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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

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Hormones of the pituitary
HORMONES OF THE PITUITARY

  • NEUROHYPOPHYSIS--POSTERIOR PITUITARY

  • ADENOHYPOPHYSIS--ANTERIOR PITUITARY


Hormones of the neurohypophysis
HORMONES OF THE NEUROHYPOPHYSIS

  • STORES AND SECRETES NEUROHORMONES PRODUCED BY HYPOTHALAMUS

  • ANTIDIURETIC HORMONE

  • OXYTOCIN


Antidiuretic hormone
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
ANTIDIURETIC EFFECT

  • AFFERENT VAGAL NERVES

  • DROP IN PRESSURE STIMULATES ADH SECRETION

  • INCREASE IN PRESSURE INHIBITS SECRETION


Factors that increase adh 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
FACTORS THAT DECREASE ADH SECRETION

  • DROP IN PLASMA OSMOTIC PRESSURE

  • INCREASED EXTRACELLULAR FLUID VOLUME

  • ALCOHOL


Diabetes insipidus
DIABETES INSIPIDUS

  • POLYURIA

  • POLYDYPSIA

  • LOSS OF ADH RELEASE

  • IMPAIRED WATER CONSERVATION

  • EXCESSIVE WATER LOSS IN URINE


Oxytocin
OXYTOCIN

  • WOMEN

  • MEN


Oxytocin in women
OXYTOCIN IN WOMEN

  • STIMULATES SMOOTH MUSCLE IN UTERUS

  • PROMOTES LABOR AND DELIVER

  • STIMULATES MYOEPITHELIAL CELLS OF MAMMARY GLANDS




Oxytocin in males
OXYTOCIN IN MALES

  • UNCERTAIN

  • STIMULATES SMOOTH MUSCLE CONTRACTIONS IN DUCTUS DEFERENS AND PROSTATE


Oxytocin and sex
OXYTOCIN AND SEX

  • AROUSAL AND ORGASM

  • EMISSION

  • CONTRACTIONS THAT PROMOTE SPERM TRANSPORT


Hormones of the hypothalamus adenohypophysis

ADENOHYPOPHYSEAL HORMONES

TSH

ACTH

FSH

LH

PRL

GH

MSH

LIPOTROPIN

RELEASING AND INHIBITING

HORMONES FROM THE

HYPOTHALAMUS

TRH

CRH

GnRH

GnIH

PRH/PIH

GH-RH/SOMATOSTATIN

HORMONES OF THE HYPOTHALAMUS & ADENOHYPOPHYSIS


Thyroid stimulating hormone
THYROID STIMULATING HORMONE

  • THYROTROPIN

  • RELEASE REGULATED BY THYROTROPIN RELEASING HORMONE (TRH)

  • TARGET CELLS IN THYROID

  • TRIGGERS RELEASE OF THYROID HORMONE


Adrenocorticotropic hormone
ADRENOCORTICOTROPIC HORMONE

  • DERIVED FROM PROOPIMELANOCORTIN

  • INCREASES SECRETION OF ADRENAL HORMONES

  • BINDS TO MELANOCYTES AND INCREASE PIGMENTATION OF SKIN


Other substances derived from proopimelanocortin
OTHER SUBSTANCES DERIVED FROM PROOPIMELANOCORTIN

  • LIPOTROPINS

  • BETA ENDORPHINS

  • MELANOCYTE STIMULATING HORMONE


Lipotropins
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
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
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
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



Gonadotropins1

HORMONES PROMOTE GROWTH AND FUNCTION OF GONADS

LUTEINIZING HORMONE

FOLLICLE STIMULATING HORMONE

GONADOTROPINS


Prolactin in females
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
PROLACTIN IN MALES

  • MAKES INTERSTITIAL CELLS MORE RESPONSIVE TO LUTEINIZING HORMONE


Growth hormone
GROWTH HORMONE

  • SECRETION STIMULATED BY GROWTH HORMONE RELEASING HORMONE

  • SECRETION INHIBITED BY GROWTH HORMONE INHIBITING HORMONE/SOMATOSTATIN


Growth hormone1
GROWTH HORMONE

  • STIMULATES GROWTH OF CARTILAGE AND BONE

  • INDIRECT EFFECTS

  • DIRECT EFFECTS


Indirect effects
INDIRECT EFFECTS

  • SOMATOMEDINS /INSULIN-LIKE GROWTH FACTORS

  • PEPTIDE HORMONES

  • BIND TO MEMBRANE RECEPTORS

  • SKELETAL MUSCLE, CARTILAGE AND OTHER TARGET CELLS


Direct effects
DIRECT EFFECTS

  • STIMULATES STEM CELL DIVISION AND GROWTH OF DAUGHTER CELLS


Effects of growth hormone on metabolism
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
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
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
PROTEIN SYNTHESIS BY RIBOSOMES

  • DIRECT EFFECT ON RIBOSOMES


Increased levels of rna
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
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
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

GROWTH HORMONE STIMULATES FATTY ACID METABOLISM

SPARES GLUCOSE AND AMINO ACIDS


Effects of growth hormone on carbohydrate metabolism
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
DECREASED USE OF GLUCOSE FOR ENERGY

  • PERHAPS DUE TO INCREASED MOBILIZATION AND UTILIZATION OF FATS


Enhances glycogenogenesis
ENHANCES GLYCOGENOGENESIS

  • GLUCOSE WILL BE STORED AS GLYCOGEN

  • RESERVES RAPIDLY FILL UP


Diminished glucose uptake by cells
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
SECRETION OF GROWTH HORMONE

  • 3 NANOGRAMS IN ADULT

  • 5 NANOGRAMS IN CHILD

  • REGULATED BY GH-RH AND SOMATOSTATIN



Hormones of the thyroid gland

HORMONES OF THE THYROID GLAND

THYROID HORMONE AND CALCITONIN


Thyroid hormone
THYROID HORMONE

  • THYROXINE (T4 )

  • TRIIODOTHRYONINE (T3 )


