Med Surg Ch 49: Diabetes Mellitus

Type 1 (juvenile onset DM, insulin dependent DM) -accounts for 5% of all DM -generally affects ppl under 40yrs, occurs in younger ppl -no available insulin -genetic predisposition (familial) and exposure to virus, most have no hx, have certain HLA type -autoimmune: immune mediated disease caused by autoimmune destruction of the pancreatic beta cells (site of insulin production), results in absence of insulin production -onset: autoantibodies are present for months to yrs before onset of Sxs, Sxs develop when person's pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose, once this happens the onset of Sxs is rapid and pts develop ketoacidosis, pt usually has hx of recent, sudden wt loss and polydipsia (excessive thirst), polyuria (frequent urination) and polyphagia (excessive hunger) -require insulin from outside source to sustain life, w/o insulin pt will develop DKA-life threatening condition resulting in metabolic acidosis Type 2 (adult onset DM, non-insulin dependent DM) -need insulin for glucose to enter cells, body is producing glucose but insulin isn't utilizing the glucose (insulin resistance) -most prevalent type: accounts for 90-95% of cases -RFs: *overweight or obese*, being older, family hx of type 2 DM -African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders and Native Americans have higher rates than whites -pancreas continues to produce endogenous (self made) insulin but insulin produced is either insufficient for needs of the body or poorly used by the tissues -metabolic abnormalities: 1. insulin resistance: body tissues don't respond to the action of insulin because insulin receptors are unresponsive or insufficient in number, when insulin isn't properly used the entry of glucose in cells is impeded resulting in hyperglycemia, in early stages pancreas responds to high BS by producing more insulin 2. decreased ability of pancreas to make insulin: as beta cells become fatigued from compensatory over production of insulin or when beta cell mass is lost 3. inappropriate glucose production by liver: instead of properly regulating release of glucose in response to blood levels, the liver does so in a haphazard way that doesn't correspond to body's needs at the time 4. altered hormone production by adipose tissue: adipokines cause chronic inflammation, a factor involved in insulin resistance, Type 2 DM and CV disease -characteristics: metabolic syndrome: increases risk of CV disorders and Type 2 DM, includes elevated glucose levels, abd obesity, elevated BP, high levels of triglycerides and decreased levels of high density lipoprotein -syndrome X: insulin resistance syndrome -onset: gradual, person may go many yrs w/ undetected hyperglycemia that might produce few, if any Sxs

*DM types (pg. 1154, Table 49-1, pg. 1155, Fig 49-2)

-recommended for all insulin treated pts w/ DM, other pts w/ DM use SMBG to help achieve and maintain glycemic goals and monitor for acute fluctuations in BS -pts who use multiple insulin injections or insulin pumps should monitor blood glucose 4 or more times a day -portable monitors (glucometers) -invasive: continuous glucose monitoring systems-uses a sensor inserted subQ, system displays glucose values that are updated every 1-5 min -non-invasive: disposable lancets are used to obtain a small drop of capillary blood (usually from a finger stick) that's placed onto a reagent strip, after a specific time the monitor displays a digital reading of the capillary blood glucose value -BS level reported by lab is sometimes higher than pt's home glucose monitor or hospital's portable monitor because some home monitors give cap blood glucose values from whole blood, test from lab provide plasma readings, plasma samples (venous samples) are 10-12% higher -ppl w/ type 1 DM should test BS before meals because many use insulin pumps or multiple daily injections and base the insulin dose on the CHO in a meal or make adjustments if the preprandial value is above or below target, test 2hrs after 1st bite of food to help person see how effectively they judged what was eaten or determine if bolus insulin dose was enough for that meal; BS test whenever hypoglycemia is suspected so immediate action can be taken; during sick days test BS levels at 4hr intervals to determine effects of the illness on glucose levels; test BS before and after exercise to determine effects of exercise on metabolic control (esp. for type 1)

*SMBG (pg. 1169, Table 49-11)

-hyperglycemia and diabetic ketoacidosis -hyperglycemic hyperosmolar nonketonic syndrome (HHNS) -hypoglycemia (insulin reaction, hypoglycemic rxn): worsens rapidly and is a serious threat if not taken care of immediately

*acute complications (pg. 1175, Table 49-16)

most widely used oral diabetes agent is metformin: glucophage (immediate release) -primary action is to reduce glucose production by the liver, also enhances insulin sensitivity at tissues and improves glucose transport into the cells -1st choice drug for ppl w/ type 2 DM -may cause moderate wt loss so useful for those w/ type 2 DM and preDM who are overweight or obese -pt who are undergoing surgery or any radiological procedures that involve the use of contrast medium are instructed to temporarily d/c metformin at least 24 hrs before surgery or procedure, shouldn't resume until 48 hrs afterward once their Cr has been check and is normal -pt may experience explosive diarrhea due to the intestines, they don't absorb the carbs (glucose)

*biguanides

Type 1 -onset is rapid so initial manifestations are sudden (acute) -3P's: polydipsia (excessive thirst) and polyuria (excessive urination)-due to osmotic effect of glucose, polyphagia (excessive hunger)-cellular malnourishment when insulin deficiency prevents utilization of glucose for energy -other Sxs: wt loss-body can't get glucose and turns to other energy sources such as fat and protein, weakness and fatigue-body cells lack needed energy from glucose, ketoacidosis-complication most common in untreated Type 1 DM Type 2 -non specific Sxs, may experience 3P's -fatigue, recurrent infections, recurrent vaginal yeast or candidal infections, prolonged wound healing, visual changes

