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171 Cards in this Set
- Front
- Back
What is the initial thyroid precursor? Source?
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Thyroid Diverticulum - arises from floor of primitive pharynx
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What happens to the Thyroid Diverticulum? What is it connected to?
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- Descends into neck from origin in floor of primitive pharynx
- Connected to tongue by thyroglossal duct |
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How is the Thyroid initially connected to the Tongue? What happens to this connection?
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- Thyroid diverticulum is connected to the tongue by the Thyroglossal Duct
- Normally disappears, but may persist as pyramidal lobe of thyroid - Foramen cecum is a normal remnant of the thyroglossal duct |
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What is the normal remnant of the thyroglossal duct (connects tongue to thyroid diverticulum)?
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Foramen Cecum
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What is the most common ectopic thyroid tissue site?
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Tongue
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What diagnosis should you consider in a patient presenting with an anterior midline neck mass that moves with swallowing or protrusion of the tongue?
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Thyroglossal Duct Cyst
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What diagnosis should you consider if your patient presents with a mass in their lateral neck?
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Branchial Cleft Cyst - persistent cervical sinus
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What are the adrenal cortex and medulla derived from?
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- Adrenal cortex: mesoderm
- Adrenal medulla: neural crest |
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What are the layers of the adrenal cortex from external to internal?
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- Zona Glomerulosa
- Zona Fasiculata - Zona Reticularis |
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What is the primary regulatory control of the Zona Glomerulosa? Secretory product?
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- Controlled by Renin-Angiotensin
- Secretes Aldosterone |
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What is the primary regulatory control of the Zona Fasiculata? Secretory product?
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- Controlled by ACTH and CRH
- Secretes cortisol and sex hormones |
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What is the primary regulatory control of the Zona Reticularis? Secretory product?
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- Controlled by ACTH and CRH
- Secretes sex hormones (eg, androgens) |
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What kind of cells are in the Adrenal Medulla?
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Chromaffin cells
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What is the primary regulatory control of the Adrenal Medulla? Secretory product?
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- Controlled by preganglionic sympathetic fibers
- Secretes catecholamines (epinephrine and norepinephrine) |
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What is the most common tumor of the adrenal medulla in adults? What does it characteristically cause?
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Pheochromocytoma
- Episodic hypertension |
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What is the most common tumor of the adrenal medulla in children? What does it characteristically cause?
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Neuroblastoma
- RARELY causes hypertension |
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How is the adrenal gland drained on the left side?
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Left adrenal gland → Left adrenal vein → Left renal vein → IVC
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How is the adrenal gland drained on the right side?
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Right adrenal gland → Right adrenal vein → IVC
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What tissue are the anterior and posterior pituitary made from?
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- Anterior Pituitary: oral ectoderm (Rathke pouch)
- Posterior Pituitary: neuroectoderm |
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What is the other name for the posterior pituitary? What does it secrete?
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Neurohypophysis
- Vasopressin / ADH - Oxytocin |
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What is the source of ADH and Oxytocin?
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They are both made in the hypothalamus and shipped to the posterior pituitary via the neurophysins (carrier proteins)
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What is the other name for the anterior pituitary? What does it secrete?
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Adenohypophysis
Think FLAT PiGs eat MuSH: - FSH - LH - ACTH - TSH - Prolactin - GH - MSH (Melanotropin) |
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What kind of cells are there in the anterior pituitary? Functions?
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- Acidophils: secretes Prolactin and GH
- Basophils: FSH, LH, ACTH, and TSH |
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What are the subunits of the hormones released from the anterior pituitary? Functions?
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- α subunit: hormone subunit common to TSH, LH, FSH, and hCG
- β subunit: determines hormone specificity |
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Which hormones have the same α subunit?
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- TSH
- LH - FSH - hCG |
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What part of TSH, LH, FSH, and hCG is the same? Which part determines its hormonal specificity?
