Endocrine System Pt.2 Flashcards
Thyroid gland is composed of…
-isthmus
-composed of follicles that produce glycoprotein thyroglobulin
-colloid (fluid with thyroglobulin + iodine) fills lumen of follicles and is precursor for TH
-parafollicular cells produce hormone calcitonin
Isthmus
2 lateral lobes connected by median mass
Thyroid hormone (TH) includes
Thyroxine (T4) and triiodothyronine (T3) which increase rate of cellular metabolism. Consequently, oxygen use and heat production rise
Effects of T3 and T4 on basal metabolic rate (BMR)/ temp. Regulation
Normal: promotes normal o2 use and BMR; calorigenesis; enhances effects of SNS
Hypo: BMR below normal; decreases body temp, cold intolerance; decreases appetite; weight gain; reduced sensitivity to catecholamine
Hyper: BMR above normal; increased body temp., heat intolerance; increased appetite; weight loss
Effects of T4 and T3 on carb/lipid/protein metabolism
Normal: promotes glucose catabolism; mobilizes fats: essential for protein synthesis: enhances liver’s synthesis of cholesterol
Hypo: decreases glucose metabolism; elevated cholesterol/triglyceride levels in blood; decreases protein synthesis; edema
Hyper: enhanced catabolism of glucose, proteins, and fats; weight loss; loss of muscle mass
Effects of T4 and T3 on NS
Normal: promotes normal development of NS in fetus and infant; promotes normal adult NS production
Hypo: in infant, slowed/deficient brain development, intellectual disability; in adults, mental dulling, depression, paresthesias, memory impairment, hypoactive reflexes
Hyper: irritability, restlessness, insomnia, personality changes exophthalmos (in Graves’ disease)
Effects of T4 and T3 on NS
Normal: promotes normal development of NS in fetus and infant; promotes normal adult NS production
Hypo: in infant, slowed/deficient brain development, intellectual disability; in adults, mental dulling, depression, paresthesias, memory impairment, hypoactive reflexes
Hyper: irritability, restlessness, insomnia, personality changes exophthalmos (in Graves’ disease)
Thyroid Hormone (TH)
-2 related compounds:
-T4 (thyroxine); has 3 tyrosine molecules + 4 bound iodine atoms
-T3 (triiodothyronine), has 2 tyrosines + 3 bound iodine atoms
-major metabolic hormone
-increases metabolic rate and heat production (calorigenic effect)
-regulation of tissue growth and development:
-development of skeletal and NS
-Reproductive capabilities
-maintenance of blood pressure
Effects of T4 and T3 on ❤️ system
Normal: promotes normal functioning of the ❤️
Hypo: decreased efficiency of ❤️s pumping action; low ❤️ rate and blood pressure
Hyper: increased sensitivity to catecholamines can lead to rapid ❤️ rate, palpitations, high blood pressure, and ❤️ failure
Synthesis of TH
-thyroid gland stores hormone extra cellularly
-thyroidglobulin synthesizedand discharged into follicle lumen
-iodides (I-) actively taken into cell and released into lumen
-iodides oxidized to iodine (I2)
-iodine attaches to tyrosine, mediated by perioxidase
-iodinated tyrosines link together to form T3 and T4
-colloid is endocystosed and vesicle is combined with a lysosome
-T3 and T4 are cleaved and diffused into bloodstream
Effects of T4 and T3 on muscular system
Normal: promotes normal muscular development and function
Hypo: sluggish muscle action; muscle cramps; myalgia
Hyper: muscle atrophy and weakness
Transport and regulation of TH
-T4 and T3 transported in the body by thyroxine-binding globulins (TBGs)
-both bind to target receptors, but T3 is 10x more active than T4
-peripheral tissues convert T4 to T3
-(-) feedback regulation of TH:
-rising TH levels provide (-) feedback inhibition on release of TSH
-hypothalamic thyrotropin-releasing hormone (TRH) can overcome (-) feedback during pregnancy or exposure to cold
