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Diabetes 2

Endocrine

QuestionAnswer
Diabetic w/ anorexia, anemia, wt loss, pallor may be: CRF
Gastroparesis, impotence, recurrent infections, stocking-glove paresthesia = Diabetic neuropathy: ?treat w/ TCA (amitriptyline)
Hypoglycemia despite glucose administration; increased C-peptide; may be due to: Insulinoma or extrapancreatic tumor
Hypoglycemia in alcoholic: give: Give Thiamine before glucose to prevent Wernicke encephalopathy
Whipple triad = hypoglycemia: FBS <40, sxs, immediate recovery upon glucose admin
hypoglycemia, 2/2 hereditary fructose intolerance: due to: aldolase B deficiency
DM complications: chronic hyperglycemia leads to: nonenzymatic glycation of proteins & produces tissue damage
Test for Diabetic Foot Ulcer with: 10g monofilament test ; Comprehensive foot exam
Major metabolic defects in T2DM Peripheral insulin resistance in mx & fat; Decreased pancreatic insulin secretion; Increased hepatic glucose output
DM risk factors FH. Age >45. Ethnic (AA, Hispanic, Native Am, Asian, Pacific). Physical inactivity. Meds (transplant, HIV, anti-psychotics). Obesity. Gestational. PCOS.
Obesity & DM fat cells = endocrine organs
Glycemic recommendations for non-PG adults w/ DM A1C <5.7%; FPG 70–100 (100-125 = IFG). Peak postprandial glucose <180 (1 hr) & <150 (after 2 hrs)
DM: Wt loss: Less common in: Type 2 DM
Major cause of mortality for DM pts: CVD
Leading cause of ESRD: Diabetic nephropathy (occurs in 20–40% of DM pts)
Most common cause of new blindness in pts 20–74 yo: Diabetic retinopathy
DM & ABCs of CHD prevention: A = Aspirin; ACEI; A1C control
DM & ABCs of CHD prevention: B = Beta-blockade; BP control
DM & ABCs of CHD prevention: C = Chol mgmt
DM & ABCs of CHD prevention: D = Diet; do not smoke; decrease DM risk
DM & ABCs of CHD prevention: E = Exercise
Target/recommendations: HbA1c target <7.0; <6.0 if poss w/o inducing hypoglycemia
T2DM Target: BP <130/80 (ACEI / ARB)
T2DM Target: Lipids LDL <100 (<70 optimal); HDL >40 M, >50 F; TG <150; statin for CV hx or >40 yo to lower LDL 30-40%
T2DM recommendations: ASA >40 yo or other risk factors; all w/ CV hx
T2DM recommendations: ACEI > 55 yo w/ other CV risk factor
Metabolic syndrome: Dx: 3 of 5: Waist circum >40 (M) / >35 (F); TG ≥150; HDL <40 (M) / <50 (F); BP ≥ 130/85; FPG ≥110
Major Metabolic Defects in T2DM Peripheral insulin resistance in mx & fat; Decreased pancreatic insulin secretion; Increased hepatic glucose output
DM risk factors FH; Age > 45; High-risk ethnic pop; Habitual physical inactivity; Meds (transplant, HIV, anti-psychotics); Obesity
Obesity & DM fat cells = endocrine organs
DM: Polydipsia is due to: enhanced thirst because of increased serum osmolality from hyperglycemia & hypovolemia
DM: Wt loss: Less common in: Type 2 DM
T2DM PE findings Acanthosis nigricans, skin tags
T2DM PE findings: PCOS PCOS (polycystic ovarian syndrome): hirsutism
Major cause of mortality for DM pts: CVD
Diabetic nephropathy: incidence occurs in 20–40% of DM pts
Leading cause of premature death in young patients: Diabetic nephropathy
DM retinopathy: prevalence strongly related to: the duration of diabetes
Most common cause of new blindness in pts 20–74 yo: Diabetic retinopathy
DM neuropathy: tx Specific tx for underlying nerve damage: not available; only improved glycemic ctrl (may slow progression but rarely reverses neuronal loss)
