Term
decompensation of diabetes higher stress due to illnesses (infections, fever, trauma, or other medical stresses) decreased physical activities in the hospital withholding of diabetic treatments administration of IV dextrose, parenteral or enteral nutrition administration of pharmacologic agents (glucocorticoids, vasopressors, fluroquinolones) |
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Definition
causes of inpatient hyperglycemia |
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Term
suppressed immune system impaired vascular responses hyperreactive platelets and coagulation inflammation increased oxidative stress |
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Definition
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Term
difficult to achieve very tight glucose target (80-110 mg/dL) higher rates of hypoglycemia were reported NICE-SUGAR (2009): largest study to date in critically ill patients (medical and surgical ICU), increased 90 day mortality in intensive group, more severe hypoglycemia meta-analysis (2009): no overall mortality benefit with intensive glycemic control, decreased mortality in surgical ICU patients only, 6-fold increase in severe hypoglycemia (<40 mg/dL) |
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Definition
recent studies on the effect of tight glycemic control for hospitalized patients |
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Term
has not been consistently shown to decrease mortality in critically ill patients may actually increase mortality leads to increased risk of hypoglycemia |
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Definition
why is a glycemic goal of 80-100 mg/dL not appropriate? |
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Term
ICU: 140-180 mg/dL non-ICU: preprandial = < 140 mg/dL; random = < 180 mg/dL clinically stable patients with previously successful tight glycemic control may have lower glycemic goals during the hospitalization terminally ill patients or patients with severe comorbidities may have higher glycemic goals no randomized controlled trials have been done in hospitalized patients outside of ICU setting |
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Definition
glycemic goals in hospitalized patients |
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Term
hyperglycemia: DM is typically not the primary medical problem, frequent interruptions in glucose lowering medications, nursing shortage, skepticism about the effect of good glycemic control, fear of hypoglycemia, lack of protocols/algorithms hypoglycemia: altered nutrition status (NPO, reduced oral intake, interruption in nutritional support, emesis), organ failures (renal disease), sudden reduction in corticosteroid dose, altered ability of patients to self-report symptoms lack of protocols/algorithms |
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Definition
barriers to optimal glycemic control in hospitalized patients: causes of hyper and hypoglycemia |
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Term
measure blood glucose at hospital admission in all patients identify ("flag") patients with PMH of DM measure A1C at hospital admission if: hyperglycemia is present and no PMH of DM or PMH of DM and no A1C within previous 3 months plasma glucose monitoring: in all patients with PMH of DM, hyperglycemia at admission, or at high risk for hyperglycemia; typical frequency is QID corresponding with each meal and HS; if patient NPO or receiving continuous nutrition support q4-6h is sufficient; frequency may be increased in severe illness individualized diets in patients with PMH of DM: consistent CHO diet, may use CHO counting to determine prandial insulin doses individualized DM therapy: guidelines currently recommend insulin in most hospitalized patients; may use non-insulin agents in selected patients (clinically stable, expected to consume meals at regular intervals, no newly developed contraindications) |
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Definition
general approach to management of inpatient hyperglycemia |
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Term
SFUs - hypoglycemia (especially in people with poor oral intake), long duration of action glinides - do not have clinical data for inpatient use, mainly used for post-prandial hyperglycemia so not ideal for NPO or patients with poor oral intake metformin - GI ADRs may be problematic, increased risk of lactic acidosis due to various conditions (decompensated HF, hypoperfusion, renal insufficiency, respiratory distress/failure, need for contrast in imaging tests) TZDs - delayed onset of action, increased intravascular volume a-glucosidase inhibitors - mainly reduce post-prandial hyperglycemia, high incidence of GI ADRs pramlintide/exenatide - mainly reduce postprandial hyperglycemia, nausea is the most common ADR DPP4 inhibitors - limited experience and no inpatient data |
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Definition
limitations of non-insulin agents: SFUs, glinides, metformin, TZDs, a-glucosidase inhibitors, pramlintide/exenatide, DPP4 inhibitors |
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Term
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Definition
(subcutaneous/IV) insulin is the preferred route in non-critically ill patients |
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Term
basal insulin provides coverage for basic metabolic function: if patient NPO they may not need exogenous basal insulin if patient has enough endogenous insulin synthesis, patients with insulin deficiency (T1DM) still need basal insulin even if NPO or have limited oral intake in order to prevent ketoacidosis nutritional insulin provides coverage for meals and/or other nutritional support (TPN, enteral feedings, dextrose infusion, nutritional supplement) |
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Definition
what is the difference between basal and nutritional insulin? |
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Term
need to review insulin regimen at least daily reassess regimen if insulin not at goal or if any BG < 100 mg/dL modify regimen if any BG < 70 mg/dL |