*clinical manifestations

-FBS (fasting plasma glucose): 70-110; DM >/= 126 mg/dl (fasting defined as no caloric intake for at least 8 hrs) -random BS: in pts w/ classic Sxs of hyperglycemia (3P's, unexplained wt loss) or hyperglycemic crisis, >/= 200 mg/dl -2 hr oral glucose tolerance test (postprandial glucose test): <180; DM if >/= 200 mg/dl (diagnosis of impaired glucose tolerance) -glycosylated Hbg = hemoglobin A1C, goal < 7%; DM A1C of 7% (6.5) or higher (% of total Hbg that has glucose attached to it, when BS levels are elevated over time the amount of glucose attached to Hbg molecules increases, glucose remains attached to RBC for life of cell (120 days), so test provides measurement of glycemic control over previous 2-3 months w/ increases in A1C reflecting elevated BS levels) -prediabetes = impaired glucose tolerance diagnosed if 2hr oral glucose tolerance test values are 140-199 mg/dl, impaired fasting glucose diagnosed if > 100 but < 126 mg/dl -all pts w/ DM and prediabetes should have A1C monitored regularly to determine success of current Tx plan and make changes if glycemic goals aren't achieved

*diagnosis

-SMBG every 4 hrs for all diabetics -test for ketones -*don't stop insulin or OAs* even if your vomiting -if eating normally, increase noncaloric fluids; if eating less, supplement w/ carb containing fluids -eat 10-15 g CHO q 1-2 hrs -stay hydrated: small amounts of fluids every 15-30 min to prevent dehydration and ketoacidosis (clear broth, ice chips, popsicle, half a cup of soda, orange/apple juice, ginger ale, gatorade, jello, apple sauce) -type 1: if BS > 240 mg/dl, check urine for ketones as well as BS every 3-4 hrs, call PCP if moderate to large ketones -all diabetics call MD if BS > 300 mg/dl 2 tests in a row -notify MD if illness lasts more than 24 hrs, have severe abd pain, persistent diarrhea, fever > 100, vomiting and no fluids for the last 4hrs, BS that's difficult to control, presence of ketones, SOB, chest pain, visual loss or other unexplained pains

*management of sick days (pg. 1180)

-exogenous (injected) insulin is needed when pt has inadequate insulin to meet specific metabolic needs, type 1 need exogenous insulin to survive-may need multiple daily injections (4 or more times) or continuous infusion via insulin pump to control BS levels, type 2 may need exogenous insulin during periods of severe stress (illness, surgery) or since it's progressive may be permanent part of management plan (4 or more) -insulin action: promotes transport of glucose into cells, inhibits conversion of glycogen into glucose -types: beef and pork (rarely seen), human -*onset, peak, duration* KNOW -Lantus: don't mix w/ other insulins -regimens: mealtime (bolus), long acting (basal), combination -1-4 doses/day -which insulin regimen best mimics endogenous insulin production? basal-bolus regimen which uses rapid or short acting (bolus) insulin before meals and intermediate or long acting (basal) background insulin once or twice a day -basal bolus regimen is an intensive insulin therapy (tight control): consists of multiple daily insulin injections w/ frequent self monitoring of blood glucose; goal is to achieve near normal glucose level 70-110 mg/dl before meals -at peak time of insulin is when hypoglycemia is most likely to occur

*meds: insulins (pg. 1158-1159, Table 49-3, Table 49-4, Fig. 49-3)

-may require hospitalization: if electrolyte imbalances aren't severe and BS levels are stable can be safely monitored at home-outpt management, if pt has severe illness (such as pneumonia or UTI) they're admitted to hospital -serious condition that proceeds rapidly and must be treated promptly Initial actions: O2; large bore IVs w/ fluids, NG tube to prevent vomiting w/ aspiration; labs-CBC, electrolytes, glucose, BUN, Cr, blood gases; frequent VS every 15 mins; frequent neuro assessment-LOC; cardiac monitoring; get brief hx (to search for cause)-insulin deficit, infection -pt is hyperglycemic and doesn't have enough fluid: fluids 1st before insulin to dilute sugar, *1st fluid, 2nd K, 3rd insulin (HHNS managed the same way) -fluid imbalance is potentially life threatening so the initial goal of therapy is to establish IV access and begin F&E replacement Rehydration 1st -IV saline 0.9% or .45% NaCl at a rate to restore U/O to 30-60 ml/hr and increase BP, done quickly -BS: will drop, change solution to D5W (5-10% dextrose) when BS = 250 mg/ml or less to prevent hypoglycemia and sudden drop in glucose that can be assoc. w/ cerebral edema -NG: if vomiting check bowel status -F&E to replace extra/intracellular water and correct deficits -monitor (esp. pts w/ renal and cardiac comprise): fluid I&O, S/S of fluid overload (esp. if cardiac hx)-watch for crackles -oral fluids: give as soon as tolerated, try salty broths to replace Na Reverse hypovolemic shock -albumin -plasma expanders -Na replacement IV insulin (regular insulin): directed toward correcting hyperglycemia and hyperketonemia, begun only after fluid resuscitation, adequate U/O-usually IV bolus followed by continuous insulin drip (usually 1 unit/ 1 ml), prevent rapid drops in serum glucose to avoid cerebral edema Restoring K balance -monitor K levels: get K levels before starting insulin, if hypokalemic, insulin admin will further decrease K levels making early K replacement essential, levels can decrease once therapy starts and insulin moves K into cells leading to life threatening hypokalemia, insulin allows water and K to enter cell along w/ glucose and can lead to a depletion of vascular vol. and hypokalemia-monitor pt's fluid balance and K levels -hyperkalemia usually for 1st 4 hrs: may see bradycardia, weakness, flaccid paralysis, oliguria -hypokalemia 4-24 hrs: K moves back into cells, lost in urine-watch for EKG changes, weakness, prevent cardiac arrest; as blood sugar falls, so does K Follow-up -determine precipitating cause -teach preventative measures

DKA management (pg. 1176-1177, Table 49-17, Table 49-18)

Sxs of dehydration (concentrated urine) -early signs: lethargy, weakness -progressive signs: dehydration, tachycardia, orthostatic hypotension -later signs: GI, severe dehydration, fruity breath odor, Kussmaul's respirations, hypotension, decreasing LOC, polyuria, wt loss, tachycardia, thirst, visual disturbances, abnormal lab values

