Endo 2: 7 Maloney Dm Drugs

Front 1

What are some examples of insulin preparations? 4

Back 1

1. Rapid acting = Insulin Aspart
2. Short Acting = Regular Humulin R
3. Intermediate Acting Insulin = NPH Humulin N
4. Long Acting Insulin = Insulin Glargine

Front 2

What is the onset of action, peak effect, and duration of Insulin aspart?

Back 2

1. 15 min onset
2. 0.6 hr peak
3. 3-5 hrs duration

Front 3

What is the onset of action, peak effect, and duration of Regular Insulin?

Back 3

1. 30-60 min onset
2. 1.5-4 hr peak
3. 5-8 hr duration

Front 4

What is the onset of action, peak effect, and duration of NPH Insulin?

Back 4

1. 1 - 1.5 hr onset
2. 6-12hr peak
3. 18-24 hr duration

Front 5

What is the onset of action, peak effect, and duration of Insulin glargine?

Back 5

1. 1 hr onset
2. 5-24 hr peak
3. 24 hr duration

Front 6

What is an example of an insulin regimen that incorporates the meal spikes of insulin as well as the basal level?

Back 6

1. Take a long acting insulin (eg glargine) to cover your basal rate
2. Take rapid acting insulin (eg aspart) before meals to cover the carbohydrates (aka glucose) in the meal

Front 7

What are the two ways to get insulin into the body and how can they be used?

Back 7

1. Injections
- Intermediate or long acting insulin for basal insulin
- Meal bolus with a rapid or short acting insulin
2. Insulin pump
- Rapid acting insulin only
- Continuous basal rate
- Meal bolus

Front 8

What are some adverse effects of insulin therapy? 3

Back 8

1. Insulin allergy or resistance
2. Lipohypertrophy
3. Hypoglycemia

Front 9

What is insulin allergy? Does this still happen with human and analog insulins?

Back 9

Insulin allergy is an immediate type hypersensitivity, is local or systemic urticaria results from histamine release from tissue mast cells sensitized by anti-insulin IgE antibodies. In severe cases, anaphylaxis results.

Because sensitivity is often to noninsulin protein contaminants, the human and analog insulins have markedly reduced the incidence of insulin allergy, especially local reactions.

Front 10

How does lipohypertrophy develop with insulin?

Back 10

if a pt repeatedly injects the same site

Front 11

How does insulin resistance develop?

Back 11

A low titer of circulating IgG anti-insulin antibodies that neutralize the action of insulin. Rarely, it may be associated with other systemic autoimmune processes such as lupus erythematosus.

Front 12

What are some sx of hypoglycemia that result from the activation of the SNS and could be seen in the adverse rxns of insulin? 6

Back 12

1. Sweating
2. Hunger
3. Paresthesias
4. Palpitations
5. Tremor
6. Anxiety

Front 13

What are some sx of hypoglycemia that result from insufficient glucose for the brain and could be seen in the adverse rxns of insulin? 6

Back 13

1. Difficulty concentrating
2. Confusion
3. Weakness
4. Drowsiness
5. Blurred vision
6. Loss of consciousness

Front 14

How do you treat hypoglycemia from an insulin overdose? 4

Back 14

1. Eat something: cookies, candy, orange juice
2. Glucose tablets
3. IV glucose
4. Glucagon (injected subcutaneous - take it anywhere)

Front 15

What does glucagon do? 2

Back 15

Increase glycogenolyis
Increase gluconeogensis

Front 16

What results from low blood glucose?

Back 16

- Low blood glucose stimulates alpha cells
- The alpha cells produce glucagon
- The glucagon goes to the liver: inc glycogenolysis and inc gluconeogenesis
- These produce glucose

Front 17

What happens with Type II DM?

