diabetes Flashcards

1
Q

medication classes for type 2 diabetes

A

biguanides
sulfonylureas
meglitinides(non-sulfonylurea secretagogues)
alpha-glucosidase inhibitors
thiazolidinediones (TZDs) aka Glitazones
dipeptidyl peptidase-4 (DPP-4) inhibitors
**insulin may be given in conjunction with any drug from each class above

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2
Q

metformin MOA

A

inhibits glucose production by the liver & decreases insulin resistance

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3
Q

sulfonylureas & meglitinides MOA

A

increase secretion of insulin

keep the ion channels open longer to continue the trigger for insulin release

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4
Q

alpha-glucosidase inhibitors MOA

A

delay absorption of glucose by the intestine

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5
Q

thiazolidinediones (glitazones)

A

decrease insulin resistance
change gene expression so that GLUT receptors are more effecient
-can cause CHF

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6
Q

dipeptidyl peptidase-4 (DPP-4)

A

promote the release of insulin from the pancreas after eating a meal
-slow down enzyme release

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7
Q

switch from oral diabetic medication to insulin when…

A
  • acute infx
  • in-patient surgery requiring NPO
  • pregnancy
  • for tighter glucose control
  • to avoid developing macrosomia
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8
Q

biguanides

A

metformin

-decreases hepatic glucose production, enhances insulin sensitivity in skeletal muscle

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9
Q

Metformin/ Glucophage

A

biguanide
for type II diabetics
MOA- decreases hepatic production of glucose
-similar effficacy as sulfonylureas by slight reduction in pts’s fasting glucose, non-fasting glucose, & HA1C
-may cause modest wt loss
SE- cramping & nausea, reduced by using slow release forms of the drug, metallic taste, LACTIC ACIDOSIS(mb fatal)
-DO NOT USE IN RENAL INSUFFICIENCY PT’s- monitor creatinine lvls in pts
-inc. risk of B12 def.- supplementation w/B-complex should be standard practice

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10
Q

metformin dosing

A
  • 500, 850, 100 mg tabs
  • generally dosed BID
  • usu daily dose 1500-200mg

extended release

  • 500 & 750mg
  • QD
  • 1500-2000mg daily

brand names- glucophage, fortamet- more expensive

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11
Q

sulfonylureas MOA

A

stimulate intact beta cells to release more insulin

  • interacts with ATP-sensitive K channels in the beta cell membrane- blocks them= increased calcium release= more insulin release
  • hypoglycemia is possible SE- particularly in pts with impaired renal or hepatic funx
  • wt gain MC SE
  • genreally ineffective after 5-10 yrs use d/t decline of beta cell funx
  • AVOID IN PT’s W/SULFA ALLERGY
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12
Q

meglitinides

A

AKA- non-sulfonylurea secretagogues
stimulate beta cells to release insulin
-bind to ATP-sensitive K channels= inc insulin release
-wt gain, hypoglycemia
-for combined use with metformin or drugs from glitazone class- avoid combining with sulfonylureas
-rapidly absorbed in GI- blood lvls peak in 30-60 min- rapidly cleared
-taken 3-4 times /day- not taken if a meal is missed
-Nateglinide/ starlix- less effective
-repaglinide/ prandin- equal to sulfonylureas

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13
Q

thiazolidinediones(TZD’s)/ glitazones

A

TZDs/ Glitazones
MOA- improve insulin sensitivity in skeletal muscle cells, fat cells, liver cells, decrease hepatic glucose production
-dosed QD, may take 6-14 wks to achieve full effect
-approved for use as montherapy, or combined with metformin or a sulfonylurea
-INC RISK OF CHF
-red bone density, inc fracture, wt gain- 5-10 lbs

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14
Q

specific examples of TZD’s/glitazones

A

Rosiglitazone/ avandia
pioglitazone/ ACTOS
-both can be used as monotherapy or concurrent with Metformin or sulfonylurea
-only ACTOS approved for concurrent use with insulin
-test liver funx before tx, then retest at 1 & 3 months for any rise in ALT
troglitazone/rezulin- lethal SE & removed from market

