Podcast
Questions and Answers
Within the intricate cascade of thyroid hormone synthesis, the coupling of iodinated tyrosine residues is catalyzed by which enzymatic complex, and how does its malfunction specifically disrupt the stoichiometric balance of T3 and T4 production?
Within the intricate cascade of thyroid hormone synthesis, the coupling of iodinated tyrosine residues is catalyzed by which enzymatic complex, and how does its malfunction specifically disrupt the stoichiometric balance of T3 and T4 production?
- Thyroid peroxidase; by favoring the formation of diiodotyrosine (DIT) over monoiodotyrosine (MIT), subsequently disrupting T4 synthesis. (correct)
- Thyroglobulin; by altering the tertiary structure required for efficient T3 and T4 iodination, leading to a non-selective reduction in hormone production.
- Deiodinase; by prematurely deiodinating T4 into T3 within the thyroglobulin molecule, skewing the T3/T4 ratio during synthesis.
- Pendrin; by inhibiting the transport of iodide into the follicular lumen, thus curtailing both T3 and T4 synthesis equally.
The inherent structural plasticity of the thyroglobulin molecule allows for compensatory mechanisms that maintain euthyroidism, even under conditions of severe iodine deficiency, by optimizing the coupling efficiency of available iodotyrosines.
The inherent structural plasticity of the thyroglobulin molecule allows for compensatory mechanisms that maintain euthyroidism, even under conditions of severe iodine deficiency, by optimizing the coupling efficiency of available iodotyrosines.
False (B)
Explain the paradoxical effects of high concentrations of iodide on thyroid hormone synthesis, detailing the molecular mechanisms that underlie the Wolff-Chaikoff effect and how this phenomenon is clinically relevant.
Explain the paradoxical effects of high concentrations of iodide on thyroid hormone synthesis, detailing the molecular mechanisms that underlie the Wolff-Chaikoff effect and how this phenomenon is clinically relevant.
The Wolff-Chaikoff effect is an autoregulatory phenomenon where high iodide concentrations acutely inhibit thyroid hormone synthesis by decreasing iodide trapping, iodination, and hormone release. This is clinically relevant because it can be exploited to manage hyperthyroidism and protect the thyroid gland during radiation exposure.
Given the intricate interplay between the hypothalamus, pituitary, and thyroid glands, a lesion in the ______ that selectively disrupts TRH secretion, while sparing other hypothalamic functions, would result in secondary hypothyroidism characterized by reduced TSH and thyroid hormone levels.
Given the intricate interplay between the hypothalamus, pituitary, and thyroid glands, a lesion in the ______ that selectively disrupts TRH secretion, while sparing other hypothalamic functions, would result in secondary hypothyroidism characterized by reduced TSH and thyroid hormone levels.
Match each cell type in the pancreatic islets of Langerhans with its corresponding primary hormonal product and delineate the specific physiological stimulus that triggers its release:
Match each cell type in the pancreatic islets of Langerhans with its corresponding primary hormonal product and delineate the specific physiological stimulus that triggers its release:
In the context of adrenal steroidogenesis, what is the rate-limiting step regulated by ACTH, and which specific enzymatic deficiency would most selectively impair glucocorticoid and androgen synthesis while relatively sparing mineralocorticoid production?
In the context of adrenal steroidogenesis, what is the rate-limiting step regulated by ACTH, and which specific enzymatic deficiency would most selectively impair glucocorticoid and androgen synthesis while relatively sparing mineralocorticoid production?
The clinical presentation of primary hyperaldosteronism invariably includes both profound hypokalemia and metabolic alkalosis due to the obligate renal potassium wasting and enhanced hydrogen ion excretion induced by excessive mineralocorticoid activity.
The clinical presentation of primary hyperaldosteronism invariably includes both profound hypokalemia and metabolic alkalosis due to the obligate renal potassium wasting and enhanced hydrogen ion excretion induced by excessive mineralocorticoid activity.
Delineate the molecular mechanisms through which cortisol exerts its permissive effects on the actions of other hormones, providing specific examples of how cortisol modulates receptor expression, signal transduction pathways, and enzymatic activities to facilitate these hormonal interactions.