Back 17

1. Insulin resistance
2. Reduced GLP-1 secretion -> helps reg blood glucose levels and secreted when you eat.
3. Pancreatic beta cell dysfunction -> Reduced insulin secretion and reduced amylin secretion

Front 18

What are the oral antidiabetic drugs? 7

Back 18

1. Biguanides (Metformin)
2. Meglitinides
3. Sulfonylureas
4. Thiazolidinediones
5. Incretin mimetics
6. Amylin analog
7. a-glucosidase inhibitors

Front 19

A 52-year-old male is newly diagnosed with type 2 diabetes mellitus. He begins lifestyle modifications. What will be the initial drug therapy for this patient?

Back 19

Biguanides (Metformin) - it will tx the insulin resistance from type II DM

Front 20

What is the first line drug for the tx of Type II diabetes? KNOW!

Back 20

Biguanides - Metformin

Front 21

What is the first line tx for Type I diabetes?

Back 21

Insulin.

Front 22

What is the MOA of Biguanide (Metformin)?

Back 22

It targets the insulin resistance from type II DM and is ineffective in the absence of insulin.

In skeletal muscle and adipose tissue there is impaired insulin induced glucose uptake and clearance. And in the liver, there is a failure of insulin to suppress excessive heptic glucose production.

Metformin (Biguanide) activates AMPK an intracellular signal of depleted cellular energy stores that has been implicated in stimulation of skeletal muscle glucose uptake and inhibition of hepatic gluconeogenesis.

Front 23

What does insulin do to skeletal muscle and liver?

Back 23

1. skeletal muscle - inc glucose uptake
2. liver - dec glucose release

Front 24

MOA summary of Metformin - Biguanide? In the liver (2) and the skeletal m. and adipose (3)

Back 24

1. Liver
Decrease hepatic glucose output - inc glycogen stores and alleviating hyperglycemia
Probably reduces gluconeogenesis
2. Skeletal muscle and adipose tissue
Enhances insulin stimulated glucose uptake
Enhances utilization of glucose
Decreases insulin resistance

Front 25

What will happen to serum insulin concentrations with metformin?

Back 25

decrease slightly

Front 26

What will happen to post-prandial glucose concentrations with metformin?

Back 26

Decrease. It is an “insulin sensitizer” because glucose levels improve without stimulation of insulin secretion

Front 27

What is important for shutting down glucose release from the liver postprandially?

Back 27

Insulin!

Front 28

What happens when you consume food (carbs)? (alpha cells, beta cells, and liver) How does Metformin change this reaction?

Back 28

Blood glucose inc. causing the alpha cell to secrete less glucagon and the beta cell to secrete more insulin. The liver in turn releases less glucose. However, with Metformin there is an even greater neg effect on the liver to release even smaller amounts of glucose.

Front 29

What will happen to fasting blood glucose (FBG) levels with metformin?

Back 29

Decrease. Usually while fasting the alpha cell is releasing more glucagon, while the beta cell is releasing less insulin. The liver releases more glucose. However with Metformin the liver does not release as much glucose.

Front 30

With Type II DM is there an increase or decrease in postprandial and fasting glucagon levels? What about glucose levels?

Back 30

With T2DM there is an increase in both postprandial and fasting glucagon levels. And a dec in both postprandial and fasting glucose.

Front 31

What are the pharmacokinetics of Metformin (Biguanide)? When do you take it?

Back 31

1. excreted in the urine
2. half life = 2 hrs
3. Given 2-3/day w/ meals to prevent side effects

Front 32

What is the clinical use of metformin?

Back 32

1. T2DM
2. Lower the risk for developing T2DM in pre-diabetic pts ( but doesn't work as well as lifestyle changes)

Front 33

What are the adverse effects of Metformin (Biguanide)? 4

Back 33

1. D/V/ anorexia
2. metallic taste
3. lactic acidosis (rare)
4. megaloblastic anemia from impaired absorption of B12 (rare)

Front 34

Is lactate produced from aerobic or anaerobic glucose metabolism?

Back 34

anaerobic

Front 35

How can lactic acidosis occur?

