Endocrine Physiology

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jknell
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206115
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Endocrine Physiology
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2013-04-05 12:28:51
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Endocrinology embriology, anatomy, physiology
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  1. Thyroid development
    Thyroid diverticulum arises from floor of primitive pharynx, descends into neck

    Connected to tongue by thyroglossal duct; nl disappears, but may persist as pyramidal lobe of thyroid

    Foramen cecum is normal remnant of thyroglossal duct

    *Most common site of ectopic thyroid tissue: tongue

    Thyroglossal duct cysts present as mass in anterior midline neck, moves when swallowing

    Branchial cleft cyst in lateral neck from persistent cervical sinus

  2. Fetal adrenal gland
    • Outer adult zone and inner active fetal zone
    • -Adult zone is dormant during early fetal life
    • -begins secreting cortisol late in gestation

    • Cortisol secretion is controlled by ACTH and CRG from fetal pituitary AND placenta
    • -Cortisol is responsible for fetal lung maturation and surfactant production
  3. Adrenal anatomy
    layers, developmental origin
    • Cortex (from mesoderm)
    • Medulla (from neural crest)
  4. Adrenal anatomy and function
    • -Zona Glomerulosa → Aldosterone (Salt/Na+)
    • -Zona Fasciculata → Cortisol/glucocorticoids, sex hormones (Sugar)
    • -Zona Reticularis → Sex hormones, e.g. androgens (Sex)

    *GFR ... the deeper you go, the sweeter it gets

    -Medulla → Catecholamines (Epi, NE)

  5. Adrenal
    primary regulatory control
    • Renin-angiotensin → Zona glomerulosa (Aldosterone→salt)
    • ACTH, hypothalamic CRH → Zona fasciculata (Glucocorticoids → sugar)
    • ACTH, hypothalamic CRH → Zona Reticularis (androgens → sex)
    • Preganglionic sympathetic fibers → Medulla (Catecholamines)
  6. Tumors of the adrenal medulla
    Phyochromocytoma and neuroblastoma
    • Phyocromocytoma:
    • -Most common tumor of the adrenal medulla in adults
    • -Cause episodic hypertension

    • Neuroblastoma:
    • -Most common tumor of the adrenal medulla in children
    • -Do NOT cause episodic hypertension
  7. Adrenal gland drainage
    Left adrenal → left adrenal vein → left renal vein → IVC

    Right adrenal → right adrenal vein → IVC

    *Same as left and right gonadal
  8. Pituitary gland
    segments, origin
    • Posterior pituitary (neurohypophysis)
    • -Derived from neuroectoderm

    • Anterior pituitary (adenophyophysis)
    • -Derived from oral ectoderm (Rathke's pouch)
  9. Posterior pituitary
    • Secretes vasopressin (ADH) and oxytocin
    • -both made in hypothalamus
    • -delivered to posterior pituitary via neurophysins (carrier proteins)

    Derived from neuroectoderm
  10. Anterior pituitary
    • Secretes: FLAT PiG
    • -FSH
    • -LH
    • -ACTH
    • -TSH
    • -Prolactin
    • -GH
    • -Melanotropin (MSH)

    • α subunit: hormone subunit common to TSH, LH, FSH, and hCG
    • β subunit: determines hormone specificity

    • Acidophils: GH, prolactin
    • *B-FLAT: Basophils → FSH, LH, ACTH, TSH
  11. Endocrine pancreas
    • Islets of Langerhans are collections of α, β, and δ endocrine cells
    • -Islets arise from pancreatic buds

    • -α = glucagon (peripheral)
    • -β = insulin (central)
    • -δ = somatostatin (interspersed)

    *Insuline (β cells) are inside

  12. Insulin
    Source
    • Released from pancreas:
    • -Glucose is major regulator of insulin release
    • -ATP generated by glucose metabolism closes K+ channels and depolarizes β cell membrane → opens voltage gated Ca2+ channels
    • -Calcium influx stimulates insulin secretion

