Diabetes Mellitus: Type 1, Type 2 & Gestational Diabetes
What does Diabetes look like in the US?
-100 million people with DM or pre-diabetes -30 million Americans (9.4%) with DM -25% of those over 65, 28% undiagnosed -84 million with pre-diabetes -cost estimate $322 billion annually
What is the normal control of blood glucose?
-food intake: glucose (from carbohydrates), fatty acids (from fats), amino acids (from protein) -liver: controls storage & mobilization of body's energy stores, hormones stimulate release and storage (glucagon) -exercise: enhances the utilization of glucose by the body
What are some ways to manage diabetes?
-lifestyle: nutrition & exercise -pharmacologic: insulin & non-insulin therapies
What are the goals of nutrition and exercise therapy in the management of diabetes?
-near normal blood glucose -normal body weight (7% loss of initial body weight) -normal blood lipids--cholesterol & triglycerides -regular exercise, start slow with medical clearance (150 min/wk)
What are some ways of tailoring treatment to reduce disparities with DM?
-providers should assess social context, including potential food insecurity, housing stability, and financial barriers, and apply that information to treatment decisions -patients should be referred to local community resources when available -patients should be provided with self-management support from lay health coaches, navigators, or community health workers when available
Why do diabetics get deep, rapid breathing?
-regulation of excess metabolic acids (ketones) by exhaling excess H+ ions (CO2) -excess H+ ions in the plasma > triggers the respiratory center (medulla) > increased RR and depth...Kussmaul respirations
What is Diabetes Mellitus?
-set of disorders characterized by elevated levels of glucose in the blood (hyperglycemia) -affects many body systems and has major physical, social, and economic consequences: the leading cause of end-stage renal disease, and non-traumatic amputations and blindness in working-age adults
What is Diabetic neuropathy?
1. (50% of those with DM). May be caused by demyelinization and/or vascular changes to nerve 2. Complications: Charcot Foot- weakening of bones in the foot; necrotic tissue needing amputation 3. Two types
What is the pathophysiology of hyperglycemia in T1DM?
1. *No insulin* > increased circulating glucose > hyperosmolar 2. osmotic effects of hyperglycemia - 3 P's 3. osmotic diuresis > (cellular) dehydration, loss of electrolytes esp. K, glucosuria 4. protein breakdown > gluconeogenesis > weight loss > increased blood nitrogen (BUN) 5. body cells cannot utilize glucose > fat breakdown > ketone produced (acidic, ketonuria) > metabolic acidosis > DKA 6. DKA (metabolic acidosis) > N & V, Kussmaul respirations (deep & rapid), fruity breath, renal failure, hypovolemic shock, coma, death
What is hypoglycemia? What are the causes? Symptoms?
1. *alert value: BG < 70 mg/dL* 2. *clinically significant BG < 54 mg/dL* 3. causes: -too much insulin -too little food -too much exercise 4. symptoms: hunger, confusion, belligerence -may or may not have Sympathetic Nervous System (SNS) symptoms (Sx): tachycardia, sweating, trembling -*hypoglycemia unawareness syndrome*
What are the screening recommendations for Type 2 DM?
1. *all adults > 45 years of age, every 3 years* 2. obese- BMI greater than or = to 25 kg/m^2 or greater than or = to 23 kg/m^2 in Asian Americans with 1 or more of the following: -first degree relative with DM -sedentary lifestyle -hypertension, hyperlipidemia (esp. TG > 250) -high risk race/ethnicity: African American, American Indian, Latinx, Asian American, Pacific Islander -history of CVD -women who are pregnant or have polycystic ovary syndrome -other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans)
What is Gestational Diabetes Mellitus (GDM)? Who should be screened?
1. *screening of all pregnant women* -high risk: strong family hx of type 2 DM, obesity, glycosuria (glucose in urine), PCOD (polycystic ovarian disease), prior hx of GDM or previous large-for-gestation infant -if high risk, test ASAP -low risk: screen all others at 24-28 weeks of gestation
How is exercise important to diabetes management? What are some barriers to and risks of exercise for diabetics?