Back 35

If production exceeds utilization, primarily in the liver, the anion gap increases and a state of lactic acidosis exist. Lactic acidosis is most often due to circulatory failure, hypoxia, and mitochondial dysfunction resulting in decreased tissue ATP (type A lactic acidosis). The result is increased anaerobic glycolysis and rate of reactinon of pyruvate to lactate.

Front 36

How could metformin biguanide cause lactic acidosis?

Back 36

Biguanides act by fixation to mitochondrial membranes, leading to lower intracellular adenosine triphosphate and higher adenosine monophosphate concentrations. Glucose is metabolized anaerobically. The resulting pyruvate is reduced to lactate, which is usually metabolized quickly in the liver. The patient might show a moderate lactatemia but no lactic acidosis. If this mechanism fails, severe lactic acidosis will develop, followed by multiple-organ dysfunction, a complication associated with a poor prognosis

Front 37

Metformin (Biguanide) is contraindicated with...4

Back 37

1. Renal disease *major concern*
2. Hepatic disease or alcohol abuse
3. lactic acidosis
4. dec tissue perfusion or hemodynamic instability (acute MI, lect ventricular failure, hypoxic lung disease, or septicemia)

Front 38

What should be discontinued before IV contrast media or surgery? and why?

Back 38

Metformin or Biguanide b/c they predispose to lactic acidosis.

Front 39

While lactic acidosis is very rare or essentially zero without a predisposing condition, why is this such a big deal?

Back 39

Potentially fatal
High number of people have a contraindication

Front 40

Two of the biggest concerns in treating type 2 diabetes mellitus is whether or not the drug causes hypoglycemia or weight gain. What effect will metformin most likely have on these parameters?

Back 40

- Doesn’t cause hypoglycemia
- Causes either weight loss or stabilization

Front 41

What are some "extra positive" Metformin (Biguanide) effects? 5

Back 41

1. No hypoglycemia
2. Decrease circulating insulin levels
3. Weight loss or stabilization
- Absence of hyperinsulinemic effects
- GI upset – less food intake
4. Shown to prevent macrovascular complications
5. Decrease TG, total and LDL-C
- Decrease VLDL synthesis

Front 42

If your patient developed significant renal impairment or their blood glucose level was not adequately controlled with metformin, what can you use?

Back 42

Pretty much any of the other drugs except rosiglitazone

Front 43

What part of the T2DM web does thiazolidinedione target?

Back 43

insulin resistance, enhance the action of insulin at target tissues

Front 44

Thiazolidinediones aka - TZDs or Glitazones. What are the agents? 2

Back 44

1. Pioglitazone (Actos)
2. Rosiglitazone (Avandia)

Front 45

What is the MOA for Thiazolidinediones (glitazones)?

Back 45

Stimulate peroxisome proliferator-activated receptor-g (PPAR-g)

Front 46

What is peroxisome proliferator-activated receptor-gamma (PPAR-gamma)?

Back 46

Intracellular receptor that increases transcription

Front 47

Where is PPAR-g located? Function?

Back 47

Lots in adipose tissue and some in skeletal muscle and liver.

- Serves as the master regulator of adipose cell differentiation and plays an important role in lipid metabolism. The increased storage of fatty acids in adipose tissue allows other tissues – such as the liver – to lower their fat content, lower their glucose production, and increase their insulin sensitivity.

Front 48

What is the thazolidinediones' (glitazones) end result in adipose, muscle, and liver tissue?

Back 48

1. Adipose tissue
Increased insulin stimulated glucose uptake
Lower free fatty acids
2. Muscle
Increased insulin stimulated glucose uptake
3. Liver
Inhibit gluconeogenesis (improves insulin-mediated suppression of hepatic glucose production)

Front 49

What is the MOA of thiazolidinediones?(glitazones) 5

Back 49

1. Liver, skeletal m., and adipose tissue
2. activates PPAR-gamma
3. inc transcription of GLUT4
4. inc uptake and utilization of glucose in adipose and skeletal m.
5. in the liver, it inhibits gluconeogenesis

Front 50

What happens to insulin resistance with thiazolidiones (glitazones) ?

