Pharm For Dm

Front 1

median age of DM onset =

Back 1

12

Front 2

type 2 DM is how much % of DM?

Back 2

85-90

Front 3

when does DM 2 onset generally?

Back 3

>30

Front 4

DM 2 hyperglycemia due to what?

Back 4

insulin resistance.

genetics.

hepatic glucose production.

Beat cell deficiency.

Front 5

beta cell deficiency phase 1 tx?

Back 5

Go to metformin 1st

Go to insulin if more is needed

Front 6

beta cell deficiency in Phase 2 insulin secretion characteristics?

Back 6

(steady insulin secretion as long as there is glucose stimulation).

Front 7

tx for DM type 2

Back 7

a. Diet, exercise and weight loss

b. Oral medications

c. Insulin(as disease progresses and B cell insulin secretion worsens)

Front 8

4 normal functions of insulin

Back 8

1. transport of glucose from blood to cell

2. conversion of glucose to glycogen (glycogenesis)

3. conversion of glucose to fatty acids (lipogenesis)

4. stimulates protein synthesis

Front 9

3 Strategies for controllingblood glucose

Back 9

A. increase circulating insulin levels

B. improve insulin sensitivity

C. regulate glucose production in liver

e. decrease postprandial glucose.

diet and exercise are always essential components

Front 10

screening per ADA begins at what age?

Back 10

45 year old w/ retesting every 3 years.

test earlier with risk factors.

Front 11

2 hour plasma glucose test for DM diagnosis.

2-h plasma glucose ≥ ___ mg/dL (11.1 mmol/L) during an OGTT. 75 g anhydrous glucose dissolved in water.*

Back 11

200

Front 12

Fasting plasma glucose for DM diagnosis.

FPG ≥ ____ mg/dL (7.0 test mmol/L). Fasting is defined as no caloric intake for at least 8 h.*

Back 12

126

Front 13

A1C % test for DM diagnosis

A1C ≥ ___ % (48 mmol/mol). The test should be performed in a laboratory using a method that is NGSP certified and standardized to the Diabetes Control and Complications Trial assay.*

Back 13

6.5

Front 14

In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥ ___ mg/dL (11.1 mmol/L).

Back 14

200

Front 15

where does insulin come from?

Back 15

Pigs. Bovine can give mad cow.

Now a days most insulin is genetically engineered by e coli and techniques using insertion of human AA's.

Front 16

Somogyi effect

Back 16

Nocturnal hypoglycemia. The body secretes glucagon to get more glucose and that ends up giving hyperglycemia in the morning. Add less insulin at night to fix this problem morning .

Front 17

Dawn Phenomenon

Back 17

More common than somogyi

impaired sensitivity. Both dawn and somogyi can happen at the same time. 75% of pt caused by tissue insensitivity to insulin occurring b/w 5am and 8 am.. Maybe due to spikes of GH released at sleep onset. Pt gets a mild hyperglycemia from dawn phenomenon.

Front 18

when to consider insulin for DM type 2

Back 18

if initial treatment if FPG > 250 mg/dL or HbA1c > 10% or ketonuria or symptoms of hyperglycemia)

Front 19

Lispro is what?

Onset time?

Peak effect?

DOA?

Back 19

Insulin

Onset time: 15-30 min

Peak onset time: 0.5-2.5 hour

DOA: 3-6.5 hours

Front 20

Aspart is what?

Onset time?

Peak effect?

DOA?

Back 20

Insulin

Onset time:10-20 minutes

Peak effect: 1-3 hours

DOA: 3-5 hours

Front 21

Glulisine is what?

Onset time?

Peak effect?

DOA?

Back 21

Insulin

Onset time:10-15 minutes

Peak effect: 1-1.5 hours

DOA: 3-5 hours

Front 22

Reular insulin is what?

Onset time?

Peak effect?

DOA?

Back 22

Insulin

Onset time:0.5-1 hour

Peak effect: 1-1.5 hour

DOA: 6-10 hours

Front 23

NPH insulin is what?

Onset time?

Peak effect?

DOA?

Back 23

Insulin

Onset time:1-2 hours

Peak effect: 6-14 hours

DOA: 16-24 hours

Front 24

Glargine is what?