DKA manifestations

often prevented w/ DCCT guidelines -caused by end organ due to damaged blood vessels (angiopathy) secondary to chronic hyperglycemia (chronic blood vessel dysfunction) -risk for complications could be significantly reduced by keeping BS levels near to normal as possible for as much of the time as possible (tight glucose control), those who maintained glucose control reduced their risk for developing retinopathy and nephropathy (the most common micro complications), management of DM-maintain BS levels WNL; those w/ DM need scheduled and ongoing monitoring for the detection and prevention of chronic complications, pts need regular follow up exams *Macrovascular: -diseases of the large and medium size blood vessels that occur w/ greater frequency and w/ an earlier onset in ppl w/ DM -includes atherosclerosis, CAD, HTN, CVA (cardiovascular/cerebrovascular), TIA, PVD -pts can decrease many RFs assoc. w/ these complications such as smoking, HTN, high fat intake and sedentary lifestyle; smoking is especially injurious to ppl w/ DM and greatly increases their risk for blood vessel and cardiovascular disease, stroke and LE amputation -optimize BP control helps prevent CV and renal disease, treating HTN results in decease in macro and micro complication (HTN in diabetics causes increase in mortality)-target BP less than 130/80 mmHg recommended for diabetics -pts w/ DM have an increase in lipid abnormalities which contributes to the increase in CV disease, target levels: LDL cholesterol < 100 mg/dl, trigylcerides < 150 mg/dl, HDL cholesterol > 40 mg/dl in men and > 50 mg/dl in women, Tx of hyperlipidemia-lifestyle interventions including nutritional therapy, exercise, wt loss and smoking cessation, meds-statins for those who don't meet lipid goals and for ppl over 40 w/ other CV disease RFs -insulin resistance w/ dyslipidemia contributes to greater risk of CV disease in pts w/ DM *Microvascular: -result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia, differ from macro because they are specific to DM, mostly affects the eyes (retinopathy), kidneys (nephropathy) and the skin (dermopathy) -diabetic retinopathy: damage to the retina due to chronic hyperglycemia, nephropathy and HTN in pts w/ DM, leading cause of blindness, most common in Type 1, nonproliferative-(most common form) partial occlusion of the small blood vessels in the retina causes microaneurysms to develop in capillary walls, the walls of these microaneurysms are so weak that capillary fluid leaks out causing retinal edema and eventually hard exudates or retinal hemorrhage, vision may also be affected if macula is involved; proliferative-(most severe form) involves retina and vitreous, when retinal capillaries become occluded the body compensates by forming new blood vessels to supply retina w/ blood (neovasculartization), these new vessels are very fragile and hemorrhage easily producing vitreous contraction, eventually light is prevented from reaching the retina as the vessels become torn and bleed into vitreous cavity, pt sees black or red sports or lines, if new blood vessels pull the retina while vitreous contracts causing a tear then partial or complete retinal detachment will occur, if macula is involved vision is lost, w/o Tx most go blind; other visual problems-glaucoma and cataracts; early detection and Tx, annual dilated eye exam (looks at back of retina), laser photocoagulation, prevention by maintaining good glycemic control and managing HTN -nephropathy: assoc. w/ damage to the small blood vessels that supply the glomeruli of the kidney, kidney disease can be greatly reduced when near normal BS control is maintained, HTN greatly accelerates progression, aggressive BP management for all pts w/ DM, tight BS control is critical in prevention and delay of nephropathy -neuropathy: damage that occurs because of metabolic derangements, most common type that affects diabetics is sensory neuropathy which leads to loss of protective sensation in LEs and increases risk for complications that result in lower limb amputation; persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage resulting in reduced nerve conduction and demyelinization as well as ischemic damage by hyperglycemia in blood vessels that supply peripheral nerves --sensory: distal symmetric polyneuropathy that affects hands and/or feet, characteristics-loss of sensation, abnormal sensations, pain and parethesias; pain described as burning, cramping, crushing or tearing is usually worse at night and occurs only at that time, parethesias may be assoc. w/ tingling, burning and itching, pt may report feeling of walking on pillows or numb feet, loss of sensitivity to touch and temp., foot injury and ulcerations can occur w/o pt ever having pain-neuropathy causes atrophy of small muscle of hands and feet causing deformity and limiting fine movement Tx: tight control of BS --autonomic: can affect nearly all body systems and lead to hyperglycemic unawareness, bowel incontinence and diarrhea and urinary retention, gastroparesis (delayed gastric emptying)-complication that can produce ANV, gastroesophageal reflux and persistent feelings of fullness, can trigger hypoglycemia by delaying food absorption; CV abnormalities include postural hypotension, resting tachycardia and painless MI, assess pts for postural hypotension to determine fall risk, change positions slowly; ED in men is usually 1st sign for autonomic, decreased libido, candidal or nonspecific vaginitis for women; neurogenic bladder-sensation in inner bladder wall decreases causing urinary retention leading to infrequent voiding, difficulty voiding and weak stream, empty bladder every 3 hrs in sitting position helps prevent stasis and infection Management: tight control of BS -complications of feet and LE: those w/ DM are at high risk for foot ulcerations, LE amputations, injury and serious infection, RFs include sensory neuropathy and PAD; sensory neuropathy: major RF for LE amputation, loss of protective sensation prevents pt from being aware that a foot injury has occurred, improper footwear and injury from stepping on foreign objects while barefoot are common causes of undetected foot injury, annual screening using monofilament (apply thin, flexible filament to several spots on plantar surface of foot and asking pt to report if felt, insensitivity to monofilament shows greatly increased risk for diabetic foot ulcers that can lead to amputation); PAD increases risk for amputation by causing reduction blood flow to LEs, when blood flow is decreased O2, WBCs and vital nutrients aren't available to tissues, wounds take longer to heal and risk for infection increases, signs of PAD (pg. 1184), management-control or reduction of RFs, particularly smoking, high cholesterol intake and HTN, bypass of graft surgery for some pts; for patients w/ LOPS or PAD teach pt how to prevent foot ulcers (pg. 1184, Table 49-21): selection of proper footwear, carefully avoid injury to foot, practice diligent skin and nail care, inspect foot thoroughly each day, treat small problems promptly; proper care of diabetic foot ulcers is critical for wound healing-casting to redistribute wt on plantar surface of foot, wound control for ulcer (debridement, dressings, skin grafting); neuropathic arthropathy or Charcot's foot results in ankle and foot changes that ultimately lead to joint dysfunction and foot drop -ESRD: most common cause; patho-damage to glomeruli; management