Back 50

dec

Front 51

Is insulin required for the glucose lowering effect of pioglitazone?

Back 51

yes,

Front 52

What is the clinical use of Thiazolidinediones (glitazones)? When do you take it?

Back 52

1. T2DM - effective in dec both fasting and postprandial glucose
2. taken once a day

Front 53

Will pioglitazone tend to cause hypoglycemia?

Back 53

Pancreas shuts off insulin production so it will not cause this. no.

Front 54

Will Thiazolidinediones (glitazones) cause weight gain?

Back 54

Yes, it could be adipose tissue mass or fluid retenton.

1. glitazone => PPAR-y activation => differentiation of pre-adipocytes into mature fat cells => weight gain

2. glitazone => PPAR-y activation => collecting tubules => inc activity of Na channels => Na reabsorption => edema => wt gain

Front 55

Would you use pioglitazone in a patient with bad heart failure?

Back 55

No, b/c of the edema.

Front 56

Will Thiazolidinediones (glitazones) cause dec bone density and inc bone fractures?

Back 56

Yes, glitazone => PPAR-y activation => Bone => bone marrow stromal cells are diverted from osteoblast lineage into the adipocyte lineage => more fractures.

Front 57

What are the 5 adverse effects of Thiazolidinediones (glitazones)?

Back 57

1. Fluid retention - Contraindicated in NYHA Class III and IV heart failure
2. Weight gain
3. Increased risk fracture - Women only
4. Anemia
5. Hepatotoxicity - Troglitazone taken off the market
Newer TZDs less hepatotoxicity

Front 58

Which Thiazolidinediones (glitazones) has very restricted use and why?

Back 58

Rosiglitazone b/c Data suggesting an increased risk of cardiovascular events, such as myocardial infraction and stroke

Front 59

Where do the Sulfonylureas and the Meglitinides target in T2DM?

Back 59

Reduced insulin secretion

Front 60

What are the sulfonylurea drugs? 3

Back 60

1. Glimepiride
2. Glipizide
3. Glyburide

These are the second generation, the first gen. is no longer used.

Front 61

The release of insulin from pancreatic beta cells summary. 6

Back 61

1. Glucose enters pancreatic beta cells via GLUT 2.
2. Glucose metabolism generates ATP and inc the intracellular ATP/ADP ratio.
3. This ratio modulates the activity of the ATP sensitive K channel on the beta cell plasma membrane.
4. A high intracellular ATP/ADP ratio closes the channel.
5. This depolarizes the cell, which opens a voltage gated Ca channel on the plasma membrane.
6. The increase in intracellular Ca stimulates exocytosis of insulin containing vesicles, thereby releasing insulin.

Front 62

MOA of sulfonylurea Drugs 3

Back 62

1. The K channel of pancreatic beta cells contains a subunit that is a receptor for sulfonylureas
2. Binding causes K channel to close, preventing its efflux
3. This depolarizes the cell, opening a voltage gated Ca channel that causes activates the secretion of insulin

Front 63

Do sulfonylureas have an effect on pulsatile secretion of insulin or basal? 2

Back 63

- increases the amount of insulin secreted with each pulse, but doesn't inc the frequency of pulses
- no effecton basal insulin secretion

Front 64

A person with type 2 diabetes took glipizide which increased insulin release from pancreatic b cells. What effect will that have on glucagon secretion from pancreatic a cells?

Back 64

dec

Front 65

What is the major and minor roles of sulfonylurea drugs?

Back 65

1. major role - stimulates insulin release from the pancreatic B cells
2. minor role - dec glucagon secretion - from enhanced release of both insulin and somatostatin

Front 66

Describe the clinical uses of Sulfonylurea drugs. Why is it used? When do you take it? Why do ppl stop taking it?

Back 66

1. T2DM
2. once a day
3. this drug usually fails or stops working in 1-2 yrs

Front 67

Will a sulfonylurea cause hypoglycemia and weight gain?

Back 67

Yes, hypoglycemia and weight gain.