1. A 7% weight loss makes significant impact on glucose regulation and BG levels -exercise plan must be individualized -active lifestyle (walk, take steps, stand, move) 2. Barriers: -dangerous neighborhood > walk in a shopping mall -mobility issues > PT 3. Risks: -HYPOGLYCEMIA -CV EVENT--screen for "silent" CV disease before starting!!
How is hypoglycemia treated?
1. Assess symptoms 2. Test blood glucose 3. Treat -15 g Carbohydrate -- 4-6 oz juice or regular soda, 8 oz low-fat milk -IV 50% dextrose per provider's order (preferred) -1 mg glucagon IM if unable to swallow 4. Re-test blood glucose -repeat blood glucose after 15-20 minutes (*Rule of 15*: 15 g carbohydrates, 15 min)
What are non-insulin medications?
1. Criteria: must have some circulating endogenous insulin to work ~ Type 2 2. Can be used in combinations and with insulin: -Biguanides -Sulfonylureas -Meglitinides -DDP-4 inhibitors -GLP-1 agonist -Sodium-glucose Co-transporter 2
How is Pre-Diabetes diagnosed?
1. FPG levels between 100-125 mg/dL > increased risk of developing diabetes in 5 years 2. associated with: -obesity -dyslipidemia with high triglycerides and/or low HDL -hypertension 3. HbA1C 5.7-6.4% (normal < 5.6%) Complications of diabetes thought to start in this stage!
How is diabetes (types 1 & 2) diagnosed?
1. Fasting Plasma Glucose (FPG) greater than or = to 126 mg/dL -fasting at least 8 hours OR 2. 1-3 hr Prandial Glucose (PG) greater than or = to 200 mg/dL -test measures body's ability to remove glucose in 2 hours (75g dose/300 mL water) -need serial tests OR 3. HgbA1C (glycosylated hemoglobin) greater than or = to 6.5% -test measures glucose attached to RBC for life span (120 days) -very good test of long-term glucose control (or lack of it!)
How is DKA treated?
1. IV hydration (0.9% normal saline, isotonic) until urine output resumes 2. then IV regular insulin until BG = 250 mg/dL > stop insulin due to its persistent affect 3. replace fluids & electrolytes (esp. potassium)
What are the signs & symptoms of Type 1 Diabetes Mellitus?
1. clinical symptoms -- rapid onset 2. "3 P's": -polyuria = excessive urination -polydipsia = excessive thirst -polyphagia = excessive hunger 3. weight loss is hallmark 4. fatigue 5. blurred vision 6. children: nocturnal enuresis 7. Ketosis (fruity breath), hyperglycemia
How is the Autonomic Nervous System affected with Diabetic Neuropathy?
1. delayed gastric emptying 2. diabetic diarrhea 3. altered bladder function 4. impotence 5. orthostatic hypotension 6. heart rate variability
What is the macrovascular complication of DM?
1. due to atherosclerosis and CAD (coronary artery disease): -inflammation in blood vessel walls -thickening and plaque deposition -rupture and thrombosis 2. increased risk: -stroke -PVD (peripheral vascular disease) 3. treatment: -*aggressive lifestyle modification to reduce risk factors*: obesity, smoking, sedentary lifestyle -medication to lower cholesterol and manage DM
What is the order when considering non-insulin medications?
1. first: lifestyle management 2. monotherapy: one drug (metformin) 3. dual therapy: two drugs--metformin + "other" drug -many factors to consider 4. triple therapy
What is the hormonal regulation of blood glucose?
1. food 2. amylin & insulin secretion 3. inhibition of gastric emptying 4. increased satiety and food utilization
How does the body use carbohydrates for energy?
1. glucose, a six carbon molecule + oxygen is converted to carbon dioxide and water -4 kcal/g of stored energy -blood glucose homeostasis is 70-99 mg/dL 2. Glucose is the brain's only source of metabolic fuel! -moderate hypoglycemia > symptoms of brain dysfunction 3. 2/3 of glucose is stored in the liver and skeletal muscle as glycogen 4. Excess glucose is stored as fatty acids (triglycerides) in adipose tissue
What are the signs & symptoms of T2DM?
