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CORTISOL DEFICIENCY
HYPOGLYCEMIA
ALDOSTERONE Extracellular water balance KIDNEY ADRENAL CORTEX OF Increased aldosterone INCREASED Na+
(MINERALOCORTICOIDS o Adjusts blood Na+ reabsorption THE ADRENAL GLAND secretion DECREASED H+ and K+
) pressure and water ZONA LOW blood volume
-under tonic control of volume reabsorption GLOMERULOSA (hence low blood ALDOSTERONE EXCESS
ACTH Na+ and K+ homeostasis H+ and K+ excretion pressure) HYPERTENSION
-regulated separately by Na+ deficiency HYPOKALEMIA
RAAS and K+ levels HIGH K+ levels METABOLIC ALKALOSIS
TESTOSTERONE Stimulates GH SECRETION at TESTES TESTIS Negative feedback on Pubertal growth spurt
puberty Reinforce LEYDIG CELLS in anterior pituitary Differentiation of
Causes eventual EPIPHYSEAL spermatogenic males epididymis, vas deferens
CLOSURE effects of FSH in and seminal vesicles
DEVELOPMENT OF MALE Sertoli cells THECA CELLS in Growth of penis and
SECONDARY SEX females seminal vesicles
CHARACTERISTICS MUSCLES Libido
Stimulates PROTEIN Protein synthesis Deepening of voice
SYNTHESIS in males
Stimulates DESCENT OF
TESTES BEFORE BIRTH
Regulates SPERM
PRODUCTION
ESTROGEN Stimulates GH SECRETION at OVARY OVARY Negative feedback on Growth of axillary and pubic
puberty Follicular phase of anterior pituitary hair
Causes eventual EPIPHYSEAL menstrual cycle
CLOSURE (by ESTRADIOL)
GROWTH, DEVELOPMENT Luteal phase of
AND MAINTENANCE OF menstrual cycle
FEMALE SECONDARY SEX (by
CHARACTERISTICS PROGESTERONE)
Regulate FEMALE
REPRODUCTIVE CYCLE
Maintain PREGNANCY
THYROID HORMONE Increases BMR BONES THYROID GLAND Increased TH secretion HYPERTHYROIDISM
-permissive effects on Accelerates BODY GROWTH Skeletal growth FOLLICULAR LOW TH levels INCREASED BMR
catecholamines CALORIGENIC ACTION CELLS LOW BMR Weight LOSS
-permissive for GH o Stimulate PROTEIN MUSCLES Conditions that Negative nitrogen balance
secretion and action SYNTHESIS Protein synthesis increase ATP SWEATING
-permissive for CNS o Increase LIPOLYSIS DEMAND: cold INCREASED cardiac output
development o Increase GLUCOSE ADIPOCYTES environment, DYSPNEA
and FA utilisation Lipolysis hypoglycaemia, TREMORS, WEAKNESS
for ATP high altitude, EXOPHTHALMUS
PRODUCTION CNS pregnancy GOITER
Enhances CHOLESTEROL Maturation
EXCRETION HYPOTHYROIDISM
DEVELOPMENT OF CNS DECREASED BMR
Weight GAIN
Positive nitrogen balance
COLD SENSITIVITY
DECREASED cardiac output
HYPOVENTILATION
LETHARGY, MENTAL
SLOWNESS
DROOPING EYELIDS
MYXEDEMA
MENTAL RETARDATION,
STUNTED BONE GROWTH
GOITER
INSULIN Increases GLUCOSE UPTAKE ADIPOCYTES PANCREAS Increased insulin DECREASED BLOOD GLUCOSE
into cells Glucose uptake BETA CELLS OF secretion (because glucose is no longer
Increases GLYCOGEN and utilisation THE ISLETS OF INCREASED blood in the blood but is inside the
SYNTHESIS Triglyceride LANGERHANS glucose cell where it is utilised for ATP
Decreases GLYCOGENOLYSIS synthesis INCREASED amino production)
and GLUCONEOGENESIS acids, fatty acid
LIVER GLUCAGON DECREASED FATTY ACID,
Increases PROTEIN Glucose uptake KETOACID, AMINO ACID
SYNTHESIS Glycogen Insulin secretion
Increases TRIGLYCERIDE synthesis inhibited HYPOKALEMIA (due to
SYNTHESIS and FAT DECREASED blood potassium intake as an action
DEPOSITION MUSCLE glucose of insulin)
Decreases LIPOLYSIS Glucose uptake SOMATOSTATIN
Increases POTASSIUM and utilisation
UPTAKE into cells Glycogen
synthesis
Stimulates FETAL GROWTH Protein synthesis
Stimulates POSTNATAL
GROWTH by stimulating
secretion of IGF-1
GLUCAGON Increases GLYCOGENOLYSIS ADIPOCYTES PANCREAS Increased glucagon INCREASED BLOOD GLUCOSE
and GLUCONEOGENESIS Lipolysis ALPHA CELLS OF secretion INCREASED FATTY ACID,
Increases LIPOLYSIS and THE ISLETS OF DECREASED blood KETOACID
KETOACID PRODUCTION LIVER LANGERHANS glucose
Glycogenolysis INCREASED amino
Gluconeogenesis acids