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- α subunit is the same
- β subunit gives specificity |
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What are the types of pancreatic cells with endocrine function?
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Islets of Langerhans:
- α cells - β cells - δ cells |
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What is the source of Islets of Langerhans in the pancreas?
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Arise from pancreatic buds
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What is the function of the α, β, and δ cells in the Islets of Langerhans in the pancreas? Relative locations in Islet?
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- α cells: glucagon (peripheral)
- β cells: insulin (central) = Insulin is Inside - δ cells: somatostatin (interspersed) |
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How is insulin synthesized? Where?
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Takes place in β cells in Islets of Langerhans:
- Preproinsulin is synthesized in RER - Cleavage of "presignal" generates Proinsulin - Proinsulin is stored in secretory granules - Cleavage of Proinsulin → exocytosis of Insulin and C-peptide |
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If you see both elevated Insulin and C-peptide vs only elevated Insulin, how does this help your differential?
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- Elevated Insulin and C-peptide: Insulinoma
- Elevated Insulin without C-peptide: Exogenous Insulin administration |
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How does insulin mediate its effects?
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1. Binds insulin receptors (tyrosine kinase activity)
2. Induces glucose uptake (carrier-mediated transport) in insulin dependent tissues - Also induces gene transcription |
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What happens when insulin binds to its receptor?
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- Tyrosine phosphorylation
- Phosphoinositide-3 kinase pathway - Induces glycogen, lipid, and protein synthesis - Vesicles containing GLUT-4 are placed in membrane to allow entry of glucose into cell INsulin moves glucose INto cells |
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What are the anabolic effects of insulin?
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- ↑ Glucose transport in skeletal muscle and adipose tissue
- ↑ Glycogen synthesis and storage - ↑ Triglyceride synthesis - ↑ Na+ retention (kidneys) - ↑ Protein synthesis (muscles, proteins) - ↑ Cellular uptake of K+ and amino acids - ↓ Glucagon release |
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What are the insulin-dependent glucose transporters? Locations?
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GLUT-4: adipose tissue and skeletal muscle
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What are the insulin-independent glucose transporters? Locations?
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- GLUT-1: RBCs, brain, cornea
- GLUT-5 (fructose): spermatocytes, GI tract - GLUT-2 (bidirectional): β islet cells, liver, kidney, small intestine |
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What type of glucose transporters are in the adipose tissue? Characteristics?
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GLUT-4: insulin-dependent glucose transporter
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What type of glucose transporters are in the skeletal muscle? Characteristics?
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GLUT-4: insulin-dependent glucose transporter
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What type of glucose transporters are in RBCs? Characteristics?
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GLUT-1: insulin-independent glucose transporter
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What type of glucose transporters are in the brain? Characteristics?
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GLUT-1: insulin-independent glucose transporter
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What type of glucose transporters are in the cornea? Characteristics?
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GLUT-1: insulin-independent glucose transporter
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What type of sugar transporters are in the spermatocytes? Characteristics?
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GLUT-5 (fructose): insulin-independent transporter
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What type of sugar transporters are in the GI tract? Characteristics?
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- GLUT-5 (fructose): insulin-independent transporter
- GLUT-2 (bidirectional): insulin-indepdent transporter - small intestine |
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What type of sugar transporters are in the β islet cells? Characteristics?
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GLUT-2 (bidirectional): insulin-indepdent transporter
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What type of sugar transporters are in the liver? Characteristics?
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GLUT-2 (bidirectional): insulin-indepdent transporter
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What type of sugar transporters are in the kidneys? Characteristics?
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GLUT-2 (bidirectional): insulin-indepdent transporter
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What kind of fuel does the brain use?
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- Glucose for metabolism normally
- Ketone bodies during starvation |
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What kind of fuel do RBCs use?
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Always utilize glucose because they lack mitochondria fro aerobic metabolism
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How do you remember the sites of insulin-indepdent glucose uptake?