Importance of thyroglobulin
IMPORTANCE OF THYROGLOBULIN

  • GLYCOPROTEIN

  • CONTAINS 140 TYROSINE AMINO ACIDS

  • SUBSTRATE IODINE BINDS WITH

  • HORMONES FORM WITHIN THYROGLOBULIN MOLECULE


Importance of iodine
IMPORTANCE OF IODINE

  • USED ONLY TO MAKE THYROID HORMONES

  • STORED IN THYROID

  • IDODIDE PUMP TRAPS IODIDE


The wedding of thyroglobulin and iodide ions
THE WEDDING OF THYROGLOBULIN AND IODIDE IONS

  • OCCURS AT THE COLLOID-CELL INTERFACE AS THYROGLOBULIN IS SECRETED


Mit and dit
MIT AND DIT

  • MONOIODTYROSINE

  • DIIODOTYROSINE

  • THYROXINE

  • TRIIODOTHRYRONINE


Thyroglobulin storage
THYROGLOBULIN STORAGE

  • IN COLLOID OF FOLLICLE

  • ONLY HORMONE STORED EXTRACELLULARLY

  • 1-3 MONTH SUPPLY IN COLLOID


Release of thyroid hormone into the blood
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
TRANSPORT IN THE BLOOD

  • THRYOXINE BINDING GLOBULIN

  • ALBUMINS


Thyroid hormones at the cells
THYROID HORMONES AT THE CELLS

  • ENTERS CELLS

  • BINDS WITH INTRACELLULAR PROTEIN RECEPTOR

  • THYROXINE HAS GREATER AFFINITY


Importance of latency and duration of action
IMPORTANCE OF LATENCY AND DURATION OF ACTION

  • T4 -- TWO OR THREE DAY LATENT PERIOD

  • MAXIMUM ACTIVITY IN 10-12 DAYS

  • T3 --- 6 TO 12 HOURS

  • MAXIMUM ACTIVITY IN 2-3 DAYS


Major effects of thyroid horomone
MAJOR EFFECTS OF THYROID HOROMONE

  • GROWTH IN CHILDREN

  • INCREASE IN METABOLIC RATE


Effects on growth
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
GENERALIZED EFFECTS ON METABOLISM

  • AFFECT METABOLISM OF ALMOST ALL CELLS OF BODY

  • CALORIGENIC EFFECT


Effect of thyroid hormone on protein synthesis
EFFECT OF THYROID HORMONE ON PROTEIN SYNTHESIS

  • PHASE ONE--INCREASED TRANSLATION

  • PHASE TWO--INCREASED TRANSCRIPTION


Effect of thyroid hormone on cellular enzyme systems
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
EFFECTS ON CELLULAR ORGANELLES

  • INCREASED ACTIVITY OF MITOCHONDRIA

  • INCREASED NUMBER OF MITOCHONDRIA


Effects on active transport
EFFECTS ON ACTIVE TRANSPORT

  • Na-K ATPase PUMPS INCREASE

  • INCREAED TRANSPORT OF SODIUM AND POTASSIUM


Effects on carbohydrate metabolism
EFFECTS ON CARBOHYDRATE METABOLISM

  • RAPID UPTAKE OF GLUCOSE

  • INCREASED GLYCOLYSIS

  • INCREASED GLUCONEOGENESIS

  • INCREASED GI ABSORPTION

  • INCREASED INSULIN SECRETION


Effect on fat metabolism
EFFECT ON FAT METABOLISM

  • LIPOGENESIS

  • LIPOLYSIS

  • MOBILIZATION OF LIPIDS


Effects on body mass
EFFECTS ON BODY MASS

  • INCREASED THYROID HORMONE DECREASES

  • DECREASED THYROID HORMONE INCREASES


Effects on cardiovascular system
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
EFFECTS ON RESPIRATION

  • INCREASED OXYGEN DEMAND

  • INCREASED CARBON DIOXIDE LEVELS

  • ACTIVATE MECHANISMS THAT INCREASE THE RATE AND DEPTH OF RESPIRATION


Effect on gastrointestinal tract
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
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
SECRETION OF THYROID HORMONE

  • TSH FROM ADENOHYPOPHYSIS STIMULATES ITS SECRTION TRH STIMULATES TSH SECRETION


Negative feedback controls of thyroid hormone release
NEGATIVE FEEDBACK CONTROLS OF THYROID HORMONE RELEASE

  • LONG FEED BACK LOOPS

  • SHORT FEEDBACK LOOPS


Long feedback loop
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

SHORT FEEDBACK LOOPS


Thyroid stimulating hormone1
THYROID STIMULATING HORMONE RELEASING OR INHIBITING HORMONES

  • HIGH SECRETION OF TSH MAY INHIBIT SECRETION OF TRH


Specific effects of tsh
SPECIFIC EFFECTS OF TSH RELEASING OR INHIBITING HORMONES

  • 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
REGULATION OF THRYOID HORMONE SECRETION RELEASING OR INHIBITING HORMONES

  • TSH FROM PITUITARY STIMULATES SYNTHESIS AND RELEASE

  • TRH PROMOTES TSH RELEASE

  • NEGATIVE FEED BACK


Calcitonin
CALCITONIN RELEASING OR INHIBITING HORMONES

  • 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
HOW CALCITONIN REDUCES BLOOD CALCIUM LEVELS RELEASING OR INHIBITING HORMONES

  • DECREASES OSTEOLYTIC EFFECT FAVORS DEPOSITION RATHER THAN RESORPTION

  • INCREASES ACTIVITY OF OSTEOBLASTS

  • PREVENTS FORMATION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS


Children vs adults
CHILDREN VS ADULTS RELEASING OR INHIBITING HORMONES

  • MAJOR ROLE IN CHILD

  • MINOR ROLE IN ADULTS


Regulation of calcitonin secretion
REGULATION OF CALCITONIN SECRETION RELEASING OR INHIBITING HORMONES