Effects of T4 and T3 on Skeletal system
Normal: promotes normal growth and maturation of skeleton
Hypo: in child, growth retardation, skeletal stunting and retention of child’s body proportions; in adults: joint pain
Hyper: in child: excessive skeletal growth, initially, followed by early epiphyseal closure and short stature; in adult: demineralization of skeleton
Homeostatic imbalances of TH
-Hypo in adults:
-pts are cold, fatigued and overweight
-myxedema; goiter if due to lack of iodine
-hashimotos- TSH receptor is blacked by abnormal antibody
-hypo in infants- cretinism
-hyper- graves:
-underweight, hot, anxious with voracious appetite
-exophthalmos
-can have goiter
-can be caused by abnormal antibody (long acting thyroid stimulator; LATS)
-also promotes excessive thyroid growth by binding to TSH receptor
Effects of T4 and T3 in GI system
Normal: promotes normal GI motility and tone; increases secretion of digestive juices
Hypo: depressed GI motility, tone, and secretory activity; constipation
Hyper: excessive GI motility; diarrhea
Effects of T4 and T3 in GI system
Normal: promotes normal GI motility and tone; increases secretion of digestive juices
Hypo: depressed GI motility, tone, and secretory activity; constipation
Hyper: excessive GI motility; diarrhea
Calcitonin
-produced by parafollicular (c) cells
-no known physiological role in humans
-antagonist to parathyroid hormone (PTH)
-at higher than normal doses:
-inhibits osteoclast activity and release of Ca2+ from bone matrix
-stimulates Ca2+ uptake and incorporation into bone matrix
Calcitonin
-produced by parafollicular (c) cells
-no known physiological role in humans
-antagonist to parathyroid hormone (PTH)
-at higher than normal doses:
-inhibits osteoclast activity and release of Ca2+ from bone matrix
-stimulates Ca2+ uptake and incorporation into bone matrix
Effects of T4 and T3 on. Reproductive system
Normal: promotes normal female reproductive ability and lactation
Hypo: depressed ovarian function: sterility; depressed lactation
Hyper: in females: depressed ovarian function; in males; impotence
Effects of T4 and T3 on integumentary system
Normal: promotes normal hydration and secretory activity of skin
Hypo: skin pale, thick, and dry; facial edema; hair coarse and thick
Hyper: skin flushed, this, and moist; hair fine and soft; nails soft and thin
Parathyroid glands
-4-8 tiny glands embedded in posterior aspect of thyroid
-Contain oxyphil cells (function unknown) and parathyroid cells that secrete parathyroid hormone (PTH) or parathormone
-PTH—most important hormone in Ca2+ homeostasis
Secretion of thyroid hormone, promoted by TSH, requires…
Follicular cells to take up the stored colloid and split the hormones from the colloid for release. Rising levels of TH feedback to inhibit the anterior pituitary and hypothalamus
Parathyroid hormone
Functions
• Stimulates osteoclasts to digest bone matrix and release Ca2+ to:
-Enhances reabsorption of Ca2+ and secretion of phosphate by kidneys
-Promotes activation of vitamin D (by kidneys); increases absorption of Ca2+ by intestinal mucosa
• Negative feedback control: rising Ca2+ in blood inhibits PTH release
Homeostatic imbalances of PTH
-Must regulate Ca2+ levels very closely
-Hyperparathyroidism due to tumor
-Bones soften and deform
-Elevated Ca2+ depresses nervous system and contributes to formation of kidney stones
-Hypoparathyroidism following gland trauma or removal or dietary magnesium deficiency
-Results in tetany, respiratory paralysis
What is the difference between T3 and T4? Which one of these is referred to as thyroxine?
T4 has 4 bound iodine atoms, and T3 has 3. T4 is the major hormone secreted, but T3 is more potent. T4=thyroxine
Why does TH require plasma proteins in order to move through blood? Where are the receptors for TSH located?