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15
Q

Alpha-glucosidase inhibitors

A

MOA- inhibit the alpha-glucosidase enzymes that line the brush border of SI- interfere with hydrolysis of CHO- delays absorp. of glucose & monosaccharides
-must be TAKEN WITH MEALS!
SE- from unabsorbed CHO(osmotic, fermentation)- abd pn, diarrhea, flatulence
-hypoglycemia with these drugs must be treated with glucose, not sucrose
-CI in pts w/GI dz- IBS, colonic ulceration, intestinal obstruction

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16
Q

2 alpha-glucosidase inhibitors

A

acarbose/ precose -high doses can lead to moderate inc transaminase, rarely fatal hepatic failure
miglitol/ glyset

17
Q

Sitagliptin/ Januvia

A

MOA- inhibits dipetidyl peptidase 4(DPP-4) which breaks down GLP-1 & GIP- gastrointestinal hormones that are released in response to a meal= GLP-1 & GIP preservation and potentiates the secretion of insulin & suppresses glucagon. normalizes insulin & glucagon lvls as blood glucose lvls normalize+ less hypoglcemic events than other agents

  • can be combined with metformin, sulfonylurea or TZD- not with insulin
  • 25, 50, 100 mg tabs, 100mg QD is typical dose
18
Q

millers order of drug tx

A

1) metformin
2) metformin + glimepiride or glipizide
3) glimepiride
4) glipizide
5) metformin + amaryl + insulin
6) actos(pioglitazone) last option, but risk of CHF is relevant

19
Q

injectable drugs

A

pramlintide- synthetic amylin

exenatide- synthetic exendin-4(hormone of gila moster saliva)

20
Q

pramlintide/ symlin

A

for both type 1 & 2 diabetes pts
1st drug approved for lowering blood sugar in type 1 diabetes since insulin in the 1920’s
allows for less use of insulin, but still lowers blood sugar lvls, reduces rise in blood sugar after meals
-IV- must be injected separately from insulin
-injected at meal times, dec A1C lvls w/o inc hypoglycemia or wt gain- may promote modest wt loss
SE- nausea which improves overtime as the pt finds optimal dose

21
Q

exenatide/ byetta

A

1st incretin mimetics
-for type 2 diabetes- works on intact beta cells
MOA- inc insulin secretion- only in the presence of elevated blood glucose(= no hypoglycemia)
-hypoglycemia may occur if used in conjunction with another hypoglycemic agent like sulfonylureas

22
Q

insulin

A
required tx for type 1 diabetes
needed in those type 2 diabetics whose lifestyle chx and pharm interventions have failed to control blood glucose lvls
-given SQ, IM, IV- NOT ORAL!(it's a protein hormone- cannot survive proteolytic breakdown). as of 2006 there is a nasal delivery system(exubera)- but was not accepted
-4 categories based on onset of action:
-rapid acting
-short acting
-intermediate acting
-long acting
-combos of the above
23
Q

rapid acting insulin

A
Lispro/ Aspart
Humulog/ Novalog
onset- <0.25hrs (15 min)
peaks- 0.5-1.5hrs
duration- 3-5hrs
24
Q

short acting insulin

regular

A

humulin R
onset- 0.5hrs
peaks- 2-4hrs
duration- 4-12hrs

25
Q

intermediate acting insulin

NPH

A

Humulin N
onset- 1-3hrs
peaks- 6-12hrs
duration- 24-28hrs

26
Q

long acting insulin

A
glargine
Lantus
onset- 4-6hrs
peaks- flat(doesn't peak)
duration- 24hrs
27
Q

insulin dosing methods

A

several common methods:

1) NPH & regular insulin before breakfast & dinner
2) regular insulin before meals, NPH or ultralente in afternoon
3) lispro for rapid onset of effects before meals ~15min before meals
4) lantus for prolonged effect to last while sleeping

28
Q

insulin absorption

A

can vary based on injection site-
depends on amount of blood flow to the area, fibrosis of the area(from frequent use)
SE- wt gain is common, hypoglycemia is MC feared SE can lead to seizures, coma & death. hypokalemia may occur from stimulation of K entry into the cells. injection site atrophy possible

29
Q

insulin dosing units

A

initial dose of 0.4-0.6units per Kg/day is typical- divided into doses approximate to normal postprandial insulin peaks & basal release