    *Insulin moves glucose Into cells

    Insulin does not cross the placenta
  13. Glucose uptake and transporters
    Insulin independent uptake
    • *BRICK L (insulin-independent glucose uptake):
    • -Brain - GLUT-1 (insulin independent)
    • -RBCs - GLUT-1 (insulin independent)
    • -Intestine - GLUT-2 (bidirectional)
    • -Cornea
    • -Kidney - GLUT-2 (bidirectional)
    • -Liver - GLUT-2 (bidirectional)

    • -β islet cells have GLUT-2 (bidirectional)
    • -GLUT-4 (insulin dependent): adipose tissue, skeletal muscle

    • *Insulin does not cross the placenta
  14. Insulin
    Function
    • Anabolic effects of insulin:
    • ↑ glucose transport in SKM and adipose
    • ↑ glycogen synthesis and storage
    • ↑ triglyceride synthesis and storage
    • ↑ Na+ retention (kidneys)
    • ↑ protein synthesis (muscles)
    • ↑ Cellular uptake of K+ and amino acids
    • ↓ glucagon release
  15. Insulin
    Regulation
    • Hyperglycemia, GH, and β2-antagonists → ↑ insulin
    • Hypoglycemia, somatostatin, and α2-agonists → ↓ insulin

  16. Insulin-dependent organs
    • GLUT-4 (insulin-dependent transporter)
    • -Resting SKM
    • -Adipose tissue
  17. Insulin-independent organs
    • GLUT-1 (insulin-independent transporter)
    • -Brain
    • -RBCs

    -Brain depends on glucose metabolism under normal circumstances; ketone bodies in starvation

    -RBCs always depend on glucose; no mitochondria for aerobic metabolism
  18. Glucagon
    Source, function, regulation
    Source: α cells in pancreas

    • Function: Catabolic effects...
    • -Glycogenolysis, gluconeogenesis
    • -Lipolysis and ketone production

    • Regulation:
    • -Secreted in response to hypoglycemia
    • -Inhibited by insulin, hyperglycemia, somatostatin
  19. Hypothalamic-pituitary hormone regulation
    • -TRH → TSH, prolactin
    • -Dopamine → (-) prolactin
    • -CRH → ACTH, melanocyte-stimulating hormone, β-endorphin
    • -GHRH → GH
    • -Somatostatin → (-) GH, TSH
    • -GnRH → FSH, LH
    • -Prolactin → (-) GnRH
  20. Prolactin
    Source, function, regulation
    Source: anterior pituitary

    • Function:
    • -stimulates milk production
    • -inhibits ovulation/spermatogenesis by inhibiting GnRH synthesis and release

    • Regulation:
    • -secretion is tonically inhibited by dopamine from hypothalamus
    • -Prolactin in turn inhibits its own secretion (by increasing dopamine synthesis and secretion)
    • -TRH ↑ prolactin secretion

    *Dopamine antagonists (antipsychotics) and estrogens (OCPs, pregnancy) stimulate prolactin secretion

  21. Prolactinoma
    tx
    Dopamine agonists (bromocriptine) inhibit prolactin secretion
  22. Growth Hormone (somatotropin)
    source, function, regulation
    Source: Anterior pituitary

    • Function:
    • -Stimulates linear growth and muscle mass through Insulin like Growth Factor (IGF-1)/somatomedin secretion
    • -Increases insulin resistance (diabetogenic)

    • Regulation:
    • -Pulsatile release in response to GHRH
    • -Secretion ↑ during exercise and sleep
    • -Secretions inhibited by glucose and somatostatin
  23. Excess secretion of GH
    e.g. pituitary adenoma
    • Acromegaly in adults
    • Gigantism in children (...no, not Jordan)
  24. Adrenal steroids
    zones/steroids, enzymes needed
    • *All steroids require
    • -hydroxysteroid dehydrogenase

    • Glomerulosa = mineralocorticoids (Aldosterone)
    • -Enzymes required: 21-hydroxylase, 11β-hydroxylase

    • Fasciculata = glucocorticoids (Cortisol)
    • -Enzymes: 17α-hydroxylase, 21-hydroxylase, 11β-hydroxylase

    • Reticularis = Androgens (Testosterone, DHT)
    • -Testosterone → DHT (conversion requires 5α-reductase)