TH must be carried through🩸by plasma proteins b/c it is lipid soluble and so does not readily dissolve in 🩸, which is mostly💧. The receptors for TSH are located on plasma membrane of the thyroid follicle cells (on the sides facing away from colloid- TSH is 💧-soluble hormone from anterior pituitary)
Adrenal (suprarenal) glands
-Paired, pyramid-shaped organs atop kidneys
-Structurally and functionally are two glands in one
-Adrenal medulla—nervous tissue; part of sympathetic nervous system
-Adrenal cortex—three layers of glandular tissue that synthesize and secrete corticosteroids
Parathyroid glands
-Located on dorsal aspect of thyroid gland
-secrete PTH- increases 🩸calcium levels
-targets bone, kidneys, and small intestine (indirectly via Vit D activation)
-PTH= key hormone for calcium homeostasis
Adrenal cortex
-Three layers and corticosteroids produced
1) Zona glomerulosa—mineralocorticoids
2) Zona fasciculata—glucocorticoids
3) Zona reticularis—gonadocorticoids
PTH release and inhibit
Falling 🩸calcium levels trigger PTH release; rising 🩸 calcium levels inhibit its release
Mineralocorticoids
-Regulate electrolytes (primarily Na+ and K+) in ECF
-Importance of Na+: affects ECF volume, blood volume, blood pressure, levels of other ions
-Importance of K+: sets RMP
-Aldosterone most potent mineralocorticoid
-Stimulates Na+ reabsorption and water retention by kidneys; elimination of K+
-Increases blood volume
-Increases blood Na+
-Decreases blood K+
Hyperparathyroidism results in…
Hypercalcemia and extreme bone wasting
Hypoparathyroidism leads to…
Hypocalcemia, evidenced by tetany and respiratory paralysis
Aldosterone
Release triggered by:
• Decreasing blood volume and blood pressure
• Rising blood levels of K+
Paired adrenal (suprarenal) glands
Sit atop the kidneys. Each adrenal gland has 2 functional portions, the cortex and medulla
Indicated general functions of parathyroid hormone
-raises 🩸 calcium
-stimulates release of calcium from bones
-indirectly increases activity of AND # of osteoclasts
-stimulates reabsorption of calcium by kidneys
-stimulates final conversion of vit d in kidneys
-calcidiol into calcitriol
-calcitriol aids calcium absorption in small intestines
-decreases 🩸 phosphate
-stimulates release of phosphate from bones and absorption of phosphate in the gut
-stimulates secretion of phosphate by kidneys
-amount secreted by kidneys exceeds the amount being released/reabsorbed, leading to OVERALL decrease in 🩸 phosphate levels
Mechanisms of aldosterone secretion
Renin-angiotensin-aldosterone mechanism: decreased blood pressure stimulates kidneys to release renin, triggers formation of angiotensin II, potent stimulator of aldosterone release
• Plasma concentration of K+: increased K+ directly influences zona glomerulosa cells to release aldosterone
• ACTH: causes small increases of aldosterone during short-term stress
• Atrial natriuretic peptide (ANP): blocks renin and aldosterone secretion to decrease BP
What is the major effect of TH? PTH? Calcitonin?
TH: increase basal metabolic rate (and heat production) in the body.
PTH: increases 🩸 Ca2+ levels in variety of ways
Calcitonin at high levels (pharmacological) has Ca2+- lowering, bone-sparing effects (at normal levels, no effects on humans)
Homeostatic imbalances of aldosterone
Aldosteronism—hypersecretion due to adrenal tumors
• Hypertension and edema due to excessive Na+
• Excretion of K+ leading to abnormal function of neurons and muscle
Name the cells that release TH, PTH, and calcitonin?
-thyroid follicular cells release TH
-parathyroid cells in parathyroid gland release PTH
-parafollicular (C) cells in the thyroid gland release calcitonin
Glucocorticoids
-Keep blood glucose levels relatively constant
-Maintain blood pressure by increasing action of vasoconstrictors
-Cortisol (hydrocortisone)
-Cortisone
-Corticosterone
-Normal levels maintained by negative feedback
Glucocorticoids
-Keep blood glucose levels relatively constant
-Maintain blood pressure by increasing action of vasoconstrictors
-Cortisol (hydrocortisone)
-Cortisone
-Corticosterone
-Normal levels maintained by negative feedback
List hormones produced by adrenal gland and their physiological effects
Aldosterone- helps kidneys control their amount of salt in the 🩸 and tissues in the body
Cortisol- helps the body manage and use carbs, proteins, and fats.
Adrenaline
List the 3 classes of hormones released from the adrenal cortex and briefly state the major effects of each?-
Glucocorticoids are stress hormones that, among many effects, increase 🩸 glucose.
