOPHYSIS--ANTERIOR PITUITARY

HORMONES OF THE NEUROHYPOPHYSIS
STORES AND SECRETES NEUROHORMONES PRODUCED BY HYPOTHALAMUS ANTIDIURETIC HORMONE OXYTOCIN

ANTIDIURETIC HORMONE ADH VASOPRESSIN PREVENTS DIURESIS (LOSS OF URINE)
CONSTRICTS ARTERIOLES AND RAISES BLOOD PRESSURE SYNTHESIZED IN SUPRAOPTIC NUCLEI OF HYPOTHALAMUS CARRIED IN HYPOTHALAMOHYPOPYSEAL TRACT STORED IN AXON TERMINALS IN PITUITARY

ANTIDIURETIC EFFECT AFFERENT VAGAL NERVES
DROP IN PRESSURE STIMULATES ADH SECRETION INCREASE IN PRESSURE INHIBITS SECRETION

FACTORS THAT INCREASE ADH SECRETION
EMOTIONAL STRESS PHYSICAL STRESS BLOOD VOLUME INCREASED PLASMA OSMOTIC PRESSURE DECREASED EXTRACELLULAR FLUID VOLUME STRENUOUS EXERCISE NICOTINE AND BARBITUATES

FACTORS THAT DECREASE ADH SECRETION
DROP IN PLASMA OSMOTIC PRESSURE INCREASED EXTRACELLULAR FLUID VOLUME ALCOHOL

DIABETES INSIPIDUS POLYURIA POLYDYPSIA LOSS OF ADH RELEASE
IMPAIRED WATER CONSERVATION EXCESSIVE WATER LOSS IN URINE

OXYTOCIN WOMEN MEN

OXYTOCIN IN WOMEN STIMULATES SMOOTH MUSCLE IN UTERUS
PROMOTES LABOR AND DELIVER STIMULATES MYOEPITHELIAL CELLS OF MAMMARY GLANDS

OTHER SOURCES OF OXYTOCIN
FETUS UTERUS

NEUROENDOCRINE REFLEXES CONTROL

OXYTOCIN IN MALES UNCERTAIN
STIMULATES SMOOTH MUSCLE CONTRACTIONS IN DUCTUS DEFERENS AND PROSTATE

OXYTOCIN AND SEX AROUSAL AND ORGASM EMISSION
CONTRACTIONS THAT PROMOTE SPERM TRANSPORT

HORMONES OF THE HYPOTHALAMUS & ADENOHYPOPHYSIS
RELEASING AND INHIBITING HORMONES FROM THE HYPOTHALAMUS TRH CRH GnRH GnIH PRH/PIH GH-RH/SOMATOSTATIN ADENOHYPOPHYSEAL HORMONES TSH ACTH FSH LH PRL GH MSH LIPOTROPIN

THYROID STIMULATING HORMONE
THYROTROPIN RELEASE REGULATED BY THYROTROPIN RELEASING HORMONE (TRH) TARGET CELLS IN THYROID TRIGGERS RELEASE OF THYROID HORMONE

ADRENOCORTICOTROPIC HORMONE
DERIVED FROM PROOPIMELANOCORTIN INCREASES SECRETION OF ADRENAL HORMONES BINDS TO MELANOCYTES AND INCREASE PIGMENTATION OF SKIN

OTHER SUBSTANCES DERIVED FROM PROOPIMELANOCORTIN
LIPOTROPINS BETA ENDORPHINS MELANOCYTE STIMULATING HORMONE

LIPOTROPINS SECRETED FROM SAME CELLS AS ACTH
BIND TO MEMBRANE RECEPTORS OF ADIPOSE CELLS CAUSE FAT BREAKDOWN & RELEASE OF FATTY ACIDS INTO CIRCULATION

BETA ENDORPHINS SAME EFFECT AS OPIATES
IMPORTANT FOR ANALGESIA IN RESPONSE TO STRESS AND EXERCISE MAY BE INVOLVED IN BODY TEMPERATURE FOOD INTAKE WATER BALANCE STRESS INCREASES SECRETION ALONG WITH ACTH

MELANOCYTE STIMULATING HORMONE
BINDS TO MELANOCYTES STIMULATES DEPOSITION OF MELANIN NOT WELL UNDERSTOOD IN HUMANS IMPORTANT REGULATOR IN OTHER VERTEBRATES PRODUCED IN PARS INTERMEDIA IN HUMANS PARS INTERMEDIA MERGES WITH PARS DISTALIS

RELATIONSHIP BETWEEN MELANOCYTE STIMULATING HORMONE AND ACTH
MSH IS SECRETED ALONG WITH ACTH USUALLY NOT IN QUANTITIES LARGE ENOUGH TO HAVE A SIGNIFICANT EFFECT MAY BE SIGNIFICANT IN ADDISON’S DISEASE

GONADOTROPINS

GONADOTROPINS HORMONES PROMOTE GROWTH AND FUNCTION OF GONADS
LUTEINIZING HORMONE FOLLICLE STIMULATING HORMONE

PROLACTIN IN FEMALES STIMULATES THE DEVELOPMENT OF DUCT SYSTEM IN MAMMARY GLANDS WITH OTHER HORMONES STIMULATES MILK PRODUCTION USUALLY INHIBITED BY PROLACTIN INHIBITING HORMONE STIMULATED BY PROLACTIN RELEASING HORMONE

PROLACTIN IN MALES MAKES INTERSTITIAL CELLS MORE RESPONSIVE TO LUTEINIZING HORMONE

GROWTH HORMONE SECRETION STIMULATED BY GROWTH HORMONE RELEASING HORMONE SECRETION INHIBITED BY GROWTH HORMONE INHIBITING HORMONE/SOMATOSTATIN

GROWTH HORMONE STIMULATES GROWTH OF CARTILAGE AND BONE
INDIRECT EFFECTS DIRECT EFFECTS

INDIRECT EFFECTS SOMATOMEDINS /INSULIN-LIKE GROWTH FACTORS
PEPTIDE HORMONES BIND TO MEMBRANE RECEPTORS SKELETAL MUSCLE, CARTILAGE AND OTHER TARGET CELLS

DIRECT EFFECTS STIMULATES STEM CELL DIVISION AND GROWTH OF DAUGHTER CELLS

EFFECTS OF GROWTH HORMONE ON METABOLISM
INCREASED PROTEIN SYTHESIS INCREASED MOBILIZATION OF FATTY ACIDS FROM ADIPOSE TISSUE INCREASED USE OF FATTY ACIDS FOR ENERGY DECREASED USE OF GLUCOSE THROUGHOUT BODY SPARING GLUCOSE FOR THE BRAIN

EFFECTS OF GROWTH HORMONE ON PROTEIN SYNTHESIS
AMINO ACID TRANSPORT AT THE CELL PROTEIN SYNTHESIS BY RIBOSOMES INCREASED LEVELS OF RNA DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS

AMINO ACID TRANSPORT AT THE CELL
ENHANCES TRANPORT OF AMINO ACIDS WORKS WITH INSULIN INCREASED AMINO ACID LEVELS LEAD TO INCREASED PROTEIN SYNTHESIS

PROTEIN SYNTHESIS BY RIBOSOMES
DIRECT EFFECT ON RIBOSOMES

INCREASED LEVELS OF RNA
INCREASES TRANSCRIPTION RATE OVER TIME INCREASES LEVELS OF RNA INCREASED RNA MEANS INCREASED PROTEIN SYNTHESIS

DECREASED CATABOLISM OF PROTEINS AND AMINO ACIDS
DECREASE IN BREAKDOWN OF PROTEINS TO AMINO ACIDS DECREASE OF USE OF AMINO ACIDS FOR ENERGY SOURCE MAY BE DUE TO MOBILIZATION OF FATTY ACIDS SPARING PROTEIN

EFFECTS OF GROWTH HORMONE ON FAT METABOLISM
CAUSE LIPOLYSIS AND THE RELEASE OF FATTY ACIDS INTO BODY FLUIDS AND CIRUCLATION ENHANCES CONVERSION OF FATTY ACIDS TO ACETYL CO A INCREASES USE OF ACETYL CO A FOR ENERGY FAT METABOLISM FAVORED OVER CARBOHYDRATE AND PROTEIN METABOLISM

GROWTH HORMONE STIMULATES FATTY ACID METABOLISM
SPARES GLUCOSE AND AMINO ACIDS

EFFECTS OF GROWTH HORMONE ON CARBOHYDRATE METABOLISM
DECREASES USE OF GLUCOSE FOR ENERGY ENHANCES GLYGOGENESIS DIMINISHES GLUCOSE UPTAKE BY CELLS

DECREASED USE OF GLUCOSE FOR ENERGY
PERHAPS DUE TO INCREASED MOBILIZATION AND UTILIZATION OF FATS

ENHANCES GLYCOGENOGENESIS
GLUCOSE WILL BE STORED AS GLYCOGEN RESERVES RAPIDLY FILL UP

DIMINISHED GLUCOSE UPTAKE BY CELLS
INITIAL INCREASED GLUCOSE UPTAKE UNTIL GLYCOGEN RESERVE IS FILLED THEN UPTAKE DIMINISHES GREATLY INCREASED BLOOD GLUCOSE LEVELS

SECRETION OF GROWTH HORMONE
3 NANOGRAMS IN ADULT 5 NANOGRAMS IN CHILD REGULATED BY GH-RH AND SOMATOSTATIN

FEEDBACK CONTROL OF GROWTH HORMONE SECRETION

HORMONES OF THE THYROID GLAND
THYROID HORMONE AND CALCITONIN .