    Periphery = Estrogen (Estradiol)
  25. Adrenal steroids
  26. 17α-hydroxylase deficiency
    steroid levels, presentation
    • 17α-hydroxylase deficiency:
    • -↑ mineralocorticoids
    • -↓ cortisol
    • -↓ sex hormones

    • Presentation:
    • -hypertension, hypokalemia
    • XY: ↓ DHT → pseudohermaphroditism (ambiguous genitalia, undescended testes)
    • XX: external phenotype female; normal internal sex organs. lacks 2° sex characteristics
  27. 21-hydroxylase deficiency
    steroid levels, presentation
    • 21-hydroxylase deficiency:
    • -↓ mineralocorticoids
    • -↓ cortisol
    • -↑ sex hormones

    • Presentation: *most common form
    • -Hypotension, hyperkalemia, ↑ renin activity, volume depletion
    • -Masculinization, leading to pseudohermaphroditism in female
  28. 11β-hydroxylase deficiency
    steroid levels, presentation
    • 11β-hydroxylase deficiency
    • -↓ aldosterone; ↑11-deoxycorticosterone
    • -↓ cortisol
    • -↑ sex hormones

    • Presentation:
    • -Hypertension (11-deoxycorticosterone is a mineralocorticoid and is secreted in excess)
    • -Masculinization
  29. Adrenal enzyme deficiencies
    common features
    All are characterized by enlargement of both adrenal glands due to ↑ ACTH stimulation due to ↓ Cortisol
  30. Cortisol
    Source, Function, Regulation
    • Source: Zona fasciculata
    • -Bound to corticosteroid-binding globulin (CBG)

    • Function: Cortisol is BBIIG
    • -Maintains Blood pressure: upregulates α1-receptors on arterioles to increase sensitivity to NE and EPI
    • -↓ Bone formation
    • -Anit-Inflammatory/Immunosuppressive:
    •      -Inhibits production of leukotrienes and PGs
    •      -Inhibits leukocyte adhesion → neutrophilia
    •      -Blocks histamine release from mast cells
    •      -Reduces eosinophils
    •      -Blocks IL-2 production
    • -↑ Insulin resistance (diabetogenic)
    • -↑ Gluconeogenesis, lipolysis, proteolysis
    • -Inhibits fibroblasts (causes striae)

    • Regulation:
    • -CRH (hypothalamus) stimulates ACTH release (pituitary) → cortisol production in adrenal ZF
    • -Excess cortisol → ↓ CRH, ACTH, and cortisol secretion
    • -Chronic stress induces prolonged secretion
  31. PTH
    Source, Function, Regulation
    Source: Chief cells - parathyroid gland

    • Function: ↑ serum Ca2+, ↓ serum (PO43-), ↑ urine (PO43-)
    • *"PTH Phosphate Trashing Hormone"
    • -↑ bone resorption of calcium and phosphate

    • -↑ kidney reabsorption of calcium in distal convoluted tubule
    • -↓ reabsorption of phosphate in proximal convoluted tubule

    -↑ 1,25-(OH)2 D3 (calcitriol) production by stimulating kidney 1α-hydroxylase

    *↑ production of M-CSF and RANK-L in osteoblasts, stimulating osteoclasts
  32. PTH
    Regulation
    • ↓ serum Ca2+ → ↑ PTH secretion
    • ↓ serum Mg2+ → ↑ PTH secretion
    • ↓↓ serum Mg2+ → ↓ PTH secretion
    •       -↓ Mg2+ from diarrhea, aminoglycosides, diuretics, alcohol abuse
  33. Phosphate homeostasis
  34. Calcium homeostasis
  35. Vitamin D
    Source, function, regulation
    • Source: D3 from sun exposure in skin
    • -D2 ingested (plants)
    • -Both converted to 25-OH in liver, and 1,25-(OH)2 (active form) in kidney

    • Functionincreases absorption of both Ca2+ and PO43- in the gut
    • -↑ absorption of dietary Ca2+ and PO43-
    • -↑ bone resorption of Ca2+ and PO43-

    • Regulation:
    • -↑ PTH, ↓ [Ca2+], ↓ PO43- causes ↑ 1,25-VitD production
    • -1,25-VitD inhibits its own production (neg. feedback)