1. gradual onset--months/years 2. blurred vision 3. fatigue 4. poor wound healing, prone to infections 5. symptoms of neuropathy 6. 3 P's not as pronounced 7. client adjusts to symptoms--denial!!
What is glucagon? What does it do?
1. hypoglycemia (low blood glucose) and stress stimulates SNS release of glucagon from pancreatic alpha cells 2. elevates blood glucose by: -glycogenolysis: transformation of glycogen to glucose -gluconeogenesis: transport of amino acids (AA) into the liver > conversion to glucose...conversion of a non-carbohydrate into glucose
What is Type 1 Diabetes Mellitus?
1. incidence & prevalence is increasing 2. autoimmune destruction of beta cells secondary to genetic predisposition and/or other factors (? viral) > NO INSULIN 3. islet auto-antibodies measureable prior to overt symptoms 4. can be measured in family members of those with type 1 in clinical study 5. can be idiopathic...no autoimmune component or genetic component *Genetic predisposition + Environmental factor = T1DM* most common pediatric chronic disease!
What are some consequences of Metabolic Syndrome?
1. increased CRP (c-reactive protein a sign of vascular inflammation) 2. clotting abnormalities 3. endothelial dysfunction 4. *all leading to an increased risk of CV disease (MI, stroke, PVD)*
What are Nursing Diagnoses for DM?
1. ineffective self-health management R/T inadequate knowledge or knowledge deficit 2. imbalance nutrition: more than body requirements 3. self-esteem disturbance R/T lifestyle changes 4. fear 5. risk for peripheral neurovascular dysfunction 6. risk for injury 7. powerlessness 8. risk for noncompliance
What is the Patient Education Plan and how is it used to treat diabetes?
1. information about disease: causes, progression, treatments, monitoring, complications -blood glucose self-monitoring is essential, 1-5 times/day -may use insulin pump or pen 2. diet & exercise: individualized plan 3. sick day plan: what to monitor, when to call medical provider 4. annual ophthalmologic examination: report any changes in vision promptly 5. annual foot exam: teach patient to check feet daily, always wear shoes
What is the effect of insulin on glucose uptake & metabolism?
1. insulin binds to the insulin receptor -when insulin is present in the blood and the cell surface receptor is functional, insulin can move across the cell membrane 2. binding activates protein cascades: -translocation of Glucose transporter-4 to the plasma membrane to allow glucose to move into the cell -influx of glucose -glycogen synthesis -glycolysis fatty acid synthesis 3. this allows normal metabolic processes to occur: -metabolism of CHO, fats, and proteins -cellular growth & differentiation and gene expression
How does Insulin Therapy for T1 & T2DM work? What information do we need to know?
1. insulin normally excreted in small pulsatile increments: basal amount + meal-related amount 2. patients are fearful of insulin -- what is the "real meaning" of being on insulin?? (source of anxiety or trepidation...life experiences...) 3. need to know onset, peak, and duration of each kind of insulin 4. all research indicates early implementation of insulin leads to better outcomes
What are alternative delivery systems of insulin?
1. insulin pump -continuous SQ administration of "basal rate" with intermittent rapid-acting insulin -individualized to client's dietary intake and activity level -used to achieve intensive insulin therapy outcomes of tight glycemic control 2. insulin pens -prefilled, portable -used by ONE person, never shared!
