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Endocrinology - Exam 2 Study Guide

by: Michelle Notetaker

Endocrinology - Exam 2 Study Guide BIOL 4110

Marketplace > University of North Texas > Biology > BIOL 4110 > Endocrinology Exam 2 Study Guide
Michelle Notetaker
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About this Document

These are comprehensive notes of Ch.3 and Ch.4 information needed for Exam 2.
Dr. Harris D Schwark
Study Guide
Endocrine system
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This 10 page Study Guide was uploaded by Michelle Notetaker on Monday October 3, 2016. The Study Guide belongs to BIOL 4110 at University of North Texas taught by Dr. Harris D Schwark in Fall 2016. Since its upload, it has received 13 views. For similar materials see Endocrinology in Biology at University of North Texas.


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Date Created: 10/03/16
Endocrinology - Exam 2 Study Guide Ch. 4 Overview: ● Calcium(Ca) & Phosphorous (inorganic phosphate(Pi)): - structure of hard tissues (bones & teeth) and metabolic regulation/signaling pathways. ● 2 primary sources of Ca & Pi: - Diet and Skeleton​. ● Calcitonin, Calcitriol (1,25-dihydroxyvitamin D) & Parathyroid hormone (PTH)​ regulate intestinal absorption and release into the blood after bone resorption of Ca & Pi. Roles of Ca & Pi Ca – Bones, teeth – Muscle contraction – Contribute to membrane potentials – Second messenger – Exocytosis – Enzyme cofactor – Part of basement membranes – Blood clotting Pi – Bones, teeth – Enzyme activator – Buffer in blood – Component of energy storage (ATP) – Component of nucleic acids, membrane phospholipids – Second messenger formation – Required for metabolism Ca & Pi plasma concentrations: ​ ● Ca​: 50% ionized, 45% protein-bound, 5% complexed. ● Pi​: 84% ionized, 10% protein-bound, 6% complexed. ● Hypocalcemia​ - too little Ca in blood (<8.5mg/dL) ● Hypercalcemia​ - too much Ca in blood (>10.5mg/dL) Regulation of Ca & Pi​: Calciotropic hormones: ● PTH - Origin​ - Parathyroid glands (principal (chief) cell). - Regulated by​ - CaSR (a GPCR) & Calcium-response element. High Ca inhibits PTH, calcitriol inhibits PTH. - Structure​ - secreted as an 84 AA; synthesized as a preproPTH; has < 5 min half-life. - Target/Receptor​ - PTH/PTHrp receptor: PTH1R – high levels in bone (osteoblasts) and kidney (proximal and distal tubules), PTH2R – high levels in CNS, pancreas, testis, placenta. - Function -​ protects against Hypocalcemia. ● Bone​: osteoblast growth/survival. high levels promotes Ca & Pi release from bone. regulates M-CSF, RANKL, and OPG production by osteoblasts. ● Kidney​: stimulates 1a-hydroxylase activity. stimulates Ca reabsorption by distal nephron (increases Ca ATPase). Inhibits Pi reabsorption by proximal nephron (represses NPT2a). ● 1,25 Dihydroxyvitamin D (Calcitriol) - Origin​ - UV light: synthesized by Cholesterol from Vit. D3 & D2. - Regulated by ​- magalin: binds to DBP, and by renal 1????-hydroxylase (CYP1????): stimulated by low serum Ca & inhibited by high serum Ca. - Structure​ - circulates blood bound to vitamin D-binding protein (DBP). - Target/Receptor​ - Small intestine, Bone, Kidney, Parathyroid gland / nuclear vitamin D receptor (VDR) that binds to Vit. D-responsive elements. ● Small intestine​ Increases Ca absorption ( by increasing TrpV channels, calbindin-D, and PMCA). Marginally increases Pi absorption. ● Bone​: Sensitizes osteoblasts to PTH. Regulates osteoid production and calcification. ● Kidney​: Minimal actions on Ca reabsorption. Promotes Pi reabsorption by proximal nephron (stimulates NPT2a). ● Parathyroid gland: ​ Directly inhibits PTH gene expression. Directly stimulate CaSR gene expression. Ca & Pi in Bones ● Bone accretion​ - osteoblasts build up bone tissue and bring Ca & Pi into bone. ● Bone resorption​ - osteoclasts break down bone tissue and release Ca & Pi into blood. ● Osteoblasts - Release (M-CSF) monocyte colony-stimulating factor, that acts with RANKL. - Derived from osteoprogenitor cells. - Contain receptors for PTH and calcitriol. - Synthesize organic bone matrix, produce alkaline phosphatase for mineralization. ● Osteocytes - Differentiated osteoblasts (trapped in matrix). - Major role in day-to-day calcium regulation. ● Osteoclasts - Multinucleate, derived from monocytes. - Contain calcitonin receptors, but no PTH or calcitriol receptors. - Produce acidic environment to resorb bone matrix. Ca & Pi in the Nephron ● Passive Ca++ reabsorption, ​ through TRP V5 & V6. ● Active Pi reabsorption, ​ through NPT2a, downregulated by PTH. - Most filtered Ca is reabsorbed. Hypocalcemic challenge: ​ - Low blood Ca (detected by CaSR on parathyroid chief cells) stimulates PTH secretion. - In the kidney, PTH increases Ca levels by increasing fractional resorption of Ca in renal distal tubules. - PTH also inhibits NPT2 activity, which increases Pi excretion. - Loss of Pi increases free ionized Ca in the blood. - At the bone, PTH stimulates osteoblasts to secrete RANKL, which increases osteoclast