Term
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Definition
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Term
| Where do we get vitamin A? How do we process it? |
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Definition
-Mostly from B-carotene
-We cleve it to two molecules of retinol, and then process it to retinoic acid; a hormone for differentiation and growth |
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Term
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Definition
-Derived from vit A
-Functions like a steroid hormone to promote growth and differentiation (esp. of epithelial cells) |
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Term
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Definition
| -Somatotroph cells of anterior pituitary |
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Term
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Definition
-It acts mainly as an antagonist, promoting gluconeogenesis and lipolysis.
-It also promotes glycogen synth, but this is the same as insulin |
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Term
| What are mechanisms of GH control? |
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Definition
Stimulated by;
-GHRH
-Hypoglycemia
-AAs like arginine
-Prolonged fasting
Inhibited by;
-Somatostatin
-Hyperglycemia |
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Term
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Definition
-Insulin-like growth factors stimulated by GH that have more potent growth effects than insulin itself
-There are two IGF-I & IGF-II
-IGF-I is linked to a tyrosine kinase receptor |
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Term
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Definition
-Caused by benign tumor of anterior pituitary after closure of epiphyseal plates (after puberty)
-Caused from excess GH secretion
-Causes an enlargement of the jaw, brow, and fingers |
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Term
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Definition
-Ant. pit benign tumor before end of growth (before puberty)
-Leads to hypersecretion of GH
-Both hypersecretion of GH diseases often lead to diabetes because of high gluconeogenesis |
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Term
| Where is vasopressin produced and stored? |
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Definition
| -Produced in hypothalamus and stored in POST. pituitary |
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Term
| Vasopressin action? Mechanism? |
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Definition
-aka ADH
-responds to high serum Na or low serum volume to increase water retention
-Leads to PKA and increased aquaporin-2 synth, which let water back in from tubules |
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Term
| ANP? Where from and action? Mechanism? |
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Definition
-Atrionatriuretic peptide
-Released from atrial cells in heart
-Increases urine output and acts as vasodilator
-Works through a cGMP pathway to activate PKG (Gt path?) |
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Term
| Aldosterone action on fluid/electrolyte levels? Where? Stimulation? Deficiency? |
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Definition
-Is a mineralocorticoid which acts to retain Na+ (water too because it follows) and secrete K+ by increasing ENaC insertion into tubule cells (Epith. Na Channel)
-Secreted by zona glomerulosa of adrenal cortex
-Stimulated by angiotensin II (and low Na/high K)
-Deficiency causes diabetes insipidus |
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Term
| What is the renin pathway and result? Where from and why? Where does a drug fit in? |
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Definition
-Released by justaglomerular cells in responce to low BP, blood volume, or Na
-Renin makes Angiotensinogen (A) to A-I
-A-I is made into A-II by angiotensin converting enzyme (ACE)
-A-II then causes vasoconstriction, aldosterone secretion, and renin inhibition (feedback inhibition)
-Overall, this path leads to increased blood pressure
-We can use ACE inhibitors to treat hypertension |
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Term
| Angiotensin II action and receptor? |
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Definition
| -Binds to Gq coupled receptor to increase PKC and lead to aldosterone secretion by zona glomerulosa of adrenal cortex |
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Term
| Vit D's most active form and action? Enzyme needed in production? |
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Definition
-Calcitriol (1,25-(OH)2D)
-Stimulates dietary Ca2+ uptake, and reabsorption in the kidneys (of phosphate too)
-Also stimulates resorption from the bones of calcium and phosphate
-needs 1a-Hydroxylase (needs sunlight) |
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Term
| PTH stimulation and action? Receptors? Excess action? |
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Definition
-Parathyroid hormone responds to low Ca2+ with high sensitivity (repressed by hypercalcemia)
-Made by chief cells of parathyroid
-It interacts with Gs+Gq receptors (for PTH-1 receptor) in bone and renal tubules to promote bone resorption and calcium retention (and phosphate excretion)
-Works in bone by increasing osteoclast levels (resorb bone)
-excess action can lead to osteoporosis and hypercalcemia |
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Term
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Definition
-Can be caused by excess PTH (chief cell adenoma) or excess vit D
-Causes "stones, bones, and moans"; stones, fractures, & fatigue
-Will also have hypophosphatemia if it's from PTH |
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Term
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Definition
-caused by PTH or Vit D def.
-Severe causes childhood rickets
-Milder caused OSTEOMALACIA later in life |
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Term
| Vit D-dependent rickets type I? |
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Definition
-Caused by mutation in gene for 1a-hydroxylase (for Vit D conversion to calcitrol, aka 1,25(OH)2D)
-Low calcitrol leads to low phosphate and Ca2+ in blood from poor intestinal absorption |
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Term
| Vit D-dependant rickets type II? |
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Definition
| -Caused by a bad receptor for calcitrol [1,25(OH)2D] |
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Term
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Definition
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Term
Receptor result for;
-Vasopressin?
-ANP
-Angiotensin II
-PTH |
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Definition
-PKA
-PKG
-PKC (Gq)
-PKA & PKC (Gq & Gs) |
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