Insulin Therapy: Combinations of insulins
1. insulins are often combined to achieve optimal blood glucose control 2. common regimens: -regular + NPH -rapid-acting + NPH -Lantus (daily) + short-acting (Regular or Rapid-acting) with meals 3. usually administered SQ -review mixing technique, administration sites -store in refrigerator (unopened) -vials stable after opened for 30 days (label) -pre-filled syringes stable up to 1 week in refrigerator
NPH (Humulin-N, Novolin-N)
1. intermediate acting 2. cloudy solution--zinc added to prolong onset and duration of activity 3. SQ injection only 4. onset 2-4 hours, peak 4-10 hours, duration 10-16 hours
glargine (Lantus) & detemir (Levemir)
1. long-acting 2. clear solution 3. SQ injection only 4. onset 1-2 hours, peak none, duration 24 + hours 5. do not mix with other insulins! 6. new--Tresiba (insulin degludec)--similar to Lantus -comes in U-100 and U-200 strengths (U-100 = 100 units/ml; U-200 = 200 units/ml)
What are the functions of insulin?
1. lowers serum glucose -pulsatile increments in response to rising serum glucose (and other stimuli) -maintains normal fasting serum glucose--70 to 99 mg/dL 2. stimulates cellular metabolism -promotes glucose transport from blood across the cell membrane to cell cytoplasm 3. stimulates storage of glucose as glycogen in liver and muscle, adipose cells (fat) 4. enhances fat deposition 5. inhibits protein degradation 6. accelerates the process of amino acid transport into cells and protein synthesis
What are the chronic complications of diabetes?
1. macrovascular 2. microvascular: -diabetic neuropathy -diabetic nephropathy -diabetic retinopathy -diabetic foot ulcers and infections
How does the body use fats for energy?
1. major energy source: 9 kcal/g of stored energy 2. stored as triglyceride in adipose: -3 fatty acid chain > lipases > glycerol & fatty acids -all cells EXCEPT brain, nervous tissue and RBC's can use fatty acids as energy! 3. fatty acids > converted into ketones (organic acid) > large amounts will lead to ketoacidosis (metabolic acidosis)
What is DKA? What does it involve? What are some results of DKA?
1. may be presenting scenario in undiagnosed T1DM -severe hyperglycemia (BG > 250 mg/dL) > serum is hyperosmolar 2. osmotic diuresis: -cellular dehydration -electrolyte imbalances (Na and K) may be masked by fluid shifts -glucosuria 3. gluconeogenesis: -protein breakdown -weight loss -increased blood nitrogen (BUN) 4. fat breakdown: -cells cannot utilize glucose -ketones produced (acidic, ketonuria) -metabolic acidosis > DKA 5. DKA (metabolic acidosis): -nausea and vomiting -Kussmaul respirations (deep, rapid) -fruity breath (from volatile ketones) -renal failure -hypovolemic shock, coma, death
What are some acute (short term) complications of DM?
1. morning hyperglycemia 2. Diabetic Ketoacidosis (DKA) 3. Hyperglycemic Hyperosmolar State (HHS) 4. Hypoglycemia
What is the incidence & prevalence of Type 2 Diabetes Mellitus?
1. multifactorial disease that causes relative insulin deficiency -recently increased numbers of children & adolescents -90-95% of those with diabetes have type 2 -80% are overweight (esp. abdominal fat) -strong genetic factor--poorly understood 2. increased prevalence with age, Native American, Hispanic, African American
Sodium-glucose Co-transporter 2 (SGLT-2) Inhibitors: canaglifozin (Invokana)
1. newest class of antidiabetic drug 2. oral medication 3. MOA: -reduces the amount of glucose reabsorbed in renal tubules -increases amount of glucose in urine (glucosuria) -promotes osmotic diuresis--polyuria may occur 4. SE: weight loss may occur, orthostatic hypotension, GU yeast infections 5. Research Update (EMPA-REG Trial): -reduces risk of major adverse cardiac events (MACE) by 11% if established CV disease -reduced risk of progression of kidney disease by 45% -reduced risk of CV death or hospitalization for HF by 23%
What are the goals and interventions in nursing care for those with DM?