THYROID HORMONE THYROXINE (T4 ) TRIIODOTHRYONINE (T3 )

IMPORTANCE OF THYROGLOBULIN
GLYCOPROTEIN CONTAINS 140 TYROSINE AMINO ACIDS SUBSTRATE IODINE BINDS WITH HORMONES FORM WITHIN THYROGLOBULIN MOLECULE

IMPORTANCE OF IODINE USED ONLY TO MAKE THYROID HORMONES
STORED IN THYROID IDODIDE PUMP TRAPS IODIDE

THE WEDDING OF THYROGLOBULIN AND IODIDE IONS
OCCURS AT THE COLLOID-CELL INTERFACE AS THYROGLOBULIN IS SECRETED

MIT AND DIT MONOIODTYROSINE DIIODOTYROSINE THYROXINE TRIIODOTHRYRONINE

THYROGLOBULIN STORAGE
IN COLLOID OF FOLLICLE ONLY HORMONE STORED EXTRACELLULARLY 1-3 MONTH SUPPLY IN COLLOID

RELEASE OF THYROID HORMONE INTO THE BLOOD
THYROGLOBULIN IS PICKED UP BY FOLLICULAR CELLS LYSOSOMES FUSE WITH PINOCYTIC VESICLES THYROXINE AND TRIIODOTHYRONINE ARE CLEAVED FROM THRYOGLOBULIN AND RELEASED

TRANSPORT IN THE BLOOD THRYOXINE BINDING GLOBULIN ALBUMINS

THYROID HORMONES AT THE CELLS
ENTERS CELLS BINDS WITH INTRACELLULAR PROTEIN RECEPTOR THYROXINE HAS GREATER AFFINITY

IMPORTANCE OF LATENCY AND DURATION OF ACTION
T4 -- TWO OR THREE DAY LATENT PERIOD MAXIMUM ACTIVITY IN DAYS T TO 12 HOURS MAXIMUM ACTIVITY IN 2-3 DAYS

MAJOR EFFECTS OF THYROID HOROMONE
GROWTH IN CHILDREN INCREASE IN METABOLIC RATE

EFFECTS ON GROWTH LACK OF THRYOID HORMONE RETARDS GROWTH
EXCESS OF THYROID HORMONE ENHANCES GROWTH IN CHILD CAUSES EPIPHYSEAL PLATES TO CLOSE PREMATURELY SO FINAL HEIGHT MAY BE SHORTENNED

GENERALIZED EFFECTS ON METABOLISM
AFFECT METABOLISM OF ALMOST ALL CELLS OF BODY CALORIGENIC EFFECT

EFFECT OF THYROID HORMONE ON PROTEIN SYNTHESIS
PHASE ONE--INCREASED TRANSLATION PHASE TWO--INCREASED TRANSCRIPTION

EFFECT OF THYROID HORMONE ON CELLULAR ENZYME SYSTEMS
INCREASED PROTEIN SYNTHEIS RESULTS IN INCREASED CELLULAR ENZYMES AS MUCH AS 6 TIMES NORMAL

EFFECTS ON CELLULAR ORGANELLES
INCREASED ACTIVITY OF MITOCHONDRIA INCREASED NUMBER OF MITOCHONDRIA

EFFECTS ON ACTIVE TRANSPORT
Na-K ATPase PUMPS INCREASE INCREAED TRANSPORT OF SODIUM AND POTASSIUM

EFFECTS ON CARBOHYDRATE METABOLISM
RAPID UPTAKE OF GLUCOSE INCREASED GLYCOLYSIS INCREASED GLUCONEOGENESIS INCREASED GI ABSORPTION INCREASED INSULIN SECRETION

EFFECT ON FAT METABOLISM
LIPOGENESIS LIPOLYSIS MOBILIZATION OF LIPIDS

EFFECTS ON BODY MASS INCREASED THYROID HORMONE DECREASES
DECREASED THYROID HORMONE INCREASES

EFFECTS ON CARDIOVASCULAR SYSTEM
INCREASED OXYGEN DEMAND INCREASED METABOLIC WASTE PRODUCTS CAUSE VASODILATION NEED FOR HEAT ELIMINATION ALSO CAUSES VASODILATION CARDIAC OUTPUT CAN INCREASE BY 50%

EFFECTS ON RESPIRATION
INCREASED OXYGEN DEMAND INCREASED CARBON DIOXIDE LEVELS ACTIVATE MECHANISMS THAT INCREASE THE RATE AND DEPTH OF RESPIRATION

EFFECT ON GASTROINTESTINAL TRACT
INCREASE ABSORPTION RATE INCREASES SECRETION OF DIGESTION JUICES INCREASES MOTILITY OF GASTROINTESTINAL TRACT TO MUCH MAY LEAD TO DIARRHEA TO LITTLE CONSTIPATION

EFFECT ON THE CENTRAL NERVOUS SYSTEM
NORMAL AMOUNTS INCREASE CEREBRATION TO LITTLE DECREASES CEREBRATION TO MUCH -- EXTREME NERVOUSNESS, PSYCHONEUROTIC TENDENCIES, MUSLE TREMOR, TIREDNESS BUT INABILITY TO SLEEP TO LITTLE -- MENTAL SLUGGISHNESS EXTREME SOMNOLENCE

SECRETION OF THYROID HORMONE
TSH FROM ADENOHYPOPHYSIS STIMULATES ITS SECRTION TRH STIMULATES TSH SECRETION

NEGATIVE FEEDBACK CONTROLS OF THYROID HORMONE RELEASE
LONG FEED BACK LOOPS SHORT FEEDBACK LOOPS

LONG FEEDBACK LOOP INHIBITORY EFFECTS OF TARGET ORGANS ON ADENOHYPOPHYSIS THYROID HORMONES COULD ACT ON HYPOTHALAMUS AND INHIBIT SECRETION OF TRH THYROID HORMONE COULD ACT ON ADENOHYPOPHYSIS AND INHIBIT ITS RESPONSE TO RELEASING HORMONES

SHORT FEEDBACK LOOPS PITUITARY HORMONES THEMSELVES INFLUENCE SECRETION OF RELEASING OR INHIBITING HORMONES

THYROID STIMULATING HORMONE
HIGH SECRETION OF TSH MAY INHIBIT SECRETION OF TRH

SPECIFIC EFFECTS OF TSH
INCREASED PROTEOLYTIC ACTIVITY IN FOLLICLES INCREASED RELEASE OF THYROID HORMONE INTO BLOOD STREAM INCREASED TRAPPING OF IODIDE IONS INCREASED IODINATION OF TYROSINE INCREAS`E IN SIZE AND ACTIVITY OF FOLLICULAR CELLS INCREASED NUMBER OF FOLLICULAR CELLS

REGULATION OF THRYOID HORMONE SECRETION
TSH FROM PITUITARY STIMULATES SYNTHESIS AND RELEASE TRH PROMOTES TSH RELEASE NEGATIVE FEED BACK

CALCITONIN POLYPEPTIDE PRODUCED BY PARAFOLLICULAR CELLS
LOWERS BLOOD CALCIUM AND PHOSPHATE LEVELS SUPRESSES BONE RESORPTION INCREASES BONE FORMATION IMPORTANT IN BONE REMODELING

HOW CALCITONIN REDUCES BLOOD CALCIUM LEVELS
DECREASES OSTEOLYTIC EFFECT FAVORS DEPOSITION RATHER THAN RESORPTION INCREASES ACTIVITY OF OSTEOBLASTS PREVENTS FORMATION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS

CHILDREN VS ADULTS MAJOR ROLE IN CHILD MINOR ROLE IN ADULTS

REGULATION OF CALCITONIN SECRETION
10% RISE IN PLASMA CALCIUM LEVELS LEADS TO 3-6 TIMES MORE CALCITONIN

OTHER IMPORTANT EFFECTS OF CALCITONIN
REDUCES LOSS OF BONE MASS DURING PROLONGED STARVATION LATE STAGES OF PREGNANCY

DIFFERENCES BETWEEN CALCITONIN AND PARATHYROID HORMONE
CALCITONIN MORE RAPID SHORT TERM REGULATOR

REGULATION OF SECRETION
PLASMA LEVELS OF CALCIUM HIGH CONCENTRATION -- INCREASED SECRETION LOW CONCENTRATION -- DECREASED SECRETION GASTRIN AND OTHER INTESTINAL HORMONES EFFECT SECRETION

PARATHYROID GLAND SMALL FLATTENED GLANDS
POSTERIOR SURFACE OF THYROID GLAND

CELLS OF PARATHYROID CHIEF CELLS OXYPHIL CELLS

PARATHYROID HORMONE PTH POLYPEPTIDE TWO OR THREE FORMS
PRINCIPAL CONTOLLER OF CALCIUM AND PHOSPHATE IN BLOOD INCREASES PLASMA CONCENTRATION OF CALCIUM DECREASES PLASMA CONCENTRATION OF PHOSPHORUS

ORGANS AFFECTED BY PARATHYROID HORMONE
BONES KIDNEY

PTH EFFECTS ON BONE OSTEOLYTIC EFFECT (BONE RESORPTION)
PROLIFERATION OF OSTEOCLASTS

PTH EFFECT ON OSTEOCLASTS
IMMEDIATE ACTIVATION OF OSTEOCLASTS PRODUCTION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS

EFFECT OF PTH ON THE KIDNEYS
EXCRETION AND REABSORPTION ACTIVATION OF VITAMIN D .

EXRETION AND REABSORPTION
IMMEDIATE AND RAPID LOSS OF PHOSPHATE IN KIDNEYS DUE TO DECREASED REABSORPTION OF PHOSPHATES INCREASED REABSORPTION OF CALCIUM IN KIDNEYS

ACTIVATION OF VITAMIN D
CALCITRIOL IMPORTANT FOR DEPOSITION IN BONES PROMOTES CALCIFICATION IMPORTANT FOR ABSORPTION OF CALCIUM IN GI TRACT

REGULATION OF PARATHYROID HORMONE RELEASE

THYMUS LOCATED UNDER MEDIASTINUM RELATIVELY LARGE IN CHILDREN
REACHES GREATEST SIZE IN PUBERTY g BEGINS TO INVOLUTE ON ITSELF AFTER PUBERTY TO 12 g AT 50 ACCELERATED BY GLUCOCORTICOIDS AND SEX HORMONES

THYMIC HORMONES THYMOSIN ALPHA THYMOSIN BETA THYMOSIN V THYMOPOIETIN
THYMULIN AND SOME OTHERS

OTHER SITES OF THYMOSIN SYNTHESIS
MACROPHAGES

EFFECTS OF THYMOSIN DEVELOPMENT OF B AND T LYMPHOCYTES
INFLUENCES HORMONES OF REPRODUCTIVE SYSTEM

HORMONES OF THE ADRENAL GLAND
CORTICAL VS MEDULLARY HORMONES

HORMONES OF THE ADRENAL MEDULLA
EPINEPHRINE NOREPINEPHRINE SIMILAR TO SYMPATHETIC GANGLION INNERVATED BY PREGANGLIONIC NERVE FIBERS FROM THE SYMPATHETIC NERVOUS SYSTEM

HORMONE SECRETION EPINEPHRINE MAKES UP 75-80 % OF SECRETION
NOREPINEPHRINE MAKES UP % OF SECRETION METABOLIC CHANGES REACH PEAK AT ABOUT 30 SECONDS AFTER HORMONE RELEASE EFFECTS MAY LAST AS LONG AS SEVERAL MINUTES

ANDRENERGIC RECEPTORS
ALPHA BETA ALL ARE G LINKED RECEPTORS NON CHANNEL LINKED RECEPTORS

NOREPINEPHRINE BINDS WITH ALPHA 1-- EFFECTIVELY ALPHA 2 -- EFFECTIVELY
BETA 1-- EFFECTIVELY BETA 2 --WEAKLY IF AT ALL

EPINEPHRINE BINDS EFFECTIVELY WITH ALPHA 1-- EFFECTIVELY
BETA 1-- EFFECTIVELY BETA 2 --EFFECTIVELY

ALPHA RECEPTORS MOST COMMON ALPHA RECEPTOR ACTIVATES Gp PROTEINS
G PROTEINS ACTIVATE ENZYMES

ALPHA 2 RECEPTORS LESS COMMON THAN ALPHA 1
ACTIVATES INHIBITORY GI PROTEINS REDUCE THE FORMATION OF cyclic AMP

ALPHA RECEPTORS VASOCONSTRICTION IRIS DILATION INTESTINAL RELAXATION
INTESTINAL SPHINCTER CONTRACTION PILOMOTOR CONTRACTION BLADDER SPHINCTER CONTRACTION

BETA 1 RECEPTORS HEART AND KIDNEYS ACTIVATES G PROTEINS
STIMULATES PRODUCTION OF cyclic AMP

BETA 2 RECEPTOR ACTIVATES STIMULATORY G PROTEINS

BETA RECEPTORS VASODILATION CARDIOACCELERATION
INCREASED MYOCARDIAL STRENGTH INTESTINAL RELAXATION UTERUS RELAXATION BRONCHIOLE DILATION CALORIGENESIS GLYCOGENOLYSIS LIPOLYSIS BLADDER RELAXATION

IMPORTANCE OF DIFFERENT RECEPTORS
AT LEAST PARTIALLY RESPONSIBLE FOR DIFFENCE IN ACTIVITY OF EPINEPHRINE AND NOREPINEPHRINE

GENERALIZED EFFECTS OF EPINEPHRINE AND NOREPINEPHRINE
MOBILIZATION OF GLYCOGEN INCREASES CATABOLISM OF GLUCOSE RESERVES IN SKELETAL MUSCLE AND LIVER LIPOLYSIS AND MOBILIZATION OF FAT RESERVES INCREASE IN RATE AND FORCE OF CARDIAC MUSCLE CONTRACTION

SOME SPECIFIC EFFECTS OF CATECHOLAMINES

VASOCONSTRICTION DUE TO CATECHOLAMINE HORMONES
VASOCONSTRICTOR MECHANISM WORKS WITH SYMPATHETIC NERVOUS SYSTEM CONSTRICT MOST BLOOD VESSELS CONSTRICT VEINS REACH AREAS SYMPATHETIC NERVOUS SYSTEM DOES NOT

VASODILATION BY EPINEPHRINE
CAUSES MILD VASODILATION IN SKELETAL IN CARDIAC

DILATION OF BRONCHIOLES BY CATECHOLAMINE HORMONES
SECRETED IN RESPONSE TO SYMPATHETIC INNERVATION RELAX BRONCHIOLES

EFFECT OF EPINEPHRNE ON GLYCOGENOLYSIS
INNERVATION ACTIVATES PHOSPHORYLASE IN LIVER AND IN MUSCLES BREAKS DOWN GLYCOGEN TO GLUCOSE

EFFECTS OF CATECHOLAMINE HORMONES ON CARDIAC MUSCLE
INCREASE RATE OF SINOATRIAL NODE DISCHARGE INCREASES RATE OF CONDUCTION INCREASES EXCITABILITY OF HEART MUSCLE INCREASES PERMEABILITY TO CALCIUM AND SODIUM

EFFECTS OF CATECHOLAMINE HORMONES ON FAT UTILIZATION
HEAVY EXERCISE BRINGS ABOUT DRAMATIC INCREASE IN FAT UTILILZATION DUE TO RAPID RELEASE OF NOREPINEPHRINE AND EPINEPHRINE DUE TO SYMPATHETIC INNERVATION OF ADRENAL MEDULLA ACTIVATE HORMONE-SENSITIVE LIPASE LYPOLYSIS AND MOBILIZATION OF FATTY ACIDS