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BRICK L:
- Brain - RBCs - Intestine - Cornea - Kidneys - Liver |
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What regulates insulin release?
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- Glucose
- GH - β2-agonists |
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How does glucose enter pancreatic β cells? What are the effects?
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3. Glucose enters β cells via GLUT-2 (bidirectional) channels
4. ↑ ATP generated from glucose metabolism 5. Closes K+ channels 6. Depolarizes β cell membrane 7. Opens voltage-gated Ca2+ channels, resulting in Ca2+ influx 8. Stimulates insulin exocytosis |
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What is the source of glucagon? Function?
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- Made by α cells of pancreas
Functions in catabolism: - Glycogenolysis and gluconeogenesis → make more glucose - Lipolysis and ketone production → make alternative sources of energy |
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What stimulates and inhibits glucagon secretion?
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- Secreted in response to hypoglycemia
- Inhibited by insulin, hyperglycemia, and somatostatin |
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What is the function of CRH?
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↑ ACTH, MSH, and β-endorphin
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What causes ↓ CRH?
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Chronic exogenous steroid use
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What is the function of Dopamine on the pituitary?
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↓ Prolactin
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What is the effect of Dopamine Antagonists (eg, anti-psychotics) on the pituitary?
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Can cause galactorrhea (↑ prolactin)
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What is the function of GnRH?
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- ↑ FSH and LH
- Tonic GnRH suppresses the HPA axis - Pulsatile GnRH leads to puberty and fertility |
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What regulates GnRH?
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Regulated by Prolactin
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What is the effect of tonic GnRH release?
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Suppresses HPA axis
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What is the effect of pulsatile GnRH release?
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Leads to puberty and fertility
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What is the function of Prolactin?
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↓ GnRH
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What are the consequences of a pituitary prolactinoma?
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Amenorrhea (↓ GnRH) and Osteoporosis
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What is the function of Somatostatin on the pituitary?
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↓ GH and TSH
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How can you treat acromegaly?
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Somatostatin analogs (↓ GH)
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What is the function of TRH?
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↑ TSH and Prolactin
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What are the effects of Prolactin?
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- Stimulates milk production in breasts
- Inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release - Excessive prolactin associated with ↓ libido |
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How is Prolactin regulated?
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- Tonically inhibited by Dopamine from hypothalamus
- Prolactin inhibits its own secretion by ↑ Dopamine synthesis and secretion - TRH ↑ Prolactin secretion |
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What drugs can be used to treat excess prolactin (such as prolactinoma)?
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Dopamine Agonists - eg, Bromocriptine
- Dopamine inhibits Prolactin secretion |
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What drugs may stimulate prolactin secretion?
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- Dopamine antagonists (eg, anti-psychotics)
- Estrogens (OCPs, pregnancy) |
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What are the effects of Growth Hormone (Somatotropin)?
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- Stimulates linear growth and muscle mass through IGF-1 / somatomedin secretion
- ↑ Insulin resistance (diabetogenic) |
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What is the effect of GH on insulin?
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GH increases insulin resistance (diabetogenic)
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What regulates Growth Hormone release?
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- Released in pulses in response to GHRH (GH releasing hormone)
- Increases during sleep and exercise - Inhibited by glucose and somatostatin |
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What can excess secretion of GH be due to? What can it cause?
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- Could be due to pituitary adenoma
- Causes acromegaly (adults) or gigantism (children) |
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What is the source of Anti-Diuretic Hormone (ADH)?
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- Synthesized in hypothalamus (supraoptic nuclei)
- Released by posterior pituitary |
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What is the function of Anti-Diuretic Hormone (ADH)?
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- Regulates serum osmolarity (V2 receptors) and blood pressure (V1 receptors)
- ↓ serum osmolarity and ↑ urine osmolarity via regulation of aquaporin channel transcription in principal cells of renal collecting duct |
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What diseases affect the levels / response to ADH?
