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HORMONES OF THE ENDOCRINE SYSTEM. HORMONES OF THE PITUITARY NEUROHYPOPHYSIS--POSTERIOR PITUITARY ADENOHYPOPHYSIS--ANTERIOR PITUITARY.

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Presentation on theme: "HORMONES OF THE ENDOCRINE SYSTEM. HORMONES OF THE PITUITARY NEUROHYPOPHYSIS--POSTERIOR PITUITARY ADENOHYPOPHYSIS--ANTERIOR PITUITARY."— Presentation transcript:

1 HORMONES OF THE ENDOCRINE SYSTEM

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

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

4 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

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

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

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

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

9 OXYTOCIN WOMEN MEN

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

11 OTHER SOURCES OF OXYTOCIN FETUS UTERUS

12 NEUROENDOCRINE REFLEXES CONTROL

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

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

15 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

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

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

18 OTHER SUBSTANCES DERIVED FROM PROOPIMELANOCORTIN LIPOTROPINS BETA ENDORPHINS MELANOCYTE STIMULATING HORMONE

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

20 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

21 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

22 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

23 GONADOTROPINS

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

25 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

26 PROLACTIN IN MALES MAKES INTERSTITIAL CELLS MORE RESPONSIVE TO LUTEINIZING HORMONE

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

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

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

30 DIRECT EFFECTS STIMULATES STEM CELL DIVISION AND GROWTH OF DAUGHTER CELLS

31 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

32 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

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

34 PROTEIN SYNTHESIS BY RIBOSOMES DIRECT EFFECT ON RIBOSOMES

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

36 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

37 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

38 GROWTH HORMONE STIMULATES FATTY ACID METABOLISM SPARES GLUCOSE AND AMINO ACIDS

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

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

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

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

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

44 FEEDBACK CONTROL OF GROWTH HORMONE SECRETION

45 HORMONES OF THE THYROID GLAND THYROID HORMONE AND CALCITONIN

46 THYROID HORMONE THYROXINE (T 4 ) TRIIODOTHRYONINE (T 3 )

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

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

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

50 MIT AND DIT MONOIODTYROSINE DIIODOTYROSINE THYROXINE TRIIODOTHRYRONINE

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

52 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

53 TRANSPORT IN THE BLOOD THRYOXINE BINDING GLOBULIN ALBUMINS

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

55 IMPORTANCE OF LATENCY AND DURATION OF ACTION T 4 -- TWO OR THREE DAY LATENT PERIOD MAXIMUM ACTIVITY IN 10-12 DAYS T 3 --- 6 TO 12 HOURS MAXIMUM ACTIVITY IN 2-3 DAYS