Onset time?

Peak effect?

DOA?

Back 24

long acting Insulin

Onset time:1-2 hours Peak effect: 6-14 hours

DOA: 24 hours

Front 25

detemir is what?

Onset time?

Peak effect?

DOA?

Back 25

long acting Insulin

Onset time:1 hour

Peak effect: none

DOA: 12-24 hours

Front 26

degludecis what?

Onset time?

Peak effect?

DOA?

Back 26

long acting Insulin

Onset time:1 hour

Peak effect: none

DOA: 24 hours

Front 27

Biguanides do what and are used for whaT?

Back 27

metformin

works in the liver to increase glucose uptake).

inhibits gluconeogenesis by liver, increase glucose uptake into muscle, increases insulin receptor sensitivity.

Used for 1st line tx of DM type 2

Front 28

contraindications for taking metformin?

Back 28

1. Contraindications:Cr > 1.5 mg/dL in males and > 1.4 mg/dL in females.

Drug can accumulate and cause lactic acidosis. Hold drug for 48 hours if receiving iodinated radiocontrast. (Creatinine clearance can be “hard stops”/contraindications)

Front 29

precautions with metformin

Back 29

1. Precautions:Use with caution in CHF, hepatic disease, pulmonary disease,MI and with ethanol abuse.

Front 30

advantages to metformin, ADR's and DDI's.

Back 30

1. Advantages– NO weight gain.

ADR's = lactic acidosis, diarrhea, nausea, bloating, metallic taste,anorexia, decreased folate and b12 absorption.

1. DDIs– sulfonylureas (incr hypoglycemia),alcohol (incr lactic acidosis risk), cimetidine, nifedipine, ranitidine,digoxin and vancomycin (all can increase metformin levels)

Front 31

A. Sulfonylureas is what used for what?

Back 31

1. Firstoral agents introduced to market for Type 2 DM – not useful in Type I DM.

1stgeneration –Rarely used now, replaced by second generation. Includes chlorpropamide, tolazamide and tolbutamide.

Front 32

glipizide.

glyburide

glimeripide

MOA?

Back 32

2nd generation Sulfonylureas .

1. MOA– stimulate insulin release from B cells and bind to specific sulfonylurea receptor, also decrease hepatic clearance of insulin. Both effects will therefore increase circulating insulin levels in body.

Front 33

precautions with glipizide. glyburide glimeripide?

Back 33

sulfur containing drugs, avoid in pts allergic to sulfa. May need to adjust doses in renal dysfunction.

Front 34

ADR's glipizide. glyburide & glimepiride?

Back 34

1. ADRs– Hypoglycemia, weight gain, CNS effects, skin reactions, GI effects, hematologic SEs, Chlorpropamide – SIADH and disulfiram-like rxn with alcohol to help with alcoholism. The drug made the alcoholics n/v when they drank alcohol.

Front 35

DDI's with glipizide. glyburide glimeripide?

Back 35

1. DDIsa. hypoglycemia – coumadin, fluconazole,H2 blockers, Mg salts, sulfonamides, tricyclic antidepressants. (If the pt ison a beta blocker you may need to increase the oral glucose stimulating drug like metformin)

b. hyperglycemia – beta blockers, calcium channel blockers, steroids, phenytoin, thiazide diuretics

Front 36

when do you take glipizide. glyburide glimeripide?

Back 36

30 minutes before meals.

Front 37

Meglitinides are what?

Back 37

used to dx DM 2 is one use.

Front 38

repaglinide nateglinide are what?

how do they work?

Back 38

1. stimulates insulin release from B cells, by closing K+ channels and opening Ca2+ channels on B cells- Not useful in Type 1 DM.

Front 39

precautions with Meglitinides?

Back 39

1. :hepatic dysfunction.

can cause weight gain.

Front 40

Thiazolidinediones do what? what do they treat

Back 40

1. Considered 2nd line for Type 2 DM per ADA.:

1. Unique,reduces insulin resistance at target tissue by increasing insulin sensitivity in muscle and adipose. Binds to specific receptors, requires presence of insulin to work. Also decreases hepatic glucose production.