Delineate the molecular mechanisms through which cortisol exerts its permissive effects on the actions of other hormones, providing specific examples of how cortisol modulates receptor expression, signal transduction pathways, and enzymatic activities to facilitate these hormonal interactions.
In the complex pathophysiology of Addison's disease, the loss of negative feedback inhibition by cortisol on the hypothalamus and pituitary leads to a compensatory increase in ______ and ______, which paradoxically contributes to hyperpigmentation due to melanocyte stimulation.
In the complex pathophysiology of Addison's disease, the loss of negative feedback inhibition by cortisol on the hypothalamus and pituitary leads to a compensatory increase in ______ and ______, which paradoxically contributes to hyperpigmentation due to melanocyte stimulation.
Match the following conditions with their underlying pathophysiological mechanisms and primary clinical manifestations:
Match the following conditions with their underlying pathophysiological mechanisms and primary clinical manifestations:
Within the complex regulation of insulin secretion from pancreatic beta cells, which intracellular signaling molecule directly triggers the exocytosis of insulin-containing granules, and how is its production modulated by alterations in glucose metabolism within the beta cell?
Within the complex regulation of insulin secretion from pancreatic beta cells, which intracellular signaling molecule directly triggers the exocytosis of insulin-containing granules, and how is its production modulated by alterations in glucose metabolism within the beta cell?
In type 2 diabetes mellitus, the primary defect is an absolute deficiency of insulin secretion resulting from autoimmune destruction of pancreatic beta cells, necessitating lifelong insulin replacement therapy from the time of diagnosis.
In type 2 diabetes mellitus, the primary defect is an absolute deficiency of insulin secretion resulting from autoimmune destruction of pancreatic beta cells, necessitating lifelong insulin replacement therapy from the time of diagnosis.
Explain the concept of 'glucotoxicity' in the context of diabetes mellitus, detailing the specific molecular and cellular mechanisms through which chronic hyperglycemia impairs pancreatic beta-cell function and contributes to the progressive decline in insulin secretion.
Explain the concept of 'glucotoxicity' in the context of diabetes mellitus, detailing the specific molecular and cellular mechanisms through which chronic hyperglycemia impairs pancreatic beta-cell function and contributes to the progressive decline in insulin secretion.
In the diagnostic evaluation of diabetes insipidus, a critical step involves assessing the patient's response to ______ administration, which helps differentiate between central and nephrogenic forms of the disease based on whether it restores urinary concentrating ability.
In the diagnostic evaluation of diabetes insipidus, a critical step involves assessing the patient's response to ______ administration, which helps differentiate between central and nephrogenic forms of the disease based on whether it restores urinary concentrating ability.
Match the following oral hypoglycemic agents with their primary mechanisms of action and key clinical considerations:
Match the following oral hypoglycemic agents with their primary mechanisms of action and key clinical considerations:
Considering the pineal gland's role in circadian rhythm regulation, what specific molecular mechanism mediates the transduction of photic information from the suprachiasmatic nucleus (SCN) to the pineal gland, ultimately influencing melatonin synthesis, and how does this pathway differ between diurnal and nocturnal species?
Considering the pineal gland's role in circadian rhythm regulation, what specific molecular mechanism mediates the transduction of photic information from the suprachiasmatic nucleus (SCN) to the pineal gland, ultimately influencing melatonin synthesis, and how does this pathway differ between diurnal and nocturnal species?
Melatonin, synthesized exclusively by the pineal gland, exerts its chronobiotic effects solely through activation of high-affinity membrane receptors located in the suprachiasmatic nucleus (SCN), with no significant intracellular targets or alternative mechanisms of action.
Melatonin, synthesized exclusively by the pineal gland, exerts its chronobiotic effects solely through activation of high-affinity membrane receptors located in the suprachiasmatic nucleus (SCN), with no significant intracellular targets or alternative mechanisms of action.
Describe the experimental evidence supporting the role of melatonin in regulating the timing of puberty in humans, detailing the specific studies that implicate melatonin signaling in the suppression of gonadotropin-releasing hormone (GnRH) secretion and the subsequent onset of sexual maturation.
