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patho chapter 37
| Question | Answer |
|---|---|
| number of people with diabetes globally in 1980 | 180 million |
| number of people with diabetes globally in 2023 | 529 million |
| 1 in how many adults have diabetes | 11 |
| how many people in the u.s. have diabetes? | 38.4 million |
| what percent of the u.s. population have diabetes? | 11.6% |
| how many adults aged 18 or older in the u.s. have diabetes? | 38.1 |
| hyperglycemia | high blood glucose |
| acute symptoms of hyperglycemia | increased thirst and urination, weight loss |
| What three things can lead to chronic complications? | hyperglycemia, insulin resistance, insulin deficiency |
| What percent of people with diabetes have type 1? | 1-5% |
| Type 1 Diabetes Mellitus | autoimmune condition, pancreas unable to make insulin, destruction of pancreatic beta cells, pharmacologic insulin therapy needed for survival |
| What percent of people with diabetes have type 2? | 90-95% |
| Type 2 Diabetes Mellitus | insulin resistance and defects in insulin secretion |
| If you have T2D are you dependent on exogenous insulin to sustain life? | no, may need insulin therapy, other medications |
| what percent of people with diabetes have monogenic DM? | 0.6-5% |
| monogenic DM | neonatal diabetes mellitus, maturity-onset diabetes of young |
| when does gestation diabetes mellitus onset? | during pregnancy |
| Ways to treat gestation diabetes mellitus? | dietary treatment, oral medications, exogenous insulin |
| What can hyperglycemia in Gestation diabetes mellitus result in? | fetal and maternal complications; infants born tend to be larger and have increased risk of developing diabetes |
| A1C | glycated hemoglobin |
| What does the A1C measure? | the percentage of hemoglobin that is bound to glucose |
| What is considered normal on the A1C test? | 5.7% |
| What is considered prediabetes on the A1C test? | 5.7-6.5% |
| What is considered diabetic on the A1C test? | greater than 6.5% |
| FPG | fasting peripheral glucose |
| what does the FPG test measure? | the concentration of glucose in your blood after a period of not eating |
| What is considered normal on the FPG test? | less than 100 mg/dL |
| What is considered prediabetes on the FPG test? | 100-126 mg/dL |
| What is considered diabetes on the FPG test? | greater than 126 mg/dL |
| What test is the gold standard test for diabetes? | A1C |
| OGTT | oral glucose tolerance test |
| oral glucose tolerance test | a two-hour test that checks your blood glucose levels before and two hours after you drink a 50-75g glucose drink |
| What is considered normal on OGTT? | less than 140 mg/dL |
| What is considered prediabetes on OGTT? | 140-220 mg/dL |
| What is considered diabetic on OGTT? | greater than 200 mg/dL |
| Prediabetes | increased risk for developing DM, primarily T2D, Impaired fasting glucose, impaired glucose tolerance |
| Impaired fasting glucose | fasting blood glucose level or hemoglobin A1C higher than normal but no diagnostic of DM |
| impaired glucose tolerance | blood glucose level two hours after oral glucose load higher than normal but not diagnostic of DM |
| What else is metabolic syndrome known as? | insulin resistance syndrome |
| What has more risk factors for diabetes than pre-diabetes? | metabolic syndrome |
| How many of the 5 features of metabolic syndrome do you need to diagnose? | 3 |
| Components of diagnosing metabolic syndrome | waist circumference or BMI, triglycerides, HDL cholesterol, blood pressure, fasting glucose |
| clinical cutoff values for waist circumference in men | greater than 102 cm (40 inches) |
| clinical cutoff values for waist circumference in women | greater than 88cm (35 inches) |
| clinical cutoff values for BMI | greater than 30kg/m2 |
| clinical cutoff values for triglycerides | greater than 150 mg/dL |
| clinical cutoff values for HDL cholesterol in men | less than 40 mg/dL |
| clinical cutoff values for HDL cholesterol in women | less than 50 mg/dL |
| clinical cutoff value for blood pressure | greater than 130 mmHg systolic BP or greater than 85 mmHg diastolic |
| clinical cutoff value for fasting glucose | greater than 100 mg/dL |
| glucose | obligate fuel for brain and CNS, need continuous supply |
| glycolysis | breakdown of carbohydrate (CHO) to form ATP; aerobic and anaerobic |
| aerobic glycolysis | mitochondria and oxygen; forms pyruvate |
| anaerobic glycolysis | no mitochondria and no oxygen; forms lactic acid |
| normal blood glucose levels | 70-110 mg/dL |
| What happens when blood glucose levels are increased? | beta cells secret insulin |