EFFECTS OF CATECHOLAMINE HORMONES ON SMOOTH MUSCLE
MOST HORMONES AFFECT SMOOTH MUSCLE VARYING DEGREES EFFECT WILL DEPEND ON TYPE OF RECEPTOR (INHIBITORY VS EXCITATORY)

THE RELATIONSHIP BETWEEN MEDULLARY HORMONES AND THE ANS
ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM USUALLY LEADS TO RELEASE OF CATECHOLAMINES BY ADRENAL MEDULLA SYMPATHETIC NERVOUS SYSTEM AND ADRENAL MEDULLA SUPPORT ONE ANOTHER

HORMONES OF THE ADRENAL CORTEX
MINERALOCORTICOIDS, GLUCOCORTICOIDS, & ANDROGENIC HORMONES

ALL ADRENOCORTICOIDS ARE STEROIDS

ALDOSTERONE VERY POTENT 95% OF MINERALOCORTICOID SECRETION
PRODUCED BY ZONA GLOMERULOSA

GENERALIZED EFFECTS OF ALDOSTERONE SECRETION
STIMULATES CONSERVATION OF SODIUM IONS STIMULATES ELIMINATION OF POTASSIUM IONS REABSORPTION OF SODIUM IONS HAS SECODARY EFFECT OF ENHANCING OSMOTIC REABSORPTION INCREASES SENSITIVITY OF TASTE BUDS IN TONGUE TO SALT

TARGET CELLS OF ALDOSTERONE
KIDNEYS SWEAT GALNDS SALIVARY GLANDS PANCREAS

EFFECT OF ALDOSTERONE ON THE KIDNEYS
MOST IMPORTANT FUNCTION CAUSES TRANSPORT OF SODIUM AND POTASSIUM THROUGH RENAL TUBULES CAUSES TRANSPORT OF HYDROGEN IONS THROUGH RENAL TUBULES .

EFFECT OF ALDOSTERONE ON TUBULAR REABSORPTION OF Na+ AND TUBULAR SECRETION OF K+
TUBULAR EPITHELIAL CELLS EXCHANGE TRANSPORT DISTAL TUBULES AND COLLECTING TUBULES CONSERVES Na+ --ELIMINATES K+

EFFECTS OF HIGH CONCENTRATIONS OF ALDOSTERONE
DECREASE SODIUM LOSS TO A FEW MILLIGRAMS PER DAY GREAT INCREASE IN POTASSIUM LOSS IN URINE

EFFECTS OF TOTAL LACK OF ALDOSTERONE
CAN INCREASE SODIUM LOSS UP TO 20 GRAMS PER DAY POTASSIUM IS CONSERVED AND LITTLE IS LOST

EFFECTS OF HIGH ALDOSTERONE ON EXTRACELLULAR WATER VOLUME
CAN INCREASE EXTRACELLULAR FLUID VOLUME UP TO 10 TO 20% OVER NORMAL

EFFECTS OF ALDOSTERONE LOSS ON EXTRAFLUID VOLUME
CAN DECREASE EXTRACELLULAR FLUID VOLUME UP TO 20 TO 25% BELOW NORMAL

EFFECTS OF EXESSIVE POTASSIUM LOSS
CAN CAUSE A SERIOUS DECREASE OF POTASSIUM HYPOKALEMIA

EFFECTS OF HYPOKALEMIA
SEVERE MUSCLE WEAKNESS MUSCLE PARALYSIS DUE TO EFFECTS ON NERVE AND MUSCLE FIBER MEMBRANES

EFFECTS OF HYPERKALEMIA
CARDIAC TOXICITY OCCURS WHEN POTASSIUM LEVELS DOUBLE SYMPTOMS WEAKNESS OF CONTRACTION ARRHYTHMIA IF LEVELS RISE FURTHER CAN LEAD TO DEATH

EFFECTS OF ALDOSTERONE ON TUBULAR SECRETION OF HYDROGEN IONS
ALSO CAUSES HYDROGEN IONS TO BE EXCHANGED FOR SODIUM IONS TO LESSER EXTENT DECREASES HYDROGEN ION CONCENTRATION IN EXTRACELLULAR FLUID NOT STRONG EFFECT CAUSES MILD DEGREE OF ALKALOSIS

EFFECTS OF ALDOSTERONE LACK ON THE CIRCULATORY SYSTEM
CAN CAUSE A 20-25% DECREASE OF BLOOD VOLUME & EXTRACELLULAR FLUIDS CAN CAUSE CIRCULATORY SHOCK WITHOUT TREATMENT MAY DIE WITH 4-8 DAYS

EFFECT OF HYPERSECRETION OF ALDOSTERONE ON THE CIRCULATORY SYSTEM
EXTRACELLULAR FLUID VOLUME INCREASES BLOOD VOLUME INCREASES CARDIAC OUTPUT INCREASES TO AS MUCH AS 20 TO 30% ABOVE NORMAL AT FIRST COMPENSATORY MECHANISMS RETURN IT DOWN TO 5-10 %

FACTORS THAT AFFECT THE REGULATION OF ALDOSTERONE SECRETION
POTASSIUM ION CONCENTRATION OF THE EXTRACELLULAR FLUID RENIN-ANGIOTENSIN SYSTEM QUANTITY OF BODY SODIUM ADENOCORTICOTROPIC HORMONE

ALDOSTERONE IS NOT AS DEPENDENT ON CRH AND ACTH
ANGIOTENSIN AND POTASSIUM LEVELS ARE THE MAJOR REGULATORS

IMPORTANCE OF POTASSIUM IONS IN ALDOSTERONE SECRETION
INCREASE IN POTASSIUM IONS CAUSES INCREASED SECRETION OF ALDOSTERONE ALDOSTERONE CAUSES ENHANCED EXCRETION OF POTASSIUM POTASSIUM LEVELS RETURN TO NORMAL

EFFECT OF RENIN-ANGIOTENSIN SYSTEM ON ALDOSTERONE SECRETION

RENIN KEY IN RENIN-ANGIOTENSIN SYSTEM
RELEASED BY JUXTAGLOMERULAR COMPLEX OF KIDNEYS SECRETED AS PRORENIN CONVERTED TO RENIN BEFORE ENTERING BLOODSTREAM

FACTORS THAT INCREASE RENIN SECRETION
SYMPATHETIC INNERVATION DECLINE IN RENAL BLOOD FLOW

EFFECTS OF RENIN CATALYZES CONVERSION OF ANGIOTENSINOGEN TO ANGIOTENSIN I ANGIOTENSIN I CONVERTED TO ANGIOTENSIN II AS PASSES THROUGH LUNGS ANGIOTENSIN CONVERTING ENZYME (ACE)

EFFECTS OF ANGIOTENSIN II
STIMULATES SECRETION OF ADH STIMULATES WATER REABSORPTION COMPLEMENTS ALDOSTERONE STIMULATES SECRETION OF ALDOSTERONE BY ADRENAL GLANDS INCREASES RETENTION OF SODIUM INCREASES LOSS OF POTASSIUM STIMULATES THIRST INCREASES FLUID CONSUMPTION INCREASES BLOOD VOLUME INCREASES CONSTRICTION OF ARTERIOLES ELEVATES SYSTEMIC BLOOD PRESSURE

EFFECTS OF ALDOSTERONE AT THE CELLULAR LEVEL
.

CORTISOL

GENERALIZED EFFECTS OF CORTISOL
CARBOHYDRATE METABOLISM PROTEIN METABOLISM FAT METABOLISM STRESS MANAGEMENT ANTI-INFLAMMATORY EFFECTS

EFFECTS OF CORTISOL ON CARBOHYDRATE METABOLISM

EFFECT OF CORTISOL ON GLUCONEOGENESIS
INCREASE 6 TO 10 TIMES INCREASES ENZYMES NEEDED TO CONVERT AMINO ACIDS TO GLUCOSE DUE TO INCREASED TRANSCRIPTION INCREASES MOBILILIZATION OF AMINO ACIDS FROM TISSUES MUSCLE MAIN SOURCE INCREASES AMINO ACID CONCENTRATON IN BLOOD

EFFECTS OF CORTISOL ON GLUCOSE UTILIZATION BY CELLS
MODERATE DECREASE IN GLUCOSE USE DECREASE OCCURS SOMEWHERE BETWEEN POINT OF ENTRY AND FINAL DEGRADATION COULD ALSO INVOLVE TRANSPORT MECHANISMS

EFFECTS OF CORTISOL ON BLOOD GLUCOSE CONCENTRATIONS
INCREASED GLUCONEOGENESIS DECREASED GLUCOSE USE RAISES BLOOD GLUCOSE LEVELS