Describe the experimental evidence supporting the role of melatonin in regulating the timing of puberty in humans, detailing the specific studies that implicate melatonin signaling in the suppression of gonadotropin-releasing hormone (GnRH) secretion and the subsequent onset of sexual maturation.
Given the intricate feedback loops governing sex hormone production, a complete androgen insensitivity syndrome (CAIS) in an XY individual, characterized by a non-functional androgen receptor, would result in elevated levels of ______ and conversion of testosterone to ______, ultimately leading to feminization despite the presence of a Y chromosome.
Given the intricate feedback loops governing sex hormone production, a complete androgen insensitivity syndrome (CAIS) in an XY individual, characterized by a non-functional androgen receptor, would result in elevated levels of ______ and conversion of testosterone to ______, ultimately leading to feminization despite the presence of a Y chromosome.
Match the following sex steroid hormones with their primary cellular sources, key physiological actions, and regulatory control mechanisms:
Match the following sex steroid hormones with their primary cellular sources, key physiological actions, and regulatory control mechanisms:
Considering the complex interplay between hormonal signaling and placental function, which specific placental hormone is structurally most similar to luteinizing hormone (LH) and serves to maintain the corpus luteum during early pregnancy, thereby ensuring continued progesterone production?
Considering the complex interplay between hormonal signaling and placental function, which specific placental hormone is structurally most similar to luteinizing hormone (LH) and serves to maintain the corpus luteum during early pregnancy, thereby ensuring continued progesterone production?
Following menopause, the primary source of estrogen production shifts from the ovaries to the adrenal glands, which significantly ramp up estradiol synthesis to compensate for the loss of ovarian function and maintain stable estrogen levels.
Following menopause, the primary source of estrogen production shifts from the ovaries to the adrenal glands, which significantly ramp up estradiol synthesis to compensate for the loss of ovarian function and maintain stable estrogen levels.
Explain the dual-cell theory of estrogen synthesis in the ovary, detailing the roles of theca and granulosa cells and the specific enzymatic activities that each cell type contributes to the overall production of estradiol.
Explain the dual-cell theory of estrogen synthesis in the ovary, detailing the roles of theca and granulosa cells and the specific enzymatic activities that each cell type contributes to the overall production of estradiol.
Flashcards
Pituitary Gland (Hypophysis)
Pituitary Gland (Hypophysis)
Located on the inferior aspect of the brain in the diencephalon region, connected to the hypothalamus by the infundibulum.
Adenohypophysis
Adenohypophysis
The anterior lobe of the pituitary gland; derived from a pouch of epithelial tissue, releases hormones.
GH (Growth Hormone)
GH (Growth Hormone)
Growth hormone; stimulates body growth, stimulates secretion of IGF-1, stimulates lipolysis.
TSH (Thyroid-Stimulating Hormone)
TSH (Thyroid-Stimulating Hormone)
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ACTH (Adrenocorticotropic Hormone)
ACTH (Adrenocorticotropic Hormone)
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Dwarfism
Dwarfism
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Thyroid hormone
Thyroid hormone
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Thyroid Follicles
Thyroid Follicles
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Parafollicular cells
Parafollicular cells
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Follicular cells
Follicular cells
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Cretinism
Cretinism
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Graves' disease
Graves' disease
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Hypothyroidism Remedy
Hypothyroidism Remedy
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Hypothyroidism
Hypothyroidism
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Parathyroid Hormone (Function)