1. nutritional status 2. maintenance of skin integrity 3. basic diabetes self-care skills 4. preventive care to avoid chronic complications
What are the causes of chronic hyperglycemia? (T2DM)
1. pancreas: -decreased beta-cell insulin and amylin secretion -increased alpha-cell glucagon secretion 2. adipose tissue: -decreased insulin-dependent glucose uptake -increase lipolysis -decreased adiponectin -increased leptin & resistin -macrophage accumulation and inflammation 3. liver: -increased hepatic gluconeogenesis 4. digestive system: -decreased GLP-1 and GIP -decreased stomach secretion of ghrelin 5. kidney: -increased glucose reabsorption and gluconeogenesis 6. muscle: -decreased insulin sensitivity -decreased glucose uptake -increased lipid accumulation 7. brain: -neurotransmitter dysfunction -altered insulin-signaling -altered lipid-sensing
What are the overarching diabetes care concepts?
1. patient centeredness -"one size does not fit all" -efforts aimed to reduce cardiovascular risk 2. care across the lifespan -increased numbers of those with T1DM living much longer -increased numbers of those with T2DM diagnosed much younger and living much longer -limited research in these groups 3. advocacy for patients with diabetes -promote funding and policy formation to support patient care and research -EBP grading must guide prioritization of funding and future research
What are the Metabolic Defects of T2DM?
1. production of hormones by adipose tissue 2. insulin resistance (insulin receptor dysfunction) -hyperglycemia ensues -hyper-insulinemia -abnormal blood glucose regulation (pre-diabetes) 3. inappropriate glucose production by liver -especially fasting...sleep, between meals 4. LATE STAGE: pancreas loses ability to produce insulin -eventual beta cell exhaustion: may take time -about 50% have decreased insulin production at time of Dx (diagnosis)
How does the body use protein for energy?
1. protein is essential for the formation of all body structures: muscle, bone, blood cells 2. protein (4 kcal/g) > amino acids -limited storage ability 3. When metabolic need exceeds food intake > amino acids (AA) are the major component used in gluconeogenesis -muscle is broken down into amino acids in starvation!
lispro (Humalog) and aspart (NovoLog)
1. rapid-acting 2. structure nearly identical to natural human insulin 3. routes: subcutaneous (SQ) injection or SQ infusion (pump) 4. clear solution 5. onset 0.25 hours, peak 1 hour, duration 3-4 hours
What is diabetic nephropathy?
1. renal impairment > *kidney failure* > dialysis 2. Risk factors: *family history, smoking, hypertension,* poor glycemic control, minority group (African American, Native American, Hispanic American) 3. *Early sign: albuminuria (protein in urine)* 4. Prevention is key. Use of *ACE inhibitors* recommended
What is diabetic retinopathy?
1. retinal disease leading to blindness -abnormal vascular permeability -microaneurysm formation -neovascularization (new small fragile blood vessels on retina)
What are some consequences of chronic hyperglycemia? (T2DM)
1. retinopathy & cataracts 2. neuropathy 3. hypertension, PVD, stroke 4. heart disease 5. steatohepatitis, biliary disease 6. gastroparesis 7. nephropathy, glomerulosclerosis, chronic kidney disease 8. oxidative stress, immunosuppression, infection, cancer 9. decreased cognition
How can diabetes be managed using psychosocial aspects?
1. screen for depression 2. screen for sleep behaviors 3. screen for barriers/access to high quality food, transportation, medication, BG monitoring equipment and safe areas for exercise
Regular (Humulin-R, Novolin-R)
1. short-acting 2. can be administered: SQ injection, SQ infusion, IV infusion 3. clear solution 4. SQ onset 0.5-1 hour, SQ peak 2-3 hours, SQ duration 3-6 hours
What is Hyperglycemic Hyperosmolar State (HHS)? How does it manifest? What is the treatment?
1. similar to DKA, but *T2DM*, acute pancreatitis, severe infection 2. hyperglycemia is *profound (> 600 mg/dL)!!!* -no ketoacidosis--some glucose uptake into muscle cells 3. hyperosmolar state -mental confusion -profound glycosuria and water loss 4. treatment: -IV fluids -IV regular insulin -electrolyte replacement -close observation for cerebral edema with fluid replacement...*mortality high*
What are some special issues for those with DM?
1. surgery and acute illness creates special risks 2. hospitalization creates a potential for unstable blood sugar levels
How do you test for GDM?