DM chronic complications (pg. 1180, Fig 49-13)

Collab care: (similar to DKA) -medical emergency and has high mortality rate -great volumes of fluid replacement, -pts are commonly older w/ cardiac or renal compromise requiring hemodynamic monitoring to avoid fluid overload during fluid replacement -when BS levels fall to 250 mg/dl, IV fluids containing glucose are administered to prevent hypoglycemia -electrolytes monitored and replaced as needed, hypokalemia isn't as significant in HHS as it is in DKA -immediate IV admin insulin and either 0.9% or 0.45% NaCL -assess VS, I&O, tissue turgor, lab values and cardiac monitoring to check efficacy of F&E replacement which includes monitoring osmolality and frequently assessing cardiac, renal and mental status Tx: once pt is stabilized initate attempts to detect and correct underlying cause Nursing management: -monitor BS and U/O and ketones -monitor admin of IV fluids to correct dehydration, insulin therapy to reduce BS and serum ketone levels and electrolytes given to correct electrolyte imbalance -assess renal status and cardiopulmonary status r/t hydration and electrolyte levels, monitor LOC -assess for signs of K imbalance resulting from hypoinsulinemia and osmotic diuresis, when insulin Tx starts the K level may decrease rapidly as K moves into cells once insulin become available, this movement into and out of extracellular fluid influences cardiac functioning-cardiac monitoring helps detect hyperkalemia and hypokalemia (changes in ECG indicate K excess or deficit), assess VS often to identify fever, hypovolemic shock, tachycardia and Kussmaul respirations

HHNS collaborative care/nursing management

Characteristics: lack of ketones in urine -main difference between them is that HHS usually has enough circulating insulin so that ketoacidosis doesn't occur -extreme hyperglycemia: 600-2000 mg/dl -profound dehydration: loss of 10-15% of body wt -mild or NO ketosis (ketone bodies) in urine -no acidosis -concentrated plasma: hyperosmolar -increased BUN -blood glucose levels greater than 600 mg/dl and marked increase in serum osmolality -HHS produces fewer Sxs in earlier stages so BS levels can climb very high before problem is noticed, the higher BS increases osmolality and produces more severe neurological Sxs such as somnolence, coma, seizures, hemiparesis and aphasia, Sxs resemble stroke so immediate determination of glucose levels is critical Tx: determine cause, vigorous fluid replacement, insulin and electrolytes

HHNS vs DKA

acarbose (Precose) -"starch blockers" -work by slowing down absorption of CHO in small intestine -taken w/ 1st bite of each main meal, most effective in lowering postprandial blood glucose -effectiveness is measured by 2hr postprandial glucose levels

alpha glucosidase inhibitors

pramlintide (Symlin) -amylin, hormone secreted by beta cells of pancreas in response to food intake, slows gastric emptying, reduces glucagon secretion and increases satiety -used in addition to mealtime insulin in pts w/ type 1 DM or type 2 DM who don't have good glucose control on ideal insulin therapy (only used concurrently w/ insulin and isn't a replacement) -administered before major meals subQ into thigh or abdomen, can't be injected into arm because absorption from this site is to variable -can't be mixed in the same syringe w/ insulin, concurrent use of pramlintide and insulin increases risk of severe hypoglycemia during the 3 hrs after injection esp. in pts w/ type 1 DM; teach pt to eat a meal w/ at least 250 calories and keep form of fast acting glucose on hand in case this happens

amylin analog

-prevention: immune studies, secondary prevention, RF reduction -maintain BS levels as near to normal as possible: type 1-requires insulin, type 2-proper nutrition, regular physical activity, maintenance of desirable body wt -*self monitoring of blood glucose (SMBG): critical necessity for DM management -home BS: usually 12% lower than lab values -interdisciplinary team: MD, RN, diabetes educator/dietician, physical therapist, counselor, wound care specialist -goals for Tx: FBS 70-110 mg/dl; PPBS < 180 mg/dl; HbgA1C <7%

collaborative management (pg. 1158, Table 49-2)

-for those who want to use only 1 or 2 injections per day -a short or rapid acting insulin is mixed w/ intermediate acting insulin (NPH) in the same syringe, this allows the pt to have both mealtime and basal coverage w/o having to administer 2 separate injections (think about the peaks of both insulins, has 2 peaks) -may be more convenient but most achieve better control w/ basal bolus therapy -can use premixed formula or pen: helpful to those who lack visual, manual or cognitive skills to mix insulin themselves, the convenience of these formulas sacrifices the potential for optimal blood glucose control because there's less opportunity for flexible dosing based on need

combo insulin therapy

1. smoking cessation 2. BP control 3. metmorfin therapy 4. lipid reduction 5. glycemic control

diabetes 2 interventions

-chronic multisystem disease r/t abnormal insulin production, impaired insulin utilization or both -ethnic groups: highest in Native Americans, then Hispanics, then Caucasians -5th leading cause of death in US -complications: more prevalent in Native Americans and African Americans, leading cause of adult blindness, end stage kidney disease an non-traumatic lower limb amputations -major contributing factor to heart disease and stroke -primarily a disorder of glucose metabolism r/t absent or insufficient supply and/or poor utilization of insulin that is available

diabetes mellitus

*control BS*: give IV fluids and insulin (if needed) immediately before, during and after surgery when there's no oral intake; unconscious surgical pt receiving insulin-watch for hypoglycemic signs such as sweating, tachycardia and tremors, frequently monitor BS -preop: need to be well regulated before surgery; labs-HbgA1C, electrolytes, renal function, CBC, EKG, CXR; surgery should be early in the morning, pt is NPO so no oral hypoglycemics, IV D5W w/ insulin, if insulin dependent BS within 1 hr of going to OR, call report to MD -intraop: may need to give regular insulin IV as needed -postop: administer IV insulin until pt can take po, when able to tolerate po intake give calorie foods, check BS 4-6 times daily, resume normal insulin schedule asap, watch for hypoglycemia in postop pt (drop in BP, increased HR), avoid bladder cath insertion to prevent infection, change dressings w/ strict sterile technique, assess wound for early signs of infection, watch for skin breakdown

