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28 Cards in this Set
- Front
- Back
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Preprandial glucose reflects hepatic glucose ___ and hepatic ___ to insulin
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1. production
2. sensitivity |
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Postprandial glucose reflects preprandial glucose, ___ load from meal, insulin __ and ____ in peripheral tissues
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1. glucose load from meal
2, 3. Insulin secretion and insulin sensitivity |
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HbA1C= ___ Hb, b/c the half life of an RBC is about __ days we get a good idea of glycemic control for that period.
Microvascular damage to the eyes, peripheral nerves, and kidneys begins at HbA1C level of __ |
1. glycosylated Hb
2. 60 days 3. 6.7 but the lower the Hb A1C the better |
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Glucagon- produced by __ cells of pancreas
Role? |
1. alpha
2. glucagon mobilized glucose |
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Insulin- produced by __ cells of pancreas
Role? Manner of secretion? |
1. beta
2. insulin stores away glucose in liver and peripheral tissues 3. Physiologically will be basally secreted and will secrete boluses in response glucose loads |
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Amylin- ___ w/ insulin and influences the amt of glucose that appears in the serum by reducing ____ secretion in the postprandial period.
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1. cosecreted
2. by reducing xs glucagon secretion in postprandial period |
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Incretin hormone released in response to food intake. Regulates ___ of glucagon adn insulin secretion
- also encourages proliferation and discourages apoptosis of __. - GIP and GLP 1 -- secreted jejunum cells in response to ___ and ___ meal. These hormones then in turn stimulate ___ secretion and suppress __ secretion, slow gastric emtpying, and ____ beta cell mass & fx, improves ___ sensitivity, and reduces food intake |
1. rate
2. beta cells of pancreas 3,4. fatty and carb-y meal 5. increases insulin 6. suppresses glucagon 7. improves insulin sensitivity |
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Adipokines-- fat cells (especially visceral fat) which release ___, IL 6, which encourage ___ resistance and endothelial dysfx.
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1. angiotensinogen
2. insulin |
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LIspro, aspart, and gluisine- MOA, PK
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MOA: BOLUS insulin, must be adjusted if postprandial glucose is not ideal, small alterations in aa structure counter insulins tendency to aggregate giving very speedy absorption
PK: RAPID acting, 3-4 hrs, convenient before meals |
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Lispro, aspart, and gluisine- AE
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- b/c so RAPID acting, there may some late post prandial hyperglycemia after the effect wears off
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Short acting insulin-MOA, Dosing
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MOA: used as BOLUS insulin post
prandial Dosing: 3-6 hr life-- not often used b/c requires inconvienient administration. Hypoglycemia if meal is delayed for 8 h so may also give late postprandial hypoglycemia |
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NPH- Use, PK, AE
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Use:intermed insulin, basal insulin which lasts for 10-16 hrs. can be mixed w/ other formulatoins
AE: do not mimic basal insulin profile b/c more peaks, variable absorption and less than 24 hr duration of action - unpredictable hyypoglycemia |
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Glargine- Use, PK, When to adjust?
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Use: basal insulin, good b/c fewer nighttime hypoglycemia episodes as compared to NPH
PK: LONG ACTING, >24 hrs -- acidic insulin into basic pH gives gradual release pattern from injection site and a peakless 24 hr profile. Cannot mix w/ other insulin formulations. Adjust: adjust glargine dose if pts FASTING glucose is not ideal |
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Determir- Use, PK
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Use: basal insulin, good b/c fewer nighttime hypoglycemic episodes as compared to NPH
PK: long acting, 16-24 hrs. Slef association and ALBUMIN binding keeps from crossing semi permeable membranes in capillaries |
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Sulfonylureas- MOA, Use
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Use: use w/ a sensitizer if insulin is very high, must have functioning beta cells, used in DM2
MOA: an insulin secretagogue that stimulates both basal and postprandial insulin secretion AE: severe hypoglycemia, weight gian, sulfa allergy |
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Sulfonylureas- Drugs
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- GLImeprimride, GLIpizide XL, GLYburide-- causes CV dz, not used
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Megltinides- Drugs
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Repaglinide, nateglinide
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Repaglinide, nateglinide- Class, MOA
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Class: Meglitinides
MOA: an insulin secretagogue that stimulates both basal and post prandial insulin secretion |
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METFORMIN- CLASS, MOA, Use
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Class: Biguanides
MOA: decreases hepatic glucose production in response to insulin Use: all pts w/ mild hyperglycemia, MUST have insulin already around. Will also cause wt loss, decrease CV risk, decreases LDL adn TGs. Take w/ meals. |
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Metformin- AE, CI
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AE: diarrhea, metallic tase, lactic acidosis
CI: renal dysfx (d/c before IV contrast), congestive heart failure, liver dz |
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Acarbose, migitol- Class, MOA, Use
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Class: Alpha glucosidase inhibitors
MOA: blocks proximal carb absorption in the duodenum Use: pts w/ marked POSTPRANDIAL hyperglycemia, will not work unless pt has this sx |
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Acarbose, migitol- AE
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- flatulence, LFTs,
CI: intestinal or liver dz |
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Rosiglitazone, pioglitazone- Class, MOA
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Class: thiazolidenediones
MOA: bind to nuclea PPAR gamma receptor and enhances the # of GLUT 4 transporters to bring glucose into the cells. THis enhances muscle and adipose tissue response to insulin |
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Rosiglitazone, pioglitazone-Use
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- Must have insulin!! Most effective on the obese with marked insulin resistance.
- Lowers bp, reduces inflammatory cytokines, preserves the β-cells and helps to redistribute fat. - Pioglitazone does a better job at lowering cholesterol than some other agents in its class. |
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Rosiglitazone, pioglitazone- AE, CI
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- edema, wt gain, anemia, liver failure
CI: heart failure adn liver dysfx |
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Exenatide- MOA, PK
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- : analog of GLP-1 that is resistant to breakdown by DPP-IV
- Is like GLP-1 does: lowers postprandial glucose, reduced fasting glucose, persistently lowers HgBA1C and persistently reduces weight Pk: sub Q as pt continues oral meds AE: N/V?D |
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Sitagliptan- MOA, Use
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- MO: reversibly inhibits DDP-IV to enhance the level of incretins (GLP-1 & GIP) for 24hrs
- Does almost all the things GLP-1 does: lowers postprandial glucose, reduced fasting glucose and persistently lowers HgBA1C Use: best as an add-on to metformin |
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If target HbA1C <7% not achieved then?
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- use intensive insulin
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