diabetes

Question 1

what happens to the islets in T2D?

Answer 1

alpha cells secrete an abnormally high amount of glucagon, there are fewer beta cells as the mass declines over time. they secrete insufficient levels of insulin over time.

Question 2

what is marker of T2D after meals?q

Answer 2

there is a blunted insulin response and an overzealous glucagon release.

Question 3

what are incretins?

Answer 3

synthesized in L cells in the ileum and colon. they are produced in response to incoming nutrients and stimulate insulin secretion.

Question 4

what is the most important incretin?

Answer 4

glucagon-like peptide 1

Question 5

what are the actions of GLP-1

Answer 5

enhances glucose dependent insulin secretion. slaws gastric emptying. suppresses glucagon secretion. promotes satiety. receptors are found on islet cells and CNS.

Question 6

what happens to uncertain secretion during T2D?

Answer 6

it is reduced.

Question 7

when to treat T2D with metformin?

Answer 7

at the time of diagnosis.

Question 8

when to treat T2D with insulin?

Answer 8

patients with marked symptoms or elevated blood glucose or A1c levels.

Question 9

what class is metformin?

Answer 9

biguanide

Question 10

metformin mechanism?

Answer 10

activates AMP-kinase and inhibits mito isoform of glycerophosphate dehydrogenase. decreases hepatic glucose production

Question 11

what are the advantages of metformin?

Answer 11

low cost, no weight gain, no hypoglycemia, reduction in cardiovascular and mortality risks.

Question 12

what class for glibenclamide/glyburide, glipizide, gliclazide, glimepiride

Answer 12

sulfonylurea

Question 13

mechanism for the sulfonylureas

Answer 13

closes the KATP channel on beta cell membranes. and increases insulin secretion.

Question 14

side effects for metformin

Answer 14

GI side effects, lactic acidosis, b12 deficiency, contraindicated with renal malfunction.

Question 15

disadvantages of sulfonylurea

Answer 15

there is hypoglycemia risk, weight gain, may blunt myocardial ischemic preconditioning.

Question 16

class for repaglinide and nateglinide

Answer 16

meglitinides

Question 17

mechanism for the meglitinides

Answer 17

closes KATP channels on the beta cell membranes. and increases insulin secretion

Question 18

disadvantages of the meglitinides

Answer 18

there is hypoglycemia risk, weight gain, may blunt myocardial ischemic preconditioning.

Question 19

class for pioglitazone

Answer 19

thiazolidinediones

Question 20

mechanism for pioglitazone

Answer 20

activates the nuclear transcription factor PPAR-gamma. to increase the peripheral insulin sensitivity

Question 21

advantages of pioglitazone

Answer 21

no hypoglycemia. increases HDL, decreases triglycerides, reduction in MI

Question 22

disadvantages of pioglitazone

Answer 22

weight gain, edema, HF, bone fractures, increased bladder cancer.

Question 23

class for rosiglitazone

Answer 23

thiazolidinediones

Question 24

mechanism for rosiglitazone

Answer 24

activates the nuclear transcription factor PPAR-gamma. to increase the peripheral insulin sensitivity

Question 25

advantages to rosiglitazone

Answer 25

no hypoglycemia

Question 26

disadvantages to rosiglitazone

Answer 26

increases in LDL, weight gain, edema, HF, none fractures, cardiovascular events, no CHF patients

Question 27

class for acarbose and miglitol

Answer 27

glucosidase inhibitors.

Question 28

mechanism for acarbose and miglitol

Answer 28

inhibits the intestinal glucosidase and slows intestinal carbohydrate metabolism

Question 29

advantages of acarbose and miglitol

Answer 29

not systemic, decreases the rise in postprandial glucose. weight neutral. no hypoglycemia

Question 30

disadvantages of acarbose and miglitol

Answer 30

GI, dosing frquency, only modest reduction in the A1c

Question 31

class for exenatide, liraglutide, albiglutide, dulaglutide.

Answer 31

GLP-1 receptor angonists. activates the incretin receptors.

