Term
| what complication do most people w/DM die of? |
|
Definition
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|
Term
| what age group has had the smallest increase in rate of DM dx since 1958? |
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Definition
|
|
Term
| are men or women more affected by DM? |
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Definition
| the rates among genders are generally equal |
|
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Term
| what is type 1 DM? type 2? |
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Definition
| type 1: B-cell destruction = lack of insulin. type 2: insulin resistance w/decreased secretion. |
|
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Term
| when does gestational diabetes occur? what is it due to? |
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Definition
| ~28 wks, due to human placental lactogen which can antagonize insulin |
|
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Term
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Definition
| latent adult autoimmune diabetes: adults w/immunologic patterns of type I DM |
|
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Term
| what is type one and a half diabetes? |
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Definition
| a type II DM pt who develops antibodies to their beta cells |
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Term
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Definition
| type I DM pts w/DM type II family members |
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Term
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Definition
| maturity onset diabetes of youth: obese pts who have a mild case of DM (due to enzymatic deficiencies) and may be treated via oral monotherapy |
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Term
| what do pts have who are at risk of developing DM? |
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Definition
| impaired glucose tolerance |
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Term
| what is metabolic syndrome? |
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Definition
| obesity, low HDLs, high TGs, HTN, and hyperglycemia |
|
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Term
| what are the 4 ways of diagnosing DM? |
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Definition
| 1) random plasma glucose > 200 mg/dl on 2 separate occasions + polyuria/polydipsia/unexplained wt loss. 2) FPG > 126 on 2 separate occasions. 3) 2 hour plasma glucose > 200 during OGTT for gestational diabetes. 4) Hgb A1C greater than or at 6.5%. |
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Term
| what is a normal fasting glucose? postprandial? |
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Definition
| normal: < 100, postprandial: < 140 |
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Term
| what two changes occur in terms of insulin regulation in DM type 2? |
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Definition
| insulin resistance and reduced insulin secretion occur |
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Term
| what occurs as a result of insulin resistance as seen in DM type 2? |
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Definition
| decreased peripheral glucose uptake, increased hepatic glucose production, and increased FFA/TG production |
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Term
| what is the pathophysiology of type 1 DM? |
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Definition
| *genetic factors: increased susceptibility to beta cell damage - seen in types 1+2 and *environmental factors: viral infections, nutrition, and chemical agents |
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Term
| how does insulin secretion normally occur? how is this affected in type 2 DM? |
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Definition
| normally there is a 1st and 2nd phase of glucose secretion, the first within a couple minutes and the second in about an hour. in type 2 DM pts, the first phase response is lost initially and the 2nd phase may eventually also be lost as well. |
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Term
| does beta cell function decline over time in type II DM pts? |
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Definition
| yes, often pts may have 50% function at time of dx and be down to 0% function 8 years later (a state which requires insulin). |
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Term
| what is thought to contribute to progressive beta cell failure in DM pts? |
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Definition
| increasing insulin resistance and increasing blood glucose levels overwork a decreasing population of beta cells, leading to their eventual failure |
|
|
Term
| can beta cell function be improved through current medical means? |
