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Pharm 2 - Exam 2 > Lecture 2 - DM > Flashcards

Lecture 2 - DM Flashcards

1
Q

Ultra Short acting Insulin

A

Lispro
Aspart
Glulisine

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2
Q

Rapid acting insulin

A

Standard

Humulin- R

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3
Q

Intermediate acting insulin

A

Novolin- N

Humulin - N

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4
Q

Long acting insulin

A

Determir

Glargine

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5
Q

What are the adverse effects of insulin?

A

hypoglycemia (<70)

hypersensitivity reaction

no risk found in pregnancy

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6
Q

Primary treatment for Type 1 DM

A

Insulin replacement

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7
Q

Where does normal insulin produced in the pancreas go first after secretion?

A

The liver

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8
Q

“Dawn effect”

A

An increase in glucose in the morning in response to cortisol

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9
Q

What is the first line treatment for DM type 2?

A

Diet restriction and exercise

If that doesnt work move to Metformin

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10
Q

Where is the majority of glucose taken up?

A

In the muscle

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11
Q

What is the MOA of metformin?

A 
Activates AMPK: 
In the liver:
-decreases gluoconeogensis 
-decrease lipogenesis 
-increase fatty acid oxidation

-increase glucose uptake in muscle/fat

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12
Q

What are the contraindications of metformin?

A

In pts with renal dysfunction or severe liver disease

D/c before radiograph producers with contrast dyes d/t potential renal dysfunction

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13
Q

Insulin secretagogues

A

Bind to potassium channel - blocking it in Beta cells —-increase insulin release

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14
Q

Repaglinide

A

Insulin secretagogues - K(ATP) Channel Modulator - Non - Sulfonylureas

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15
Q

TZD

A

Thiazolidinediones (pioglitazone)

Increase insulin sensitivity in target tissues

NOT hypoglycemic

Works on liver o decrease glucose output

Increases glucose utilization in skeletal muscle and adipose

Decrease FFA in adipose

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16
Q

What is the MOA of Repaglinide?

A

Increase insulin release from pancreas beta cells
Bind to SUR on ATP-sensitive beta cell K+ channel

Requires functional beta cells

Rapid absorption/peak insulin 30-60 min
-administer right before meal

17
Q

When do you tell your pt to take repaglinide?

A

Right before meal

18
Q

What are the adverse effects of Thiazolidinediones?

A

Fluid retention - edema, anemia

Weight gain

Decrease bone density

Increase risk of bladder cancer/heart failure?

Not a go to drug unless you have to

19
Q

Which drugs are glucose dependent insulin secretion and why is this a good thing?

A

Exenatide (GLP-1 Mimetic)

Prevents the risk of hypoglycemia

20
Q

What are the adverse effects of GLP-1 Mimetics

A

N/V/D
Increase risk of hypoglycmeia when combined with insulin secretagogues (alone there wouldn’t be this risk)

Acute pancreatitis
May decrease GI absorption of other drugs

Contraindicated in pts with gastroparesis

21
Q

Incretin based agent

A

DDP-4 inhibitors

Sitagliptin

22
Q

What is the MOA of sitagliptin?

A

Prolong endogenous GLP-1 action
Increase glucose mediated insulin secretion

Weight neutral

23
Q

Canagliflozin

A

Newest drugs in treating type 2 DM

Renal SGLT-2 inhibitors

sodium-dependent glucose co-transporter in kidney (prox renal tubule)

inhibition suppresses glucose re-absorption, lowers blood glucose
decrease A1c 1-1.5%

nearly all glucose is reabsorbed in the kidney so we target one of those two transporters and increase excretion glucose in the urine

24
Q

What are the adverse effects of DPP-4 inhibitors?

A

increase risk of hypoglycemia when combined with insulin secretagogues
cleavage not specific to incretins
acute pancreatitis
hepatic failure (can be fatal)
hypersensitivity rx
longer term safety unknown
joint pain that can be severe and disabling

pregnancy: no risk has been found in humans

25
Q

What are the adverse effects of renal SGLT-2 inhibitors?

A 
genital mycotic infections 
recurrent UTIs
hyperkalmeia; hypermagnesemia
hyperphosphatemia
long term safely unknown --increase risk of bone fx?
may lead to ketoacidosis

pregnancy: risk can not be rule out

metabolized by UDP-GT - inducers (rifampin, phenobarbital, phenytoin, ritonavir) can decrease blood levels

26
Q

Acarbose

A

alpha - glucosidase inhibitors

decrease GI glucose absorption
decrease postprandial glycemia (must be taken with meal)

decrease A1c by 0.5-1%

27
Q

What are the adverse effects of alpha - glucosidase inhibitors?

A

abdominal pain; diarrhea; flatulence
alleviated with dose titration/continued use
elevated liver function tests/hepatic failure (acarbose)
increased risk of hypoglycemia when taken with sulfonylureas/insulin

contraindicated in chronic intestinal disease

28
Q

Amylin agonists

A

amylin is released by beta cells to inhibit glucagon release

29
Q

Intermediate vs long acting insulin composition affecting function

A

Intermediate acting (NPH) have protein bound to it that slows its onset down

Detimir (long acting) has fatty acid that binds to albumin to slow it down

30
Q

What is the MOA of TZD?

A

Thiazolidinediones –Pioglitazone

PPAR-gamma ligand in nucleus –alters expression of insulin responsive genes

insulin sensitizer

31
Q

What is the MOA of exenatide?

A

GLP-1 Mimetic –incretin based agent

these increase insulin release in the intestine when glucose is present

must be injected since they are peptide based

32
Q

secreatgogue

A

means they act on the Beta cell to enhance secretion of insulin

these include:
sulfonylureas
nonsulfonylurea secretagogeus
DDP-4 inhibitors (doesn’t work at beta cell but rather prevents the incretins in the intestine from getting degraded, thus they act long at increasing insulin release in response to glucose)

33
Q

sensitizers

A

enhance the effect of insulin
this includes
metformin
TZDs (not an ideal drug d/t SEs)

these drugs dont have the risk of hypoglycemia that secretogogues have since they are simply enhancing the insulin that is already present, and not increasing amount of insulin

34
Q

Which has the greatest risk of hypoglycemia, sulfonlyureas or non-sulfonylureas?

A

sulfonlyureas since they are slower

nons work so fast that the hypoglycemia would be transient at best

35
Q

DDP-4 enzyme

A

degrades incretins in the intestine

DDP4 inhibitors like sitagliptin prevent this degrading thus prolonging the function of incretins (increase insulin release in response to glucose)

36
Q

What do canagliflozin and acarbose have in common?

A

the decrease the amount of glucose present in the blood by decreasing its absorption (acarbose) or reabsoprtion (canagliflozin)

Pharm 2 - Exam 2 (7 decks)

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