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- 1° Polydipsia: ADH is suppressed
- Central Diabetes Insipidus (DI): ADH ↓ - Nephrogenic Diabetes Insipidus (DI): ADH ↑ (kidney is resistant to its effects) |
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What can cause nephrogenic diabetes insipidus?
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Resistance to ADH can be mediated by a mutation in the V2 receptor (regulates serum osmolarity)
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How do you treat central diabetes insipidus?
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Desmopressin (ADH analog) - central DI is caused by insufficient production of ADH
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What are the types of receptors that ADH acts on? Effects?
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- V2 receptor: regulates serum osmolarity
- V1 receptor: regulates blood pressure |
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How is ADH regulated?
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- Osmoreceptors in hypothalamus (1°)
- Hypovolemia (2°) |
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What is the first step in production of adrenal steroids?
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Conversion of Cholesterol → Pregnenolone via Cholesterol Desmolase
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How do you produce Aldosterone?
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1. Cholesterol → Pregnenolone (Cholesterol Desmolase)
2. Pregnenolone → Progesterone (3β-hydroxysteroid dehydrogenase) 3. Progesterone → 11-deoxycorticosterone (21-hydroxylase) 4. 11-deoxycorticosterone → Corticosterone (11β-hydroxylase) 5. Corticosterone → Aldosterone (Aldosterone Synthase) |
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What are the molecules on the way from Cholesterol to Aldosterone?
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1. Cholesterol
2. Pregnenolone 3. Progesterone 4. 11-deoxycorticosterone 5. Corticosterone 6. Aldosterone |
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What are the enzymes on the way from Cholesterol to Aldosterone?
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1. Cholesterol Desmolase
2. 3β-hydroxysteroid dehydrogenase 3. 21-hydroxylase 4. 11β-hydroxylase 5. Aldosterone Synthase |
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How do you produce Cortisol?
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1. Cholesterol → Pregnenolone (Cholesterol Desmolase)
2. Pregnenolone → 17-hydroxypregnenolone (17α-hydroxylase) 3. 17-hydroxypregnenolone → 17-hydroxyprogesterone (3β-hydroxysteroid dehydrogenase) 4. 17-hydroxyprogesterone → 11-deoxycortisol (21-hydroxylase) 5. 11-deoxycortisol → Cortisol (11β-hydroxylase) Steps 2 and 3 can be switched around, but need both enzymes |
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What are the molecules on the way from Cholesterol to Cortisol?
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1. Cholesterol
2. Pregnenolone 3. 17-hydroxypregnenolone 4. 17-hydroxyprogesterone 5. 11-deoxycortisol 6. Cortisol OR 3. Progesterone (depending on order of enzymes) |
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What are the enzymes on the way from Cholesterol to Aldosterone?
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1. Cholesterol desmolase
2. 17α-hydroxylase 3. 3β-hydroxysteroid dehydrogenase 4. 21-hydroxylase 5. 11β-hydroxylase (Enzymes 2 and 3 can be done in either order) |
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How do you produce Estradiol?
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1. Cholesterol → Pregnenolone (Cholesterol Desmolase)
2. Pregnenolone → 17-hydroxypregnenolone (17α-hydroxylase) 3. 17-hydroxypregnenolone → Dehydroepiandrosterone (DHEA) 4. DHEA → Androstenedione 5. Androstenedione → Estrone (Aromatase) 6. Estrone → Estradiol OR 5. Androstenedione → Testosterone 6. Testosterone → Estradiol (Aromatase) |
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What are the actions of Aromatase?
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- Androstenedione → Estrone
- Testosterone → Estradiol |
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What are the actions of 5α-Reductase?