Question 32

mechanism for the GLP-1 agonists

Answer 32

activates the receptor, increases insulin, decreases glucagon, slows gastric emptying increases satiety.

Question 33

advantages of the GLP-1 agonists

Answer 33

weight reduction and potential for the beat-cell mass regeneration.

Question 34

disadvantages of the GLP-1 agonists

Answer 34

GI, pancreatitis, hypoglycemia, caution in RD, C-cell hyperplasia and medullary thyroid tumors. has to be injected.

Question 35

what is the class for sitagliptin, alogliptin, saxaliptin, linagliptin

Answer 35

DPP-4 inhibitors, incretin enhancer

Question 36

mechanism of sitagliptin, alogliptin, saxaliptin, linagliptin

Answer 36

inhibit DPP-4 activity, increases the active GLP1, active GIP, insulin secretion, decreases glucagon.

Question 37

advantages for sitagliptin, alogliptin, saxaliptin, linagliptin

Answer 37

no hypoglycemia, weight neutral.

Question 38

disadvantagres for sitagliptin, alogliptin, saxaliptin, linagliptin

Answer 38

urticaria and angioedema, pancreatitis, long term unknown

Question 39

class for the "flozins"

Answer 39

SGLT2 inhibitors. they reduce the reabsorption in the kidney.

Question 40

advantages to the flozins

Answer 40

weight loss, and no hypoglycemia

Question 41

disadvantages of the flozins

Answer 41

hypokalemia, volume depletion, mycotic infections (UTI), HSR, increased LDL, long term unknown.

Question 42

colesevelem class

Answer 42

bile acid sequester ants. these decrease hepatic glucose production

Question 43

when is hypoglycemia a problem?

Answer 43

more common with sulfonylurea and insulin therapy. more common in T1D. increased risk if over 60, impaired renal function, poor nutrition, liver disease, increased activity, longer duration DM.

Question 44

symptoms of hypglycemia

Answer 44

confusion, slurred speech, dizziness, weakness, shaking, palpitations, nervousness, sweating, extreme hunger, HA, mood or behavior swings, tingling of hands tongue or lips, vision changes, poor coordination, unresponsiveness, unconsciousness, or seizures.

Question 45

what are the treatment recommendations for hypoglycemia

Answer 45

glucose! IF THEY ARE CONSCIOUS. people at high risk for hypo should be given glucagon prescription.

Question 46

when is the glucagon emergency kit given

Answer 46

when the patient is unconscious or unable to swallow.

Question 47

who should always have a script for glucagon?

Answer 47

T1D and severe low blood sugar in T2D.

Question 48

what do we give in the hospital for severe hypoglycemia

Answer 48

IV dextrose

Question 49

amylin

Answer 49

peptide released with insulin from beta cells in response to eating. absent in T1D, variable in T2D. slows gastric emptying, suppresses postprandial glucagon secretion, may reduce appetite.

Question 50

pramlitide

Answer 50

synthetic amylin. inject before meals. for use with insulin. may give weight loss. significant risk for hypoglycemia. GI SE. especially nausea.

Question 51

when is insulin indicated for T2D

Answer 51

glucose toxicity, insufficient endogenous production. contraindication for oral therapy. significant hyperglycemia at presentation. maximum dose of oral agents. surgery, pregnancy, decompensation, serious renal or hepatic disease.

Question 52

rapid acting insulin analogs

Answer 52

lispro insulin, aspart, glulisine,

Question 53

intermediate acting insulin analogs

Answer 53

determir insulin, neutral protamine lispro, neutral protamine aspart.

Question 54

insulin determir characteristics

Answer 54

duration of action dose dependent. lower doses are intermediate acting, higher doses last 24hr. once or twice daily, delayed release from subcut injection site.

Question 55

glargine insulin

Answer 55

long acting, is a basal formulation.

Question 56

insulin storage

Answer 56

refrigeration is best. can be stable at RT for up to one month. never freeze and avoid sunlight.

Question 57

what is lipohypertrophy

Answer 57

atrophy of the subcutaneous fat at the injection site.