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Definition
|
|
Term
| how can insulin resistance be decreased? |
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Definition
| insulin sensitivity can be improved by reducing carbohydrate intake (10-15 g/day), TZDs, and exercise |
|
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Term
| what minority populations have higher risks of DM? |
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Definition
| black americans: 50-100% increased risk compared to whites and hispanic americans: 130-200% increase compared to whites w/a higher rate of long term complications |
|
|
Term
| what factors can lead to insulin resistance? |
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Definition
| genetics, obesity/inactivity, aging, medications, rare disorders |
|
|
Term
| what are the general outcomes of insulin resistance? |
|
Definition
| type 2 DM, HTN, dyslipidemia, atherosclerosis, and PCOS |
|
|
Term
| how does decreased insulin affect the liver? |
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Definition
| the liver will increase gluconeogenesis (insulin usually suppresses this) |
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Term
| how do type 1+2 DM compare in terms of mode of onset, acanthosis, DKA, insulin reserve, and autoantibodies? |
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Definition
| mode of onset: type 1 acute/2 insidious, acanthosis nigricans: type 1 absent/2 present, DKA: type 1 present/2 usually absent, insulin reserve: type 1 absent/2 present, and autoantibodies type 1 present/2 absent |
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Term
| what are common methods of monitoring DM therapy efficacy? |
|
Definition
| Hgb A1C - which should generally be less than 7%. FPG - should be 110 mg/dl or lower. |
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|
Term
| what complications can glycemic control decrease incidence of? |
|
Definition
| retinopathy, nephropathy, and neuropathy |
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|
Term
| what are nutrition-related strategies for improved metabolic control? |
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Definition
| reduced caloric intake, spreading food intake out throughout the day, placing more importance on total carbohydrate vs carbohydrate source, decreased sat fat and total fat, increased physical activity, moderate wt loss, and monitoring of blood glucose |
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|
Term
| what is the primary tx for type 1 DM pts? |
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Definition
| insulin therapy and/or amylin (a pancreatic peptide which is co-secreted w/insulin which reduces glucagon/blood sugar and increases satiety) |
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|
Term
| what is used to lower blood sugar in type I DM pts? |
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Definition
| long acting/peakless analog insulins such as glargine or detimir - which establish a baseline insulin level |
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Term
| what therapy would be taken at mealtime in type I DM pts? |
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Definition
| rapid-acting insulin analogs or a premixed analog (containing both rapid and long acting analogs) |
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Term
| what is the primary tx for type 2 DM pts? |
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Definition
| oral hypoglycemics (sulfonylureas, biguanides, TZDs, alpha glucosidase inhibitors, dpp4-inhibitors), incretins (exenatide and liraglutide - GLP analogues), amylin, and insulin |
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Term
| what are the 4 general steps in DM type 2 therapy? |
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Definition
| 1) diet/exercise/nutrition therapy. 2) oral agents (mono/combo). 3) add/change insulin. 4) intensify insulin. |
|
|
Term
| what ADRs are associated with acarbose/alpha-glucosidase inhibitors? |
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Definition
|
|
Term
| what ADRs are associated with metformin/biguanides? |
|
Definition
| some GI disturbances, possible weight loss, and rarely: lactic acidosis |
|
|
Term
| what ADRs are associated with sulfonylureas? |
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Definition
|
|
Term
| what ADRs are associated with troglitazone/TZDs? |
|
Definition
|
|
Term
| what MOA is associated with metformin/biguanide? |
|
Definition
| reduction of hepatic glucose output and lipolysis = increased sensitization to blood sugar |
|
|
Term
| what MOA is associated with metformin/biguanide and troglitazone/TZDs? |
|
Definition
| reduction of hepatic glucose output and lipolysis = increased sensitization to blood sugar. also increased glucose uptake in the musculature. |
|
|
Term