Parathyroid Hormone (Function)
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Hyperparathyroidism
Hyperparathyroidism
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Hypoparathyroidism
Hypoparathyroidism
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Adrenal Glands Location
Adrenal Glands Location
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Fight-or-flight Response
Fight-or-flight Response
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Corticosteroids
Corticosteroids
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Gulcocorticoids
Gulcocorticoids
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Hyperaldosteronism
Hyperaldosteronism
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Alpha (α) Pancreatic cells
Alpha (α) Pancreatic cells
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Beta (β) Pancreatic cells
Beta (β) Pancreatic cells
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Diabetes Symptoms
Diabetes Symptoms
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Study Notes
- The pituitary gland, or hypophysis, sits on the inferior aspect of the brain in the diencephalon region
- It is about 1.3 cm (0.5 in.) in diameter
- It attaches to the hypothalamus by a stalk called the infundibulum
- The adenohypophysis derives from a pouch of epithelial tissue known as Rathke's pouch
Anterior Pituitary Gland (Adenohypophysis)
- The anterior pituitary lobe is large
- It releases hormones, including growth hormone (GH)
- Other hormone releases include, Thyroid Stimulating hormone (TSH) and Adenocorticotropic hormone (ACTH)
- It releases Lutenizing hormone (LH)
- Other secretions include Follicle stimulating hormone (FSH)
- It secretes Melanocyte stimulating hormone (MSH)
- The anterior pituitary also the releases Prolactin (PRL)
- Somatotropes produce growth hormone (GH; somatotropin) which is a single chain of 191 amino acids
- GH stimulates body growth, stimulates the secretion of IGF-1, stimulates lipolysis, and inhibits the actions of insulin on carbohydrate and lipid metabolism
Posterior Pituitary Gland (Neurohypophysis)
- The posterior pituitary lobe is small
- It stores hormones, including oxytocin
- It also stores Anti-Diuretic hormone (ADH)
- Corticotropes produce Adrenocorticotropic hormone (ACTH; corticotropin) which is a single chain of 39 amino acids
- ACTH stimulates the production of glucocorticoids and androgens in the adrenal cortex
- This maintains the size of the zona fasciculata and zona reticularis of cortex
Thyroid-Stimulating Hormone (TSH)
- Thyrotropes produce this with is a Glycoprotein of two subunits, a (89 amino acids) and β (112 amino acids)
- TSH stimulates the production of thyroid hormones by thyroid follicular cells
- It also maintains the size of follicular cells
Gonadotropins
- Gonadotropes produce Follicle-stimulating hormone (FSH), which is a Glycoprotein of two subunits, α (89 amino acids) and β (112 amino acids)
- FSH stimulates the development of ovarian follicles and regulates spermatogenesis in the testis
- Lactotropes/Mammotropes make Prolactin (PRL) which is a Single chain of 198 amino acids
Prolactin
- Prolactin stimulates milk secretion and production
Pituitary Gland Disorders
- Hypersecretion of hGH in childhood leads to gigantism
- The hypersecretion of hGH in adulthood leads to acromegaly
- Hyposecretion of human growth leads to dwarfism
Thyroid Hormone
- Thyros is greek for "shield"
- It secretes Thyroxine and T3 (Tri- iodo -thyronine)
- The thyroid regulates proper growth and development
- It regulates the basal metabolic rate (BMR)
Thyroid Structure
- The Larynx sits above the thyroid isthmus
- The right and left thyroid lobes sit on either side of the trachea
Cells of the Thyroid
- Thyroid follicles are numerous spherical hollow sacs
- Parafollicular cells secrete Calcitonin/ thyrocalcitonin)
- Follicular cells Secrets (Thyroxine)
Production and Action of Thyroid Hormones
- Iodide trapping takes place
- Synthesis of thyroglobulin is next
- Oxidation of Iodide
- Next, Iodination of tyrosine coupling of T1 and T2
- Pinocytosis and digestion of colloid occurs next
- Secretion of thyroid hormone and transporting in the blood is last
Thyroid Hormone and Amphibians
- Thyroxine stimulates metamorphosis in amphibians with TRHÃ TSH