  • 10% RISE IN PLASMA CALCIUM LEVELS LEADS TO 3-6 TIMES MORE CALCITONIN


Other important effects of calcitonin
OTHER IMPORTANT EFFECTS OF CALCITONIN RELEASING OR INHIBITING HORMONES

  • REDUCES LOSS OF BONE MASS DURING PROLONGED STARVATION LATE STAGES OF PREGNANCY


Differences between calcitonin and parathyroid hormone
DIFFERENCES BETWEEN CALCITONIN AND PARATHYROID HORMONE RELEASING OR INHIBITING HORMONES

  • CALCITONIN MORE RAPID

  • SHORT TERM REGULATOR


Regulation of secretion
REGULATION OF SECRETION RELEASING OR INHIBITING HORMONES

  • PLASMA LEVELS OF CALCIUM

  • HIGH CONCENTRATION -- INCREASED SECRETION

  • LOW CONCENTRATION -- DECREASED SECRETION

  • GASTRIN AND OTHER INTESTINAL HORMONES EFFECT SECRETION


Parathyroid gland
PARATHYROID GLAND RELEASING OR INHIBITING HORMONES

  • SMALL FLATTENED GLANDS

  • POSTERIOR SURFACE OF THYROID GLAND


Cells of parathyroid
CELLS OF PARATHYROID RELEASING OR INHIBITING HORMONES

  • CHIEF CELLS

  • OXYPHIL CELLS


Parathyroid hormone
PARATHYROID HORMONE RELEASING OR INHIBITING HORMONES

  • 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
ORGANS AFFECTED BY PARATHYROID HORMONE RELEASING OR INHIBITING HORMONES

  • BONES

  • KIDNEY


Pth effects on bone
PTH EFFECTS ON BONE RELEASING OR INHIBITING HORMONES

  • OSTEOLYTIC EFFECT (BONE RESORPTION)

  • PROLIFERATION OF OSTEOCLASTS


Pth effect on osteoclasts
PTH EFFECT ON OSTEOCLASTS RELEASING OR INHIBITING HORMONES

  • IMMEDIATE ACTIVATION OF OSTEOCLASTS

  • PRODUCTION OF NEW OSTEOCLASTS FROM PROGENITOR CELLS


Effect of pth on the kidneys
EFFECT OF PTH ON THE KIDNEYS RELEASING OR INHIBITING HORMONES

  • EXCRETION AND REABSORPTION

  • ACTIVATION OF VITAMIN D


Exretion and reabsorption
EXRETION AND REABSORPTION RELEASING OR INHIBITING HORMONES

  • IMMEDIATE AND RAPID LOSS OF PHOSPHATE IN KIDNEYS DUE TO DECREASED REABSORPTION OF PHOSPHATES

  • INCREASED REABSORPTION OF CALCIUM IN KIDNEYS


Activation of vitamin d
ACTIVATION OF VITAMIN D RELEASING OR INHIBITING HORMONES

  • CALCITRIOL

  • IMPORTANT FOR DEPOSITION IN BONES PROMOTES CALCIFICATION

  • IMPORTANT FOR ABSORPTION OF CALCIUM IN GI TRACT


Regulation of parathyroid hormone release
REGULATION OF PARATHYROID HORMONE RELEASE RELEASING OR INHIBITING HORMONES


Thymus
THYMUS RELEASING OR INHIBITING HORMONES

  • LOCATED UNDER MEDIASTINUM

  • RELATIVELY LARGE IN CHILDREN

  • REACHES GREATEST SIZE IN PUBERTY -- 40 g

  • BEGINS TO INVOLUTE ON ITSELF AFTER PUBERTY TO 12 g AT 50

  • ACCELERATED BY GLUCOCORTICOIDS AND SEX HORMONES


Thymic hormones
THYMIC HORMONES RELEASING OR INHIBITING HORMONES

  • THYMOSIN ALPHA

  • THYMOSIN BETA

  • THYMOSIN V

  • THYMOPOIETIN

  • THYMULIN

  • AND SOME OTHERS


Other sites of thymosin synthesis
OTHER SITES OF THYMOSIN SYNTHESIS RELEASING OR INHIBITING HORMONES

  • MACROPHAGES


Effects of thymosin
EFFECTS OF THYMOSIN RELEASING OR INHIBITING HORMONES

  • DEVELOPMENT OF B AND T LYMPHOCYTES

  • INFLUENCES HORMONES OF REPRODUCTIVE SYSTEM


Hormones of the adrenal gland

HORMONES OF THE ADRENAL GLAND RELEASING OR INHIBITING HORMONES

CORTICAL VS MEDULLARY HORMONES


Hormones of the adrenal medulla
HORMONES OF THE ADRENAL MEDULLA RELEASING OR INHIBITING HORMONES