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Testosterone → Dihydrotestosterone (DHT)
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Which enzyme deficiency would cause:
- Mineralocorticoids: ↑ - Cortisol: ↓ - Sex Hormones: ↓ |
17α-Hydroxylase (A)
Glucocorticoid and Androgen/Estrogen precursors cannot be produced, which shuttles more Pregnenolone / Progesterone substrate through the Aldosterone pathway |
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Which enzyme deficiency would cause:
- Mineralocorticoids: ↓ - Cortisol: ↓ - Sex Hormones: ↑ |
21-Hydroxylase (B)
Progesterone and 17-Hydroxyprogesterone cannot continue towards formation of Aldosterone and Cortisol, so they get shuttled to the sex hormone pathway |
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Which enzyme deficiency would cause:
- Mineralocorticoids: ↓ / ↑ - Cortisol: ↓ - Sex Hormones: ↑ |
11β-Hydroxylase (C)
- ↓ Aldosterone - ↑ 11-deoxycorticosterone (results in ↑ BP) - Cortisol can't be made - Sex hormones increased due to extra substrate |
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What is similar about 17α-hydroxylase, 21-hydroxylase, and 11β-hydroxylase deficiencies?
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All congenital adrenal enzyme deficiencies → enlargement of both adrenal glands due to ↑ ACTH stimulation (due to ↓ cortisol)
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What labs are associated with 17α-hydroxylase deficiency?
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- ↑ Mineralocorticoids
- ↓ Cortisol - ↓ Sex hormones (↓ DHT) - Hypertension - Hypokalemia |
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How does a patient with 17α-hydroxylase deficiency present?
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↑ Mineralocorticoids, ↓ Cortisol, and ↓ Sex hormones causes:
- XY: pseudo-hermaphroditism (ambiguous genitalia, undescended testes) - XX: lack secondary sexual development - Both: hypertension, hypokalemia |
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What labs are associated with 21-hydroxylase deficiency?
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- ↓ Mineralocorticoids
- ↓ Cortisol - ↑ Sex hormones (↑ 17-hydroxy-progesterone) - Hypotension - Hyperkalemia - ↑ Renin activity |
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How does a patient with 21-hydroxylase deficiency present?
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↓ Mineralocorticoids, ↓ Cortisol, and ↑ Sex Hormones causes:
- Presents in infancy with salt-wasting or in childhood with precocious puberty - XX: virilization - Hypotension, hyperkalemia, ↑ Renin activity |
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What labs are associated with 11β-hydroxylase deficiency?
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- ↓ Aldosterone
- ↑ 11-deoxycorticosterone (results in ↑ BP) - Hypertension - Low renin - ↓ Cortisol - ↑ Sex hormones |
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How does a patient with 11β-hydroxylase deficiency present?
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↓ Aldosterone, ↑ 11-deoxycorticosterone, ↓ Cortisol, and ↑ Sex hormones causes:
- XX: virilization - Hypertension |
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What diagnosis should you consider in an XY patient who presents with pseudo-hermaphroditism (ambiguous genitalia, undescended testes)? Other findings?
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17α-hydroxylase deficiency
- Hypertension - Hypokalemia - ↓ Sex hormones (↓ DHT) - ↓ Cortisol - ↑ Aldosterone |
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What diagnosis should you consider in an XX patient lacking secondary sexual development? Other findings?
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17α-hydroxylase deficiency
- Hypertension - Hypokalemia - ↓ Sex hormones (↓ DHT) - ↓ Cortisol - ↑ Aldosterone |
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What diagnosis should you consider in an infant presenting with salt wasting? Other findings?
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21-Hydroxylase deficiency
- Hypotension - Hyperkalemia - ↓ Mineralocorticoids - ↓ Cortisol - ↑ Sex hormones |
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What diagnosis should you consider in an child with precocious puberty? Other findings?
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21-Hydroxylase deficiency
- Hypotension - Hyperkalemia - ↓ Mineralocorticoids - ↓ Cortisol - ↑ Sex hormones |
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What diagnosis should you consider in an XX patient with virilization? Other findings?