Front 68

What are the adverse effects of Sulfonylurea Drugs? 5

Back 68

1. N/V
2. Allergic skin rxns
3. Cholestatic jaundice
4. Leukopenia, thrombocytopenia, hemolytic anemia
5. hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)

Front 69

What are the meglitinide drugs? 2

Back 69

1. Repaglinide
2. Nateglinide

Front 70

What is the MOA of Meglitinide (Repaglinide and Nateglinide) drugs?

Back 70

- Binds to a different site on the channel subunit than the sulfonylureas
- Inhibit the ATP-sensitive K channels in the same manner as the sulfonylureas.

Front 71

Meglitinide (Repaglinide and Nateglinide) drugs Pharmacokinetics?

Back 71

1. very fast onset: 15-30 min
2. short duration - major effect is reduce postprandial hyperglycemia, and should give before meals.
-Nateglinide:
- Repaglinide

Front 72

Meglitinide (Repaglinide and Nateglinide) drugs clinical uses ?

Back 72

1. Type 2 diabetes mellitus
2. Take before meal to control postprandial glycemia

Front 73

What effect will nateglinide have on overnight or fasting glucose levels?

Back 73

Little effect. Nateglinide may have a special role in the treatment of individuals with isolated postprandial hyperglycemia, but it has minimal effect on overnight or fasting glucose levels.

Front 74

Meglitinide (Repaglinide and Nateglinide) drug adverse effect?

Back 74

Hypoglycemia (Lower risk of hypoglycemia than SFU, but weight gain still issue)

Front 75

What portion of the diabetic disease does Incretins (GLP-1 mimetics) target?

Back 75

Reduced GLP-1 secretion

Front 76

How does giving IV glucose differ from giving oral glucose?

Back 76

IV glucose – smaller spike in insulin release vs oral glucose

Front 77

What is GLP-1 and what does it do?

Back 77

- GLP-1 is released from L cells during nutrient absorption in the GI tract.

- Secretion is impaired in type 2 DM

-Liver – decreased glucagon reduces hepatic glucose production (secondary effect from GLP-1)

-High doses – delays gastric emptying and induces satiety.

Front 78

How does the body get rid of GLP-1?

Back 78

Dipeptidyl peptidase-IV
(DPP-IV)

Front 79

How can you increase GLP-1 effects in the body?

Back 79

1. Prevent the metabolism of GLP-1
2. Give GLP-1

Front 80

What are the GLP-1 Mimetics? 5

Back 80

1. GLP-1 agonists
- Exenatide (Byetta)
- Liraglutide (Victoza)
2. DPP-IV inhibitors
- Sitagliptin (Januvia )
- Saxagliptin (Onglyza)
- Linagliptin (Tradjenta)

Front 81

Which can cause a higher concentration of ‘GLP-1’ (greater GLP-1 effect)?

Back 81

Exenatide; You can give a lot of it. Verus just inhibiting the breakdown…there’s only so much there.

Front 82

What is the GLP-1 Mimetics MOA for low and high concentrations of GLP-1? 2

Back 82

1. lower GLP-1 concentrations
- inc glucose stimulated beta cell secretory activity
- reduces alpha cell secretory activity
2. Higher GLP-1 conc
- delays gastric emptying
- inc satety

Front 83

Which agent will most likely reduce appetite and food intake?

Back 83

Exenatide

Front 84

What is the MOA for GLP-1 agonists and DPP-IV inhibitors? 2

Back 84

1. Increases glucose stimulated b-cell secretory activity
2. Reduces a-cell secretory activity

Front 85

What is the MOA for GLP-1 agonists? 2

Back 85

1. Delays gastric emptying
2. Increases satiety

Front 86

What is the advantage of increasing glucose stimulated insulin release?

Back 86

Less chance of causing hypoglycemia...mimics the natural course of the body.

Front 87

What is the advantage of decreasing glucagon release?

Back 87

Reduce hepatic glucose production

Front 88

What is the advantage of delayed gastric emptying?