1. test using 1 or 3 hours oral glucose tolerance test (OGTT): normal less than or = to 140 mg/dL at 1-2 hour test 2. threshold is lower for GDM! 3. all hyperglycemia is detrimental to maternal & fetal health! 4. test for persistence at 4-12 week follow-up appointment with OB provider
What should a nursing assessment of a diabetic include?
1. the primary problem 2. hypoglycemia & hyperglycemia 3. skin 4. diabetes self-care skills
What do we mean when we say that diabetes is a risk continuum?
The lower the values for blood glucose the better, not just under the limits for diagnosing diabetes mellitus!
What is gluconeogenesis?
When stored glycogen is used up, fat (or muscle) is used
What is glycogenolysis?
When the fasting body uses stored glycogen
What is the Healthy People 2020 Goal related to Diabetes? What are the opportunities to accomplish this goal?
Goal: reduce the disease and economic burden of DM and improve the quality of life for all persons who have, or are at risk for, DM Opportunities to reduce the health and economic burden of DM: -primary prevention: movement from no diabetes to diabetes -testing & early diagnosis: movement from unrecognized to recognized diabetes -access to care for all persons with diabetes: movement from no diabetes care to access to appropriate diabetes care -improved quality of care: movement from inadequate to adequate care
What also triggers glucagon secretion to increase conversion of amino acids to glucose?
high protein meals and strenuous exercise
What are counter-regulatory hormones?
hormones that raise blood glucose during stressful times, sleep, and periods of fasting: -glucagon -epinephrine -growth hormone -cortisol -somatostatin
When does insulin secretion increase?
in response to ingestion of foods -spikes at breakfast, lunch, & dinner -baseline of insulin secreted between meals and during sleep never goes to zero; 1/2 of all insulin is basal rate -insulin is needed whether or not the patient is eating -varying heights of plasma insulin depending on various amounts of quick-acting glucose foods (OJ) and high quality carbs (whole grains & veggies) and protein
How do you measure insulin?
indirectly through the c-peptide chain
Biguanide: metformin (Glucophage)
1. MOA -reduces glucose production by liver -enhances insulin sensitivity at tissue level 2. PO 3. Does not promote weight gain 4. Withhold preoperatively or if IV contrast used and for 48 hours after 5. Not to be used in those with renal impairment 6. Good effect on plasma lipids (cholesterol) 7. SE: GI (decreased appetite, nausea, diarrhea), vitamin B12 deficiency (test for this occasionally), lactic acidosis (rare, but life-threatening)
Incretin mimetic (GLP-1 RA): exenatide (Byetta, Bydureon); semaglutide (Ozempic)
1. MOA: -*stimulate incretin hormone (GLP-1 receptor agonist)* -decreases glucagon production -increased satiety, slows gastric emptying 2. *SQ injection (daily; semaglutide weekly)* 3. not used with insulin therapy 4. can be used with oral agents 5. SE: May cause nausea, vomiting--start with low dose, hypoglycemia, pancreatitis, renal impairment
Thiazoledinediones (TZDs): pioglitazone (Actos)
1. MOA: decreases insulin resistance by promoting glucose uptake by skeletal muscle and adipose tissue, & may decrease glucose production in liver 2. Mainly an add-on to metformin therapy 3. Not started much anymore d/t risk of MI, sudden death 4. SE: headaches, sinusitis, myalgia, upper respiratory tract infection (URI) 5. Adverse effects (AE): heart failure d/t renal fluid retention
DPP-4 inhibitors: sitagliptin (Januvia)
1. MOA: enhances incretin hormone system -inhibits DDP-4: an enzyme that inactivates the incretin hormones -stimulates release of insulin from pancreas -suppresses post-prandial release of glucagon 2. oral medication 3. no weight gain 4. SE: well-tolerated, rare pancreatitis
Sulfonylureas: glipizide (Glucotrol)
1. MOA: increase insulin production from the pancreas 2. Oral medication 3. First generation (not use any more) -may cause hypoglycemia 4. Second generation (used widely) -give 30 min before meal -less risk of hypoglycemia -Glipizide (Glucotrol, Glucotrol XL) 5. SE: hypoglycemia; flushing, palpitations, nausea when combined with alcohol (a disulfuram-type reaction), beta-blockers diminish effectiveness of drug
What are the causes of morning hyperglycemia and how is it managed?