- TRH rises during premetamorphosis and prometamorphosis
Diseases of the Thyroid
- A lack of iodine causes hypothyroidism, and the resulting elevation in TSH secretion stimulates the excessive growth of the thyroid aka Goiter
- Children with underactive thyroid glands are therefore stunted in their growth and suffer severe mental retardation aka Cretinism
- Hypothyroidism is inadequate secretion of thyroid hormones
- Symptoms of hypothyroidism include an abnormally basal metabolic rate, weight gain and lethargy
- Severe hypothyroidism in adults is called Myxedema
- Mucoproteins (glycosaminoglycans) and fluid accumulate in connective tissues and viscera, producing edema
- Swelling of the hands, feet, face, and tissue around the eyes is also Myxedema
Reasons and Remedies for Hypothyroidism
- A thyroid gland defect is a reason
- Insufficient thyrotropin-releasing hormone (TRH) secretion from the hypothalamus can also cause it
- Insufficient TSH secretion from the anterior pituitary is another cause
- Remedies for Hypothyroidism include, iodine supplements and Thyroxine taken in pill form
- Increasing uptake of protein, natural healthful fat may help too
Hyperthyroidism
- Graves' disease is a type of hyperthyroidism
- It is an autoimmune disorder where circulating auto-antibodies bind to TSH receptors on thyroid cells and overstimulate the thyroid gland
- Exophthalmos is also another symptom
Symptoms of Hyperthyroidism
- A high BMR accompanied by weight loss, nervousness, irritability, intolerance to heat are all symptoms
Parathyroid Glands
- Parathyroid glands secrete Parathyroid hormone
- Helps to bring the blood Calcium concentration up
- The parathyroid glands sense low serum calcium and increase PTH secretion
Action of Parathyroid
- PTH signals the bone to release calcium and the kidney to calcitriol formation and decreases excretion of calcium
- Vitamin D taken into the liver becomes calcidiol
- Once in the kidney, becomes Calcitriol which drives small intestines to Increase calcium absorption and increases serum calcium
Function of Calcium
- Required for Function of Muscles
- Required for Neuromuscular excitability
- Required for Functioning of the nervous and endocrine systems
- Required for Blood coagulation
Hyperparathyroidism
- Hypercalcemia
- Can lead to Kidney stones and Osteoporosis
- Hyperparathyroidism symptoms include fatigue, memory loss, and bone aches
Hypoparathyroidism
- Decreased function of the parathyroid glands with underproduction of parathyroid hormone
- The cause is low levels of calcium in the blood,
- Causing cramping and twitching of muscles or tetany (involuntary muscle contraction)
Adrenal Glands
- Adrenal glands are both adrenal and suprarenal glands
- The adrenal glands sit above the kidneys and have cortex and medulla regions
- They are paired organs that cap the superior borders of the kidneys
- Outer part is Cortex, inner part is Medulla
- Adrenal Medulla is responsible for "flight or fight or freeze" response
Fight-or-flight Response
- Stimulates sympathetic nervous system via the hypothalamus
- Activates adrenal medulla and adrenal cortical system by releasing CRF
Cortex-Histology
- Histologically from outer to inner layers have: Zona Glomerulosa, Zona Fasciculata, Zona Reticulata and Medulla
- The hypothalamus drives the fight or flight response, and in the next step, the Pituitary gland secretes hormone ACTH
Adrenal Cortex Layers
- The inner 3 Layers are responsible for making hormones and Cortex comes from Mesoderm
- From Outer to Inner the Layers are: Zona Glomerulosa, Fasciculata and then Reticularis
Adrenal Medulla Reactions
- Impulses activate glands and smooth muscles, releasing norepinephrine and epinepherine to bloodstream
- Neural activity combines with hormones in the bloodstream to constitute fight-or-flight response, and these hormones arrive at the adrenal cortex and release approximately 30 hormones
Adrenal Cortex
- derived from mesoderm
- It secretes Cortiocoids/corticosteroids
Zona Glomerulosa
- This is where the body secretes Mineralcorticoids
- Regulates Na + and K + balance
- Aldosterone is a potent mineralcorticoid here
- Stimulates: The kidneys to retain Na + and water while excreting K + in the urine
- The effects includes Increase blood volume and, Regulates blood electrolyte balance