ADRENAL DIABETES INCREASE COULD BE AS LARGE AS 50 % ABOVE NORMAL
SIMILAR TO PITUITARY DIABETES BUT DIFFERENT FROM INSULIN DEFICIENCY

EFFECT OF CORTISOL ON PROTEIN METABOLISM

EFFECTS OF CORTISOL ON CELLULAR PROTEINS STORES
REDUCES PROTEIN STORES EXCEPT IN LIVER DECREASED PROTEIN SYNTHESIS DECREASE IN FORMATION OF RNA INCREASED CATABOLISM OF PROTEIN DECREASED TRANSPORT OF AMINO ACIDS INTO TISSUES OTHER THAN LIVER

EFFECTS OF CORTISOL ON THE LIVER AND PLASMA PROTEIN CONCENTRATIONS
SYNTHESIS OF PROTEINS IN LIVER INCREASES INCREASED ACTIVITY OF LIVER ENZYMES PLASMA PROTEINS PRODUCED ARE RELEASED INTO BLOOD

EFFECTS OF CORTISOL ON MOVEMENTS OF AMINO ACIDS INTO AND OUT OF THE BLOOD AND BLOOD AMINO ACID CONCENTRATIONS DEPRESSES UPTAKE BY MUSCLE AND OTHER CELLS INCREASED UPTAKE BY LIVER INCREASES PLASMA CONCENTRATIONS OF AMINO ACIDS

EFFECTS OF INCREASED PLASMA CONCENTRATIONS OF AMINO ACIDS ON LIVER UTILIZATION OF AMINO ACIDS
INCREASED DEAMINATION OF AMINO ACIDS INCREASED PROTEIN SYNTHESIS INCREASED SYNTHESIS OF PLASMA PROTEINS INCREASED GLUCONEOGENESIS

EFFECTS OF CORTISOL ON FAT METABOLISM

EFFECT OF CORTISOL ON THE MOBILIZATION OF FATS
INCREASES MOBILIZATION OF FATTY ACIDS FROM ADIPOSE TISSUE INCREASES PLASMA FATTY ACID CONCENTRATIONS MODERATELY INCREASES OXIDATION OF FATTY ACIDS SHIFTS BODY TO FAT METABOLISM IN STARVATION OR STRESS EFFECT DEVELOPS OVER SEVERAL HOURS GLYCOGEN AND GLUCOSE SPARER

OTHER EFFECTS OF CORTISOL

EFFECTS OF CORTISOL IN STRESSFUL SITUATION
ANY KIND OF STRESS INCREASES ACTH SECRETION INCREASED SECRETIONS OF CORTISOL IN MINUTES

EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
INFLAMMATION IS TRIGGERED BY TRAUMA, INFECTION OR A VARIETY OF OTHER MECHANISMS CORTISOL CAN BLOCK INFLAMMATION CAN EVEN REVERSE MANY OF ITS EFFECTS

SPECIFIC EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE
STABILIZES LYSOSOMAL MEMBRANES BLOCKS MOST OF THE FACTORS CAUSING INFLAMMATION INCREASES HEALING PROCESS

IMPORTANCE OF CORTISOL IN FIGHTING DISEASE
RHEUMATOID ARTHRITIS RHEUMATIC FEVER ACUTE GLOMERULONEPHRITIS

CONTROL OF CORTISOL SECRETION
ACTH IS THE MAJOR FACTOR CAUSING CORTISOL SECRETION

EFFECT OF CORTICOTROPIN RELEASING HORMONE IN ACTH SECRETION
SMALL PEPTIDE FROM HYPOTHALAMUS LITTLE ACTH IS SECRETED IN THE ABSENCE OF CRH

EFFECTS OF PHYSIOLOGICAL STRESS ON ACTH SECRETION
CAN LEAD TO INCREASE ACTH CAN RESULT IN INCREASED LEVELS OF CORTISOL WITHIN A FEW MINUTES REGULATED BY HYPOTHALAMUS AND THE RELEASE OF CRH

FEEDBACK CONTROLS ON ACTH SECRETION
CORTISOL HAS A DIRECT NEGATIVE FEEDBACK EFFECT ON HYPOTHALAMUS DECREASING CRH ON ANTERIOR PITUITARY DECREASING ACTH

HORMONES OF THE PANCREAS

PANCREATIC HORMONES GLUCAGON INSULIN SOMATOSTATIN
PANCREATIC POLYPEPTIDE

SOMATOSTATIN PRODUCED BY DELTA CELLS IDENTICAL TO BRAIN FORM
SUPPRESSES RELEASE OF GLUCAGON AND INSULIN SLOWS RATE OF FOOD ABSORPTION SLOWS RATE OF ENZYME SECRETION

PANCREATIC POLYPEPTIDE
INHIBITS GALLBLADDER CONTRACTIONS REGULATES PRODUCTION OF SOME PANCREATIC ENZYMES MAY HELP IN CONTOLLING RATE OF ABSORPTION IN GI TRACT

INSULIN POLYPEPTIDE HORMONE SECRETED BY BETA CELLS
WHEN GLUCOSE LEVELS RISE ABOVE NORMAL LEVELS OR WHEN ELEVATED LEVELS OF ARGININE, LEUCINE AND OTHER HORMONES ARE PRESENT IN THE BLOOD

INSULIN DEPENDENT CELLS
MOST ALL THE CELL IN BODY

INSULIN INDEPENDENT CELLS
BRAIN KIDNEYS LINING OF GI TRACT RED BLOOD CELLS

GENERALIZED EFFECTS OF INSULIN
ACCELERATION OF GLUCOSE UPTAKE IN ALL TARGET CELLS ACCELERATION OF GLUCOSE UTILIZATION IN ALL TARGET CELLS ENHANCED ATP PRODUCTION IN ALL TARGET CELLS STIMULATION OF GLYCOGENESIS IN SKELETAL AND LIVER CELLS STIMULATION OF AMINO ACID ABSORPTION IN ALL TARGET TISSUES STIMULATION OF PROTEIN SYNTHESIS IN ALL TARGET TISSUES STIMULATION OF LIPOGENESIS IN ALL TARGET TISSUES

INSULIN REDUCES THE BLOOD GLUCOSE LEVEL

INSULIN IS A PROTEIN AND FAT SPARER

SPECIFIC EFFECTS OF INSULIN`

EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM
RAPID UPTAKE OF GLUCOSE STORAGE OF GLUCOSE AS GLYCOGEN CATABOLISM OF GLUCOSE ESPECIALLY IN ADIPOSE, LIVER AND SKELETAL TISSUES

EFFECTS OF INSULIN ON THE UPTAKE, STORAGE AND USE OF GLUCOSE BY THE LIVER
MOST OF GLUCOSE ABSORBED AFTER MEAL IS STORED IN LIVER AS GLYCOGEN ACTS AS A RESERVE TO SUPPLY GLUCOSE BETWEEN MEALS

MECHANISMS OF GLUCOSE UPTAKE
INSULIN INHIBITS PHOSPHORYLASE ENHANCES UPTAKE OF GLUCOSE BY HEPATOCYTES INCREASES ACTIVITY OF GLUCOKINASE ENZYME PHOSPHORYLATES GLUCOSE TRAPPING IT INSIDE CELL INCREASES ACTIVITY OF ENZYMES PROMOTING GLYCOGENESIS NET EFFECT IS TO INCREASE GLYOGEN LEVELS IN LIVER

GLYCOGEN STORAGE IN LIVER
ABOUT 5-6 PERCENT OF LIVER MASS USUALLY 100 GRAMS

OTHER EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM IN THE LIVER
PROMOTES CONVERSION OF LIVER GLUCOSE INTO FATTY ACIDS FATTY ACIDS ARE THEN TRANSPORTED TO ADIPOSE TISSUES AND DEPOSITED INHIBITS GLUCONEOGENESIS DECREASES ACTIVITIES OF ENZYMES

EFFECTS OF INSULIN ON GLUCOSE METABOLISM IN MUSCLE CELLS
MUSCLES GENERALLY USE FATTY ACIDS AS THEIR ENERGY SOURCE RESTING MEMBRANE IS ALMOST IMPERMEABLE TO GLUCOSE UNTIL STIMULATED BY INSULIN

CONDITIONS WHERE MUSCLES USE CONSIDERABLE GLUCOSE
DURING PERIODS OF HEAVY EXERCISE DURING THE FIRST FEW HOURS AFTER A MEAL WHEN INSULIN LEVELS ARE HIGH

