Presentation on theme: "Chapter 33 Diabetes Mellitus and the Metabolic Syndrome"— Presentation transcript:
1Chapter 33 Diabetes Mellitus and the Metabolic Syndrome Essentials of PathophysiologyChapter 33 Diabetes Mellitus and the Metabolic Syndrome
2Pre lecture Quiz Type 2 diabetes is more common than type 1. FType 2 diabetes is more common than type 1.All cells can use fatty acids interchangeably with glucose for energy.Insulin is produced by the pancreatic beta cells in the islets of Langerhans.Hyperglycemia is characterized by headache, difficulty in problem solving, disturbed or altered behavior, coma, and seizures.Chronic complications of diabetes mellitus refer only to type 1 diabetes mellitus.
3Pre lecture Quiz Alpha Insulin ketoacidosis Metabolic one ______________ lowers the blood glucose concentration by facilitating the movement of glucose into body tissues.Glucagon, a polypeptide molecule produced by the _____________ cells of the islets of Langerhans, maintains blood glucose between meals and during periods of fasting.Type __________ diabetes mellitus is characterized by destruction of the pancreatic beta cells and is characterized by an absolute lack of insulin, an elevation in blood glucose, and a breakdown of body fats and protein.The ________________ syndrome is a condition of abnormalities that are identified through specific criteria such as abdominal obesity, elevated triglycerides, elevated blood pressure, elevated fasting plasma glucose, and decreased high-density lipoprotein cholesterol (HDL).Diabetic ____________________ occurs when ketone production by the liver exceeds cellular use and renal excretion.AlphaInsulinketoacidosisMetabolicone
4Anabolism and Catabolism available foodstuffsAnabolismstored foodstuffs(in blood)insulin,(in cells)anabolicsteroidsglucoseglycogenCatabolismamino acidsproteinsglucagon,epinephrine,free fatty acidscortisoltriglyceridesliver can convert amino acidsand free fatty acids intoketones
5Insulin and Glucagon Are the Main Controls available foodstuffsAnabolismstored foodstuffs(in blood)insulin,(in cells)anabolicsteroidsglucoseglycogenCatabolismamino acidsproteinsglucagon,epinephrine,free fatty acidstriglyceridescortisolliver can convert amino acidsand free fatty acids intoketones
6QuestionTell whether the following statement is true or false. Anabolic reactions release energy.
7AnswerFalse Rationale: Anabolic reactions use energy to build/produce/synthesize (like building proteins from amino acids). Catabolic reactions break down substances, releasing energy in the process (like digestion).
8Scenario Two women have benign pancreatic tumors. In one, the tumor is an insulinoma that secretes insulinIn the other, the tumor is a glucagonoma that secretes glucagonQuestions:What differences do you expect to see between these two women? Why?Both of the women have arthritis, but only one is being treated with corticosteroids. Which one? Why is the other not receiving corticosteroids?
9The Pancreas pancreas exocrine endocrine pancreas pancreas releases digestivereleases hormonesjuices through ainto the bloodductto theduodenum
12Functions of Pancreatic Hormones Glucagon: causes cells to release stored food into the bloodInsulin: allows cells to take up glucose from the bloodAmylin: slows glucose absorption in small intestine; suppresses glucagon secretionSomatostatin: decreases GI activity; suppresses glucagon and insulin secretion
15AnswerInsulinRationale: Insulin allows cells to take glucose from the blood and use it for energy/to make ATP. Because it stimulates movement of glucose out of the blood and into the cells, blood glucose levels decrease when insulin is released.
16Discussion Think back on your day so far. When do you think you had your highest insulin levels?When do you think you had your lowest insulin levels?When did you have your highest glucagon levels?
18Review the figure on insulin’s actions. DiscussionReview the figure on insulin’s actions.If someone lacks insulin, what happens to his:Blood glucose levels?Blood amino acid levels?Blood pH?Intracellular fat levels?Intracellular protein levels?Cell growth?
19DiscussionReview the following diagrams on anabolism/catabolism and insulin’s mechanism of action.Questions:Identify five things that could go wrong to cause increased blood glucoseWhich of the cases you identified would be least likely to respond to insulin?
20Anabolism and Catabolism available foodstuffsAnabolismstored foodstuffs(in blood)insulin,(in cells)anabolicsteroidsglucoseglycogenCatabolismamino acidsproteinsglucagon,epinephrine,free fatty acidscortisoltriglyceridesliver can convert amino acidsand free fatty acids intoketones
21Types of Diabetes Mellitus Type 1: pancreatic beta cell destruction predominantly by an autoimmune processType 2: a combination of beta cell dysfunction and insulin resistanceOtherGenetic defects in insulin productionGenetic defects in insulin actionDiabetes secondary to other diseasesDrug interactionsGestational diabetes mellitus
23QuestionTell whether the following statement is true or false. Type 2 DM is more common than type 1 DM.
24AnswerTrue Rationale: Type 1 DM is autoimmune (juvenile diabetes is type 1), and affects only 5–10% of the diabetic population. Type 2 DM is associated with risk factors like obesity, poor diet, and sedentary lifestyle; 90–95% of diabetics suffer from this type.
28Acute Complications of Diabetes (cont.) DiscussionHow would hyperglycemia with ketoacidosis cause:Heavy breathing?Polyuria?Dehydration?Which of these would you not see in hyperglycemia without ketoacidosis?
29Scenario You find a man collapsed on the sidewalk. He is wearing a diabetic alert bracelet and has an insulin syringe in his briefcaseQuestions:Does he need insulin?Why or why not?What signs might help you tell whether he has a hyperglycemic or hypoglycemic problem?
30Chronic Complications of Diabetes Mellitus Increased glucose levels allow glucose to bind to proteins in:Hemoglobin Hb A1C has higher O2 affinityBasement membranes of blood vesselsNephropathyRetinopathyMay cause increased risk of atherosclerosisLens cataracts(Porth, C. M. . Pathophysiology [7th ed.]. Lippincott Williams & Wilkins andGreenspan, F. & Gardner, D. G. . Basic and clinical endocrinology [7th ed.]. McGraw-Hill.)
32Osmolarity in Diabetes Mellitus When blood glucose is high, increased blood osmolarity can cause cells to shrinkNerve cells produce intracellular osmoles to keep their osmolarity balanced with the bloodHypotonic cell A shrinksABCell B is in osmotic balance(Porth, C. M. . Pathophysiology [7th ed.]. Lippincott Williams & Wilkins.)
33Osmolarity in Diabetes Mellitus (cont.) When the client brings blood glucose back to normal, the nerve cells are hyperosmolar to the blood and gain water, swellingNerve damage may be caused by swelling, demyelination, and lack of O2 secondary to vascular diseaseACell A is in osmotic balanceBHypertoniccell B swells(Porth, C. M. . Pathophysiology [7th ed.]. Lippincott Williams & Wilkins.)
34Diabetic Neuropathy Somatic neuropathy Autonomic neuropathy Diminished perception of vibration, pain, and temperatureHypersensitivity to light touch; occasionally, severe “burning” painAutonomic neuropathyDefects in vasomotor and cardiac responsesImpaired motility of the gastrointestinal tractInability to empty the bladderSexual dysfunction
35QuestionWhich of the following is not a complication of diabetes mellitus?NephropathyRetinopathyNeuropathyAll of the above are complications of DM.
36AnswerAll of the above are complications of DM.Rationale: Nephropathy and retinopathy are caused by increased blood glucose levels that cause binding of excess glucose to the basement membranes of the blood vessels of the kidneys and eyes. Neuropathy is due to swelling and demyelination of nervous tissue.