Mineralocortoids increase 🩸 Na+ (and 🩸 pressure) and decrease 🩸 K+
Gonadcorticoids are male and female sex hormones that are thought to have a variety of effects
Glucocorticoids: cortisol
Released in response to ACTH, patterns of eating and activity, and stress
• Prime metabolic effect is gluconeogenesis—formation of glucose from fats and proteins
-Promotes rises in blood glucose, fatty acids, and amino acids
• “Saves” glucose for brain
• Enhances vasoconstriction à rise in blood pressure to quickly distribute nutrients to cells
• Powerful anti-inflammatory – reduces effects of histamine
• Suppresses the immune system – reduces the activity of T and B cells
• Inhibits healing
• Alters mood
• Increases appetite
Mineralocortoids (chiefly aldosterone) regulation of release
Stimulates by renin-angiotensin-aldosterone mechanism (activated by decreasing 🩸volume or 🩸 pressure), elevated 🩸 K+ levels, and ACTH (minor influence)
Mineralocortoids (chiefly aldosterone/ adrenocortical hormones) regulation of release
Stimulates by renin-angiotensin-aldosterone mechanism (activated by decreasing 🩸volume or 🩸 pressure), elevated 🩸 K+ levels, and ACTH (minor influence)
Inhibited by increasing 🩸 pressure, decreases 🩸 K+ levels
Homeostatic imbalances of glucocorticoids
-Hypersecretion—Cushing’s syndrome/disease
-Depresses cartilage and bone formation
-Inhibits inflammation
-Depresses immune system
-Disrupts cardiovascular, neural, and gastrointestinal
-Fat redistribution
-Buffalo hump
-Hyposecretion—Addison’s disease
-Decrease in glucose and Na+ levels
-Difficulty handling chronic stress
-Extreme fatigue
-Weight loss
-Hyperpigmentation
-Also involves deficits in mineralocorticoids
-Decreased Na+ levels
-Severe dehydration, and hypotension
Homeostatic imbalances of glucocorticoids
-Hypersecretion—Cushing’s syndrome/disease
-Depresses cartilage and bone formation
-Inhibits inflammation
-Depresses immune system
-Disrupts cardiovascular, neural, and gastrointestinal
-Fat redistribution
-Buffalo hump
-Hyposecretion—Addison’s disease
-Decrease in glucose and Na+ levels
-Difficulty handling chronic stress
-Extreme fatigue
-Weight loss
-Hyperpigmentation
-Also involves deficits in mineralocorticoids
-Decreased Na+ levels
-Severe dehydration, and hypotension
Mineralcorticoids target organ and effects
Kidneys: increase 🩸 levels of Na+ and b decrease 🩸 levels of K+
Since 💧 reabsorption usually accompanies sodium retention, 🩸 volume and 🩸 pressure rise
Gonadocorticoids (Sex Hormones)
-Most weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens
-May contribute to:
-Onset of puberty
-Appearance of secondary sex characteristics
-Sex drive in women
Gonadocorticoids (Sex Hormones)
-Most weak androgens (male sex hormones) converted to testosterone in tissue cells, some to estrogens
-May contribute to:
-Onset of puberty
-Appearance of secondary sex characteristics
-Sex drive in women
Mineralocorticoids effects of hyper and hypo secretion
Hyper: aldosteronism
Hypo: Addison’s disease
What are the 2 major stimuli for aldosterone release? What is the major stimulus for cortisol release?