  • EPINEPHRINE

  • NOREPINEPHRINE

  • SIMILAR TO SYMPATHETIC GANGLION

  • INNERVATED BY PREGANGLIONIC NERVE FIBERS FROM THE SYMPATHETIC NERVOUS SYSTEM


Hormone secretion
HORMONE SECRETION RELEASING OR INHIBITING HORMONES

  • EPINEPHRINE MAKES UP 75-80 % OF SECRETION

  • NOREPINEPHRINE MAKES UP 20-25 % OF SECRETION

  • METABOLIC CHANGES REACH PEAK AT ABOUT 30 SECONDS AFTER HORMONE RELEASE

  • EFFECTS MAY LAST AS LONG AS SEVERAL MINUTES


Andrenergic receptors
ANDRENERGIC RECEPTORS RELEASING OR INHIBITING HORMONES

  • ALPHA

  • BETA

  • ALL ARE G LINKED RECEPTORS

  • NON CHANNEL LINKED RECEPTORS


Norepinephrine
NOREPINEPHRINE RELEASING OR INHIBITING HORMONES

  • BINDS WITH

    • ALPHA 1-- EFFECTIVELY

    • ALPHA 2 -- EFFECTIVELY

    • BETA 1-- EFFECTIVELY

    • BETA 2 --WEAKLY IF AT ALL


Epinephrine
EPINEPHRINE RELEASING OR INHIBITING HORMONES

  • BINDS EFFECTIVELY WITH

    • ALPHA 1-- EFFECTIVELY

    • ALPHA 2 -- EFFECTIVELY

    • BETA 1-- EFFECTIVELY

    • BETA 2 --EFFECTIVELY


Alpha receptors
ALPHA RECEPTORS RELEASING OR INHIBITING HORMONES

  • MOST COMMON ALPHA RECEPTOR

  • ACTIVATES Gp PROTEINS

  • G PROTEINS ACTIVATE ENZYMES


Alpha 2 receptors
ALPHA 2 RECEPTORS RELEASING OR INHIBITING HORMONES

  • LESS COMMON THAN ALPHA 1

  • ACTIVATES INHIBITORY GI PROTEINS

  • REDUCE THE FORMATION OF cyclic AMP


Alpha receptors1
ALPHA RECEPTORS RELEASING OR INHIBITING HORMONES

  • VASOCONSTRICTION

  • IRIS DILATION

  • INTESTINAL RELAXATION

  • INTESTINAL SPHINCTER CONTRACTION

  • PILOMOTOR CONTRACTION

  • BLADDER SPHINCTER CONTRACTION


Beta 1 receptors
BETA 1 RECEPTORS RELEASING OR INHIBITING HORMONES

  • HEART AND KIDNEYS

  • ACTIVATES G PROTEINS

  • STIMULATES PRODUCTION OF cyclic AMP


Beta 2 receptor
BETA 2 RECEPTOR RELEASING OR INHIBITING HORMONES

  • ACTIVATES STIMULATORY G PROTEINS


Beta receptors
BETA RECEPTORS RELEASING OR INHIBITING HORMONES

  • VASODILATION

  • CARDIOACCELERATION

  • INCREASED MYOCARDIAL STRENGTH

  • INTESTINAL RELAXATION

  • UTERUS RELAXATION

  • BRONCHIOLE DILATION

  • CALORIGENESIS

  • GLYCOGENOLYSIS

  • LIPOLYSIS

  • BLADDER RELAXATION


Importance of different receptors
IMPORTANCE OF DIFFERENT RECEPTORS RELEASING OR INHIBITING HORMONES

  • AT LEAST PARTIALLY RESPONSIBLE FOR DIFFENCE IN ACTIVITY OF EPINEPHRINE AND NOREPINEPHRINE


Generalized effects of epinephrine and norepinephrine
GENERALIZED EFFECTS OF EPINEPHRINE AND NOREPINEPHRINE RELEASING OR INHIBITING HORMONES

  • 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

SOME SPECIFIC EFFECTS OF CATECHOLAMINES RELEASING OR INHIBITING HORMONES


Vasoconstriction due to catecholamine hormones
VASOCONSTRICTION DUE TO CATECHOLAMINE HORMONES RELEASING OR INHIBITING HORMONES

  • VASOCONSTRICTOR MECHANISM

  • WORKS WITH SYMPATHETIC NERVOUS SYSTEM

  • CONSTRICT MOST BLOOD VESSELS

  • CONSTRICT VEINS

  • REACH AREAS SYMPATHETIC NERVOUS SYSTEM DOES NOT


Vasodilation by epinephrine
VASODILATION BY EPINEPHRINE RELEASING OR INHIBITING HORMONES

  • CAUSES MILD VASODILATION

  • IN SKELETAL

  • IN CARDIAC


Dilation of bronchioles by catecholamine hormones
DILATION OF BRONCHIOLES BY CATECHOLAMINE HORMONES RELEASING OR INHIBITING HORMONES

  • SECRETED IN RESPONSE TO SYMPATHETIC INNERVATION

  • RELAX BRONCHIOLES


Effect of epinephrne on glycogenolysis
EFFECT OF EPINEPHRNE ON GLYCOGENOLYSIS RELEASING OR INHIBITING HORMONES

  • INNERVATION

  • ACTIVATES PHOSPHORYLASE

  • IN LIVER AND IN MUSCLES

  • BREAKS DOWN GLYCOGEN TO GLUCOSE


Effects of catecholamine hormones on cardiac muscle
EFFECTS OF CATECHOLAMINE HORMONES ON CARDIAC MUSCLE RELEASING OR INHIBITING HORMONES

  • 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
EFFECTS OF CATECHOLAMINE HORMONES ON FAT UTILIZATION RELEASING OR INHIBITING HORMONES

  • 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
EFFECTS OF CATECHOLAMINE HORMONES ON SMOOTH MUSCLE RELEASING OR INHIBITING HORMONES

  • 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
THE RELATIONSHIP BETWEEN MEDULLARY HORMONES AND THE ANS RELEASING OR INHIBITING HORMONES

  • 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

HORMONES OF THE ADRENAL CORTEX RELEASING OR INHIBITING HORMONES

MINERALOCORTICOIDS, GLUCOCORTICOIDS, & ANDROGENIC HORMONES


All adrenocorticoids are steroids
ALL ADRENOCORTICOIDS ARE STEROIDS RELEASING OR INHIBITING HORMONES


Aldosterone
ALDOSTERONE RELEASING OR INHIBITING HORMONES

  • VERY POTENT

  • 95% OF MINERALOCORTICOID SECRETION

  • PRODUCED BY ZONA GLOMERULOSA


Generalized effects of aldosterone secretion
GENERALIZED EFFECTS OF ALDOSTERONE SECRETION RELEASING OR INHIBITING HORMONES

  • 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
TARGET CELLS OF ALDOSTERONE RELEASING OR INHIBITING HORMONES

  • KIDNEYS

  • SWEAT GALNDS

  • SALIVARY GLANDS

  • PANCREAS


Effect of aldosterone on the kidneys
EFFECT OF ALDOSTERONE ON THE KIDNEYS RELEASING OR INHIBITING HORMONES

  • 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
EFFECT OF ALDOSTERONE ON TUBULAR REABSORPTION OF Na RELEASING OR INHIBITING HORMONES+ 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
EFFECTS OF HIGH CONCENTRATIONS RELEASING OR INHIBITING HORMONES OF ALDOSTERONE