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21-Hydroxylase deficiency
- Hypotension - Hyperkalemia - ↓ Mineralocorticoids - ↓ Cortisol - ↑ Sex hormones OR 11β-Hydroxylase deficiency - Hypertension (d/t ↑ 11-deoxycorticosterone) - ↓ Aldosterone - ↓ Cortisol |
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What is the source of Cortisol? What does it bind in the blood?
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- Adrenal Zona Fasciculata
- Binds to corticosteroid-binding globulin |
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What are the effects of Cortisol?
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Cortisol is a BIG FIB:
- ↑ BP - ↑ Insulin resistance - ↑ Gluconeogenesis, lipolysis, and proteolysis - ↓ Fibroblast activity - ↓ Inflammatory and immune responses - ↓ Bone formation |
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How does cortisol affect BP?
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↑ BP: upregulates α1-receptors on arterioles → ↑ sensitivity to NE and Epi
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How does cortisol affect insulin?
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↑ Insulin resistance → diabetogenic
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How does cortisol affect stored forms of energy?
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- ↑ Gluconeogenesis
- ↑ Lipolysis - ↑ Proteolysis |
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How does cortisol affect fibroblasts? Effect?
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↓ Fibroblast activity → causes striae
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How does cortisol affect inflammation / immune responses?
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↓ Inflammatory and Immune responses:
- Inhibits production of leukotrienes and prostaglandins - Inhibits leukocyte adhesion → neutrophilia - Blocks histamine release from mast cells - Reduces eosinophils - Blocks IL-2 production |
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How does cortisol affect bones?
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↓ Bone formation due to ↓ Osteoblast activity
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What infections can be reactivated after administration of exogenous corticosteroids? How?
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Reactivation of TB and Candidiasis
- Due to blocked IL-2 production |
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How is Cortisol regulated?
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- CRH (hypothalamus) stimulates ACTH release (pituitary), causing cortisol production in adrenal zona fasciculata
- Excess cortisol ↓ CRH, ACTH, and cortisol secretion |
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What is the effect of chronic stress on cortisol?
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Chronic stress induces prolonged secretion of Cortisol
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What is the source of Parathyroid Hormone (PTH)?
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Chief cells of parathyroid gland
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What are the effects of PTH?
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- ↑ Bone resorption of Ca2+ and PO4(3-)
- ↑ Kidney reabsorption of Ca2+ in distal convoluted tubule - ↓ Reabsorption of PO4(3-) in proximal convoluted tubule - ↑ 1,25-(OH)2-D3 (Calcitriol) production by stimulating kidney 1α-hydroxylase |
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How does PTH affect the nephron? Which parts?
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- ↑ Kidney reabsorption of Ca2+ in distal convoluted tubule
- ↓ Reabsorption of PO4(3-) in proximal convoluted tubule |
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How does PTH affect the bones?
|
↑ Bone resorption of Ca2+ and PO4(3-)
- ↑ Production of macrophage colony-stimulating factor and RANK-L (receptor activator of NF-κB ligand) - RANK-L secreted by osteoblasts and osteocytes binds RANK (receptor) on osteoclasts and their precursors → stimulates osteoclasts and ↑ Ca2+ |
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How does PTH affect the kidney, besides its action on the nephron?
|
↑ 1,25-(OH)2-D3 (Calcitriol) production by stimulating kidney 1α-hydroxylase
|
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Which enzyme produces 1,25-(OH)2-D3 (calcitriol) in the kidney?