Aldosterone:
1) decrease in 🩸 blood volume or 🩸 pressure, which triggers the renin-angiotensin-aldosterone mechanism
2)increase in plasma K+ levels
Cortisol:
ACTH from anterior pituitary- in turn is controlled by CRH from hypothalamus. CRH release follows a diurnal (day-night) rhythm and is increased in response to various stressors, as well as by hypoglycemia and fever
Gonadocortoids hypersecretion
-Adrenogenital syndrome (masculinization)
-Not noticeable in adult males
-Females and prepubertal males
-Boys – reproductive organs mature; secondary sex characteristics emerge early
-Females – beard, masculine pattern of body hair; clitoris resembles small penis
Glucocorticoids (chiefly cortisol/ adrenocortical hormone) regulation of release
Stimulated by ACTH
Inhibited by feedback inhibition exerted by cortisol
Adrenal medulla
-Medullary chromaffin cells synthesize epinephrine (80%) and norepinephrine (20%)
-Effects
-Vasoconstriction
-Increased heart rate
-Increased blood glucose
-Blood diverted to brain, heart, and skeletal muscle
-Released in response to acute (short term) stress (fight or flight)
-Responses brief
-Epinephrine stimulates metabolic activities, bronchial dilation, and blood flow skeletal muscles and the heart
-Norepinephrine influences peripheral vasoconstriction and blood pressure
-Tends to increase BP to maintain profusion during fight or flight response
Glucocorticoids target organ and effects
Body cells: promotes gluconeogenrsis and hyperglycemia; mobilizes fats for energy metabolism; stimulate protein catabolism; assist body to resist stressors; depress inflammatory and immune responses
Stress and the general adaptive syndrome
-Any condition, Physical or emotional, that threatens homeostasis is a form of STRESS
-Exposure to stressors will produce the same general pattern of hormonal and physiological adjustments
-These responses are part of the general adaptive syndrome aka the stress response
-It can be divided into three phases
▪ The Alarm Phase
▪ The Resistance Phase
▪ The Exhaustion Phase
Glucocorticoids effects of hyper and hyposecretion
Hyper: Cushing’s
Hypo: Addison’s
The Alarm Phase
-The immediate short-term response to a crises which involves:
▪ General sympathetic activation
▪ With epinephrine and norepinephrine release from the adrenal medulla
-This leads to:
▪ Increased mental alertness
▪ Increased energy use by all cells
▪ Glycogen and lipid reserve mobilization
▪ Changes in circulation
▪ Decreased digestive activity and urine production
▪ Increased sweat gland secretion
▪ Increases in heart and respiratory rates
Gonadocorticoids (chiefly androgens, converted to testosterone or estrogens after release/ Adrenocortical hormones) regulation of release
Stimulated by ACTH; mechanism of inhibition incompletely understood, but feedback inhibition not seen
The Resistance Phase
-The long-term metabolic adjustments which involves:
-The release of GHRH and CRH (same as ACTHRH) from the hypothalamus
-This inhibits the release of Growth Hormone and glucocorticoids (by way of ACTH).
-Sympathetic stimulation causes the activation of the Renin-Angiotensin system to produce Aldosterone and ADH
-For the conservation of water and salts
-K+ and H+ are lost
-GH and glucocorticoids together:
-Mobilize the remaining energy reserves
-Lipids from dipose tissue
-Amino acids from skeletal muscle
- Conserve Glucose
-Peripheral tissues break down lipids or energy
-Not neural tissue
-Glucocorticoids and Glucagon (from the pancreas) together:
-Elevate blood Glucose Concentration:
-Liver synthesizes glucose from:
-Lipids
-Carbohydrates
Gonadocorticoids target organ and effects
Insignificant effects in males; contributes to female libido; development of pubic and axillary hair in females; source of estrogens after menopause
Exhaustion Phase
▪ When the resistance phase ends homeostatic regulation breaks down
▪ Unless action is taken immediately, organ systems will begin to fail Due to:
-Exhaustion of energy reserves
-Inability to produce glucocorticoids
-Failure of electrolyte balance (Why?)
-Cumulative damage to vital organs
▪ If not treated immediately it will lead to death
Gonadocorticoids effects of hypersecretion
Hyper: masculinization of females (adrenogenital syndrome)
Pineal Gland
-Small gland hanging from roof of third ventricle
-Pinealocytes secrete melatonin, derived from serotonin
-Melatonin may affect
-Timing of sexual maturation and puberty
-Day/night cycles
-In darkness melatonin is released causing sleepiness
-Light impulses from the retina suppress melatonin release
– Physiological processes that show rhythmic variations (body temperature, sleep, appetite) –(Supplements?)