  • DECREASE SODIUM LOSS TO A FEW MILLIGRAMS PER DAY

  • GREAT INCREASE IN POTASSIUM LOSS IN URINE


Effects of total lack of aldosterone
EFFECTS OF TOTAL LACK OF ALDOSTERONE RELEASING OR INHIBITING HORMONES

  • 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
EFFECTS OF HIGH ALDOSTERONE ON EXTRACELLULAR WATER VOLUME RELEASING OR INHIBITING HORMONES

  • CAN INCREASE EXTRACELLULAR FLUID VOLUME

  • UP TO 10 TO 20% OVER NORMAL


Effects of aldosterone loss on extrafluid volume
EFFECTS OF ALDOSTERONE LOSS ON EXTRAFLUID VOLUME RELEASING OR INHIBITING HORMONES

  • CAN DECREASE EXTRACELLULAR FLUID VOLUME

  • UP TO 20 TO 25% BELOW NORMAL


Effects of exessive potassium loss
EFFECTS OF EXESSIVE POTASSIUM LOSS RELEASING OR INHIBITING HORMONES

  • CAN CAUSE A SERIOUS DECREASE OF POTASSIUM

  • HYPOKALEMIA


Effects of hypokalemia
EFFECTS OF HYPOKALEMIA RELEASING OR INHIBITING HORMONES

  • SEVERE MUSCLE WEAKNESS

  • MUSCLE PARALYSIS

  • DUE TO EFFECTS ON NERVE AND MUSCLE FIBER MEMBRANES


Effects of hyperkalemia
EFFECTS OF HYPERKALEMIA RELEASING OR INHIBITING HORMONES

  • CARDIAC TOXICITY OCCURS WHEN POTASSIUM LEVELS DOUBLE

  • SYMPTOMS WEAKNESS OF CONTRACTION ARRHYTHMIAIF LEVELS RISE FURTHER CAN LEAD TO DEATH


Effects of aldosterone on tubular secretion of hydrogen ions
EFFECTS OF ALDOSTERONE ON TUBULAR SECRETION OF HYDROGEN IONS RELEASING OR INHIBITING HORMONES

  • 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
EFFECTS OF ALDOSTERONE LACK ON THE CIRCULATORY SYSTEM RELEASING OR INHIBITING HORMONES

  • 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
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
FACTORS THAT AFFECT THE REGULATION OF ALDOSTERONE SECRETION SYSTEM

  • 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

ALDOSTERONE IS NOT AS DEPENDENT ON CRH AND ACTH SYSTEM

ANGIOTENSIN AND POTASSIUM LEVELS ARE THE MAJOR REGULATORS


Importance of potassium ions in aldosterone secretion
IMPORTANCE OF POTASSIUM IONS IN ALDOSTERONE SECRETION SYSTEM

  • INCREASE IN POTASSIUM IONS CAUSES INCREASED SECRETION OF ALDOSTERONE

  • ALDOSTERONE CAUSES ENHANCED EXCRETION OF POTASSIUM

  • POTASSIUM LEVELS RETURN TO NORMAL



Renin
RENIN SYSTEM

  • 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
FACTORS THAT INCREASE RENIN SECRETION SYSTEM

  • SYMPATHETIC INNERVATION

  • DECLINE IN RENAL BLOOD FLOW


Effects of renin
EFFECTS OF RENIN SYSTEM

  • 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
EFFECTS OF ANGIOTENSIN II SYSTEM

  • 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



Cortisol
CORTISOL SYSTEM


Generalized effects of cortisol
GENERALIZED EFFECTS OF CORTISOL SYSTEM

  • CARBOHYDRATE METABOLISM

  • PROTEIN METABOLISM

  • FAT METABOLISM

  • STRESS MANAGEMENT

  • ANTI-INFLAMMATORY EFFECTS



Effect of cortisol on gluconeogenesis
EFFECT OF CORTISOL ON GLUCONEOGENESIS SYSTEM

  • 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
EFFECTS OF CORTISOL ON GLUCOSE UTILIZATION BY CELLS SYSTEM

  • 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
EFFECTS OF CORTISOL ON BLOOD GLUCOSE CONCENTRATIONS SYSTEM

  • INCREASED GLUCONEOGENESIS

  • DECREASED GLUCOSE USE

  • RAISES BLOOD GLUCOSE LEVELS


Adrenal diabetes
ADRENAL DIABETES SYSTEM

  • INCREASE COULD BE AS LARGE AS 50 % ABOVE NORMAL

  • SIMILAR TO PITUITARY DIABETES BUT DIFFERENT FROM INSULIN DEFICIENCY



Effects of cortisol on cellular proteins stores
EFFECTS OF CORTISOL ON CELLULAR PROTEINS STORES SYSTEM

  • 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
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
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

EFFECTS OF CORTISOL ON FAT METABOLISM ON LIVER UTILIZATION OF AMINO ACIDS


Effect of cortisol on the mobilization of fats
EFFECT OF CORTISOL ON THE MOBILIZATION OF FATS ON LIVER UTILIZATION OF AMINO ACIDS

  • 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

OTHER EFFECTS OF CORTISOL ON LIVER UTILIZATION OF AMINO ACIDS


Effects of cortisol in stressful situation
EFFECTS OF CORTISOL IN STRESSFUL SITUATION ON LIVER UTILIZATION OF AMINO ACIDS

  • ANY KIND OF STRESS INCREASES ACTH SECRETION

  • INCREASED SECRETIONS OF CORTISOL IN MINUTES


Effects of cortisol on the inflammatory response
EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE ON LIVER UTILIZATION OF AMINO ACIDS

  • 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
SPECIFIC EFFECTS OF CORTISOL ON THE INFLAMMATORY RESPONSE ON LIVER UTILIZATION OF AMINO ACIDS

