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Stack #38875
RRC Maintenance - Diabetes Mellitus
| question | answer |
|---|---|
| DM1: etiology | progressive destruction of pancreatic beta-cells due to autoimmune process in susceptible individuals |
| when do clinical manifestations appear in those with DM1? | when the individual is no longer able to produce insulin in their pancreas |
| 3 P's of diabetes | polydipsia (excessive thirst), polyuria (frequent urination) and polyphagia (excessive hunger) |
| source of insulin needed in DM1 | exogenous (outside source) |
| complication of DM1 in those without insulin | diabetic ketoacidosis |
| 3 metabolic abnormalities in DM2 | insulin resistance, impaired glucose tolerance/marked decrease in the ability of the pancreas to produce insulin as beta cells become fatigued from compensatory overproduction of insulin, inappropriate glucose production by liver |
| impaired glucose tolerance | where blood glucose levels are higher than normal, however not high enough to diagnose diabetes |
| Syndrome X | insulin resistance, elevated insulin levels, abdominal obesity, elevated BP, high triglycerides, dyslipidemia (high LDL, low HDL) |
| What does syndrome X significantly increase the risk of? | cardiovascular disease |
| Risk factors for syndrome X | obesity, sedentary lifestyle, polycystic ovary syndrome, urbanization/Westernization, family history, gestational diabetes, increased age |
| What type of insulin is produced in DM2? Why does the person develop DM2? | endogenous - however it is poorly utilized by tissues or insufficient for body's needs |
| Causes of hypoglycemia | ETOH intake, too little food, too much diabetic medication, too much exercise without compensation, diabetic medication/food taken at wrong time, loss of weight without a change in medication, use of beta blocker that interfere with recognition of symptom |
| why does hypoglycemia occur? | low blood glucose occurs when there is too much insulin in proportion to glucose in blood |
| hypoglycemia | <3.9mmol/L |
| Why is mental functioning often affected with hypoglycemia? | brain requires a constant supply of glucose in sufficient quantities |
| What are caused of hyperglycemia? | too much food, too little or no diabetes meds, inactivity, emotional/physical stress, poor absorption of insulin, non-compliance, undiagnosed DM |
| Why can emotional/physical stress contribute to hyperglycemia? | release of epinephrine and cortisol will cause the liver to convert glycogen to glucose which will increase the serum glucose in the blood as a result of the "fight-or-flight" response |
| diabetic ketoacidosis | profound deficiency of insulin and characterized by hyperglycemia, ketosis, acidosis and dehydration |
| precipitating factors of DKA | illness, infection, inadequate insulin dosage, undiagnosed DM1, poor self-management, neglect |
| why does DKA happen? | when circulating supply of insulin is insufficient, glucose can't be broken down so body breaks down fats stores as secondary source of fuel |
| what are ketones | acidic byproduct of fat metabolism that can alter blood pH causing metabolic acidosis to develop |
| ketouria | ketones in the urine |
| classic signs of DM1 | polyuria, polydipsia, polyphagia, weight loss, weakness/fatigue |
| classic signs of DM2 | non-specific, may experience s+sx of DM1, fatigue, recurrent infection, prolonged wound healing, visual changes |
| clinical manifestations of hypoglycemia | confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, cold/clammy skin, numb fingers, toes, mouth, tachycardia, headache, unsteady gait, slurred speech, seizure, coma |
| clinical manifestation of hyperglycemia | increase in urination, increase in appetite followed by lack of appetite, weakness/fatigue, blurred vision, headache, glucouria, nausea/vomiting, abdominal cramping |
| clinical manifestations of DKA | poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension, lethargy, weakness, soft/sunken eyeballs, abdominal pain with anorexia and vomiting, kausmall resps to reverse acidosis, acetone breath, ketones in urine/blood, blood pH <7.35 |
| goal of diabetes management | optimal glycemic control to prevent complications |
| ABC of diabetes | A1C <7%, BP <130/80, cholesterol --> LDL <2.5mmol/L, total chol/HDL ratio < 4 |
| A1C | reflects glycemia over usual 120day lifespan of RBC and represent avg free glucose attached to RBC over 3 months, measures treatment effectiveness |
| renal function tests | BUN, creatinine, urine for protein and microalbuminuria, albumin/creatinine ratio |
| EKG | silent MI due to neuropathy, rule out ischemia |
| dilated eye exam | retinopathy |
| ankle-brachial index | PVD |
| pedal monofilament test | neuropathy |
| casual plasma glucose level diagnostic of DM | >=11mmol/L |
| fasting plasma glucose diagnostic of DM | >=7mmol/L |
| how does one monitor their blood glucose at home? | accucheck monitoring |
| target A1C for diabetic | <=7% |
| target blood sugar level pre-meal for diabetic | 4-7mmol/L |
| target blood glucose value 2hrs post-meal for diabetic | 5-10mmol/L |
| Why is it important to monitor BP and cholesterol in addition to blood sugars for those with diabetes? | to prevent microvascular and macrovascular complications |
| BP treatment | lifestyle modifications, ACE inhibitor, ARB, beta blocker, thiazide diuretic |
| cholesterol treatment | lifestyle modification, then statin if LDL not @ target, statin or fibrate if LDL at target, low HDL, elevated triglyc. fibrate if high triglycerides |
| retinopathy | retinal blood flow determined by need for O2 -> small retinal vessels have no means to control flow; hypoxia cause engorgement of vessels resulting in retinal HTN which results in development of small aneurysms...this damages retinal cells |
| nephropathy | due to decreased renal flow, glomerular permeability increases in uncontrolled DM, glomerular HTN develops r/t increased GFR |
| What BP meds have been shown to be renal-protective? | ACE inhibitors with those without renal disease, ARB in those with renal disease |
| complications of neuropathy | skin breakdown, ulcers, gangrene, neuropathic pain |
| risk factors for diabetic foot ulcers | previous ulcer, increased age, neuropathy, PVD, structural deformity, renal transplantation, poor SES, smoking, poor foot care |
| What do clients need to taught to assess for when check their feet daily? | changes in skin color, swelling, sores, ingrown toenails, cracks and cuts |
| biguanides | metformin; glucophage |
| mechanism of action: biguanide | release glucose by decreasing production of glucose in liver and also enhances glucose uptake and utilization by muscle |
| site of action: biguanide | liver |
| thiazoldinediones | actos, avantia |
| site of action: thiazoldinediones | muscle |
| mechanism of action: thiazoldinediones | increases glucose sensitivity and increases the ability of target cells to respond to insulin |
| alpha glucosidase inhibitor | acarbose |
| site of action: alpha glucosidase inhibitor | intestines |
| mechanism of action: alpha glucosidase inhibitor | slows digestion of CHO thereby reducing the rise in blood glucose post-meals...inhibits enzyme responsible for breaking complex carbs into monosaccharides |
| sulfonylureas | glyberide |
| site of action: sulfonylureas | pancreas |
| mechanism of action: sulfonylureas | increases insulin release and may also increase tissue response to insulin |
| site of action: meglitinides | pancreas |
| mechanism of action: meglinides | stimulates pancreatic insulin release |
| goal of insulin therapy | mimic normal insulin secretion |
| advantage of insulin therapy | safe, effacious and well understood, biological replacement, multiple effects (not just for glucose), may reduce serious events, no contraindications, no drug interactions, easily titratible and predictable |
| disadvantages of insulin therapy | fear of injections, often insulin is viewed as end of line ("failures" go on insulin), pt and dr non-acceptance, risks include hypoglycemia/weight gain, not used effectively for DM2 -> resistant to high doses |
Created by:
bella83
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