– production of antioxidant and detoxification molecules in the liver
Catecholamines (epinephrine and norepinephrine/ adrenal medullary hormone)
Stimulated by preganglionic fibers of SNS
Pancreas
• Triangular gland partially behind stomach
• Has both exocrine and endocrine cells
-Acinar cells (exocrine) produce enzyme-rich juice for digestion
-Pancreatic islets (islets of Langerhans) contain endocrine cells
-Alpha (a) cells produce glucagon (hyperglycemic hormone)
-Beta (b) cells produce insulin (hypoglycemic hormone)
-PP cells (formerly F cells) produce pancreatic polypeptide - regulates pancreatic and gastric function
Catecholamines target organ and effects
SNS target organs: effects mimic SNS activation; increase ❤️ rate and metabolic rate; increase 🩸 pressure by promoting vasoconstriction
Glucagon
• Major target liver
• Causes increased blood glucose levels
• Effects
-Glycogenolysis—breakdown of glycogen to glucose
-Gluconeogenesis—synthesis of glucose from lactic acid and noncarbohydrates
-Release of glucose to the 🩸
Glucagon
• Major target liver
• Causes increased blood glucose levels
• Effects
-Glycogenolysis—breakdown of glycogen to glucose
-Gluconeogenesis—synthesis of glucose from lactic acid and noncarbohydrates
-Release of glucose to the 🩸
Catecholamines effects of hypersecretion
Hyperglycemia, increased metabolic rate, rapid heartbeat and palpitations, hypertension, intense nervousness, sweating (prolonged fight or flight)
Catecholamines effects of hypersecretion
Hyperglycemia, increased metabolic rate, rapid heartbeat and palpitations, hypertension, intense nervousness, sweating (prolonged fight or flight)
Insulin
• Effects of insulin (51 Amino Acid protein)
-Lowers blood glucose levels
-Enhances membrane transport of glucose into fat and muscle cells
-Inhibits glycogenolysis and gluconeogenesis
-Participates in neuronal development and learning and memory
• Not needed for glucose uptake in liver, kidney or brain
-These organs are insulin independent
Adrenal cortex, adrenal medulla, anterior pituitary, and posterior pituitary: which part of the glands release steroid hormones? Amino acids-based hormones?
Adrenal cortex released steroid hormones
Adrenal medulla, anterior, and posterior pituitary release amino acid-based hormones
ACTH from anterior pituitary acts to cause release of steroid hormones from the adrenal cortex. Both adrenal medulla and posterior pituitary are composed of nervous tissue rather than glandular tissue, that other glands are made of
Adrenal cortex, adrenal medulla, anterior pituitary, and posterior pituitary: which part of the glands release steroid hormones? Amino acids-based hormones?
Adrenal cortex released steroid hormones
Adrenal medulla, anterior, and posterior pituitary release amino acid-based hormones
ACTH from anterior pituitary acts to cause release of steroid hormones from the adrenal cortex. Both adrenal medulla and posterior pituitary are composed of nervous tissue rather than glandular tissue, that other glands are made of
Insulin action on cells
• Activates tyrosine kinase enzyme receptor
• Cascade an increased glucose uptake into increased glycogen synthesis
• Triggers enzymes to:
-Catalyze oxidation of glucose for ATP production – first priority
-Polymerize glucose to form glycogen – next priority
-Convert glucose to fat (particularly in adipose tissue) – last priority
• Also works as growth hormone, promoting:
-increased amino acid uptake
-to increase protein synthesis
Insulin action on cells
• Activates tyrosine kinase enzyme receptor
• Cascade an increased glucose uptake into increased glycogen synthesis
• Triggers enzymes to:
-Catalyze oxidation of glucose for ATP production – first priority
-Polymerize glucose to form glycogen – next priority
-Convert glucose to fat (particularly in adipose tissue) – last priority
• Also works as growth hormone, promoting:
-increased amino acid uptake
-to increase protein synthesis
Pineal gland
-located in the diencephalon
-primary hormone is melatonin which influences daily rhythm in body temp., sleep, and appetite and may have an antigonadotropic effect in children
Pineal gland
-located in the diencephalon
-primary hormone is melatonin which influences daily rhythm in body temp., sleep, and appetite and may have an antigonadotropic effect in children
Factors that influence insulin release
• insulin release is stimulated by:
-Elevated blood glucose levels – primary stimulus
-Remember Insulin: Lowers blood glucose levels by driving it into cells, burning it as fuel, storing it as glycogen and fat
-Rising blood levels of amino acids and fatty acids
-Release of acetylcholine by parasympathetic nerve fibers (Does this make sense?)