1. May be caused by: -Dawn phenomenon (T1 or 2): normal BG until around 3 am, then BG increases until awakening -Somogyi effect (T1): normal BG until around 3 am when BG drops > subsequent increase secondary to counter-regulatory hormone surge 2. Nurse must wake up client to check BG at 3 am!
What nutritional changes should diabetics make to their diet?
1. Medical Nutrition Therapy (MNT): Individualized meal plan 2. consistent intake = meal plan (reduction of calorie intake) 3. Glycemic Index (GI): avoid foods with high GI--potatoes, white bread, pasta, rice, simple sugars 4. Home blood glucose monitoring is essential -patient may *self monitor BG values 1-5 times/day (SMBG)*
What are the different commercially available insulins?
1. Rapid acting--lispro (Humalog), aspart (NovoLog) 2. Short acting--regular (Humulin-R), (Novolin-R) 3. Intermediate acting--NPH (Humulin-N), (Novolin-N) 4. Long acting--glargine (Lantus)
What are the two types of diabetic neuropathy?
1. Somatic (peripheral) neuropathy: -with or without pain -loss of feeling, sense of temperature, or tingling paresthesia -stocking-glove pattern 2. Autonomic neuropathies: disorder of SNS or PNS -loss of vasomotor function, GI, GU or sexual dysfunction
What are the types of Diabetes Mellitus?
1. Type 1 diabetes (T1DM): -characterized by autoimmune destruction of pancreatic beta cells -results in absolute insulin deficiency 2. Type 2 diabetes (T2DM): -characterized by progressive loss of beta cell insulin secretion -preceded/accompanied by insulin resistance 3. Gestational diabetes mellitus (GDM): -diabetes diagnosed during the second or third trimester of pregnancy (not present prior to gestation) *All types result in Fasting Plasma Glucose (FPG) > 126 mg/dL (hyperglycemia)*
What things should diabetics know on a food label?
1. What is the serving size? 2. How many calories in that serving? 3. How many servings are you eating? How many calories from fat? 4. Limit fat, cholesterol and sodium intake -fat: 1/3 of calories or less -sodium and cholesterol: may need to restrict 5. Include lots of fiber 6. How much of the daily amount am I getting in this serving?
Why are diabetics at an increased risk for infection?
1. alterations in: -senses: vision, touch -oxygenation: prone to tissue hypoxia secondary to PVD, CVD -pathogens: increased glucose -immune response: innate & adaptive responses defective
What are the 4 types of pancreatic cells? What are they stimulated by?
4 types of pancreatic cells: 1. acinar: digestive enzymes (amylase, lipase, and proteolytic (trypsin) 2. alpha cells: glucagon 3. beta: insulin & amylin 4. delta cells: gastrin & somatostatin stimulated by both PNS and SNS
What leads to a diagnosis of Metabolic Syndrome?
At least 3 of the follow 5 traits: 1. hyperglycemia (FPG > 100 mg/dL) 2. visceral obesity -- increased waist circumference (> 40" men, > 35" women) 3. hypertension (>130/85 mmHg) 4. increased serum triglycerides (greater than or = to 150 mg/dL) 5. decreased serum HDL cholesterol (<40 mg/dL men, <50 mg/dL women)
How does obesity contribute to the metabolic defects of T2DM?
obesity > increased free fatty acids (FFA) > cause beta cell dysfunction > inhibit glucose uptake & storage, reduce hepatic insulin sensitivity > increase hepatic glucose production > "fatty liver" may result
What are gut derived hormones? What do they do?
the incretins (GLP1 and GIP) GLP1 stimulates glucose-dependent insulin release and suppresses postprandial glucagon release