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

57 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

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

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

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

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

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

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

64 EFFECT ON FAT METABOLISM LIPOGENESIS LIPOLYSIS MOBILIZATION OF LIPIDS

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

66 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%

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

68 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

69 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

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

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

72 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

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

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

75 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

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

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

78 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

79 CHILDREN VS ADULTS MAJOR ROLE IN CHILD MINOR ROLE IN ADULTS

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

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

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

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

84 PARATHYROID GLAND SMALL FLATTENED GLANDS POSTERIOR SURFACE OF THYROID GLAND

85 CELLS OF PARATHYROID CHIEF CELLS OXYPHIL CELLS

86 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

87 ORGANS AFFECTED BY PARATHYROID HORMONE BONES KIDNEY

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

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

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

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

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

93 REGULATION OF PARATHYROID HORMONE RELEASE

94 THYMUS 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

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

96 OTHER SITES OF THYMOSIN SYNTHESIS MACROPHAGES

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

98 HORMONES OF THE ADRENAL GLAND CORTICAL VS MEDULLARY HORMONES

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

100 HORMONE SECRETION 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

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

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

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

104 ALPHA RECEPTORS MOST COMMON ALPHA RECEPTOR ACTIVATES G p PROTEINS G PROTEINS ACTIVATE ENZYMES

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

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

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

108 BETA 2 RECEPTOR ACTIVATES STIMULATORY G PROTEINS

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

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

111 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

112 SOME SPECIFIC EFFECTS OF CATECHOLAMINES

113 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

114 VASODILATION BY EPINEPHRINE CAUSES MILD VASODILATION IN SKELETAL IN CARDIAC

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

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

117 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

118 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

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

120 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

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

122 ALL ADRENOCORTICOIDS ARE STEROIDS

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

124 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

125 TARGET CELLS OF ALDOSTERONE KIDNEYS SWEAT GALNDS SALIVARY GLANDS PANCREAS

126 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

127 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 +

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

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

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

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

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

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

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

135 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

136 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

137 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 %

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

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

140 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

141 EFFECT OF RENIN- ANGIOTENSIN SYSTEM ON ALDOSTERONE SECRETION

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

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

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

145 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

146 EFFECTS OF ALDOSTERONE AT THE CELLULAR LEVEL

147 CORTISOL

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

149 EFFECTS OF CORTISOL ON CARBOHYDRATE METABOLISM

150 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

151 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

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

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

154 EFFECT OF CORTISOL ON PROTEIN METABOLISM

155 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

156 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

157 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

158 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

159 EFFECTS OF CORTISOL ON FAT METABOLISM

160 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

161 OTHER EFFECTS OF CORTISOL

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

163 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

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

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

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

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

168 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

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

170 HORMONES OF THE PANCREAS

171 PANCREATIC HORMONES GLUCAGON INSULIN SOMATOSTATIN PANCREATIC POLYPEPTIDE

172 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

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

174 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

175 INSULIN DEPENDENT CELLS MOST ALL THE CELL IN BODY

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

177 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

178 INSULIN REDUCES THE BLOOD GLUCOSE LEVEL

179 INSULIN IS A PROTEIN AND FAT SPARER

180 SPECIFIC EFFECTS OF INSULIN`

181 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

182 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

183 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

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

185 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

186 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

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

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

189 EFFECTS OF INSULIN CAUSES RAPID TRANSPORT OF GLUCOSE INTO THE CELLS

190 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

191 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

192 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

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

194 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

195 SYMPTOMS OF HYPOGLYCEMIC SHOCK PROGESSIVE IRRITABILITY FAINTING CONVULSIONS COMA DEATH

196 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

197 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

198 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

199 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

200 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

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

202 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

203 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

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

205 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

206 INSULIN GREATLY ENHANCES PROTEIN SYNTHESIS AND DECREASES DEGRADATION OF PROTEINS

207 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

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

209 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 400 - 600 mg/100ML SECRETION DECREASES RAPIDLY AS BLOOD GLUCOSE LEVELS RETURN TO FASTING LEVEL

210 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

211 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

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

213 GLUCAGON PRODUCED BY ALPHA CELLS

214 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

215 GLUCAGON IS A GLUCOSE SPARER

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

217 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

218 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

219 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

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

221 IMPORTANCE OF BLOOD GLUCOSE REGULATION ITS ALL FOR THE BRAIN

222 IN NORMAL INDIVIDUAL 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

223 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

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

225 PINEAL GLAND PEA SIZED EPITHALAMUS ROOF OF DIENCEPHALON NEUROENDOCRINE TRANSDUCER

226 CONVERTS SIGNALS RECEIVED THROUGH NERVOUS SYSTEM INTO AN ENDOCRINE SIGNAL

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

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

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

230 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

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

232 THE HORMONES OF THE TESTES TESTOSTERONE INHIBIN

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

234 HORMONES OF THE PLACENTA TEMPORARY ORGAN ESTROGEN PROGESTERONE HUMAN CHORIONIC GONADOTROPIN

235 HORMONE OF THE UTERUS RELAXIN

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

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

238 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

239 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

240 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

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

242 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

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

244 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

245 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

246 HUMAN CHORIONIC SOMATOMAMMOTROPIN SECRETION BEGINS AT ABOUT 4 TH 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

247 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

248 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

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

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

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

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

253 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

254 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

255 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

256 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

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

258 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

259 ENDOCRINE FUNCTION OF THE DIGESTIVE SYSTEM

260 HORMONES OF THE DIGESTIVE SYSTEM GASTRIN SECRETIN CHOLECYSTOKININ

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

262 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

263 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

264 HORMONES OF THE KIDNEYS

265 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

266 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

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

268 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

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

270 LEPTIN A NEW HORMONE

271 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


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