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1α-Hydroxylase
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What is the net effect of PTH on Ca2+ and PO4(3-) in the serum and urine?
|
- ↑ Serum Ca2+
- ↓ Urine Ca2+ - ↓ Serum PO4(3-) - ↑ Urine PO4(3-) (Phosphate Trashing Hormone = PTH) |
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What peptide is similar to PTH? Source?
|
PTH-related peptide (PTHrP)
- Functions like PTH - Commonly ↑ in malignancies (eg, paraneoplastic syndrome) |
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How is PTH regulated?
|
- ↓ Serum Ca2+ → ↑ PTH
- ↓ Serum Mg2+ → ↑ PTH - ↓↓ Serum Mg2+ → ↓ PTH |
|
What are common causes of ↓ Mg2+?
|
- Diarrhea
- Aminoglycosides - Diuretics - Alcohol abuse |
|
What is the effect of PTH on the intestine?
|
- Increases intestinal Ca2+ absorption
- Increases intestinal PO4(3-) absorption |
|
What are the forms of calcium in the plasma? What percent is in each form?
|
- Ionized (~45%)
- Bound to albumin (~40%) - Bound to anions (~15%) |
|
How does pH affect calcium homeostasis in the plasma?
|
↑ in pH → ↑ affinity of albumin (negative charge) to bind Ca2+
Clinical manifestations of hypocalcemia: - Cramps - Pain - Paresthesias - Carpopedal spasm |
|
What are the sources of Vitamin D? Activation?
|
- D3 from sun exposure in skin
- D2 ingested from plants - Both converted to 25-OH in liver and to 1,25-(OH)2 (active form) in kidney - 24,25-(OH)2-D3 is an inactive form |
|
What is the function of Vitamin D (Cholecalciferol)?
|
- ↑ Absorption of dietary Ca2+ and PO4(3-)
- ↑ Bone resorption → ↑ Ca2+ and PO4(3-) |
|
How is Vitamin D regulated?
|
- Increased 1,25-(OH)2-D production by: ↑ PTH, ↓ [Ca2+], ↓ [PO4(3-)]
- 1,25-(OH)2 feedback inhibits its own production |
|
What are the implications of a deficiency of Vitamin D?
|
- Rickets in kids
- Osteomalacia in adults |
|
What can cause a Vitamin D deficiency?
|
- Malabsorption
- ↓ Sunlight - Poor diet - Chronic kidney failure |
|
What is the source of Calcitonin?
|
Parafollicular cells (C cells) of Thyroid
|
|
What is the function of Calcitonin?
|
↓ Bone resorption of Ca2+ → Tones down Ca2+ levels
|
|
What regulates Calcitonin?
|
↑ Serum Ca2+ causes Calcitonin secretion (to tone down Ca2+ levels in serum)
|
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How do PTH and Calcitonin relate?
|
- Calcitonin opposes actions of PTH
- Calcitonin is not important in normal Ca2+ homeostasis |
|
Which endocrine hormones signal via "cAMP"?
|
FLAT ChAMP + CGG:
- FSH - LH - ACTH - TSH - CRH - hCG - ADH (V2 receptor) - MSH - PTH - Calcitonin - GHRH - Glucagon |
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Which endocrine hormones signal via "cGMP"?
|
Think vasodilators:
- ANP - NO (EDRF) |
|
Which endocrine hormones signal via "IP3"?
|
GOAT HAG:
- GnRH - Oxytocin - ADH (V1 receptor) - TRH - Histamine (H1 receptor) - Angiotensin II - Gastrin |
|
Which endocrine hormones signal via "steroid receptors"?
|
VETTT CAP:
- Vitamin D - Estrogen - Testosterone - T3 and T4 - Cortisol - Aldosterone - Progesterone |
|
Which endocrine hormones signal via "intrinsic tyrosine kinase"?
|
MAP kinase pathway, think growth factors
- Insulin - IGF-1 - FGF - PDGF - EGF |
|
Which endocrine hormones signal via "receptor-associated tyrosine kinase"?
|
JAK/STAT pathway, think acidophiles and cytokines (PIG)
- Prolactin - Immunomodulators: IL-2, IL-6, IL-8, IFN - GH |
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What kind of signaling pathway is important for the MAP kinase pathway?