-Hyperglycemic hormones like glucagon, epinephrine, growth hormone, thyroxine, glucocorticoids
-indirectly stimulate insulin release
-by increasing glucose levels
-Insulin release is Inhibited by:
-Low blood sugar
-Somatostatin (GHIH)
-Secreted by Delta (d) Islet Cells
-sympathetic nervous system
Short-term stress
The hypothalamus activates the adrenal medulla via neural stimuli
1) APs triggered by the hypothalamus in response to stressors activate the SNS
2) APs travel along preganglionic sympathetic axons to adrenal medulla
3) adrenal medulla secrete amino acid-based hormones: epinephrine (80%) and some norepinephrine (20%)
4)epinephrine and norepinephrine reinforce other sympathetic responses to ready the body for exertion (fight or flight)
Homeostatic imbalances of insulin
• Hyposecretion = Hyperglycemia
-Signs and Symptoms include:
-Polyuria—increased urine output with glycosuria
-Glucose acts as osmotic diuretic
-Polydipsia—increased thirst
-From water loss due to polyuria
-Polyphagia—•increased appetite (why?)
-Cells cannot take up glucose; are “starving”
-Since glucose can not be burned as fuel in most…
-liver increases its burning of fats to generate auxiliary fuels or ketone bodies (acidic) Þketoacidosis
-Untreated ketoacidosis Þ hyperpnea; disrupted heart activity and O2 transport; depression of nervous system Þ coma and death possible
Long-term stress
The hypothalamus activates the adrenal cortex via hormonal stimuli. This greatly reinforces the continuing short-term stress response.
1)stressors cause hypothalamic neurons to release corticotropin-releasing hormone (CRH)
2)CRH travels via the portal system of blood vessels to the anterior pituitary
3) anterior pituitary cells (corticotrophs) release adrenocorticotropic hormone (ACTH)
4) ACTH travels in blood to the adrenal cortex
5) the adrenal cortex synthesizes and releases glucorticoids, e.g. cortisol (and Mineralocorticoids, e.g., aldosterone)
Diabetes mellitus
• Group of disorders characterized by High Blood Sugar with glycosuria
• Type 1 – insulin dependent
–Childhood onset
–beta cells do not produce insulin
–May be caused by autoimmune reaction to a viral infection
–Must replace insulin by multiple injections or continuous infusion
•Type 2 – insulin independent
–Usually later onset
–Associated with obesity
–beta cell produce normal amounts of insulin but cells become resistant to it
–May be controlled through diet and exorcize
–Oral medicines to lower blood glucose
•Uncontrolled (?) Diabetes can lead to chronic medical problems
Pancreas type of gland
Exocrine and endocrine. Endocrine portion (pancreatic islets) releases insulin and glucagon and smaller amounts of other hormones to the 🩸
Hypersecretion of insulin- hyperinsulinism
• Causes:
• –Hypoglycemia (Low blood glucose)
• –Anxiety, nervousness, disorientation, unconsciousness, even death
• Treated by sugar ingestion
• The body cells need glucose!
• NOTE: Hypoglycemia is much more serious than hyperglycemia since cells, especially neurons, can die in absence of sufficient glucose
Pancreas: glucagon released by
Alpha cells when 🩸 levels of glucose are low, stimulates the liver to release glucose to the blood
Ovaries and placenta
• Gonads produce steroid sex hormones
– Same as those of adrenal cortex
• Ovaries produce estrogens and progesterone
– Estrogen
-Maturation of reproductive system
-Appearance of secondary sexual characteristics
-With progesterone, causes breast development and cyclic changes in uterine mucosa
• Placenta secretes estrogens, progesterone, and human chorionic gonadotropin (hCG)
Pancreas: insulin is released by…
Beta cells when 🩸 levels of glucose (and amino acids) are rising. It increases the rate of glucose uptake and metabolism by most body cells. Hyposecretion or hyperactivity of insulin results in diabetes; cardinal signs are Polyuria, polydipsia, and polyphagia
Pancreas: insulin is released by…
Beta cells when 🩸 levels of glucose (and amino acids) are rising. It increases the rate of glucose uptake and metabolism by most body cells. Hyposecretion or hyperactivity of insulin results in diabetes; cardinal signs are Polyuria, polydipsia, and polyphagia
Testes
• Testes produce testosterone
-initiates maturation of male reproductive organs
-Causes appearance of male secondary sexual characteristics and sex drive
-Necessary for normal sperm production
-Maintains reproductive organs in functional state
Adipose tissue
Leptin – appetite control; stimulates increased energy expenditure
Thymus
-Located: upper thorax
-releases the paracrines thymulin, thymosins, and thymopoietins, which are important tissues the normal development of the immune response
Enteroendocrine cells of GI
• Gastrin stimulates release of HCl
• Secretin stimulates liver and pancreas
• Cholecystokinin stimulates pancreas, gallbladder, and hepatopancreatic sphincter
• Serotonin acts as paracrine
Enteroendocrine cells of GI
• Gastrin stimulates release of HCl
• Secretin stimulates liver and pancreas
• Cholecystokinin stimulates pancreas, gallbladder, and hepatopancreatic sphincter
• Serotonin acts as paracrine
❤️
Atrial natriuretic peptide (ANP) decreases blood Na+ concentration, therefore blood pressure and blood volume
Kidneys
• Erythropoietin signals production of red blood cells
• Renin initiates the renin-angiotensin-aldosterone mechanism
Kidneys
• Erythropoietin signals production of red blood cells
• Renin initiates the renin-angiotensin-aldosterone mechanism
Skeleton (osteoblasts)
Osteocalcin
• Prods pancreas to secrete more insulin; restricts fat storage; improves glucose handling; reduces body fat
• Activated by insulin
• Low levels of osteocalcin in type 2 diabetes – perhaps increasing levels may be new treatment
Skin
Cholecalciferol, precursor of vitamin D
Skin
Cholecalciferol, precursor of vitamin D
Which hormones does ❤️ produce and what is its function?