DM lifestyle mods: Months 1–6: 16 individual sessions with a registered dietitian (RD)
DM lifestyle mods: Months 7–36: Minimum of 1 session every other month with RD; additional support as needed
DM lifestyle mods: Focus of sessions Review food & activity records; Problem-solve difficulties; Praise participant's effort
Modest wt loss & DM modest wt loss reduces incidence of new-onset DM in at-risk popn
When to Start Insulin: T2DM: Insulin can: (when used in adequate doses) decrease any level of elevated A1C to, or close to, the therapeutic goal
When to Start Insulin: T2DM: insulin max dose Unlike other blood glucose–lowering medx, there is no max dose of insulin beyond which a tx effect will not occur
When to Start Insulin: T2DM: Large insulin doses Relatively lg doses of insulin (1 unit/kg), cf w/ those required to tx T1DM, may be necessary to overcome the insulin resistance of T2DM and lower A1C to the target level
MOA: Biguanides Decrease hepatic glucose output/gluconeogenesis. Increase skeletal muscle uptake of glucose
MOA: TZDs Mx & adipose tissue: decrease insulin resistance, increase insulin sensitivity. Increase glucose uptake. Inhibit hepatic glucose production
MOA: Sulfonylurea & Repaglinide (eg, glipizide) Pancreas: increase insulin secretion
GLP-1 is secreted from: L-cells of the jejunum & ileum
GLP-1 stimulates glucose-dependent insulin secretion; suppresses glucagon secretion; slows gastric emptying; leads to reduction in food intake; increases insulin sensitivity
GLP-1: long-term effects in animal models increase in beta cell mass; improved beta fn
Contraindications to continuing certain oral DM agents Worsened hepatic fn; advanced CHF
Oral DM agents: If creatinine >1.5 (1.4): stop metformin
Oral DM agents: Contrast dye load / cardiac catheterization: hold metformin
Target/recommendations: HbA1c target <7.0; <6.0 if poss w/o inducing hypoglycemia
Target/recommendations: BP <130/80 (ACEI / ARB)
Target/recommendations: Lipids LDL <100 (<70 optimal); HDL >40 M, >50 F; TG <150; statin for CV hx or >40 yo to lower LDL 30-40%
Target/recommendations: ASA >40 yo or other risk factors; all w/ CV hx
Target/recommendations: ACEI > 55 yo w/ other CV risk factor
Abx tx for diabetic foot (ulcer <2 cm) TMP-SMX-DS plus Pen VK
MOA: Alpha-glucosidase inhibitors (Precose, Glyset) decrease glucose (starch) absorption in intestines
Tx for impaired insulin secretion (ie, secretagogues) = Sulfonylureas (glyburide, glimepiride, glipizide). Meglitinides (repaglinide/Prandin, nateglinide/Starlix). Insulin
Tx for insulin resistance = biguanides; TZDs
Tx for decreased glucose absorption = alpha-glucosidase inhibitors
Eruptive xanthomas Occur when TGs are very high. on flexor surface of limbs & buttocks. -> skin infxns
GLP-1 agonist (secretins) names (2) = exenatide (Byetta) and liraglutide (Victoza)
Pramlintide = Synthetic amylin (beta cell hormone) analogue. Given SQ
DPP-4 inhibitors (incretins) MOA Prolong action of endogenous GLP-1 (sitagliptin and saxagliptin). Slow the inactivation of incretin hormones released from intestine. Inhibit post-prandial glucagon
Earliest sign of DM nephropathy microalbuminura (may -> nephrotic syndrome, hypoalbuminemia, edema, worse GFR)
Meglitinide MOA nonsulfonurea agent that stimulates release of insulin from pancreas. Natglinide (Starlix), repaglinide (Prandin)
Created by: Abarnard