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Definition
how often should an insulin regimen be reviewed for a patient in a hospital? |
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Term
supplemental/correctional insulin |
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Definition
refers to additional insulin injections between scheduled doses to correct for unexpected hyperglycemia, usually dosed based on patient's blood glucose level |
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Term
regular insulin: inexpensive, longer duration may be problematic rapid-acting insulin: ideal preparation for isolated hyperglycemia without affecting subsequent glucose readings, expensive |
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Definition
comparison of the types of insulin used for supplemental/correctional insulin |
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Term
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Definition
usually refers to the use of regular insulin dosed based on BG without any scheduled insulin ineffective for hyperglycemia when used as monotherapy gives no incentive to adjust scheduled therapy usually not individualized dosing reactive approach rather than proactive often leads to fluctuation in BG levels |
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Term
continuous IV infusion uses regular insulin |
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Definition
(subcutaneous/continuous IV infusion) is the preferred route for ICU patients |
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Term
advantages: most effective in achieving pre-specified BG levels, allows rapid dosing adjustment, has been shown to decrease mortality and morbidity in some studies disadvantages: very labor intensive (requires q1-2h glucose monitoring), increases risk of hypoglycemia |
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Definition
advantages and disadvantages to IV insulin infusions |
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Term
CRITICAL ILLNESS HYPERGLYCEMIC CRISIS preoperative, intraoperative, and postoperative care post heart surgery post organ transplant cardiogenic shock high dose glucocorticoid therapy prolonged NPO in T1DM |
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Definition
indications of IV insulin infusions |
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Term
first dose of SC insulin should be given before IV insulin is discontinued if intermediate or long acting insulin is used alone, administer 2-3 hours prior if combination of basal and preprandial insulin, basal insulin can be initiated at any time of the day administer short or rapid acting insulin 1-2 hours prior to discontinuing IV infusion |
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Definition
transition from CIII to SC |
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Term
increased insulin sensitivity: T1DM, elderly decreased insulin clearance: renal failure patients, patients with organ failure, liver disease diminished glycogen stores: malnourished patients |
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Definition
in what patients would you use less aggressive insulin dosing? |
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Term
hyperglycemia in patients with prior DM: if A1C is elevated at admission, preadmission regimens need to be revised hyperglycemic patients without prior DM (A1C should be used to differentiate between stress hyperglycemia and undiagnosed DM): patients with newly diagnosed DM should receive appropriate education and follow up, patients with stress hyperglycemia still need appropriate follow up with a physician |
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Definition
follow up upon discharge from the hospital |
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Term
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Definition
a medical emergency in which severe lack of insulin results in the breakdown of body fat for energy, which leads to accumulation of ketones in the body |
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Term
hyperosmolar hyperglycemic state |
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Definition
a medical emergency in which extremely high serum glucose level results in increased urination, which leads to severe dehydration and impaired renal function |
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Term
causes: absolute deficiency in insulin OR insufficient insulin coupled with increased counterregulatory stress hormones hyperglycemia -> glucosuria -> osmotic diuresis -> dehydration and loss of Na and K increased lipolysis -> increased FFA -> increased ketone bodies -> increased ketonemia and metabolic acidosis evolves over a short period of time (< 24 hours) |
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Definition
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Term
causes: insufficient insulin AND insulin resistant residual insulin is sufficient enough to inhibit lipolysis therefore minimizing ketosis, but not hyperglycemia hyperglycemia -> glucosuria -> osmotic diuresis -> severe dehydration (hyperosmolality), loss of electrolytes, and impaired renal function reduction in urinary excretion of glucose leads to more severe hyperglycemia than in DKA evolves over days and weeks |
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Definition
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Term
hyperglycemia (HHS>DKA) dehydration (HHS>DKA) Na and K are the main electrolytes affected sodium: decreased Na and water reabsorption and increased urinary Na loss lead to net loss of total body Na (need to calculate a corrected Na based on glucose level before accessing total Na deficit) potassium: dehydration and acidosis (in DKA) cause shifting of K out of cells, insulinopenia leads to impaired K entry into cells, increased K in ECF leads to increased urinary loss serum Na and K concentrations depend on degree of dehydration other electrolytes effected include: Cl, Phos, Ca, Mg metabolic acidosis = DKA hyperosmolality = HHS |