Glucagon secretion
inhibited
INCREASED blood
glucose
INCREASED amino
acids, ketoacids
INSULIN
SOMATOSTATIN
OTHER ORGANS
Protein synthesis
increase in organ size
INSULIN Increases GLUCOSE UPTAKE ADIPOCYTES PANCREAS Increased insulin DECREASED BLOOD
into cells Glucose uptake and BETA CELLS OF THE secretion GLUCOSE (because
Increases GLYCOGEN utilisation ISLETS OF INCREASED blood glucose is no longer in
SYNTHESIS Triglyceride synthesis LANGERHANS glucose the blood but is inside
Decreases GLYCOGENOLYSIS INCREASED amino the cell where it is
and GLUCONEOGENESIS LIVER acids, fatty acid utilised for ATP
Glucose uptake GLUCAGON production)
Increases PROTEIN Glycogen synthesis
SYNTHESIS Insulin secretion DECREASED FATTY
Increases TRIGLYCERIDE MUSCLE inhibited ACID, KETOACID,
SYNTHESIS and FAT Glucose uptake and DECREASED blood AMINO ACID
DEPOSITION utilisation glucose
Decreases LIPOLYSIS Glycogen synthesis SOMATOSTATIN HYPOKALEMIA (due to
Increases POTASSIUM Protein synthesis potassium intake as an
UPTAKE into cells action of insulin)
THYROID HORMONE Increases BMR BONES THYROID GLAND Increased TH secretion HYPERTHYROIDISM
-permissive effects on Accelerates BODY GROWTH Skeletal growth FOLLICULAR CELLS LOW TH levels INCREASED BMR
catecholamines CALORIGENIC ACTION LOW BMR Weight LOSS
-permissive for GH o Stimulate PROTEIN MUSCLES Conditions that Negative nitrogen
secretion and action SYNTHESIS Protein synthesis increase ATP balance
-permissive for CNS o Increase LIPOLYSIS DEMAND: cold SWEATING
development o Increase GLUCOSE ADIPOCYTES environment, INCREASED cardiac
and FA utilisation for Lipolysis hypoglycaemia, high output
ATP PRODUCTION altitude, pregnancy DYSPNEA
Enhances CHOLESTEROL CNS TREMORS,
EXCRETION Maturation WEAKNESS
DEVELOPMENT OF CNS EXOPHTHALMUS
GOITER
HYPOTHYROIDISM
DECREASED BMR
Weight GAIN
Positive nitrogen
balance
COLD SENSITIVITY
DECREASED
cardiac output
HYPOVENTILATION
LETHARGY,
MENTAL
SLOWNESS
DROOPING
EYELIDS
MYXEDEMA
MENTAL
RETARDATION,
STUNTED BONE
GROWTH
GOITER
ESTROGEN Stimulates GH SECRETION at OVARY OVARY Negative feedback on Growth of axillary and
puberty Follicular phase of anterior pituitary pubic hair
Causes eventual EPIPHYSEAL menstrual cycle (by
CLOSURE ESTRADIOL)
GROWTH, DEVELOPMENT Luteal phase of
AND MAINTENANCE OF menstrual cycle (by
FEMALE SECONDARY SEX PROGESTERONE)
CHARACTERISTICS
Regulate FEMALE
REPRODUCTIVE CYCLE
Maintain PREGNANCY
CORTISOL DEFICIENCY
HYPOGLYCEMIA
INTESTINE
Stimulates calcium,
phosphate and magnesium
absorption
LH secretion inhibited
TESTOSTERONE,
ESTROGEN,
PROGESTERONE
(negative feedback)
TESTOSTERONE Stimulates GH SECRETION TESTES LEYDIG CELLS in Testosterone secretion Pubertal growth spurt
at puberty Reinforce spermatogenic males inhibited Differentiation of
Causes eventual effects of FSH in Sertoli TESTOSTERONE epididymis, vas
EPIPHYSEAL CLOSURE cells THECA CELLS in (negative feedback) deferens and seminal
DEVELOPMENT OF MALE females vesicles
SECONDARY SEX MUSCLES Growth of penis and
CHARACTERISTICS Protein synthesis seminal vesicles
Stimulates PROTEIN Libido
SYNTHESIS in males Deepening of voice
ESTROGEN Stimulates GH SECRETION OVARY Converted from Increased estrogen Maturation and
(ESTRADIOL) at puberty Follicular phase of TESTOSTERONE secretion maintenance of the
Causes eventual menstrual cycle ESTROGE fallopian tubes,
EPIPHYSEAL CLOSURE CORPUS uterus, cervix and
DEVELOPMENT OF UTERUS LUTEUM, Estrogen secretion vagina
FEMALE SECONDARY SEX Proliferation of uterine PLACENTA, inhibited Development of
CHARACTERISTICS lining during follicular FETAL ADRENAL ESTROGEN (negative breasts
Maintains PREGNANCY phase of menstrual cycle GLAND feedback) FSH and Up-regulates
Lower UTERINE LH suppressed estrogen, LH and
THRESHOLD TO progesterone
CONTRACTILE STIMULI receptors
DURING PREGNANCY Proliferation and
development of
ovarian granulosa
cells