diabetic pt having surgery

incretin hormones are released by intestines throughout the day but levels increase in response to meals, when glucose levels are normal or elevated incretins increase insulin synthesis and release from pancreas, decreases hepatic glucose production, hormone is inactivated by DPP-4 sitagliptin (Januvia) -"gliptin" drugs -blocks action of DPP-4 enzyme which is responsible for inactivating incretin hormones -results in increase in insulin release, decrease in glucagon secretion and decrease in hepatic glucose production -glucose dependent drug so they lower potential for hypoglycemia, absence of wt gain as a SE

dipeptidyl peptidase-4 (DPP-4) inhibitors

-*RFs: (esp. Type 2) obesity, high fat, reduced physical activity

etiology and patho

-30 min for 5 days/wk of moderate intensity aerobic physical activity, resistance training 3 times a wk -benefits: decreases insulin resistance and can have a direct effect on lowering BS levels, contributes to wt loss further decreasing resistance, helps reduce triglyceride and LDL cholesterol levels, increases HDL, reduces BP, improves circulation -pts who use insulin, sulfonylureas or meglitinides are at increased risk for hypoglycemia when they increase physical activity esp. if they exercise at the time of peak drug action or eat too little to maintain adequate BS levels -glucose lowering effects of exercise can last up to 48hrs after activity, pts who use meds that can cause hypoglycemia should schedule exercise 1hr after a meal or carry a 10-15g CHO snack and check for BS before exercising, eat small CHO snacks every 30 min during exercise to prevent hypoglycemia, if taking these meds always carry a fast acting source of CHO (glucose tabs, hard candies) when exercising -avoid strenuous exercise: can be perceived as a stress causing release of counterrregulatory hormones and temporary elevation of BS -exercise can worsen conditions of a pt w/ type 1 DM who is hyperglycemic and ketotic, vigorous activity should be avoided if BS is over 250 mg/dl and ketones are present in urine -don't exercise: if BS > 250 w/ ketones or > 300 w/o ketones; if BS < 100 -prior to beginning exercise program/session: hydrate 1st, then check BS

exercise (pg. 1168, Table 49-10)

exenatide (Byetta) -increase insulin synthesis and release from pancreas, inhibit glucagon secretion, decrease gastric emptying and reduce food intake by increasing satiety -administered by subQ injection in prefilled pen, given twice a day -delayed gastric emptying may affect absorption of oral meds, advise pt to take fast acting oral meds at least 1hr before injecting exenatide

glucagon-like peptide receptor agonists: incretin hormone

-mostly seen in Type 1 -caused by a great deficiency in insulin and characterized by hyperglycemia, ketosis, acidosis and dehydration -precipitating factors: illness and infection, inadequate insulin dose, undiagnosed Type 1 DM, poor self management and neglect Causes: -too little insulin -omitting insulin -increased, unmet need -insulin resistance Patho: -deficient insulin supply so glucose can't be properly used for energy -body compensates by fat/protein breakdown as a secondary source of fuel, ketones formation (acidic by products of fat metabolism): ketosis alters pH balance causing metabolic acidosis, ketonuria-ketone bodies are excreted in urine causing electrolyte depletion -deficiency: impairs protein synthesis and causes excessive protein degradation resulting in nitrogen losses from tissues, stimulates production of glucose from amino acids (from proteins) in liver and leads to further hyperglycemia (because of deficiency the added glucose can't be used and BS level rises more adding to the diuresis) -if not treated pt will develop severe depletion of Na, K, Cl, Mg and phosphate, vomiting caused by acidosis results in more F&E losses, eventually hypovolemia followed shock occurs, renal failure occurs from hypovolemic shock and causes retention of ketones and glucose, acidosis progresses, untreated pt becomes comatose due to dehydration, electrolyte imbalance and acidosis -dehydration: manifestations of poor skin turgor, dry mucous membranes, tachycardia and orthostatic hypotension; early Sxs: lethargy and weakness; as pt becomes severely dehydrated the skin becomes dry and loose, eyes become soft and sunken, abd pain accompanied by ANV, Kussmaul's respirations (rapid, deep breathing assoc. w/ dyspnea)-body's attempt to reverse metabolic acidosis through exhalation of excess CO2, acetone-sweet, fruity breath odor -labs: blood glucose level >/= 250 mg/dl, arterial blood pH < 7.3, HCO3 level < 16 mEq/L, large ketones in urine or serum -3 major resulting abnormalities: *diuresis*-causes dehydration and electrolyte imbalance, *hypovolemic shock, acidosis*

hyperglycemia and diabetic ketoacidosis: causes, patho

-same as DKA but no ketones -life threatening syndrome that can occur in pts w/ diabetes who are able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion -occurs most often in elderly (> 60) w/ Type 2 diabetics -common causes: UTI, pneumonia, sepsis, any acute illness and newly diagnosed Type 2 DM, often r/t impaired thirst sensation and/or a functional inability to replace fluids, usually a hx of inadequate fluid intake, increasing mental depression and polyuria -higher mortality than DKA: probably due to elderly pop. -occurs in undiagnosed diabetics: often induced by meds such as glucocorticoids, diuretics, IV glucose solutions for prolonged periods

hyperglycemic hyperosmolar non-ketotic syndrome (HHNS)