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Definition
major components of DKA and HHS (hyperglycemia, dehydration, Na, K, pH, osmolality) |
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Term
INFECTION (PNEUMONIA, UTI, SEPSIS) inappropriate insulin therapy (omission, inadequate dose, or insulin pump problems) new onset of DM CVD pregnancy trauma hyperthyroidism pancreatitis drugs |
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Definition
precipitating factors for DKA and HHS |
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Term
symptoms: history of polyuria, polydipsia, and weight loss; N/V, abdominal pain; fruity odorous breath (DKA); weakness and muscle cramps; altered mental status (drowsy, stupor, coma, hemiparesis, hemianopsia, and seizure) signs: dehydration (signs and symptoms include dry mucous membranes, reduced skin turgor, sunken eyes, altered mental status, weight loss, hypotension, tachycardia, prolonged capillary refill and even shock); hyperventilation, coma (more frequent in HHS) |
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Definition
clinical presentation of DKA or HHS |
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Term
plasma glucose: > 250 mg/dL serum Na: low serum K: low-high ARTERIAL PH: < 7.3 SERUM BICARB: 10-18 URINE KETONES: PRESENT SERUM KETONES: PRESENT serum osmolality: variable ANION GAP: > 10-12 |
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Definition
diagnosis of DKA based on lab levels |
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Term
PLASMA GLUCOSE: > 600 mg/dL serum Na: normal or increased serum K: low - high arterial pH: > 7.3 serum bicarb: > 18 urine ketones: small serum ketones: small SERUM OSMOLALITY: > 320 (normal 275-290) anion gap: variable |
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Definition
diagnosis of HHS based on lab values |
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Term
risk of mortality increases in very young or very old negative prognosis factors: hypotension, hypothermia, coma |
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Definition
negative prognosis factors for DKA and HHS |
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Term
correction of hyperglycemia correction of dehydration correction of electrolytes (sodium and potassium) correction of metabolic acidosis in DKA treatment of underlying cause |
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Definition
general approach to treatment of DKA or HHS |
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Term
continuous IV insulin infusion: if plasma glucose does not fall by 50-75 mg/dL in the 1st hour, increase infusion rate every hour until steady decline is reached maintenance insulin infusion when plasma glucose reaches 200 mg/dL in DKA or 300 mg/dL in HHS once plasma glucose is at 200 (DKA) or 300 (HHS) then decrease insulin drip and add dextrose to IV fluids adjust infusion rate and dextrose amount to maintain 150-200 mg/dL until acidosis resolves (DKA) or 250-300 mg/dL until hyperosmolality resolves and mental status improves (HHS) intermittent SC rapid-acting insulin may be used in mild DKA: bolus dose and q1-2h injections to achieve glucose around 250 mg/dL then dose adjust until DKA resolves no differences in efficacy compared to IV insulin in mild DKA allows treatment on general medicine floor or ED which cuts costs MUST HOLD INSULIN IF K < 3.3 MEQ/L!!! |
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Definition
correction of hyperglycemia in DKA and HHS |
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Term
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Definition
at what K level must insulin be held? |
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Term
need repletion of both intravascular and estravascular volume 0.9% NaCl (normal saline) should be infused subsequent fluid depends on serum Na concentrations: normal or elevated Na - 0.45% NaCl; low Na - 0.9% NaCl when plasma glucose reaches 200 mg/dL in DKA or 300 mg/dL in HHS, switch to D5W in 1/2NS infusion rate must be adjusted for cardiac and renal dysfunction monitor BP and I/O to better assess fluid status |
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Definition
correction of dehydration in DKA and HHS |
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Term
sodium: replaced adequately with fluid replacement potassium: usually depleted due to urinary loss but serum concentration may be low, normal, or high replacement dose depends on serum K level low (<3.3): treatment immediately with K and HOLD INSULIN THERAPY until K > 3.3 normal (>3.3 but <5.2): give supplemental K in IV fluids while patient is on IV insulin high (>5.2): no replacement until level drops (usually 1-2 hours after treatment) and recheck q2h must consider renal function goal K level = 4-5 mEq/L |
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Definition
correction of electrolytes (Na and K) in DKA and HHS |
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Term
acidosis will correct with insulin therapy sodium bicarbonate may be necessary only in SEVERE acidosis pH < 6.9: bicarb should be given until pH > 7 pH >/= 6.9: no bicarb needed need to monitor K and replace accordingly |
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Definition
correction of metabolic acidosis in DKA |
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Term
SC insulin may be initated when blood glucose < 200 mg/dL and DKA resolves (serum bicarbonate >/= 15 mEq/L, pH > 7.3, and anion gap = 12 mEq/L) or HHS resolves (osmolality and metal status normalizes) SC insulin should provide basal and prandial coverage first dose of SC insulin should be given before IV insulin is discontinued, depending on type of SC insulin: if intermediate or long acting insulin used alone, administer 2-3 hours prior to discontinuation of IV insulin; administer short or rapid acting insulin 1-2 hours prior to discontinuing IV infusion |
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Definition
transition from IV insulin to SC for DKA and HHS |
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