EFFECTS OF HEAVY EXERCISE ON MUSCLE CELLS
DOES NOT REQUIRE LARGE AMOUNTS OF INSULIN MEMBRANE PERMEABILITY CHANGES DUE TO CONTRACTILE PROCESS

EFFECTS OF INSULIN CAUSES RAPID TRANSPORT OF GLUCOSE INTO THE CELLS

EFFECT OF INSULIN ON THE STORAGE OF GLYCOGEN IN MUSCLE CELLS
IN RESTING MUSCLES AFTER MEAL GLUCOSE IS STORED AS MUSCLE GLYCOGEN CONCENTRATION CAN BE AS MUCH AS 1-2 % OF CELL MASS CAN BE USED AS ENERGY RESERVE

DIFFERENCES BETWEEN LIVER GLYCOGEN AND MUSCLE GLYCOGEN
MUSCLE GLYCOGEN CANNOT BE RECONVERTED TO GLUCOSE AND RELEASED INTO BLOOD STREAM WHILE LIVER CELLS CAN MUSCLE CELLS DO NOT HAVE GLUCOSE PHOSPHATASE LIVER CELLS HAVE GLUCOSE PHOSPHATASE

MECHANISM BY WHICH INSULIN INCREASES GLUCOSE TRANSPORT IN MUSCLE CELLS
SOME GLUCOSE TRAPPING BY GLUCOKINASE ENHANCES FACILITATED DIFFUSION OF GLUCOSE THROUGH MEMBRANE TAKES ONLY A FEW SECONDS

EFFECTS OF GLUCOSE ON THE BRAIN
INSULIN INDEPENDENT PERMEABLE TO GLUCOSE WITH OR WITHOUT INSULIN BRAIN DEPENDENT ON GLUCOSE

BLOOD GLUCOSE LEVELS ARE MAINTAINED DUE TO THE BRAINS NEED FOR GLUCOSE
BLOOD GLUCOSE LEVELS MUST ALWAYS MAINTAIN A CRITICAL LEVEL LEVELS IN A RANGE OF mg/100 ml CAUSES HYPOGLYCEMIC SHOCK

SYMPTOMS OF HYPOGLYCEMIC SHOCK
PROGESSIVE IRRITABILITY FAINTING CONVULSIONS COMA DEATH

EFFECT OF INSULIN ON FAT METABOLISM
MAY NOT BE AS DRAMATIC AS CARBOHYDRATE BUT IS MORE IMPORTANT INSULIN IS A PROTEIN SPARER EFFECTS OF INSULIN ARE BEST SEEN WHEN THERE IS A LACK OF INSULIN

EFFECTS OF INSULIN ON EXCESS FAT SYNTHESIS AND STORAGE
SEVERAL EFFECTS LEAD TO AN INCREASE IN FAT STORAGE INCREASE IN GLUCOSE UTILIZATION BY MANY OF BODY’S CELLS INSULIN ALSO PROMOTES FATTYACID SYNTHESIS IN LIVER INSULIN PROMOTES A SMALL AMOUNT OF FATTY ACID SYNTHESIS IN THE ADIPOSE CELLS

FACTORS THAT LEAD TO AN INCREASE IN FATTY ACID SYNTHESIS IN THE LIVER
INCREASED TRANSPORT OF GLUCOSE INTO HEPATOCYTES EXCESS CITRATE AND ISOCITRATE IONS ARE FORMED BY CITRIC ACID CYCLE TRANSPORT OF FATTY ACIDS TO THE ADIPOSE TISSUES

INCREASED TRANSPORT OF GLUCOSE INTO THE LIVER
PHOSPHORYLATION CONVERSION OF GLUCOSE TO PYRUVATE CONVERSION OF PYRUVATE TO ACETYL-coA SYTHESIS OF FATTY ACIDS FROM ACETYL coA

EXCESS CITRATE AND ISOCITRATE IONS FROM THE CITRIC ACID CYCLE
FORMED WHEN EXCESSIVE AMOUNTS OF GLUCOSE ARE BEING USED FOR ENERGY DIRECTLY ACTIVATE ACETYL-coA CARBOXYLASE CATALYZES FIRST STAGE OF FATTY ACID SYNTHESIS

FATTY ACIDS ARE THEN TRANSPORTED TO THE ADIPOSE TISSUES
REMOVES THEM AND PREVENTS A NEGATIVE FEEDBACK EFFECT ON ACETYL-co CARBOXYLASE

EFFECTS OF INSULIN OF FAT STORAGE AT THE ADIPOSE TISSUES
SAME EFFECT AS IN THE LIVER BUT SMALLER ONE TENTH AS MUCH GLUCOSE IS TRANSPORTED INTO ADIPOSE CELLS

ESSENTIAL EFFECTS OF INSULIN ON FAT STORAGE IN THE ADIPOSE TISSUES
INHIBITS THE ACTIVITY OF HORMONE SENSITVE LIPASE CATALYZES LIPOLYSIS PROMOTES TRANSPORT OF GLUCOSE INTO CELLS SAME AS IN MUSCLE CELLS USED TO FORM GLYCEROL

WHEN INSULIN IS NOT AVAILABLE FAT STORAGE IS GREATLY INHIBITED IF NOT BLOCKED

EFFECTS OF INSULIN ON PROTEIN METABOLSISM
WITH GH PROMOTES UPTAKE OF AMINO ACIDS INTO CELLS DIRECTLY AFFECTS RIBOSOME TO CAUSE TRANSLATION INCREASES (OVER TIME) TRANSCRIPTION INHIIBITS CATABOLISM OF PROTEINS INHIBITS GLUCONEOGENESIS ENZYMES IN LIVER

INSULIN GREATLY ENHANCES PROTEIN SYNTHESIS AND DECREASES DEGRADATION OF PROTEINS

EFFECT OF INSULIN ON GROWTH
INSULIN WORKS WITH GROWTH HORMONE SYNERGISTIC EFFECT ANIMALS DEPRIVED OF EITHER PITUITARY OR PANCREAS DISPLAY STUNTED GROWTH BOTH NEED TO BE PROVIDED FOR NORMAL GROWTH

CONTROL OF INSULIN SECRETION
BY BLOOD GLUCOSE LEVELS IN THE BLOOD BY AMINO ACID LEVELS IN THE BLOOD BY GASTROINTESTINAL HORMONES

EFFECTS OF BLOOD GLUCOSE LEVELS ON INSULIN SECRETION
80-90 mg/100ML--MINIMAL INSULIN SECRETION ABOVE 100mg/100ML --INSULIN SECRETION RISES QUICKLY CAN REACH AS MUCH AS mg/100ML SECRETION DECREASES RAPIDLY AS BLOOD GLUCOSE LEVELS RETURN TO FASTING LEVEL

EFFECT OF AMINO ACIDS ON INSULIN SECRETION
SOME OF THE AMINO ACIDS CAUSE INCREASED SECRETION IE ARGININE AND LEUCINE AMINO ACIDS ADMINISTERED WITHOUT AN ACCOMPANYING RISE IN BLOOD GLUCOSE WILL CAUSE ONLY A SMALL RISE IN SECRETION IF BOTH ARE PRESENT INSULIN SECRETION MAY BE DOUBLED

EFFECT OF GASTROINTESTINAL HORMONES ON INSULIN SECRETION
GASTRIN SECRETIN CCK GASTRIC INHIBITORY PEPTIDE RELEASED AFTER EATING SEEM TO CAUSE AN ANTICIPITORY RISE IN INSULIN SECRETION ALMOST DOUBLE SECRETION OF INSULIN AFTER A MEAL

CARBOHYDRATE VS FATTY ACID (LIPID) METABOLISM
INSULIN DETERMINES WHICH WILL OCCUR

GLUCAGON PRODUCED BY ALPHA CELLS

GENERALIZED EFFECTS OF GLUCAGON
GLYCOGENOLYSIS IN SKELETAL AND LIVER CELLS LIPOLYSIS AND FATTY ACID MOBILIZATION IN ADIPOSE TISSUES GLUCONEOGENESIS AT THE LIVER REDUCTION OF GLUCOSE UTILIZATION INCREASE IN BLOOD GLUCOSE LEVELS

GLUCAGON IS A GLUCOSE SPARER

GLYCOGENOLYSIS AND INCREASED BLOOD GLUCOSE LEVELS CAUSED BY GLUCAGON
MOST DRAMATIC EFFECT INCREASES BLOOD GLUCOSE LEVELS IN MINUTES