-etiology/RFs: insulin overdose, skipping a meal, sleeping late, exercise w/o CHO supplement, N/V, alcohol intake, effect of meds -Type 1 most susceptible -Pathophysiology: low BS occurs when there's too much insulin in proportion to available glucose in blood causing BS level to drop to < 70 mg/dl, suppression of insulin secretion and production of glucagon and E (not as effective) provide defense against hypoglycemia (E causes Sxs of shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger and pallor)

hypoglycemia

-brain needs a constant supply of glucose in sufficient amounts to function properly so hypoglycemia can affect mental functioning, Sxs includes difficulty speaking, visual disturbances, stupor, confusion and coma -mimics ETOH intoxication -if left untreated can progress to loss of consciousness, seizures, coma and death -hypoglycemic unawareness: condition where a person doesn't experience the warning S/S of hypoglycemia until glucose levels reach a critical point, then the person may become incoherent and combative or lose consciousness; pt's at risk: those had repeated episodes of hypoglycemia, older pts, pts who use beta andrenergic blockers; using tight BS control not best goal because of hypoglycemia that can occur, usually managed w/ BS goals that are somewhat higher than those who are able to detect and manage onset of hypo -causes: often r/t mismatch in timing of food intake and peak action of insulin or OA that increase endogenous insulin secretion -balance between BS and insulin can be disrupted by administering too much insulin or medication ingesting too little food, delaying the time of eating and performing unusual amounts of exercise -can occur at any time but most episodes occur when OA or insulin is at its peak of action or when pt's daily routine is disrupted w/o adequate adjustments in diet, meds and activity -Sxs may occur when a very high BS level fall too rapidly (BS level of 300 mg/dl falling to 180 mg/dl)-BS is above normal but sudden metabolic shift can evoke Sxs, too vigorous management of hyperglycemia can cause this

hypoglycemia: clinical manifestations

*return BS to normal* -at 1st sign test BS, immediately begin Tx for hypoglycemia if < 70 -mild rxn: treat w/ 15 g CHO, check BS every 15 min, repeat if < 70; make 15g of carbs (6 oz of regular soda, 6-8 lifesavers, 1 tbs syrup or honey, 4 tsp jelly, 4 oz orange juice, tube of cake icing or paste) -if > 70, give snack of cheese and crackers, peanut butter and crackers (given after hypoglycemia is corrected) -severe rxn: if unconscious, give IV glucose or glucagon immediately -*conscious hypoglycemia: rule of 15 for Tx-blood glucose less than 70mg/dl eat 15g of simple (fast acting) carbs such as 4-6 oz of fruit juice or a regular soft drink every 15 min, can also use gels or tabs, recheck BS 15 min later after initial ingestion of food, if value is still < 70 mg/dl eat 15g more grams of CHO and recheck the BS in 15 min, if no significant improvement occurs after 2-3 doses of 15g of simple CHO contact HCP; because of potential for rebound hypoglycemia after an acute episode have the pt ingest a complex CHO after recovery to prevent another hypoglycemic attack -avoid w/ carbs that contain fat (such as candy bars, cookies, whole milk, ice cream)-fat slows the absorption of glucose and delays the response to Tx, avoid overTx w/ large amounts of quick acting carbs so that rapid fluctuation to hyperglycemia doesn't occur -*unconscious hypoglycemia: admin 50% glucagon IV (irritating to the blood vessels) -in an acute care setting pts may be treated w/ 20-50 ml of 50% dextrose IV push; if pt isn't alert enough to swallow and no IV access is available administer 1 mg of glucagon by IM or subQ injection-IM injection in a site such as the deltoid muscle will result in quicker action -glucagon stimulates a strong liver response to convert glycogen to glucose making glucose quickly available, nausea is a common rxn after glucagon injection-to prevent aspiration if vomiting occurs turn pt on side until he/she becomes alert, pts w/ minimal glycogen stores won't respond to glucagon (those w/ alcohol related liver disease, starvation and adrenal insufficiency -once stabilized: determine cause, teach prevention: check for BBs, 1/3 of all diabetics may not recognize Sxs

hypoglycemia: medical management (pg. 1179, Table 49-19)

-diabetics are more susceptible to infections because of defect in mobilization of white blood cells and an impaired phagocytosis by neutrophils an monocytes, difficult to manage when it appears -3 main contributing factors: impaired leukocyte activity, neuropathies, vascular insufficiency - if all 3 are present infected areas heal more slowly, infection increases insulin need, at increased risk for DKA -UTI: most common type of infection in DMs, caused by glucosuria and neurogenic bladder w/ retention -diabetic foot: 40% of infections require amputation, 10% die -antibiotic therapy -foot care: don't use creams, rubs, ointments, chemicals or other OTCs on corns or callouses because they increase risk of infection, examine feet daily (use mirror if needed), don't walk barefoot, schedule regular podiatrist visits, wear shoes w/ material that breaths, wash feet daily w/ mild soap, water and dry well, test water temp. before bathing, avoid prolonged foot soaks, heating pads and hot water bottles, wear proper fitting shoes and hosiery, break new shoes in gradually, use mild moisturizer cream (none between the toes) -teach measures to prevent infection: practicing good hygiene, avoiding exposure to individuals who have a communicable illness, getting flu/pneumonia vaccine

infections

-routine doses are usually administered by subQ injection, regular insulin can be given IV when immediate onset of action is desired, insulin isn't taken orally because it's inactivated by gastric juices -insulin injection (pg. 1161, Table 49-5, Fig. 49-4) -site selection: fastest subQ absorption is from abdomen, followed by back of arm, thigh and buttock, abd is preferred site, caution pt about injecting into a site that's to be exercised-exercise of injection site w/ increased body heat and circulation generated by exercise may increase rate of absorption and speed the onset of insulin action -rotate injection site within 1 anatomic site (abd for at least 1 wk before using different site like right arm), allows for better insulin absorption -higher the gauge number the smaller the diameter resulting in a more comfortable injection -self injection at home: use of an alcohol swab on site before self injection isn't needed, routine hygiene such as washing w/ soap and rinsing w/ water is adequate, applies only to pt self injection technique (when done in hospital use alcohol to prevent HAI) -perform injections at 45 (if skinny) to 90 degree angle depending on thickness of pt's fat pad