  • STABILIZES LYSOSOMAL MEMBRANES

  • BLOCKS MOST OF THE FACTORS CAUSING INFLAMMATION

  • INCREASES HEALING PROCESS


Importance of cortisol in fighting disease
IMPORTANCE OF CORTISOL IN FIGHTING DISEASE ON LIVER UTILIZATION OF AMINO ACIDS

  • RHEUMATOID ARTHRITIS

  • RHEUMATIC FEVER

  • ACUTE GLOMERULONEPHRITIS


Control of cortisol secretion
CONTROL OF CORTISOL SECRETION ON LIVER UTILIZATION OF AMINO ACIDS

  • ACTH IS THE MAJOR FACTOR CAUSING CORTISOL SECRETION


Effect of corticotropin releasing hormone in acth secretion
EFFECT OF CORTICOTROPIN RELEASING HORMONE IN ACTH SECRETION ON LIVER UTILIZATION OF AMINO ACIDS

  • SMALL PEPTIDE FROM HYPOTHALAMUS

  • LITTLE ACTH IS SECRETED IN THE ABSENCE OF CRH


Effects of physiological stress on acth secretion
EFFECTS OF PHYSIOLOGICAL STRESS ON LIVER UTILIZATION OF AMINO ACIDSON 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
FEEDBACK CONTROLS ON ACTH SECRETION ON LIVER UTILIZATION OF AMINO ACIDS

  • CORTISOL HAS A DIRECT NEGATIVE FEEDBACK EFFECT

    • ON HYPOTHALAMUS DECREASING CRH

    • ON ANTERIOR PITUITARY DECREASING ACTH


Hormones of the pancreas

HORMONES OF THE PANCREAS ON LIVER UTILIZATION OF AMINO ACIDS


Pancreatic hormones
PANCREATIC HORMONES ON LIVER UTILIZATION OF AMINO ACIDS

  • GLUCAGON

  • INSULIN

  • SOMATOSTATIN

  • PANCREATIC POLYPEPTIDE


Somatostatin
SOMATOSTATIN ON LIVER UTILIZATION OF AMINO ACIDS

  • 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
PANCREATIC POLYPEPTIDE ON LIVER UTILIZATION OF AMINO ACIDS

  • INHIBITS GALLBLADDER CONTRACTIONS

  • REGULATES PRODUCTION OF SOME PANCREATIC ENZYMES

  • MAY HELP IN CONTOLLING RATE OF ABSORPTION IN GI TRACT


Insulin
INSULIN ON LIVER UTILIZATION OF AMINO ACIDS

  • POLYPEPTIDE HORMONE

  • SECRETED BY BETA CELLS

  • WHEN GLUCOSE LEVELS RISE ABOVE NORMAL LEVELSOR

  • WHEN ELEVATED LEVELS OF ARGININE, LEUCINE AND OTHER HORMONES ARE PRESENT IN THE BLOOD


Insulin dependent cells
INSULIN DEPENDENT CELLS ON LIVER UTILIZATION OF AMINO ACIDS

  • MOST ALL THE CELL IN BODY


Insulin independent cells
INSULIN INDEPENDENT CELLS ON LIVER UTILIZATION OF AMINO ACIDS

  • BRAIN

  • KIDNEYS

  • LINING OF GI TRACT

  • RED BLOOD CELLS


Generalized effects of insulin
GENERALIZED EFFECTS OF INSULIN ON LIVER UTILIZATION OF AMINO ACIDS

  • 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 REDUCES THE BLOOD GLUCOSE LEVEL ON LIVER UTILIZATION OF AMINO ACIDS


Insulin is a protein and fat sparer
INSULIN IS A PROTEIN AND FAT SPARER ON LIVER UTILIZATION OF AMINO ACIDS


Specific effects of insulin
SPECIFIC EFFECTS OF INSULIN` ON LIVER UTILIZATION OF AMINO ACIDS


Effects of insulin on carbohydrate metabolism
EFFECTS OF INSULIN ON CARBOHYDRATE METABOLISM ON LIVER UTILIZATION OF AMINO ACIDS

  • 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
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
MECHANISMS OF GLUCOSE UPTAKE BY THE LIVER

  • 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
GLYCOGEN STORAGE IN LIVER BY THE LIVER

  • ABOUT 5-6 PERCENT OF LIVER MASS

  • USUALLY 100 GRAMS


Other effects of insulin on carbohydrate metabolism in the liver
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
EFFECTS OF INSULIN ON GLUCOSE METABOLISM IN MUSCLE CELLS LIVER

  • 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
CONDITIONS WHERE MUSCLES USE CONSIDERABLE GLUCOSE LIVER

  • 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
EFFECTS OF HEAVY EXERCISE ON MUSCLE CELLS LIVER

  • DOES NOT REQUIRE LARGE AMOUNTS OF INSULIN

  • MEMBRANE PERMEABILITY CHANGES DUE TO CONTRACTILE PROCESS


Effects of insulin
EFFECTS OF INSULIN LIVER

  • CAUSES RAPID TRANSPORT OF GLUCOSE INTO THE CELLS


Effect of insulin on the storage of glycogen in muscle cells
EFFECT OF INSULIN ON THE STORAGE OF GLYCOGEN IN MUSCLE CELLS LIVER

  • 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
DIFFERENCES BETWEEN LIVER GLYCOGEN AND MUSCLE GLYCOGEN LIVER

  • 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
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
EFFECTS OF GLUCOSE ON THE BRAIN MUSCLE CELLS

  • 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 ARE MAINTAINED DUE TO THE BRAINS NEED FOR GLUCOSE

  • BLOOD GLUCOSE LEVELS MUST ALWAYS MAINTAIN A CRITICAL LEVEL

  • LEVELS IN A RANGE OF 20-50 mg/100 ml CAUSES HYPOGLYCEMIC SHOCK


Symptoms of hypoglycemic shock
SYMPTOMS OF HYPOGLYCEMIC SHOCK FOR GLUCOSE

  • PROGESSIVE IRRITABILITY

  • FAINTING

  • CONVULSIONS

  • COMA

  • DEATH


Effect of insulin on fat metabolism
EFFECT OF INSULIN ON FAT METABOLISM FOR GLUCOSE