| what MOA is associated w/alpha-glucosidase inhibitors? |
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Definition
|
|
Term
| what MOA is associated w/sulfonylureas and meglitinides? |
|
Definition
| increasing insulin secretion |
|
|
Term
| what are the goals for DM type II tx? |
|
Definition
| FPG: 80-120 (normal: <110), PPG: 100-140 (normal: <120), and HbA1C: <6.5 (normal: <6) |
|
|
Term
| what metric would more likely be associated with HbA1C 3 month avg increasing? |
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Definition
|
|
Term
| what metric would more likely be associated with HbA1C 3 month avg decreasing? |
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Definition
|
|
Term
| what is the MOA for incretins? |
|
Definition
| incretins or GLPs (glucagon-like polypeptide) stimulate insulin secretion, improve postprandial control and area associated w/wt loss. (these are not oral hypoglycemics) |
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|
Term
| can even a 1% drop in HbA1c reduce long-term DM complications? |
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Definition
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|
Term
| how does high blood glucose cause complications in DM? |
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Definition
| glucose is converted to sorbitol by aldose reductase. sorbitol (an alcohol) accumulates in optic, vascular, and nerve tissue - attracting water and causing damaging swelling. AGEs (advanced glycation end products) also cause damage in these tissues. both sorbitol and AGEs generally cause microangiopathic disease. |
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|
Term
| what microvascular retinopathy is associated w/DM? |
|
Definition
| impaired vision and blindness |
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|
Term
| what microvascular nephropathy is associated w/DM? |
|
Definition
| HTN, proteinuria, nephrotic syndrome, and renal failure |
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|
Term
| what microvascular peripheral neuropathy is associated w/DM? |
|
Definition
| pain, paresthesias, hyperesthesias, and weakness |
|
|
Term
| what microvascular autonomic neuropathy is associated w/DM? |
|
Definition
| GI dysfunction, orthostatic HTN, *cardiorespiratory arrest*, bladder dysfunction, and impotence |
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|
Term
| what do microvascular complications in DM generally boil down to? |
|
Definition
| damage due to high blood glucose |
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|
Term
| what is the #1 cause of end stage renal disease in the US? |
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Definition
|
|
Term
| what can intercostal mononeuropathy cause in DM pts? |
|
Definition
| cardiac and/or intra-abdominal dysfunction and pain |
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|
Term
| are DM pts at more of a risk for silent MIs? |
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Definition
|
|
Term
| what is the sequence of autonomic abnormalities seen in DM pts? |
|
Definition
| thermoregulatory function and sweating, impotence/bladder dysfunction, CV reflex problems, sweating, hypoglycemia unawareness, and postural hypotension in gastric problems |
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|
Term
| what is the clinical presentation of CV disorders related to DM? |
|
Definition
| postural hypotension, resting tachycardia, and silent MI |
|
|
Term
| can DM cause connective tissue complications? |
|
Definition
| yes including osteoporosis, carpal-tunnel, limited joint mobility, adhesive capsulitis, etc |
|
|
Term
| what are the 3 types of macrovascular changes seen in DM type 2 and their respective effect? |
|
Definition
| *CAD (MI), *cerebrovascular (stroke), and *peripheral vascular disease (intermittent claudication/gangrene) |
|
|
Term
| does lowering glucose help w/macrovascular complications due to DM? |
|
Definition
| yes, some - however not as much as lowering lipids/BP |
|
|
Term
| how does DM affect MI survival in men/women? |
|
Definition
| DM pts survive MIs less often overall w/women DM pts being the worst affected. |
|
|
Term
| what does diabetic ketoacidosis (DKA), the most common endocrine emergency consist of? |
|
Definition
| hyperglycemia (> 250 mg/dl), ketosis (ketonemia/ketonuria), acidosis (pH < 7.3, HCO3 < 15 mEq/L) |
|
|
Term
| what are the common presentations of diabetic ketoacidosis (DKA)? |
|
Definition
| either a DM1 pt who didn't take enough of their medicine (or at all) or a new DM1 dx |
|
|
Term
| what are the 2 greatest causes of mortality in DKA pts? |
|
Definition
| acidosis and dehydration (osmotic diuresis) |
|
|
Term
|
Definition
| hydration (normal saline) and IV insulin |
|
|
Term
| what is the clinical presentation of DKA pts? |
|
Definition
| dehydrated (dry/sunken eyes), possible abdominal pain due to pancreatitis, and shallow rapid breathing (kussmaul's - creates a compensatory alkalosis) |