| What is increased when beta cells secrete insulin? | rate of glucose transport into target cells, rate of glucose utilization and ATP generation, conversion of glucose to glycogen, amino acid absorption and protein synthesis, triglyceride synthesis in adipose tissue |
| What happens when blood glucose levels are decreased? | alpha cells secrete glucagon |
| What happens when alpha cells secrete glucagon? | increased breakdown of glycogen to glucose, increased breakdown of fat to fatty acids, increased synthesis and release of glucose |
| How is glucose transported into a cell? | facilitated transport mediated by glucose transporter (GLUT) |
| Where is glucose transporter (GLUT4) located in skeletal muscle and adipocytes? | in the cytosol |
| What do GLUT4 vesicles need to translocate to the membrane? | insulin stimuli |
| GLUT2 | located at the cell membrane of several organs in particular pancreas and liver, does not require insulin to be translocate |
| GLUT2 pancreas | GLUT2 transport glucose into the cell and that stimulates a signaling pathway to secret insulin |
| GLUT2 liver | GLUT2 transport glucose into the cell and insulin activates a pathway to convert glucose as glycogen |
| glycogen | storage form of glusose |
| where is glycogen primarily located? | skeletal muscle and liver |
| glycogenolysis | conversion of liver and muscle glycogen to glucose |
| lipolysis | process through which triglycerides are hydrolyzed to fatty acids and glycerol |
| gluconeogenesis | formation of glucose or glycogen from non-CHO sources |
| precursors of gluconeogenesis | pyruvate, amino acids, glycerol |
| ketogenesis | production of ketone bodies- acetoacetate, 3-hydroxybutyrate |
| Fuel metabolism in diabetes mellitus | deficiency in insulin and increase in glucagon, other counterregulatory hormones, hyperglycemia, T1D, T2D |
| Fuel metabolism T1D | increased mobilization of FFAs causes increased heaptic synthesis of ketone bodies, diabetic ketoacidosis |
| Fuel metabolism T2D | ketone bodies not sufficient for development of DKA, hyperosmolarity |
| Most common form of Type 1 diabetes mellitus | t-cell mediated autoimmune destruction of pancreatic beta cell |
| type 1 diabetes mellitus etiology | genetics (familial predisposition, HLA genes on short arm of chromosome), environment, autoimmunity (antibodies against pancreatic beta-cell components) |
| type 1 diabetes mellitus pathogenesis | environmental factors trigger immune response, autoantibodies and antigens develop, honeymoon period follows (period of endogenous insulin secretory recovery), insulin production ceases |
| treatment for type 1 diabetes mellitus | exogenous insulin |
| most common form of DM | T2D |
| type 2 diabetes mellitus etiology | genetics (if both parents have T2D, risk is 75%), ethnicity (disproportionately affects minority populations) |
| non modifiable risk factors for type 2 diabetes | family history of diabetes, age over 45 years, race and ethnicity, history of gestational diabetes |
| modifiable risk factors for type 2 diabetes | physical inactivity, high body fat or body weight, tobacco use/ pollution, unhealthy diet |
| type 2 diabetes treatment | lifestyle modifications, medications, glucose monitoring |
| lifestyle modifications for type 2 diabetes | balanced diet with more fiber rich foods, exercising (aerobic exercise and resistance exercise) |
| medications for type 2 diabetes | oral (ex. metformin), insulin- typically basal insulin is used, intermediate or long-acting forms, insulin regimens vary |
| glucose monitoring for type 2 diabetes | HbA1c test (measures average blood glucose levels), fingersticks |
| Acute complications of diabetes | diabetic ketoacidosis, hyperosmolarity syndrome, hypoglycemia |
| what is diabetic ketoacidosis absolute or relative insulin deficiency characterized by? | hyperglycemia, metabolic acidosis, ketonemia |
| what is diabetic ketoacidosis absolute or relative insulin deficiency most commonly associated with? | T1D |
| what are the most common causes of diabetic ketoacidosis absolute or relative insulin deficiency? | disruption of insulin treatment, new onset of T1D |
| DKA insulin deficiency and CHO metabolism? | hyperglycemia, glycosuria and osmotic diuresis, dehydration and hemoconcentration, peripheral circulatory failure progressing to shock, hypotension, anuria, coma and death |
| DKA insulin deficiency and fat metabolism | mobilization of depot fat in the blood; lipemia, secondary hypertriglyceridemia; FFAs made into LDLs |
| what happens in secondary hypertriglyceridemia; FFAs made into LDLs? | ketone bodies develop into ketonemia, progressive metabolic acidosis, ketonuria, cardiovascular collapse |
