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Endocrinology-Ch.3 Notes

by: Michelle Notetaker

Endocrinology-Ch.3 Notes BIOL 4110

Marketplace > University of North Texas > Biology > BIOL 4110 > Endocrinology Ch 3 Notes
Michelle Notetaker
GPA 3.5

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About this Document

These notes cover the lecture material in more detail and in an easy-to-read format.
Dr. Harris D Schwark
Class Notes
Endocrine system
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This 7 page Class Notes was uploaded by Michelle Notetaker on Wednesday September 28, 2016. The Class Notes belongs to BIOL 4110 at University of North Texas taught by Dr. Harris D Schwark in Fall 2016. Since its upload, it has received 4 views. For similar materials see Endocrinology in Biology at University of North Texas.


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Date Created: 09/28/16
Endocrinology ­ Ch.3 Energy Metabolism 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 act to do? Lower plasma glucose Is insulin anabolic or catabolic? Anabolic ­ major anabolic hormone in the body Function of glucagon? Restore plasma glucose Function of cortisol in energy metabolism? Increase 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 adipose 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 doeincrease? ↑ synthesis of proteins, lipids and glycogen  ↑  entry of K+ and phosphate What are the effects on the liver ­ what doedecrease? ↓ cAMP, ketogenesis and gluconeogenesis ↓  production 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 prevent 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 Diabetes Mellitus. 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? by the beta cells of the islets of Langerhans in the pancreas Is DM a syndrome or a disease? A syndrome What determines carb 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 catabolic  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 catabolism of fats? Ketoacidosis List the ketone bodies Acetoacetic acid B hydroxybutyric acid Acetone What are the consequences of ketoacidosis and 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 in humans? Type 1 (IDDM, Juvenile­onset) Type 2 (NIDDM, adult onset) Type 3 (Secondary causes of diabetes) What falls under (wrt cause) type 1 Diabetes Mellitus? A combination of GENETIC predisposition and IMMUNOLOGICAL  DESTRUCTION of B cells What does this do (Diabetes Type 1) Progressive and eventually complete insulin insuffiency How do you know if someone as type 1 Diabetes? You do get hyperglycaemia and clinical signs BUT before this you  can find autoantibodies What are these autoantibodies against? Insulin B cell GAD = glutamic acid decarboxylase What is type 2 diabetes characterised by? Insulin resistance and dysfunctional B cells So compare type 1 and 2 1 = insulin insufficiency 2 = insulin resistance Origin of Type 2 defects? Thought to be genetic So why do we say fat people get it? Deleterious effects can be accentuated by environmental  factors  (e.g. obesity How do you know if someone has type 2 diabetes? Defects are actually evident for A DECADE OR LONGER before  hyperglycaemia and clinical signs develop List the potential aetiologies of Diabetes Mellitus (DM) Genetics Immune­med destruction of islet cells Obesity Infection Pancreatitis Concurrent illness Drug therapy Islet amyloidosis What signs are seen? ­ PUPD, PG, weight loss ­ Hepatomeg mm wasting ­ Bacterial infections common ­ Eye problems ­ Kidney problems ­ skin disease ­ more later if uncontrolled What bacterial infections can occur? UTI Resp tract infections What eye problems? Cataracts Retinopathy Peripheral neuropathy Kidney problems? Glomerulonephritis Skin disease Cutaneous xanthomata, ulcerative dermatosis What happens later if the disease is uncontrolled? Anorexia V+ Dehydration Why do these later signs occur? From ketoacidosis List the potential triggers of diabetic ketoacidosis Dehydration System inflammation Iatrogenic Other diseases What can cause the...dehydration? Accidental water restriction V+ Chronic Kidney Disease ...systemic inflammation? Pancreatitis UTI Pyometra Pneumonia ...iatrogenic causes? Corticosteroids Progestagens (eg proligesterone, megoestrol, acetate)


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