|
|
Term
| can lactic acidosis occur in DKA pts as well? |
|
Definition
| yes - this is occurs in combined acidosis, which is due to severe dehydration that causes hypoperfusion/hypotension. |
|
|
Term
| what is hyperosmolar hyperglycemic non-ketotic coma (HHNKC)? tx? |
|
Definition
| a condition found in DM2 pts which is considered an emergency as the glucose levels are in the thousands. the drivers here are hyperglycemia/hyperosmolarity, not ketosis. tx: fluids, insulin (but less insulin than in DKA), and any underlying causes. |
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|
Term
| what was the DM delay trial DPP1? |
|
Definition
| a study which attempted to see if giving pts at risk for DM1 insulin and immunosuppressants would lower their risk - but it didn't. |
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|
Term
| what was the DM delay trial DPP2? |
|
Definition
| TZD/metformin/lifestyle mod instructions were given to pts w/gestational diabetes. lifestyle modification was found to be most effective in delaying DM2. |
|
|
Term
| what did the accord trial discover? |
|
Definition
| not all pts could tolerate an HbA1C goal of 6.5 |
|
|
Term
| who is at risk for development of hypoglycemia? |
|
Definition
| pts w/autonomic neuropathy, DM2 on beta blockers (blocking adrenergics can mask hypoglycemia), deficiencies in counterregulatory hormones, and other factors (alcohol, irregular eating) |
|
|
Term
| what are the 2 kinds of reactive hypoglycemia? |
|
Definition
| alimentary/dumping syndrome (pts w/bowel sx: absorb food faster than insulin releases so when insulin is released = hypoglycemia) and functional (usually young, thin pts) |
|
|
Term
| what are the symptoms of reactive hypoglycemia? |
|
Definition
| the symptom complex is adrenergic (sympathetic driven), so pts are anxious, nervous, tremulous, have increased HR, and sweating w/cool skin (due to vasoconstriction). the next phase is neuro-glycopenic: staring, twitching (pts on beta-blockers may skip to this phase). |
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|
Term
| how is alimentary/dumping syndrome hypoglycemia treated? |
|
Definition
| frequent, protein meals, and avoiding simple carbohydrates. alpha glucosidase inhibitors may help with this (off label), as they delay the absorption of glucose into the small bowel. |
|
|
Term
| what is fasting/post-absorptive hypoglycemia? |
|
Definition
| this has more serious implications than reactive hypoglycemia. symptomatology is commensurate w/the level of hypoglycemia and neuroglycopenic symptoms including stroke may occur. these pts have some kind of organic pathology driving the hypoglycemia (non islet cell tumors, ). |
|
|
Term
| how can non-islet cell tumors cause fasting/post-absorptive hypoglycemia? |
|
Definition
| non-islet cell tumors can secrete insulin-like hormones. generally these are large tumors of mesodermal origin (fibrosarcoma/mesothelioma) found retro-peritoneally or in the thorax. |
|
|
Term
| what characterizes islet cell tumors as a cause of fasting/post-absorptive hypoglycemia? |
|
Definition
| usually these tumors are benign and seen in the 5th decade. if the tumor is malignant, they are not metastatic. these pts are diagnosed w/hypoglycemia and (high?) insulin levels. this may be a difficult dx if the pts are compensating by eating more. |
|
|
Term
| what is factitious hypoglycemia? |
|
Definition
| clinically, these pts present similarly to those w/insulinomas, however they are taking something like a sulfonylurea which increase endogenous insulin. even though their insulin levels are abnormally high the medication as a cause may not be immediately evident as sulfonylureas will maintain the correct C-peptide ratio. a sulfonylurea assay or detection of insulin Ab may dx this condition. |
|
|
Term
| other than alimentary/dumping syndrome hypoglycemia, what else can be caused by gastric bypass? |
|
Definition
| GLP 1 elevation = higher insulin activity = hypoglycemia |
|
|
Term
| what characterizes drug induced hypoglycemia? |
|
Definition
| this is common, usually due to alcohol (reduces glycogen stores in liver by inhibiting hepatic gluconeogenesis). pts w/out liver disease are predisposed to early morning hypoglycemia following alcohol ingestion the night before while hypoglycemia in pts w/liver disease is more serious and perhaps more prolonged. sulfonylureas and insulin may also cause this. |
|
|
Term
| if a DM1 pt's insulin requirements are dropping, what is potentially the cause? |
|
Definition
| renal disease or adrenal insufficiency |
|
|
Term
| what does the workup of hypoglycemia include? |
|
Definition
| r/o drug induced, check hx for: pre-existing hepatic/renal disease, pituitary/adrenal disease, retroperitoneal tumor, or reactive (carbohydrate/meal induced) |
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