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pharm unit 5 > diabetes > Flashcards

diabetes Flashcards

1
Q

what happens to the islets in T2D?

A

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.

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2
Q

what is marker of T2D after meals?q

A

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

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3
Q

what are incretins?

A

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

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4
Q

what is the most important incretin?

A

glucagon-like peptide 1

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5
Q

what are the actions of GLP-1

A

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

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6
Q

what happens to uncertain secretion during T2D?

A

it is reduced.

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7
Q

when to treat T2D with metformin?

A

at the time of diagnosis.

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8
Q

when to treat T2D with insulin?

A

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

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9
Q

what class is metformin?

A

biguanide

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10
Q

metformin mechanism?

A

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

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11
Q

what are the advantages of metformin?

A

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

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12
Q

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

A

sulfonylurea

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13
Q

mechanism for the sulfonylureas

A

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

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14
Q

side effects for metformin

A

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

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15
Q

disadvantages of sulfonylurea

A

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

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16
Q

class for repaglinide and nateglinide

A

meglitinides

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17
Q

mechanism for the meglitinides

A

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

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18
Q

disadvantages of the meglitinides

A

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

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19
Q

class for pioglitazone

A

thiazolidinediones

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20
Q

mechanism for pioglitazone

A

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

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21
Q

advantages of pioglitazone

A

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

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22
Q

disadvantages of pioglitazone

A

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

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23
Q

class for rosiglitazone

A

thiazolidinediones

24
Q

mechanism for rosiglitazone

A

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

25
Q

advantages to rosiglitazone

A

no hypoglycemia

26
Q

disadvantages to rosiglitazone

A

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

27
Q

class for acarbose and miglitol

A

glucosidase inhibitors.

28
Q

mechanism for acarbose and miglitol

A

inhibits the intestinal glucosidase and slows intestinal carbohydrate metabolism

29
Q

advantages of acarbose and miglitol

A

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

30
Q

disadvantages of acarbose and miglitol

A

GI, dosing frquency, only modest reduction in the A1c

31
Q

class for exenatide, liraglutide, albiglutide, dulaglutide.

A

GLP-1 receptor angonists. activates the incretin receptors.

32
Q

mechanism for the GLP-1 agonists

A

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

33
Q

advantages of the GLP-1 agonists

A

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

34
Q

disadvantages of the GLP-1 agonists

A

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

35
Q

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

A

DPP-4 inhibitors, incretin enhancer

36
Q

mechanism of sitagliptin, alogliptin, saxaliptin, linagliptin

A

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

37
Q

advantages for sitagliptin, alogliptin, saxaliptin, linagliptin

A

no hypoglycemia, weight neutral.

38
Q

disadvantagres for sitagliptin, alogliptin, saxaliptin, linagliptin

A

urticaria and angioedema, pancreatitis, long term unknown

39
Q

class for the “flozins”

A

SGLT2 inhibitors. they reduce the reabsorption in the kidney.

40
Q

advantages to the flozins

A

weight loss, and no hypoglycemia

41
Q

disadvantages of the flozins

A

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

42
Q

colesevelem class

A

bile acid sequester ants. these decrease hepatic glucose production

43
Q

when is hypoglycemia a problem?

A

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.

44
Q

symptoms of hypglycemia

A

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.

45
Q

what are the treatment recommendations for hypoglycemia

A

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

46
Q

when is the glucagon emergency kit given

A

when the patient is unconscious or unable to swallow.

47
Q

who should always have a script for glucagon?

A

T1D and severe low blood sugar in T2D.

48
Q

what do we give in the hospital for severe hypoglycemia

A

IV dextrose

49
Q

amylin

A

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.

50
Q

pramlitide

A

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

51
Q

when is insulin indicated for T2D

A

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.

52
Q

rapid acting insulin analogs

A

lispro insulin, aspart, glulisine,

53
Q

intermediate acting insulin analogs

A

determir insulin, neutral protamine lispro, neutral protamine aspart.

54
Q

insulin determir characteristics

A

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

55
Q

glargine insulin

A

long acting, is a basal formulation.

56
Q

insulin storage

A

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

57
Q

what is lipohypertrophy

A

atrophy of the subcutaneous fat at the injection site.

pharm unit 5 (12 decks)

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