Back 88

Reduce the postprandial spike in blood glucose levels, by doing this the pancreas can catch up

Front 89

Pharmaco GLP-1 Mimetics: Which 2 drugs are Subcutaneous injections and which 2 drugs are oral?

Back 89

1. Exenatide and Liraglutide - Subcutaneous injections
2. Sitagliptin and Saxagliptin - Oral

Front 90

What is the clinical use of GLP-1 Mimetic? Hint: what the entire lecture is about.

Back 90

T2DM

Front 91

What are the adverse effects of Exenatide and Liraglutide (GLP-1 Mimetic and Incretin)

Back 91

1. Nausea, vomiting
2. Hypoglycemia – low risk
3. Pruritus, urticaria, rash
4. Acute pancreatitis

Front 92

Why do the GLP-1 agonists cause nausea and vomiting?

Back 92

Delay gastric emptying

Front 93

What is an adverse effect associated with Liraglutide in particular along with the N/V, hypoglycemia, pruritus, and acute pancreatitis?

Back 93

Thyroid C-cell carcinoma = black box warning

Front 94

What are the adverse effects of DPP-IV inhibitors? 2

Back 94

1. Hypoglycemia – low risk
2. Allergic reactions - Rash, hives, angioedema, anaphylaxis, Stevens-Johnson syndrome

Front 95

What effect will exenatide and sitagliptin have on body weight?

Back 95

-Exenatide will dec body weight
- Sitagliptin will have no effecton body weight

Front 96

What part of the diabetic disease does Pramlintide target?

Back 96

Reduced amylin secretion from the pancreatic beta cell dysfunction is where Pramlintide takes action.

Front 97

What is amylin?

Back 97

It is secreted by the Pancreatic beta cell just like insulin and results in:
1. delayed gastric emptying
2. inhibited glucagon secretion
3. increased satiety

Slows and reduces the entry of glucose into circulation, working w/ insulin to control glucose levels.

Front 98

What is the Pramlintide agent? (1)

Back 98

Amylin mimetic

Front 99

What are the clinical uses for pramlintide or amylin mmetic?

Back 99

1. Type 1 and type 2 diabetics who inject insulin at mealtimes.
2. Subcutaneous injection

Front 100

What are the adverse effects of Pramlintide or amylin mimetic? 3

Back 100

1. Nausea, vomiting, anorexia
2. Headache
3. Hypoglycemia when combined with insulin

Front 101

What do Exenatide and Amylin have in common?

Back 101

both delay gastric emptying and reduce the postprandial spike in blood glucose levels

Front 102

How else can the postprandial rise in blood glucose level be reduced?

Back 102

a-Glucosidase Inhibitors

Front 103

What are the 2 alpha-Glucosidase inhibitors?

Back 103

1. Acarbose
2. Miglitol

AKA Starch blockers

Front 104

What is the MOA for alpha glucosidase inhibitors? 4

Back 104

1. Reversible inhibitor of a-glucosidase, an enzyme attached to the intestinal brush border.
2. It cleaves complex carbohydrates to yield glucose.
3. By reversibly inhibiting a glucosidase, carbohydrates that would have been absorbed in the upper small intestine are absorbed instead, in smaller quantities, throughout the length of the small intestine.
4. This increases the time required for absorption of carbohydrates which helps reduce the postprandial peak in blood sugar.

Front 105

Will acarbose reduce fasting blood glucose levels?

Back 105

No, Lower post-prandial glucose levels without causing hypoglycemia. Since carbs are absorbed more distally, malabsorption and weight loss do not occur. But increased delivery of carbs to the colon commonly result in increased gas production and GI symptoms.

Front 106

alpha-Glucosidase Inhibitors: clinical use?

Back 106

T2DM

Front 107

What are the adverse effects of alpha glucosidase? 5

Back 107

1. Flatulence
2. Bloating
3. Abdominal discomfort
4. Diarrhea
5. Elevation of liver enzymes

Front 108

what will Metformin do?

