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IOS 9 Exam 3
DM pathophysiology
| Question | Answer |
|---|---|
| Abnormalities in glucose homeostasis results from altered | metabolism of CHO, Fats, proteins which results from insufficient secretion of insulin, resistance to insulin or both |
| DM 1 associated with | Autoimmune destruction of of pancreatic B-cells, influenced by genetic and environmental factors |
| DM2 associated with | older age, obesity, Fhx, personal Hx of gestational DM, impaired glucose, physical inactivity and race |
| Complications of DM are | Macrovascular (MI, stroke, PVR), Microvascular- retinopathy, nephropathy |
| Absorptive State is | Fed State--Liver is exposed to glucose , pancrease releases insulin and insulin taken up in muscles for energy, in adipose tissues for storage |
| Post-absorptive state is | Fasting state- No glucose is absorbed from the GI, yet plasma concentrations are sustained- Catabolic or breakdown of stores-Glyconeogenolysis, gluconeogenlysis, lipolysis |
| Glycogenolysis is | Glycogen that is stored in the liver is hydrolyzed by G-6-phosphatase (only hepatocytes) to form glucose for energy |
| Gluconeogenesis is | A form of new glucose production from lactate, alanine, glycerol (2/3 of post-absorptive phase form of glucose) |
| Lipolysis is | Triglycerides are cleaved to glycerol and FA- Glycerol forms glucose and FA become ketones- This occurs in prolonged starvation, the brain can use ketones for energy |
| The key hormones that control the transition from feasting to fasting are | Insulin(anabolic) and glucagon(catabolic) control the trasition from feasting to fasting |
| B-cells produce insulin from | A single-chain peptide called pre-proinsulin (110AA). This is transported through rough ER then cleaved to form proinsulin, In the golgi- C-peptide cleaved and B and A chain fold and disulfide bonds are formed |
| Equilar amounts of C-protein and insulin are released in circulation and this serves as | Useful index of insulin secretion- This can indicate if B-cells are functioning |
| Insulin release from pancreatic B-cells | Glucose stimulates insulin secretion, which is transported via GLUT2. Glucose is phosphorylated by glucokinase, Increase in intracellular K, Voltage Ca channels open trigger insulin release in biphasic phases |
| Insulin Biphasic release | 1st phase-Reaches peak in 1-2 minutes, 2nd phase-delayed onset, but longer duration |
| Secondary mechanisms of insulin inhibition/secretion are | Activation of the ANS can suppress insulin secretion or GI hormones-Incretin, Glucagon-like-peptide-1 |
| Insulin Binds alpha subunit transmembrane receptor | It is internalized and promotes translocation of glucose via GLUT4 |
| Insulin acts to | LIVER-Stimulate Glycogen synthesis (storage), FA synthesis, FAT-Glucose uptake, Triglycerides syn and storage, MUSCLE- Glucose uptake- INHIBITS- Glycogenolysis, Glyconeogenesis, Ketogen, Lipolysis, Protein breakdown |
| Glucagon causes | Increase in Glycogenolysis,Gluconeogenesis, Plasma glucose, Fat breakdown, protein breakdown |
| Prediabets is | Impaied fasting glucose=100-126, Impaired glucose tolerance-=140-200 |
| Type 1 DM is | Absolute deficiency of insulin secretion and occurs in 5-10% of DM patients, with onset 10-14yo, autoimmune destruction of B-cells (80-90% death) |
| Destruction of B-cells MOA | Autoimmune disease, selctive destruction of by Tcytotoxc cells then triggering cytokine causing inflammation, further macrophages and autoantibodies to site of inflammation |
| Type I markers of B-cell destruction are | Antibodies- Islet cell antibodies (ICA), Glutamic acid decarboxylase antibodies (GAD), antibodies to insulin |
| Honeymoon phase is | Days or weeks after the initial diagnosis of Type 1 experience apparent remission, metabolic abnormalities recover temporily but exogenous insulin requirements are inevitable |
| Environmental factors in Type 1 | Viruses (rubella, coxsackie, CMV), Dietary factors in infancy, seasonal variation (winter), geographical (sweeden) |
| Genetic factors of Type 1 | Human leokocyte antigen genes on chromosome 6 may predisose type 1, or variation in insulin genes |
| Disease states commonly present in Type 2 DM | HTN, dyslipidemia, Obesity |
| What are the Type 2 modifiable risk factors | Obesity, inactivity, Pre-DM, HTN, Low LDL or high TG |
| What are Type 2 Non-modifiable risk factors | Race, age, FHx, Genetics, Polysystic ovary disease, gestational DM, Baby>9lbs |
| Type 2 development | Initial is insulin Resistance and hyperinsulinemia with normal glucose tolerance leadint to decline in insulin levels and impaired glucose tolerance (B-cells impaired) |
| Insulin resistance is defined as | CHO is ingested and there is resistance to the metabolic effect of insulin, and no longer does insulin inhibit the liver from secreting glucose. |
| Potential theories why Type 2 have insulin resistance | Decrease in number of insulin receptors on the cell surface, decreased affinity of insulin receptors, defects in insulin signaling, Alterations in glucose transport (GLUT 4) |
| B-cell dysfunction is | B-cells are unable to maintain elevated rate of insulin secretionto overcome insulin resistance earlies manifestaton is loss of phase 1 |
| Potential of B-cell dysfunction | B-cell exhaustation, Glucose- toxcity, Difference in B-cell mass, Aging, Genetics |
| Glucoagon In type 2 DM in the non-fasting state is | Elevated which further drives production of glucose by the liver. This is one of the dysfunctions of the Type 2 or Type 1 |
| Amylin is a hormone that is co-secreted with insulin and is involved in | Glucose regulation of neuroendocrine function, lower rate of gastric emptying, suppression of post-prandial release of glucagon and improves satiety signals. Completely gone in Type 1 and varies in Type 2 |
| Gestational DM | Glucose intolerance occurs during pregnancy, B-cell reserves cannot over come insulin resistance, can lead to teratogenic issues, risk increases in second pregnancy |
| Maturity-onset DM- MODY | Onset occurs before 25, characterized by impaired B-cell function=insulin secretion disfunction with minimal insulin resistance (genetic)- NO Antibody |
| Maturity onset DM clincal presentation | Mild, asymptomatic hyperglycemia in non-obese children, adolescents, yound adults, strong FHx |
| DM 1.5 is | A latent autoimmune DM of adulthood- a slowly progressive form of autoimmune DM, presents like Type 2 but has Type 1 clinical features- GAD antibodies |
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liza001
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