  • 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
EFFECTS OF INSULIN ON EXCESS FAT SYNTHESIS AND STORAGE FOR GLUCOSE

  • 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
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
INCREASED TRANSPORT OF GLUCOSE INTO THE LIVER 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
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
FATTY ACIDS ARE THEN TRANSPORTED TO THE ADIPOSE TISSUES CYCLE

  • REMOVES THEM AND PREVENTS A NEGATIVE FEEDBACK EFFECT ON ACETYL-co CARBOXYLASE


Effects of insulin of fat storage at the adipose tissues
EFFECTS OF INSULIN OF FAT STORAGE AT THE ADIPOSE TISSUES CYCLE

  • 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
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



Effects of insulin on protein metabolsism
EFFECTS OF INSULIN ON PROTEIN METABOLSISM INHIBITED IF NOT BLOCKED

  • 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



Effect of insulin on growth
EFFECT OF INSULIN ON GROWTH DEGRADATION OF PROTEINS

  • 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
CONTROL OF INSULIN SECRETION DEGRADATION OF PROTEINS

  • 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
EFFECTS OF BLOOD GLUCOSE LEVELS ON INSULIN SECRETION DEGRADATION OF PROTEINS

  • 80-90 mg/100ML--MINIMAL INSULIN SECRETION

  • ABOVE 100mg/100ML --INSULIN SECRETION RISES QUICKLY

  • CAN REACH AS MUCH AS 400 - 600 mg/100ML

  • SECRETION DECREASES RAPIDLY AS BLOOD GLUCOSE LEVELS RETURN TO FASTING LEVEL


Effect of amino acids on insulin secretion
EFFECT OF AMINO ACIDS ON INSULIN SECRETION DEGRADATION OF PROTEINS

  • 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
EFFECT OF GASTROINTESTINAL HORMONES ON INSULIN SECRETION DEGRADATION OF PROTEINS

  • 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

CARBOHYDRATE VS FATTY ACID (LIPID) METABOLISM DEGRADATION OF PROTEINS

INSULIN DETERMINES WHICH WILL OCCUR


Glucagon
GLUCAGON DEGRADATION OF PROTEINS

  • PRODUCED BY ALPHA CELLS


Generalized effects of glucagon
GENERALIZED EFFECTS OF GLUCAGON DEGRADATION OF PROTEINS

  • 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

GLUCAGON IS A GLUCOSE SPARER DEGRADATION OF PROTEINS


Glycogenolysis and increased blood glucose levels caused by glucagon
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
MECHANISMS OF ACTIVATING GLYCOGENOLYSIS IN THE LIVER GLUCAGON

  • 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
EFFECT OF GLUCAGON ON GLUCONEOGENESIS IN THE LIVER GLUCAGON

  • 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
REGULATION OF GLUCAGON SECRETION GLUCAGON

  • 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
EFFECTS OF AMINO ACIDS ON GLUCAGON SECRETION GLUCAGON

  • HELPS PREVENT HYPOGLYCEMIA THAT WOULD OCCUR IF YOU ATE A MEAL OF PURE PROTEIN


Importance of blood glucose regulation

IMPORTANCE OF BLOOD GLUCOSE REGULATION GLUCAGON

ITS ALL FOR THE BRAIN


In normal individual
IN NORMAL INDIVIDUAL GLUCAGON

  • BLOOD GLUCOSE LEVELS ARE TIGHTLY REGULATED

  • BETWEEN 80-90 IN THE MORNING

  • 120 TO 140 AFTER BREAKFAST

  • RETURN TO NORMAL IN ABOUT 2 HOURS AFTER MEAL


Maintenance of blood glucoses between meals
MAINTENANCE OF BLOOD GLUCOSES BETWEEN MEALS GLUCAGON