Reactions to low Blood Volume
- Caused by Dehydration, Na deficiency, or hemorrhage
- The body decreases in blood pressure which stimulates Juxtaglomerular cells of the kidneys, thus Increased renin
- This in turn Increases angiotensinogen made in liver à Increased angiotensin Ià Increased angiotensin II via ACE in the lungs
- This stimulates increased aldosterone which stimulates kidneys to uptake Na/water and release H+ in the urine
Zona Fasciculata
- This is where the body secretes Gulcocorticoids
- Regulates the metabolism of glucose and other organic molecules
- Produces Cortisol/ Hydrocortisone
- ACTH and anterior pituitary stimulate Zona
- stimulates Gluconeogenesis
- Increase blood glucose levels and Promote lipolysis
Zona Reticularis
- This is where the body secretes Sex steroids
- Produces Hormones such as DHEA (Dihydroxyepialdosterone) and Androgenic Steroids (Weak male Hormones)
- The Function as precursor hormones is to regulate, Ovaries to Estrogen and Testis to Androgens
Adrenal Gland Disorders
- Addison's Disease has the following causes, Adrenal Insufficiency,Inadequate secretion of glucocortcoids and mineralocorticoids
- Results in hypoglycemia, sodium and potassium imbalance, dehydration, hypotension, rapid weight loss, and generalized weakness
- Characterized by discoloration of the skin, smoky appearance, or various tints or shades of deep amber or chestnut brown
- Congenital Adrenal Hyperplasia increases proliferation in cells and tissue of the gland and stems from a Genetic predispositions
- In New borne Children is that they are devoid of essential enzyme necessary to produce cortisol, aldosterone
- Simultaneously, secretes excess of androgen, which may lead to male characteristics in girls and precocious puberty in boys.
- Causes for an Overactive Adrenal Glands (Excess of Cortisol lead to Cushing Syndrome
- Causes: over secretion of ACTH (tumor in anterior Pituitary)
- Characteristics include Moon face and Buffalo hump
- Accumulation of fat at the back of the neck and upper back
Overactive Adrenal Glands
- Can cause Hyperaldosteronism (Excess of Aldosterone) which is caused by overproduction of aldosterone from one or both adrenal glands
- Effects: increases blood pressure and lowers potassium levels in the blood (muscle aches, weakness and spasms)
Pheochromocytoma
- A rare adrenal tumour characterized by an Excess of Adrenaline or Noradrenaline (Adrenal medulla)
- Has a persistent Effect with pressure and Symptoms in the form Headaches, sweating, tremors, anxiety and rapid heart beat
Adrenal Cancer
- Involves formation of Malignant adrenal tumours
Pancreas
- The pancreas consist of both Exocrine and endocrine glands
- Produces digestive enzymes, bicarbonates + and Insulin and Glucagon
- A Cross-section view show Pancreatic duct
Pancreas-Histology
- The exocrine element secretes Acinar cells secrete pancreatic enzymes into pancreatic duct
- Islets of Langerhan are responsible secretions of endocrine hormones in the gland
Islets of Langerhans cell types
- 5 cell types exist
- A or α cells (~20%) are located at the periphery of the islet and secret Glucagon
- B or ẞ cells (~75%) located at the center of the islet and secret insulin\
- D or 6 cells (~5%) are located around the periphery and release Somatostatin, a paracrine inhibitor of both insulin and glucagon secretion
- F cells (<2%) produce pancreatic polypeptide which regulates among other things overall Pancreatic Activity, effect on Appetite on gastric motility
- Epsilon Cells (É› cells): Produce ghrelin, a hormone involved primarily in regulating appetite and energy balance
Insulin Funciton
- Blood glucose level declines to a set point; stimulus for insulin release diminishes
- Homeostasis maintained
- Liver takes up glucose and stores it as glycogen
- Body cells take up more glucose, and thus Insulin is made to be in hyperglycemic
Pancreatic Function
- Glucagon acts on hepatocytes (liver cells) to: convert glycogen into glucose
- Insulin acts on various body cells to: accelerate facilitated diffusion of glucose
Alpha Cells
- Alpha (a) cells of the islets secrete glucagon, which acts antagonistically to insulin
- Glucagon promotes the hydrolysis of stored glycogen in the liver and fat in adipose tissue.