Back 108

increase glucose uptake into cells

will also reduce gluconeogenesis and glycogenolysis in the liver
****major mech


HER WORDS:

Liver
Decrease hepatic glucose output
Probably reduces gluconeogenesis
Skeletal muscle and adipose tissue
Enhances insulin stimulated glucose uptake
Enhances utilization of glucose
Decreases insulin resistance

Front 109

Pioglitazone does what?

Back 109

Stimulate peroxisome proliferator-activated receptor-g (PPAR-g)

Present in liver, skeletal muscle and adipose tissue (highest levels)
Activates the nuclear peroxisome proliferator-activated receptor-g (PPAR-g)
This increases transcription of genes such as the glucose transporter, GLUT4.
In adipose tissue and skeletal muscle, it increases uptake and utilization of glucose.
In liver, it inhibits gluconeogenesis.

Class: Thiazolidinediones (TZD)

Front 110

Rosiglitazone does what?

Back 110

Stimulate peroxisome proliferator-activated receptor-g (PPAR-g)

Present in liver, skeletal muscle and adipose tissue (highest levels)
Activates the nuclear peroxisome proliferator-activated receptor-g (PPAR-g)
This increases transcription of genes such as the glucose transporter, GLUT4.
In adipose tissue and skeletal muscle, it increases uptake and utilization of glucose.
In liver, it inhibits gluconeogenesis.

Class: Thiazolidinediones (TZD)
DRUG OF LAST RESORT!

Front 111

what kind of drug is Glimepiride

Back 111

Sulfonylurea Drug

Stimulation of insulin release from pancreatic b cells by glucos

Front 112

what kind of drug is Glipizide

Back 112

Sulfonylurea Drug

Stimulation of insulin release from pancreatic b cells by glucose

Front 113

what kind of drug is Glyburide

Back 113

Sulfonylurea Drug

Stimulation of insulin release from pancreatic b cells by glucose

Front 114

Exenatide is what kind of drug?

Back 114

GLP-1 agonists

Delays gastric emptying
Increases glucose stimulated b-cell secretory activity
Reduces a-cell secretory activity
Inhibits postprandial glucagon secretion
Increases satiety

Front 115

Liraglutide is what kind of drug?

Back 115

GLP-1 agonists

Delays gastric emptying
Increases glucose stimulated b-cell secretory activity
Reduces a-cell secretory activity
Inhibits postprandial glucagon secretion
Increases satiety

causes thyroid cancer

Front 116

Sitagliptin is what kind of drug?

Back 116

DPP-IV inhibitors (increases GLP-1)

Delays gastric emptying
Increases glucose stimulated b-cell secretory activity
Reduces a-cell secretory activity
Inhibits postprandial glucagon secretion
Increases satiety

Front 117

Saxagliptin is what kind of drug?

Back 117

DPP-IV inhibitors (increases GLP-1)

Delays gastric emptying
Increases glucose stimulated b-cell secretory activity
Reduces a-cell secretory activity
Inhibits postprandial glucagon secretion
Increases satiety

Front 118

Pramlintide is what kind of drug?

Back 118

Amylin mimetic

Inhibit glucagon secretion
Delay gastric emptying
Increase satiety

Front 119

what kind of drug is Acarbose

Back 119

a-Glucosidase Inhibitors

Slower absorption of glucose-->reduced postprandial peak in blood glucose

Front 120

what kind of drug is Miglitol

Back 120

a-Glucosidase Inhibitors

Slower absorption of glucose-->reduced postprandial peak in blood glucose

Front 121

Repaglinide is what kind of drug?

Back 121

Meglitinide

Binds to a different site on the channel subunit than the sulfonylurea
Inhibit the ATP-sensitive K channels in the same manner as the sulfonylureas.

INCREASED INSULIN RELEASE

Front 122

Nateglinide is what kind of drug?

Back 122

Meglitinide

Binds to a different site on the channel subunit than the sulfonylurea
Inhibit the ATP-sensitive K channels in the same manner as the sulfonylureas.


INCREASED INSULIN RELEASE