  • 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

THEY DO IT ALL FOR THE BRAIN GLUCAGON

ALSO THE RETINA, GERMINAL EPITHELIA OF GONADS, KIDNEYS, AND OTHER INSULIN INDEPENDENT CELLS


Pineal gland
PINEAL GLAND GLUCAGON

  • PEA SIZED

  • EPITHALAMUS

  • ROOF OF DIENCEPHALON

  • NEUROENDOCRINE TRANSDUCER


Neuroendocrine transducer
NEUROENDOCRINE TRANSDUCER GLUCAGON

  • CONVERTS SIGNALS RECEIVED THROUGH NERVOUS SYSTEM INTO AN ENDOCRINE SIGNAL


Relationship to hypothalamus
RELATIONSHIP TO HYPOTHALAMUS GLUCAGON

  • INFORMATION ABOUT LIGHT AND DARK CYCLES CARRIED FROM EYES TO HYPOTHALAMUS

  • SYMPATHETIC NERVES CARRY ACTION POTENTIALS TO PINEAL GLAND


Hormones of the pineal gland
HORMONES OF THE PINEAL GLAND GLUCAGON

  • MELATONIN

  • OTHERS HAVE BEEN FOUND BUT THEY DO NOT KNOW THEIR FUNCTIONS ARGININE VASOTOCIN


Melatonin
MELATONIN GLUCAGON

  • DERIVED FROM SERATONIN

  • PRODUCTION LOWEST IN DAYLIGHT

  • PRODUCTION HIGHEST AT NIGHT


Effects of melatonin
EFFECTS OF MELATONIN GLUCAGON

  • 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
HORMONES OF THE REPRODUCTIVE TISSUES GLUCAGON

  • MALE

  • FEMALE

  • REGULATED BY FSH AND LH


The hormones of the testes
THE HORMONES OF THE TESTES GLUCAGON

  • TESTOSTERONE

  • INHIBIN


Hormones of the ovaries
HORMONES OF THE OVARIES GLUCAGON

  • ESTROGENS ESTRADIOL, ESTRIN ESTRONE

  • PROGESTINS PROGESTERONE

  • INHIBIN

  • RELAXIN


Hormones of the placenta
HORMONES OF THE PLACENTA GLUCAGON

  • TEMPORARY ORGAN

  • ESTROGEN

  • PROGESTERONE

  • HUMAN CHORIONIC GONADOTROPIN


Hormone of the uterus
HORMONE OF THE UTERUS GLUCAGON

  • RELAXIN


Hormones of pregnancy
HORMONES OF PREGNANCY GLUCAGON

  • HUMAN CHORIONIC GONADOTROPIN

  • SECRETION OF PROGESTERONE

  • SECRETION OF ESTROGEN

  • HUMAN CHORIONIC SOMATOMAMMOTROPIN


Human chorionic gonadotropin
HUMAN CHORIONIC GONADOTROPIN GLUCAGON

  • 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
DIFFUSES FROM FETAL BLOOD INTO MATERNAL BLOOD GLUCAGON

  • 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
PLACENTA TAKES OVER SECRETORY FUNCTION AT SECOND MONTH GLUCAGON

  • SECRETES ESTROGEN AND PROGESTERONE

  • PLACENTA STOPS SECRETING HUMAN CHORIONIC

    • CAUSING THE CORPUS LUTEUM TO DEGENERATE AND INVOLUTE


Importance of human chorionic gonadotropin
IMPORTANCE OF GLUCAGONHUMAN 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
PROGESTERONE SECRETION BY THE PLACENTA GLUCAGON

  • 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
ROLE OF PLACENTAL PROGESTERONE GLUCAGON

  • 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
PLACENTAL ESTROGEN GLUCAGON

  • 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
ESTROGEN FUNCTIONS GLUCAGON

  • 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
IMPORTANCE OF THE FETUS IN SECRETING PLACENTAL ESTROGEN GLUCAGON

  • 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


Human chorionic somatomammotropin
HUMAN CHORIONIC SOMATOMAMMOTROPIN GLUCAGON

  • 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
HORMONAL CHANGES IN PREGNANCY GLUCAGON

  • INHIBITION OF GONADOTROPIN

  • STIMULATION OF PROLACTIN

  • STIMULATION OFRELAXIN

  • STIMULATION OF INSULIN

  • STIMULATION OF ALDOSTERONE

  • STIMULATION OF CORTISOL

  • STIMULATION OF THYROID HORMONE


Inhibition of gonadotropins
INHIBITION OF GONADOTROPINS GLUCAGON

  • 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
STIMULATION OF PROLACTIN GLUCAGON

  • SECRETION INCREASES THROUGHOUT PREGNANCY

  • WORKS WITH ESTROGEN AND PROGESTERONE TO STIMULATE BREAST DEVELOPMENT AND MILK PRODUCTION


Stimulation of relaxin
STIMULATION OF RELAXIN GLUCAGON

  • HUMAN CHORIONIC GONADOTROPIN STIMULATES RELAXIN SECRETION BY CORPUS LUTEUM IN FIRST TWO MONTHS

  • LATER RELAXIN IS SECRETED BY THE ENDOMETRIUM


Function of relaxin
FUNCTION OF RELAXIN GLUCAGON

  • RELAXES PELVIC LIGAMENTS

  • WORKS WITH PROGESTERONE TO INHIBIT UTERINE CONTRACTIONS


Stimulation of insulin
STIMULATION OF INSULIN GLUCAGON

  • 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
STIMULATION OF ALDOSTERONE GLUCAGON

  • 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
STIMULATION OF CORTISOL GLUCAGON

  • 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
EFFECTS OF INCREASED CORTISOL LEVELS GLUCAGON

  • 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
INCREASED THYROID HORMONE GLUCAGON

  • 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
THE ENDOCRINE FUNCTION OF THE HEART GLUCAGON

  • ATRIOPEPTIN/ATRIAL NATRIURETIC PEPTIDE

  • PRODUCED BY ATRIA CARDIAC MUSCLES


Effects of atrial natriuretic peptide
EFFECTS OF ATRIAL NATRIURETIC PEPTIDE GLUCAGON

  • 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



Hormones of the digestive system
HORMONES OF THE DIGESTIVE SYSTEM GLUCAGON

  • GASTRIN

  • SECRETIN

  • CHOLECYSTOKININ


Gastrin
GASTRIN GLUCAGON

  • POLYPEPTIDE

  • SECRETED BY MUCOSAL LINING

  • STIMULATES PRODUCTION OF HCL AND PEPSIN


Secretin
SECRETIN GLUCAGON

  • 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
CHOLECYSTOKININ GLUCAGON

  • SECRETED BY WALL OF DUODENUM

  • STIMULATES CONTRACTION OF DUODENUM

  • INHIBITS GASTRIC ACID SECRETIONS UNDER CERTAIN CONDITIONS

  • STIMULATES THE RELEASE OF ENZYMES FROM THE PANCREAS



Calcitriol
CALCITRIOL GLUCAGON

  • 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
EFFECT OF CALCITRIOL GLUCAGON

  • 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
ERYTHROPOIETIN GLUCAGON

  • PEPTIDE HORMONE

  • RELEASED BY KIDNEY IN RESPONSE TO HYPOXIA IN KIDNEY TISSUES


Possible causes of hypoxia
POSSIBLE CAUSES OF HYPOXIA GLUCAGON

  • 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
EFFECT OF ERYTHROPOIETIN GLUCAGON

  • STIMULATES HEMATOPOIESIS

  • ELEVATES BLOOD VOLUME SLIGHTLY DUE TO INCREASE IN RED BLOOD CELLS

  • IMPROVES OXYGEN DELIVERY TO PERIPHERAL TISSUES


Leptin

LEPTIN GLUCAGON

A NEW HORMONE


Effects of aging
EFFECTS OF AGING GLUCAGON

  • FEW FUNCTIONAL CHANGES

  • DECLINE IN LEVELS OF REPRODUCTIVE HORMONES

  • ENDOCRINE TISSUES MAY BECOME LESS RESPONSIVE

  • SOME TARGET CELLS IN TISSUES MAY BECOME LESS RESPONSIVE


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