activity. - Osteoclast activity increases bone resorption and release of Ca & Pi into blood. Ca++/Pi & immune/inflammatory cells ● ​RANK, RANKL, osteoprotegerin​ are similar to TNFα receptor/NF-κB signaling components. - Activated T cells can express RANKL (stimulated by TNF-α, interleukins… ● Inflammatory bone disease is associated with increased RANKL-toosteoprotegerin ratios - Leads to bone erosion and osteoporosis. Regulation of Ca++/Pi metabolism by gonadal and adrenal steroid hormones ● ​Estadiol - Stimulates Ca++ absorption in intestine, reabsorption in kidney. - Promotes osteoblast survival and osteoclast apoptosis. ● ​Glucocorticoids ​have opposite effects. Disorders of Ca & Pi regulation Hyperparathyroidism • Kidney stones • Osteoporosis • GI disturbances, peptic ulcers, nausea, constipation • Muscle weakness, decreased muscle tone • Depression, lethargy, fatigue, mental confusion • Polyuria • Low serum phosphate, high serum calcium Hypoparathyroidism • Tetany, convulsions, paresthesias, muscle cramps • Decreased myocardial contractility • First-degree heart block • CNS problems, including irritability and psychosis • Intestinal malabsorption • Low serum calcium, high serum phosphate concentration Vitamin D deficiency - Results in hypocalcemia, hypomagnesemia, decreased GI absorption of Ca++ and Pi. - These changes cause increased PTH, increased bone resorption. ● Rickets: vitamin D deficiency before skeletal maturation. ● Osteomalacia: inadequate bone mineralization after skeletal growth is complete. Ch.3 What are the main three hormones involved in Energy Metabolism? Insulin Glucagon Cortisol Which other hormones are involved, but to a lesser extent? GH Progesterone Catecholamines Thyroid Hormone What does​ ​insulin​ do? ​ Decreases plasma glucose Is​ nsulin anabolic or catabolic? Anabolic ​- major anabolic hormone in the body Function of g​ lucagon​? Restore plasma glucose Function of​ cortisol ​ n energy metabolism? ​ Increases plasma glucose What stimulates the secretion of insulin? High/rising [plasma glucose] What other stimuli are included, but to a lesser extent? GI hormones Other sugars/hormones What tissues/organs does insulin act on? Adipose tissue Skeletal Muscle Liver What are the effects of insulin on a ​ dipose tissue​? Increase glucose uptake, FA synthesis, TAG storage Decrease Lipolysis What are its effects on ​skeletal muscle​? Increase glucose uptake Increase glycogen and protein synthesis Increase Ketoacid uptake What are ​the effects on the​ liver - ​ what does it ​ncrease ? ↑ synthesis of proteins, lipids and glycogen ↑​entry of K+ and phosphate What a re the effects on the liver - what does it ​ecrease ? ↓​cAMP, ketogenesis and gluconeogenesis ↓​​ roduction of glucose What type of islet cells are there in the liver? B, a, d, PP (F) What do each of these produce? B​ = insulin a ​= glucagon d ​= somatostatin PP​ = pancreatic polypeptide How does ​glucagon​ work to p ​ revent hypoglycaemia​? (resotre glucose in plasma) Acts to increase hepatic glucose output (increase gluconeogensis and glycgen breakdown) Acts on adipose tissue to increase FFA mobilisation How does ​cortisol​ ​act in ​increase glucose​ in plasma? - decrease peripheral uptake of glucose - increase hepatic output by gluconeo - increase FFZ mobilisation from AT - increase protein synthesis (makes aa.s available for gluconeogenesis) What is involved in the integrated hormone response to lowered glucose​? Glucose sparing for CNS Use of glucose reservoir (liver glycogen) Gluconeogenesis The following questions concern D ​ iabetes Mellitus (DM). ​ Give its definition A chronic state of hyperglycaemia caused by abnormalities in carb, protein and lipid metabolism - which may due to an absolute lack of insulin or to factors that oppose its action Where is the insulin secreted from? Beta cells of the islets of Langerhans in the pancreas Is DM​ ​a syndrome or a disease? A syndrome What determines c ​ arb metabolism and blood glucose? ​ Balance between: 1) Insulin (anabolic hormone) 2) Catabolic hormones - glucagon, cortisol, catehcolamines, GH What happens if the balance is tipped to the c ​ atabolic hormones? - failure of glucose uptake by tissues - catabolism esp of fats What is the consequence of failure of glucose uptake? Hyperglycaemia Osmotic diuresis What is the consequence of the c ​ atabolism of fats​? Ketoacidosis List the ​ketone bodies Acetoacetic acid B hydroxybutyric acid Acetone What are the consequences of​ k ​ etoacidosis ​ nd the PU, wrt to management? Can't maintain fluid intake Rapidly becomes dehydrated from osmotic D D + A = need emergency care if to survive How is​ ​DM classified? Type 1 (IDDM, Juvenile-onset) Type 2 (NIDDM, adult onset) Type 3 (Secondary causes of diabetes) What does Type 1 Diabetes cause? Progressive and eventually complete insulin insuffiency What is type 2 diabetes characterised by? Insulin resistance and dysfunctional B cells Compare ​Type 1​ and​ T​ ype 2 1 = insulin insufficiency 2 = insulin resistance


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