insulin administration

-hormone produced by beta cells in pancreas, continuously released into the bloodstream in small increments w/ increased release when food is ingested, lowers BS and facilitates stable, normal glucose range of 70-110 mg/dl -promotes glucose transport from the bloodstream across cell membranes into cell -rise in plasma insulin after a meal stimulates storage of glucose as glycogen in liver and muscle (promotes glycogenesis), inhibits gluconeogenesis, catabolism and ketogenesis, increases fat deposition of adipose tissue, increases protein synthesis and inhibits glycogen breakdown (glycogenolysis) -promotes anabolism (a storage hormone) -glucagon: insulin opposite -other hormones that affect blood sugar levels: E/NE, growth hormone, cortisol -all work to oppose effects of insulin (counterrregulatory hormones), they increase blood glucose levels by stimulating glucose production and output by the liver and by decreasing the movement of glucose into the cells -insulin and opposing hormones maintain BS levels WNL by regulating release of glucose for energy during food intake and periods of fasting (sleeping period)

insulin and glucagon

-programmed to deliver a continuous infusion of rapid acting insulin 24 hrs a day (basal rate) -basal insulin can be temporarily increased or decreased based on carb intake, activity changes or illness -at mealtime user programs pump to deliver bolus infusion of insulin appropriate to amount of CHO ingested and an additional amount if needed to bring down high preprandial (pre-meal) blood glucose -site insertion changed every 2-3 days, users must check blood glucose level at least 4 times/day (testing 8 times or more is common) -pump allows for tight glucose control because insulin delivery is similar to normal physiologic pattern

insulin pumps

most common diabetic skin lesion characterized by reddish brown, round or oval patches, initially scaly then they flatten out and become indented, lesions appear most frequently on shins

integumentary complications

-type 1 need mealtime insulin and long or intermediate acting insulin to control glucose levels in between meals and overnight, w/o 24 hr background insulin they're more prone to developing DKA -type 2 who use oral meds also need insulin to adequately control BS levels -long acting insulin: glargine (Lantus) and detemir (Levemir), released steadily and continuously and doesn't have a peak of action, because of lack of peak the risk for hypoglycemia is greatly reduced, can't be diluted or mixed w/ any other insulin or solution in the same syringe -intermediate acting: NPH, duration of 12-16 hrs, peak ranges from 6-8 hrs which can result in hypoglycemia, only basal insulin that can be mixed w/ short and rapid acting insulins, cloudy insulin that must be gently agitated before admin (role in between hands to mix)

long or intermediate acting (basal) background insulin

-to control postprandial blood glucose levels (BS to see if they're taking in enough glucose w/ their meals) timing of rapid and short acting insulin in relation to meals is crucial -rapid acting: lispro (Humalog), aspart (NovoLog), have an onset of action of 5-15 min and should be injected within 15 min of mealtime (inject once food is in the room), most closely mimic natural insulin secretion in response to a meal -short acting: regular insulin, onset of action of 30-60 min and should be injected 30-45 min before a meal to ensure that onset of action coincides w/ meal absorption, more likely to cause hypoglycemia because longer duration of action

mealtime insulin (bolus)

work on 3 defects of type 2 DM: insulin resistance, decreased insulin production and increased hepatic glucose production -biguanides -sulfonylureas -alpha glucosidase inhibitors -thiazolidinediones -dipeptidly peptidase-4 (DPP-4) inhibitors -glucagon-like peptide receptor agonists -amylin analog

meds: oral and non-insulin injectable agents (pg. 1164, Table 49-7)

-ADA diet no longer used, if pt has an overall healthy eating plan a person w/ DM can eat the same foods as a person who doesn't have DM -individualized goals = wt loss to increase insulin sensitivity, lower BP, lower lipid levels, maintain BS levels, modify nutrient intake and lifestyle to prevent/slow rate of chronic complications -Food guide pyramid: if followed will provide adequate overall good nutrition Type 1: meal planning should be based on individual's usual food intake and preferences and balanced w/ insulin and exercise patterns, insulin regimen should be developed w/ pt's eating habits and activity pattern in mind, teach to adjust rapid acting insulin before the meal according to BS and CHO meal content Type 2: emphasizes achieving glucose (HgA1C), lipids and BP control, wt reduction (5-7% of body wt), meal plan w/ appropriate serving sizes, reduced total fats (saturated and trans fats), low CHO and avoidance of simple sugars can decrease calorie consumption, space meals out to spread nutrient intake throughout the day, regular exercise; monitor BS levels, A1C, lipids and BP -General dietary guidelines (best taught by dietician): -CHO (< 300 g/day): includes sugars, starches and fiber, CHO (healthy) are the remaining calories including whole grains, fresh veggies and fruits, low fat milk; limit sugars -glycemic index (GI) = rise in BS after a person has eaten carb containing food (developed to compare postprandial responses to CHO containing foods): foods w/ high GI cause sharp rise in BS, foods w/ low GI raise BS at a slower rate -fiber 25-30 g/day -fat (provides energy): limit fat to < 10% of total calories, < 200-300 mg/day of cholesterol, limited trans fat -protein: 15%-20% of total calorie consumption, high protein diets aren't recommended as a wt loss method for ppl w/ DM -*limit alcohol*: alcohol inhibits gluconeogenesis (breakdown of glycogen to glucose) by liver which can cause severe hypoglycemia in pts on insulin or OA that increase insulin secretion, increases calories, triglycerides; moderate alcohol consumption-1 drink/day for women, 2 drinks/day for men -*avoid*: adding sugars, sweetened foods, inconsistent timing of food/meals (if you're consuming alcohol and the things from the avoid list, you must include them into your carb count) -Pt teaching: CHO counting-serving size of CHO is 15 g, teach pt about foods that contain CHOs, how to read food labels and appropriate serving sizes; diabetes exchange lists-meal plan w/ specific numbers of helpings from a list of exchanges for each meal and snack; myPlate-DM each meal needs 1/2 half of plate of non-starchy veggies, 1/4 of starch, 1/4 of protein, glass of non-fat milk and small piece of fresh fruit -dietary control is the 1st step before meds are prescribed

nutrition (pg. 1166, Table 49-8)