The ❤️ produces atrial natriuretic (ANP).
ANP decreases 🩸pressure by increasing the kidney’s production of salty urine
What is the main function of the hormone produced by the skin?
Major function of vit D3, produced in inactive form by the skin, is to increase intestinal absorption of calcium
Diabetes mellitus and diabetes inspidus are both due to a lack of a hormone. Which hormone causes which? What symptom do they have in common? What would you find in the urine of a pt w/ 1 but not the other.
Diabetes mellitus is due to a lack of insulin production or action, whereas diabetes inspidus is due to lack of ADH. Both conditions are characterized by production of copious amounts of urine. You would find glucose in the urine of a pt with diabetes mellitus, but not in diabetes inspidus
What chemical class of hormones do gonadal hormones belong to? Which major endocrine gland secretes hormones of the same chemical class
Gonadal hormones are steroid hormones. A major endocrine that also secretes steroid hormones is the adrenal cortex
The major stimulus for release of parathyroid hormone is…
Humoral
Important anabolic hormones; many of its effects mediated by IGFs
Growth hormone
Cause the kidneys to conserve water and/or salt
Aldosterone and ADH
Stimulates milk production
Prolactin
Tropic hormone that stimulates the gonads to secrete sex hormones
LH
Increases uterine contractions during birth
Oxytocin
Major metabolic hormones of the body
T4 and T3
Causes reabsorption of sodium ions by the kidneys
Aldosterone
Causes reabsorption of sodium ions by the kidneys
Aldosterone
Tropic hormone that stimulates the thyroid gland to secrete thyroid hormone
TSH
Secreted by posterior pituitary
ADH and oxytocin
Steroid hormone
Aldosterone
If there is adequate carb intake, secretion of insulin results in…
-lower 🩸 glucose
-increased cell utilization of glucose
-storage of glycogen
If there is adequate carb intake, secretion of insulin results in…
-lower 🩸 glucose
-increased cell utilization of glucose
-storage of glycogen
If anterior pituitary secretion is deficient in a growing child, the child will…
Become a dwarf but have fairly normal body proportions
Some hormones act by
-increasing the synthesis of enzymes
-converting an inactive enzyme into an active enzyme
-affecting only specific target organs
Lipolysis
metabolic process that breaks down fat stores in the body into glycerol and free fatty acids (FFAs)
Gluconeogenesis
Metabolic process that produces glucose from non-carb sources, such as amino acids, lactate, and glycerol
Glycogenolysis
process of breaking down glycogen into glucose to produce energy when the body needs it
What is the mechanism of action of lipid-soluble hormones?
Activation of genes, which increases protein synthesis in the cell
What keeps intracellukar receptors from binding to DNA before a hormone binds to the receptor?
Chaperone proteins (chaperonins)
What gland secretes the most important hormone controlling calcium balance in the blood?
Parathyroid
Zona glomerulosa: class of hormones it produces
Mineralocorticoids
What material is stored in the lumen of thyroid follicle?
Iodinated thyroglobulin, from which TH can be produced
What type of stimulation controls parathyroid release?
Humoral
Another name for TSH
Thyroidtropin