| DKA insulin deficiency and protein metabolism | decreased protein synthesis, overall protein catabolism, particularly in muscle, elevated levels of blood urea nitrogen BUN, net loss of K+ |
| DKA diagnosis | laboratory criteria- hyperglycemia, ketosis, metabolic acidosis |
| DKA treatment | supportive measures, intravenous insulin therapy, intravenous fluids, intravenous electrolyte replacements |
| Hyperglycemic hyperosmolar syndrome (HHS) | severe hyperglycemia and coma but without ketosis |
| HHS risk factors | IGT or T2D |
| HHS etiology and pathogenesis | ready access to fluids not available; excessive unreplaced fluid losses, severe hyperglycemia and hyperosmolarity, glycosuria, osmotic diuresis, urinary electrolyte losses, reduction in GFR from dehydration |
| HHS clinical manifestations | related to hyperglycemia, dehydration, serum hyperosmolarity more severe than in DKA, plus neurologic symptoms and vascular thrombosis |
| HHS diagnosis | laboratory criteria, profound dehydration and alteration in consciousness |
| treatment | same as DKA- insulin and fluids |
| hypoglycemia | medical emergency: decreased blood glucose levels (<60mg/dL), autonomic nervous system and neuroglycopenic symptoms |
| hypoglycemia etiology and pathogenesis | complication of T1D and insulin treated T2D, glucose-stimulated decline in plasma insulin levels |
| hypoglycemia precipitating factors | incorrect amount (too much) or type of insulin, missing meals and snacks, exercise |
| hypoglycemia clinical manifestations | ANS symptoms prompt eating, raising blood glucose level, neuroglycopenic symptoms result from glucose deprivation to CNS |
| hypoglycemia treatment | glucose |
| Microvascular complications due to hyperglycemia | retinopathy (blindness), nephropathy (kidney failure), neuropathy (limb amputation) |
| macrovascular complications due to hyperglycemia | hypertension (peripheral vascular disease) leads to heart attack (heart disease) which induces stroke (cerebrovascular disease) |
| Chronic complications of DM | microvascular diseases, macrovascular diseases |
| microvascular diseases | diseases of smaller vasculature |
| macrovascular diseases | diseases of large vasculature |
| proposed pathogenesis of microvascular complications | hyperglycemia primary factor, retinopathy, neuropathy, nephropathy |
| Proposed pathogenesis of macrovascular complications | aggressive and accelerated rates of stroke, cardiovascular disease, peripheral vascular disease; hyperglycemia; insulin resistance |
| Insulin resistance | reduced HDLs; increased triglycerides; increased LDLs; FFA induced increase in ROS; polyol pathway, hexosamine pathway, PKC, AGE precursors, atherosclerotic macrovascular disease |
| Diabetic retinopathy | disease of retina resulting in loss of vision |
| Diabetic retinopathy etiology and pathogenesis | excessive vascular occlusion or vascular permeability, subsequent macular edema, neovascularization, fibrous tissue proliferation, vitreous hemorrhage |
| Retinopathy clinical manifestations | temporary blurring of vision, refractory changes, increased risk of cataract formation |
| retinopathy management | glucose control, well-controlled blood pressure |
| Diabetic nephropathy | damage to capillary wall in kidneys causes protein molecules to spill into urine- leading cause of death in diabetic patients |
| Diabetic nephropathy classes of renal changes | glomerulosclerosis, structural vascular changes (small arterioles), tubulointerstitial disease |
| Diabetic nephropathy clinical manifestations | presence of microalbuminuria |
| Diabetic neuropathy | damage to nerve due to high blood glucose |
| Diabetic neuropathy pathogenesis | increased polyol pathway activity, Na+ retention, edema, myelin swelling, nerve degeneration |
| Diabetes related peripheral neuropathy symptoms | pain, muscle weakness, numbness, slow healing leg or foot sores, pins and needles sensation |
| Acute muscle contraction induces? | glucose uptake |
| Effect of exercise on blood glucose levels | decreases blood glucose |
| Acute effect of exercise | Adipose tissue releases FFAs during exercise which are used by skeletal muscle to produce ATP |
| Skeletal Muscle Adaptation to Exercise | increase mitochondria number and size, Increase GLUT4 concentration, decrease intracellular lipid accumulation, increase the size of the muscle fiber |
| increase mitochondria number and size | increase the capacity of muscle to metabolize glucose and lipids |
| Increase GLUT4 concentration | increase insulin sensitivity and the capacity of uptake glucose |
| decrease intracellular lipid accumulation | decrease the impairment on insulin pathway |
| increase the size of the muscle fiber | increase the site for glucose clearance under insulin stimulation |
Created by:
camrynfoster