-those diagnosed are at increased risk for developing type 2 DM -impaired glucose tolerance or impaired fasting glucose -middle stage between normal glucose homeostasis and DM where blood glucose levels are elevated but not high enough to meet criteria for DM -usually don't have Sxs -encourage pts to undergo screening and give instruction about managing RFs for DM -have blood glucose and A1C tested regularly and monitor for Sxs of DM (3P's) -management: maintain healthy wt, exercise regularly, eat healthy diet

prediabetes

-hypoglycemia -allergic rxns: local inflammatory rxns to insulin may occur such as itching, erythema and burning around injection site, rxns may be self limiting within 1-3 months or may improve w/ low dose of antihistamine, manifested by a systemic response w/ urticaria and maybe anaphylactic shock, allergies not to insulin but additives to insulin such as zinc or protamine -lipodystrophy: atrophy of subQ tissue, occurs if same injection sites are used frequently, hypertrophy (thickening of subQ tissue) eventually regresses if pt doesn't use site for at least 6 months -somogyi phenomenon: hyperglycemia in the morning may be due to this, high dose of insulin produces a decline in BS levels during night, as a result counterregulatory hormones are released stimulating lipolysis, gluconeogenesis and glycogenolysis which produces rebound hyperglycemia, the danger is that when BS levels are measured in the morning hyperglycemia is present and pt or HCP may increase the insulin dose; if pt is experiencing morning hyperglycemia, check BS levels between 2-4AM for hypoglycemia to help determine if the cause is somogyi effect, pt may report HAs when waking up, night sweats or nightmares, a bedtime snack or reduction in dose of insulin can prevent somogyi effect -dawn phenomenon: characterized by hyperglycemia that's present on awakening, counterregulatory hormones (GH, cortisol) excreted in increased amounts in the early morning are responsible Tx: somogyi-less insulin; dawn-increase in insulin or adjustment in admin time -if predawn levels of BS levels are < 60 mg/dl and S/S of hypoglycemia are present, reduce insulin; if 2-4AM BS is high, increase insulin

problems w/ insulin therapy

-primary RF for type 2 DM is obesity, modest wt loss of 5-7% of body wt and regular exercise of 30 min 5 times/wk lower risk; more RFs-age, ethnicity (NA, Hispanic, AA, Asian, Pacific Islander), having baby that weighs more than 9 lbs, having gestational DM, family hx of DM -blood sugar testing -insulin/OA: proper admin, assessment of pt's response to insulin therapy, teaching pt about admin and SEs of insulin; nursing is the same, pt shouldn't take extra pills if they have overeaten, if pt uses sulfonylureas and metformin instruct about prevention, Sx recognition and management of hypoglycemia -urine testing -medical ID (Medic alert tag) -travel: being sedentary for long periods may raise person's glucose level, encourage pt to get up and walk at least every 2 hrs to lower risk of DVT and prevent elevation of glucose levels -causes, S/S, actions r/t hypoglycemia, hyperglycemia -personal hygiene: potential for infection is increased, susceptible to periodontal disease-encourage daily brushing and flossing and regular visits to the dentist, when having dental work done pt should inform dentist that they have DM, regular bathing w/ emphasis on foot care, inspect feet daily, avoid going barefoot and wear shoes that are supportive and comfortable (firm not soft soles), if cuts, scrapes or burns occur they should be treated quickly and monitored carefully-wash area and apply non-abrasive or non-irritating antiseptic ointment, cover area w/ dry sterile pad, notify HCP immediately if injury doesn't begin to heal within 24 hrs or if signs of infection develop -how to handle sick days: don't stop taking insulin -meds -effects of stress during acute illness, injury and surgery: stress increases BS level and results in hyperglycemia (evoke counterregulatory hormone response), check glucose at least every 4 hrs if ill, test for ketones every 3-4 hrs if acutely ill pt w/ type 1 DM and glucose > 240 mg/dl; report to HCP when glucose levels are > 300 mg/dl for 2 tests in a row or urine ketone levels are moderate to large, pt w/ type 1 DM may need an increase in insulin to prevent DKA, insulin therapy may be required for pt w/ type 2 DM to prevent/treat hyperglycemic Sxs and avoid acute hyperglycemic emergency, in critically ill pts insulin therapy may be started if BS is persistently greater than 180 mg/dl; pt requires more energy during times of stress and illness, if pt can eat normally-continue w/ regular meal plan, increase intake of non-caloric fluids (water, diet gelatin, other de-caffeinated drinks) and continue taking OAs, non-insulin injectable agents and insulin; when illness causes pts to eat less than normal-continue taking OAs, non-insulin injectable agents and insulin while supplementing food intake w/ CHO containing fluids (low Na soup, juices and regular de-caffeinated soft drinks)

pt teaching (pg. 1174-1175, Table 49-14, Table 49-15)

-elderly diabetics -surgical intervention for diabetics: bariatric

special situations

-insulin is a protein, heat and freezing alter insulin molecule -insulin vials and pens currently in use may be left at room temp. for up to 4wks -prolonged exposure to direct sunlight should be avoided -unopened insulin vials and pens should be stored in the fridge -prefilled syringes containing 2 different insulins are stable for up to 1wk when stored in fridge, syringes containing only 1 type of insulin are stable up to 30 days -syringes should be stored in vertical position w/ needle pointed up to avoid clumping of suspended insulin needle, before injection gently roll syringe in hands to warm insulin and re-suspend the particles

storage of insulin

glipizide (Glucotrol), glyburide (DiaBeta) -primary action to increase insulin production by the pancreas -hypoglycemia is major SE

sulfonylureas

pioglitazone (Actos), rosiglitazone (Avandia) -"insulin sensitizers" -most effective for ppl who have insulin resistence (type 2 DM) -improve insulin sensitivity, transport and utilization at target tissues -don't increase insulin production so they don't cause hypoglycemia when used alone -rarely used because of adverse effects: rosigliatazone-assoc. w/ adverse cardiovascular events (MI), pioglitazone-can worsen HF and assoc. w/ an increased risk of bladder cancer

thizaolidinediones