    *PTH leads to ↑ Ca2+ and ↓ PO43- reabsorption in the kidney

    *24,25-VitD3 is inactive form of Vitamin D
  36. Vitamin D deficiency
    • Rickets in kids
    • Osteomalacia in adults
  37. Calcitonin
    Source, function, regulation
    Source: Parafollicular cells (C cells) of thyroid

    • Function: Calcitonin opposes actions of PTH
    • -not important in normal calcium homeostasis
    • - ↓ bone resorption of calcium
    • *"Calcitonin tones down calcium levels"

    • Regulation:
    • - ↑ serum Ca2+ causes calcitonin secretion
  38. Signalling pathways of endocrine hormones
    • cAMP
    • cGMP
    • IP3
    • Steroid receptor
    • Intrinsic tyrosine kinase
    • Receptor-associated tyrosine kinase
  39. cAMP mediated
    FLAT ChAMP

    F
    SH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH, calcitonin, GHRH, glucagon
  40. cGMP mediated
    • Think vasodilators:
    • -ANP
    • -NO (EDRF)
  41. IP3 mediated
    GGOAT

    G
    nRH, GHRH, Oxytocin, ADH (V1 receptor), TRH, histamine (H1), angiotensin II, gastrin
  42. Steroid receptor mediated
    VETTT CAP

    Vitamin D, Estrogen, Testosterone, T3/T4, Cortisol, Aldosterone, Progesterone
  43. Intrinsic tyrosine kinase mediated
    • MAP kinase pathway
    • Think growth factors

    -Insulin, IGF-1, FGF, PDGF, EGF
  44. Receptor-associated tyrosine kinase mediated
    • PIG; think acidophiles and cytokines
    • -JAK/STAT pathway

    Prolactin, Immunomodulators (e.g. cytokines IL-2, IL-6, IL-8, IFN) GH
  45. Signalling pathway of steroid hormones
    • lipophilic; circulate bound to specific binding globulins (↑ their solubility)
  46. Sex hormone-binding globulin
    SHBG
    • In men: ↑ SHBG lowers free testosterone
    • gynecomastia

    • In women: ↓ SHBG raises free testosterone
    • hirsutism
    • →SHBG levels ↑ during pregnancy
  47. Thyroid hormones
    Source, function, regulation
    Iodine-containing hormone that controls body's metabolic rate

    • Source: Follicles of thyroid
    • -Most T3 is formed in target tissue

    • Function:
    • T3 functions 4B's
    • -Brain maturation
    • -Bone growth (synergism with GH)
    • -Beta-adrenergic effects (β1 receptor on heart...↑CO, HR< SV, contractility)
    • -Basal metabolic rate ↑ (via ↑ Na+/K+-ATPase activity = ↑O2 consumption, RR, body temp)
    • -↑ glycogenolysis, gluconeogenesis, lipolysis

    • Regulation: TRH (hypothalamus) stimulates TSH (pituitary), stimulates follicular cells
    • -T3 → anterior pituitary (neg feedback) to ↓ sensitivity to TRH
  48. Thyroid-stimulating immunoglobulins (TSI)
    Graves' disease
    TSIs (like TSH) stimulate follicular cells

    Graves' disease has autoantibodies that activate follicular cells: hyperthyroidism
  49. Wolff-Chaikoff effect
    • Wolff-Chaikoff effect: excess iodine temporarily inhibits thyroid peroxidase 
    • → ↓ iodine organification 
    • → ↓ iodine organification 
    • → ↓ T3/T4 production
  50. Thyroid Peroxidase
    • Peroxidase is enzyme responsible for oxidation and organification of iodide as well as coupling of MIT and DIT
    • Propylthiouracil inhibits both peroxidase and 5'-deiodinase
    • Methimazole inhibits peroxidase only
  51. Thyroxine-binding globulin (TBG)
    • TBG binds most T3/T4
    • only free hormone is active
    • ↓TBG in hepatic failure
    • ↑TBG inpregnancy or OCP use (estrogen ↑ TBG)
  52. T4 → T3
    • T4 is the major thyroid product
    • Converted to T3 in peripheral tissue by 5'-deiodinase
    • T3 binds receptors with greater affinity than T4

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