Front 41

precautions with Thiazolidinediones?

Back 41

Liver dysfunction. Monitor LFTs every 2 months for first year and periodically thereafter.

Rosiglitazone has a black box warning for MI.

Front 42

Alpha-glucosidase inhibitors examples and MOA?

Back 42

acarbose and miglitol.

MOA – Reversible inhibitor of alpha glucosidase in the small intestine, therefore interfering with the hydrolysis of complex carbs and dietary disaccharides. Reduces intestinal absorption of starches and disaccharides and slows the absorption of carbohydrates ® lower postprandial glucose.

Front 43

contraindications for alpha-glucosidase inhibitors (Exenatide )?

when to give?

Back 43

IBD, colonic ulceration or intestinal obstruction.

Must be given with first bite of each meal. b. Really poor compliance

Front 44

(Exenatide ) glucagon like peptide 1 receptor agonist MOA

Back 44

1. incretin mimetic agent. Incretinis a peptide hormone released from cells in the gi tract in response to food.It promotes insulin release and inhibits glucagon release thereby lowering postprandial glucose2. Usedas adjunct with other oral antidiabetics in patients who have not receivedoptimal glycemic control; not for use with insulin

Front 45

ADR's of glucagon like peptide 1 receptor agonist?

comments about $$$ and when to take it

Back 45

Exenatide generic name

pancreatitis

$$$$.

Front 46

what is Exenatide/Liraglutide /Dulaglutide/albiglutide made from?

Back 46

gilamonster saliva.

Front 47

Pramlintide MOA?

Back 47

1. human amylin analog; co-secreted with insulin inresponse to food intake

2. Used as adjunct treatment in Type I and Type 2 DMpatients who use insulin at mealtimes and who have failed to achieve glucosecontrol

Front 48

Pramlintide ADR's and price?

Back 48

$$$$$

No weight gain, GI effects, hypoglycemia.

Front 49

Oral dipeptidyl peptidaseIV inhibitors (DPP-4 inhibitors)

example and MOA.

Back 49

sitagliptan , saxagliptin ,linagliptin alogliptin & alogliptin

MOA= enhance the incretin system in the body by blocking the DPP-4 enzyme

Front 50

sitagliptin , saxagliptin ,linagliptin alogliptin & alogliptin indications?

Back 50

indications: 1. Used as an adjunct to diet andexercise in pts with Type 2 DM. Can be used as monotherapy or in combinationwith metformin or glitazones.

Front 51

sitagliptin , saxagliptin ,linagliptin alogliptin & alogliptin comments

Back 51

$$$$$$

less effective at reducing A1C than other drugs on market.

Front 52

Sodium GlucoseCotransporter Type 2 (SGLT-2) Inhibitor examples and MOA

Back 52

dapagliflozin, canagliflozin & empagliflozin

1. MOA:Sodium-glucose co-transporter 2 (SGLT2), expressed in the proximalrenal tubules, is responsible for the majority of the reabsorption of filteredglucose from the tubular lumen. inhibitingSGLT2, reduces reabsorption of filtered glucose and lowers the renal thresholdfor glucose (RTG), and thereby increases urinary glucose excretion. (forcingout glucose through the kidneys)

Front 53

ADR's of dapagliflozin, canagliflozin & empagliflozin and indications?

Back 53

Lots of glucose in the urine so more UTI's.

tx for type 2 DM.

Front 54

Janumet is a combination drug and what is in it?

Back 54

Januvia + metformin

Front 55

Kombiglyze is a combination drug and what is in it?

Back 55

Onglyza + metformin

Front 56

Glucovance is a combination drug and what is in it?

Back 56

glyburide + metformin

Front 57

Jentadueto is a combination drug and what is in it?

Back 57

linagliptin plus metformin hydrochloride)

Front 58

Drugsthat can raise blood glucose?

Back 58

A. Hyperglycemia - thiazide diuretics

, thyroidhormones,

oral contraceptives,

sympathomimetics,

niacin,

INH,

phenothiazines,

corticosteroids

Front 59

Drugs that can lower blood glucose ?

Back 59

probenecid,

rifampin,

ASA,

sulfonamides