|
Intrinsic tyrosine kinase
|
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What kind of signaling pathway is important for the JAK?STAT kinase pathway?
|
Receptor-associated tyrosine kinase
|
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What is the signaling pathway of steroid hormones?
|
- Steroid hormone binds to receptor located in nucleus or cytoplasm
- Transformation of receptor to expose DNA-binding domain - Enters cell and binds to enhancer-like element in DNA - Affects gene transcription: pre-mRNA → mRNA → protein → response |
|
What happens to steroid hormones in the serum? Why?
|
Steroid hormones are lipophilic and therefore must circulate bound to specific binding globulins, which ↑ their solubility
|
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What happens to men with increased sex-hormone binding globulin (SHBG)?
|
Gynecomastia
|
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What happens to women with increased sex-hormone binding globulin (SHBG)?
|
Hirsutism
|
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What can increase the amount of sex-hormone binding globulin (SHBG)?
|
- OCPs
- Pregnancy (Free estrogen levels remain unchanged) |
|
What are the iodine containing hormones that control the body's metabolic rate?
|
Thyroid Hormones: T3/T4
|
|
What is the source of the thyroid hormones (T3/T4)?
|
- Follicles of thyroid
- Most T3 formed in target tissues |
|
What are the functions of thyroid hormones?
|
- Bone growth (synergism with GH)
- CNS maturation - ↑ CO, HR, SV, contractility - ↑ Basal metabolic rate - ↑ Glycogenolysis, gluconeogenesis, lipolysis |
|
How do thyroid hormones affect the heart? Effects?
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↑ β1 receptors in heart → ↑ CO, HR, SV, contractility
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How do thyroid hormones affect the basal metabolic rate? Effects?
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↑ BMR by ↑ Na+/K+ ATPase activity → ↑ O2 consumption, RR, and body temperature
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What are the effects of thyroid hormones on energy storage?
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↑ Glycogenolysis, gluconeogenesis, and lipolysis
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What is the mnemonic to remember the T3 functions?
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T3 functions - 4 B's:
- Brain maturation (CNS) - Bone growth - β-adrenergic effects (↑ β1 receptors) - Basal metabolic rate ↑ |
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What binds the thyroid hormones in the blood? What hormones are active?
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- Thyroxine-binding globulin (TBG) binds most T3/T4 in the blood
- Only the free hormone is active |
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What can decrease the amount of Thyroxine-Binding Globulin (TBG)?
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Hepatic Failure
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What can increase the amount of Thyroxine-Binding Globulin (TBG)?
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Pregnancy or OCP use (estrogen ↑ TBG)
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What is the major thyroid product? What happens to it?
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- T4 is the major thyroid product
- Converted to T3 in peripheral tissue by 5'-deiodinase |
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What enzyme converts T4 to T3 in the peripheral tissues?
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5'-deiodinase
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Which form of the thyroid hormones can bind receptors with greater affinity?
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T3 binds receptors with greater affinity than T4
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What enzyme is responsible for oxidation and organification of iodide?
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Peroxidase
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What enzyme is responsible for coupling of monoiodotyrosine (MIT) and diodotyrosine (DIT)?
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Peroxidase
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What drug can inhibit both peroxidase and 5'-deiodinase?
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Propylthiouracil
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What drug can inhibit peroxidase but not 5'-deiodinase?
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Methimazole
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What regulates Thyroid Hormones (T3/T4)?
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- TRH (hypothalamus) stimulates TSH (pituitary), which stimulates follicular cells
- Negative feedback by T3, T4 to anterior pituitary ↓ sensitivity to TRH - Thyroid stimulating immunoglobulins (TSIs), like TSH, stimulate follicular cells (eg, Graves disease) |
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What is the name of the effect when excess iodine temporarily inhibits thyroid peroxidase? Effect?
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Wolff-Chaikoff effect:
- ↓ Iodine organification → ↓ T3/T4 production |