MECHANISMS OF ACTIVATING GLYCOGENOLYSIS IN THE LIVER
ACTIVATES ADENYLATE CYCLASE FORMS c AMP ACTIVATES PROTEIN KINASE REGULATOR PROTEIN ACTIVATES PROTEIN KINASE ACTIVATES PHOSPHORYLASE b KINASE CONVERTS PHOSPHORYLASE b INTO PHOSPHORYLASE a PROMOTES THE PHOSPHORLYSIS OF GLYCOGEN INTO GLUCOSE 1 PHOSPHATE GLUCOSE 1 PHOSPHATE IS DEPHOSPHORYLATED AND LEAVES THE HEPATOCYTE BY FACILITATED DIFFUSION

EFFECT OF GLUCAGON ON GLUCONEOGENESIS IN THE LIVER
NONCARBOHYDRATE SUBSTRATES ARE CONVERTED TO PYRUVATE OR AN INTERMEDIATE IN THE CITRIC ACID CYCLE AMINO ACIDS ARE CONVERTED TO PYRUVATE OR PHOSPHOPHENOLPYRUVATE LIPIDS CAN BE CONVERTED TO PGA, PGAL OR ANOTHER 3 CARBON INTERMEDIATE GLUCONEOGENESIS HAS SAME INTERMEDIATES AS GLYCOLYSIS BUT ITS ENZYMES RUN IT FROM PYRUVATE TO GLUCOSE

REGULATION OF GLUCAGON SECRETION
BLOOD GLUCOSE CONCENTRATIONS OPPOSITE EFFECT THAN IT HAS ON INSULIN WHEN BLOOD GLUCOSE FALLS AS LOW AS 70mg/100ML LARGE AMOUNTS OF GLUCAGON ARE SECRETED PROTECTS THE BODY AGAINST HYPOGLYCEMIA

EFFECTS OF AMINO ACIDS ON GLUCAGON SECRETION
HELPS PREVENT HYPOGLYCEMIA THAT WOULD OCCUR IF YOU ATE A MEAL OF PURE PROTEIN

IMPORTANCE OF BLOOD GLUCOSE REGULATION
ITS ALL FOR THE BRAIN

IN NORMAL INDIVIDUAL BLOOD GLUCOSE LEVELS ARE TIGHTLY REGULATED
BETWEEN IN THE MORNING 120 TO 140 AFTER BREAKFAST RETURN TO NORMAL IN ABOUT 2 HOURS AFTER MEAL

MAINTENANCE OF BLOOD GLUCOSES BETWEEN MEALS
LIVER ACTS AS A BLOOD GLUCOSE BUFFER STORES GLUCOSE AFTER MEALS AS MUCH AS 2/3 OF GLUCOSE ABSORBED IS STORED IN LIVER AS GLYCOGEN RELEASES GLUCOSE BETWEEN MEAL INSULIN AND GLUCAGON FUNCTION AS SEPARATE CONTROL SYSTEMS IN HYPOGLYCEMIA SYMPATHETIC INNERVATION INCREASES AND STIMULATES RELEASE OF EPINEPHRINE WHICH INCREASES GLUCOSE RELEASE OVER HOURS OR DAYS--GH AND CORTISOL ARE RELEASED DECREASE GLUCOSE UTILIZATION

THEY DO IT ALL FOR THE BRAIN
ALSO THE RETINA, GERMINAL EPITHELIA OF GONADS, KIDNEYS, AND OTHER INSULIN INDEPENDENT CELLS

PINEAL GLAND PEA SIZED EPITHALAMUS ROOF OF DIENCEPHALON
NEUROENDOCRINE TRANSDUCER

NEUROENDOCRINE TRANSDUCER
CONVERTS SIGNALS RECEIVED THROUGH NERVOUS SYSTEM INTO AN ENDOCRINE SIGNAL

RELATIONSHIP TO HYPOTHALAMUS
INFORMATION ABOUT LIGHT AND DARK CYCLES CARRIED FROM EYES TO HYPOTHALAMUS SYMPATHETIC NERVES CARRY ACTION POTENTIALS TO PINEAL GLAND

HORMONES OF THE PINEAL GLAND
MELATONIN OTHERS HAVE BEEN FOUND BUT THEY DO NOT KNOW THEIR FUNCTIONS ARGININE VASOTOCIN

MELATONIN DERIVED FROM SERATONIN PRODUCTION LOWEST IN DAYLIGHT
PRODUCTION HIGHEST AT NIGHT

EFFECTS OF MELATONIN SLOWS MATURATION OF SPERM, EGGS AND REPRODUCTIVE ORGANS REDUCES RATE OF GnRH SECRETION EFFECTIVE ANTIOXIDANT MAY BE INVOLVED IN CIRCADIAN RHYTHM INCREASED SECRETION MAY CAUSE SEASONAL AFFECTIVE DISORDER

HORMONES OF THE REPRODUCTIVE TISSUES
MALE FEMALE REGULATED BY FSH AND LH

THE HORMONES OF THE TESTES
TESTOSTERONE INHIBIN

HORMONES OF THE OVARIES
ESTROGENS ESTRADIOL, ESTRIN ESTRONE PROGESTINS PROGESTERONE INHIBIN RELAXIN

HORMONES OF THE PLACENTA
TEMPORARY ORGAN ESTROGEN PROGESTERONE HUMAN CHORIONIC GONADOTROPIN

HORMONE OF THE UTERUS RELAXIN

HORMONES OF PREGNANCY HUMAN CHORIONIC GONADOTROPIN
SECRETION OF PROGESTERONE SECRETION OF ESTROGEN HUMAN CHORIONIC SOMATOMAMMOTROPIN

HUMAN CHORIONIC GONADOTROPIN
HAS STRUCTURE SIMILAR TO LUTEINIZING HORMONE FIRST SECRETED BY TROPHOBLAST CELLS OF BLASTOCYST BEFORE IMPLANTATION SECRETED BY PLACENTA ONCE ESTABLISHED

DIFFUSES FROM FETAL BLOOD INTO MATERNAL BLOOD
STIMULATES CORPUS LUTEUM PREVENTS DEGENERATION PREVENTS INVOLUTION CAUSES IT TO ALMOST DOUBLE IN SIZE STIMULATES CONTINUED SECRETION OF PROGESTERONE MAINTAINS ENDOMETRIUM LATER IN PREGNANCY STIMULATES SECRETION OF PROGESTERONE AND ESTROGEN IMPORTANT IN MAINTAINING PREGNANCY IN FIRST 7-10 WEEKS

PLACENTA TAKES OVER SECRETORY FUNCTION AT SECOND MONTH
SECRETES ESTROGEN AND PROGESTERONE PLACENTA STOPS SECRETING HUMAN CHORIONIC CAUSING THE CORPUS LUTEUM TO DEGENERATE AND INVOLUTE

IMPORTANCE OF HUMAN CHORIONIC GONADOTROPIN
PREVENTS DEGENERATION OF THE CORPUS LUTEUM STIMULATES THE CORPUS LUTEUM TO SECRETE ESTROGEN STIMULATES THE CORPUS LUTEUM TO SECRETE PROGESTERONE STIMULATES SECRETION OF STEROIDS FROM ADRENAL CORTEX OF FETUS STIMULATES FETAL GONADS TO SECRETE SUPRESSES MATERNAL LYMPHOCYTES REDUCING REJECTION OF THE FETUS

PROGESTERONE SECRETION BY THE PLACENTA
BEGINS SECRETION ABOUT THE 6TH WEEK OF PREGNANCY THIS TOTALLY REPLACES PROGESTERONE FROM THE CORPUS LUTEUM BY THE 12TH -14TH WEEKS

ROLE OF PLACENTAL PROGESTERONE
MAINTENANCE OF PREGNANCY STIMULATES GROWTH OF ENDOMETRIUM STIMULATES SECRETION OF NUTRIENTS ENDOMETRIAL GLANDS INHIBITS CONTRACTION OF THE UTERUS PREVENTS PREMATURE EXPULSION OF FETUS WORKS WITH PROLACTIN & OXYTOCIN TO STIMULATE PREPARATIONS FOR LACTATION IN BREAST SERVES AS A PRECURSOR FOR PLACENTAL ESTROGEN

PLACENTAL ESTROGEN CORPUS LUTEUM SECRETES ESTROGEN FOR FIRST MONTH
IN RESPONSE TO HUMAN CHORIONIC GONADOTROPIN AFTER 1ST MONTH HUMAN CHORIONIC GONADOTROPIN STIMULATES ESTROGEN SECRETION FROM PLACENTA LEVELS INCREASE UNTIL DELIVERY

