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Diabetes 2
Endocrine
| Question | Answer |
|---|---|
| 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
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