Glucagon
- Pancreas cells release Insulin with stimulates glucose uptake from blood by Tissue cells
- Lowers sugar level
- Liver uptakes glucose and converts to glycogen, thus lowering blood sugar
- High levels cause Promotes insulin release
Somatostatin
- Somatostatin decreases release of both insulin and glucagon thereby decreasing gastrointestinal functions by: decreasing motility, secretion, and absorption
Clinical Insulin Issues
- Type 1 insulin dependent (juvenile onset) means the autoimmune destruction is of β cells where insulin levels are low in the blood stream
- Type 2 non-insulin dependent (maturity onset) involves deficiency of insulin production or change in insulin receptors on the target cells, leading to high blood glucose levels
Diabetes Symptoms
- Symptoms include Hyperglycemia, Glucosuria, Polyuria and Polydipsia
Diabetes Treatment
- Sulphonylureas (e.g. tolbutamide): increases insulin secretion
- Glibizide /Gliburide: insulin secretion and promotes its action at cellular level
- Diabetes Drugs (orally active), include Biguanides which increasing glucose catabolism, glucose absorption in the intestine
- Thiazide diuretics, Diazxide can be used in the treatment of hypertension
- Diabetes Drugs like Leptin: Decreases basal and glucose-stimulated insulin release
Diabetes insipidus
- Causes Polyuria and, Polydipsia
- Diabetes insipidus stems from salt and water metabolism
- This results in intense thirst and heavy urination
- Di is result of brain not making enough of ADH (hormone in balance of water function,
- Diagnosis with help of Blood test + urine balance
- Vasopressin, , a synthetic hormone is the recommended treatment.
Pineal Gland
- Located: at of the third ventricle of the diencephalon which is encapsulated by the meninges covering the brain
- Weighs= 0.2 g in a child
- Long = 5 to 8 mm (0.2 to 0.3 in.)
- The gland begins to regress in size at about age seven
- Regulated by the suprachiasmatic nucleus (SCN) of the hypothalamus and regulated by the secretion of melatonin
- Plays a part in regulation of "circa-adian" rhythms
- Involved in in timing births of seasonally (animals)
Role of Melatonin release
- Pineal gland stimulation is suppressed for the day
- During night, Retinohypothalamic Stimulation stimulates SCN
- Results is Superior cervical Sympathetic neuron activity
Role of melatonin
- higher secretion of melatonin in children's (1-5 yrs)
- The time the births of seasonally breeding animals
- Lowest level at the end of puberty (decrease of 75%)
- This suggests a role for melatonin in the onset of human puberty, with peak levels in the middle of the night
Gonads
- Testes secrete Androgens
- Ovaries Secrete female hormones which are Progesterone and Estrogen
- Male organs are testis which create the most sex hormones The female hormones are mostly created from Oestrogen
Testes
- made of two compartments which include the Seminiferous tubules/and the Interstitial tissue.
- The interstitial tissue secretes Leydig cells and it involved in production of testosterone
Ovaries- Anatomy
- Located inside pelvic cavity
- Produce estrogen & progesterone
- Responsible for development & maintenance of female characteristics & menstrual cycle
Ovaries/Gonads
- Ovaries convert into a corpus at the post cycles
- The gonad secretes estradiol-17 β (estradiol-17 beta) to create esterogen where follicle can grow
- The process of ovulation makes corpus for reproduction function
Placenta Structure
- Made of Secretes Estrogens ,progesterone. human chorionic gonadotropins with helps in function with LH-like stimulation
- Also secretes human chorionic gonadotropins and somatomammotropin
Summary of Cellular interactions and Hormones
- Maturation of sperm is controlled by inhibin or Testosterone
- Follicle maturation and female production through estrogen
- Breast are prepared through the progesterone hormone
Gut Production
- Gut is responsible from the stomach acids such as HCl and pepsins, where gastric increases the volume
- Gut releases Gastric acid from stomach which produce the acids
- Secretin hormones are important in pancreatic secretions
Non-Classical Endocrine hormones
Kidney
- Responsible for production for RBC with cytokine
Heart
- responsible for lower pressure
- ANF is associated with this function
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Description
The pituitary gland attaches to the hypothalamus by the infundibulum. The adenohypophysis derives from Rathke's pouch. The anterior pituitary lobe is large and releases hormones, including growth hormone (GH).