ESTROGEN FUNCTIONS STIMULATES ENLARGEMENT OF THE UTERUS
STIMULATES BREAST GROWTH STIMULATES DEVELOPMENT OF DUCTS IN BREAST STIMULATES ENLARGEMENT OF GENITILIA STIMULATES RELAXATION OF PELVIC LIGAMENTS

IMPORTANCE OF THE FETUS IN SECRETING PLACENTAL ESTROGEN
PLACENTA LACKS ENZYME IN ESTROGEN PATHWAY FETAL ADRENAL CORTEX CONTAINS THE ENZYME NECESSARY TO CONVERT PREGNELONE TO DHEA TRANSPORTED BACK TO PLACENTA AND IS CONVERTED INTO ESTRODIOL AND RELEASED 962

HUMAN CHORIONIC SOMATOMAMMOTROPIN
SECRETION BEGINS AT ABOUT 4TH WEEK RISES THROUGHOUT PREGNANCY SIMILAR TO HUMAN GROWTH HORMONE WEAKLY STIMULATES FETAL DEVELOPMENT AND BREAST DEVELOPMENT ANTAGONISTIC TO INSULIN DECREASING MATERNAL USE OF GLUCOSE MAKES MORE GLUCOSE AVAILABLE TO FETUS CAN CAUSE GESTATIONAL DIABETES IN MOTHER PROMOTES MOBILIZATION OF FATS

HORMONAL CHANGES IN PREGNANCY
INHIBITION OF GONADOTROPIN STIMULATION OF PROLACTIN STIMULATION OFRELAXIN STIMULATION OF INSULIN STIMULATION OF ALDOSTERONE STIMULATION OF CORTISOL STIMULATION OF THYROID HORMONE

INHIBITION OF GONADOTROPINS
HIGH LEVELS OF ESTROGEN AND PROGESTERONE IN BLOOD STREAM INHIBIT SECRETION OF GONADOTROPIN RELEASING HORMONE THIS INHIBITS THE RELEASE OF FOLLICLE STIMULATING HORMONE AND LUTEINIZING HORMONE THIS PREVENTS OVULATON AND/OR MENSTRUATION

STIMULATION OF PROLACTIN
SECRETION INCREASES THROUGHOUT PREGNANCY WORKS WITH ESTROGEN AND PROGESTERONE TO STIMULATE BREAST DEVELOPMENT AND MILK PRODUCTION

STIMULATION OF RELAXIN
HUMAN CHORIONIC GONADOTROPIN STIMULATES RELAXIN SECRETION BY CORPUS LUTEUM IN FIRST TWO MONTHS LATER RELAXIN IS SECRETED BY THE ENDOMETRIUM

FUNCTION OF RELAXIN RELAXES PELVIC LIGAMENTS
WORKS WITH PROGESTERONE TO INHIBIT UTERINE CONTRACTIONS

STIMULATION OF INSULIN
DECREASED MATERNAL SENSITIVITY TO INSULIN CAUSES ITS SECRETION TO INCREASE AFTER 3RD MONTH CAN BECOME SEVERE ENOUGH TO CAUSE GESTATIONAL DIABETES NORMALLY RETURNS TO NORMAL AFTER BIRTH

STIMULATION OF ALDOSTERONE
ESTROGEN AND PROGESTERONE DIRECTLY INCREASE THE SECRETION OF ANGIOTENSIN II AND ALDOSTERONE FROM ADRENAL CORTEX PROMOTE SODIUM AND WATER RETENTION HELPS TO PROVIDE SODIUM TO FETUS ESTROGEN SEEMS TO INHIBIT THE VASCULAR EFFECTS OF HIGH LEVELS OF ANGIOTENSIN II

STIMULATION OF CORTISOL
INCREASES IN CORTISOL SECRETION AND SECRETION OF CORTISOL BINDING GLOBULIN IN RESPONSE TO STIMULATION OF ESTROGEN LEAD TO AN INCREASE IN BOTH FREE AND PROTEIN BOUND CORTISOL

EFFECTS OF INCREASED CORTISOL LEVELS
INCREASED BODY FAT DEVELOPMENT OF MAMMARY GLANDS INCREASED APPETITE INCREASED BLOOD GLUCOSE LEVELS INCREASED GLUCOSE LEVELS INCREASE INSULIN SECRETION INCREASED INSULIN SECRETION INCREASES LIPID STORAGE

INCREASED THYROID HORMONE
HIGH LEVELS OF ESTROGEN STIMULATE THYROTROPIN RELEASING HORMONE STIMULATES THYROID STIMULATING HORMONE RESULTS IN INCREASE IN GLAND SIZE, SECRETORY RATE, BASAL METABOLIC RATE, CARDIAC AND PULMONARY FUNCTION

THE ENDOCRINE FUNCTION OF THE HEART
ATRIOPEPTIN/ATRIAL NATRIURETIC PEPTIDE PRODUCED BY ATRIA CARDIAC MUSCLES

EFFECTS OF ATRIAL NATRIURETIC PEPTIDE
PROMOTES LOSS OF SODIUM IONS AND WATER AT KIDNEYS INHIBITS RENIN RELEASE INHIBITS SECRETION OF ADH AND ALDOSTERONE SUPPRESSES THIRST BLOCKS ACTION OF ANGIOTENSIN II AND NOREPINEPHRINE ON ARTERIOLES

ENDOCRINE FUNCTION OF THE DIGESTIVE SYSTEM

HORMONES OF THE DIGESTIVE SYSTEM
GASTRIN SECRETIN CHOLECYSTOKININ

GASTRIN POLYPEPTIDE SECRETED BY MUCOSAL LINING
STIMULATES PRODUCTION OF HCL AND PEPSIN

SECRETIN POLYPEPTIDE FIRST HORMONE
SECRETED BY THE MUCOSA OF THE DUODENUM STIMULATES A BICARBONATE RICH SECRETION FROM THE PANCREAS CAN INHIBIT GASTRIC SECRETIONS UNDER CERTAIN CONDITIONS STIMULATES SECRETION OF BILE

CHOLECYSTOKININ SECRETED BY WALL OF DUODENUM
STIMULATES CONTRACTION OF DUODENUM INHIBITS GASTRIC ACID SECRETIONS UNDER CERTAIN CONDITIONS STIMULATES THE RELEASE OF ENZYMES FROM THE PANCREAS

HORMONES OF THE KIDNEYS

CALCITRIOL STEROID HORMONE SECRETED IN RESPONSE TO PTH
DEPENDENT ON CHOLECALCIFEROL FROM SKIN OR DIET CARRIED BY TRANSCALCIFERIN VITAMIN D REFERS TO ALL FORMS OF THE VITAMINS

EFFECT OF CALCITRIOL STIMULATION OF CALCIUM AND PHOSPHATE ABSORPTION BY GI TRACT STIMULATE FORMATION AND DIFFERENTIATION OF OSTEOPROGENITOR CELLS AND OSTEOCLASTS STIMULATING CALCUM REABSORPTION AT THE KIDNEYS SUPPRESSES PARATHYROID HORMONE SECRETION

ERYTHROPOIETIN PEPTIDE HORMONE
RELEASED BY KIDNEY IN RESPONSE TO HYPOXIA IN KIDNEY TISSUES

POSSIBLE CAUSES OF HYPOXIA
REDUCTION IN RENAL BLOOD FLOW REDUCTION IN NUMBER OF RED BLOOD CELLS REDUCTION IN ABILITY OF RED BLOOD CELLS TO CARRY OXYGEN REDUCTION IN OXYGEN CONTENT OF AIR PROBLEMS WITH THE RESPIRATORY MEMBRANE

EFFECT OF ERYTHROPOIETIN
STIMULATES HEMATOPOIESIS ELEVATES BLOOD VOLUME SLIGHTLY DUE TO INCREASE IN RED BLOOD CELLS IMPROVES OXYGEN DELIVERY TO PERIPHERAL TISSUES

LEPTIN A NEW HORMONE

EFFECTS OF AGING FEW FUNCTIONAL CHANGES
DECLINE IN LEVELS OF REPRODUCTIVE HORMONES ENDOCRINE TISSUES MAY BECOME LESS RESPONSIVE SOME TARGET CELLS IN TISSUES MAY BECOME LESS RESPONSIVE

HORMONES OF THE ENDOCRINE SYSTEM

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HORMONES OF THE ENDOCRINE SYSTEM

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