Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sketchy Pharmacology Notecards > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What receptors are responsible for the release of insulin from beta cells in pancreas?

A

Beta 2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MOA of beta cells release of insulin in response to high serum glucose?

A

Glucose enters the beta cells, causing a rise in ATP, this leads to K channels to close shut, preventing their efflux, the cells depolarize as a result, Ca flows in and insulin vesicles are released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is released in addition to insulin and why?What is the clinical significance of this?

A

C peptide, insulin is placed in the vesicles as pro insulin where it cleaved to insulin and C peptide, we can measure c peptide levels to measure the amount of insulin in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain MOA of insulin on peripheral cells.

A

Binds to its receptor on cell surface membrane, leading to activation of tyrosine kinase, this causes the cell to express GLUT4 receptor to allow glucose to enter cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What other effects does insulin have on metabolism.

A
  1. Increases glycogenesis in liver2. Increase fat synthesis and storage in adipose tissues3. Induces protein synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the effect of insulin on serum [K] and what is the clinical significance of this?

A

Drives up K ions into the cells so it can lead to hypokalemia, can be used to treat hyperkalemia when administered together with glucose to prevent hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name short acting insulins.

A

Glusin, Aspart and Lispro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the properties of short acting insulin?

A

Rapid onset of action, useful for post prandial glycemic control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name intermediate acting insulins

A

Regular insulin and NPH - neutral protamine hagedorn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the properties of intermediate acting insulins?

A

Delayed onset and intermediate duration of action (NPH is more delayed) due to the formation of dimers and hexamers, takes time to breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do we use for diabetic ketoacidosis? what is an adverse effect of this?

A

IV insulin, have to watch out for K levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name long acting insulin and what are their properties.

A

Detemir and Glargine, have long durations of action and provide a steady background level of insulin (glargine has no peak)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA of sulfonyl ureas

A

Bind to ATP-dependent K+ channels on beta cells leading to depolarization of beta cells, lead to calcium influx and release of endogenous insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name first generation sulfonyl ureas

A

tolbutamide, chloropropramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name second generation sulfonyl ureas

A

Glyburide, glipzide and glimeperide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the shortest acting sulfonyl ureas and what is a consequence of this?

A

Glipizide, less risk of development of hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name meglitinides

A

repaglinide, nateglinide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOA of meglitinides

A

MOA similar to sulfonureas bind the ATP-dependent K+ channels on beta cells leading to depolarization, calcium influx and release of endogenous insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which ones mentioned are sulfa drugs

A

Meglitinides are not sulfa drugs, sulfonyl ureas are!

20
Q

What are the adverse effect of meglitinides and sulfanyl ureas

A

Can cause hypoglycemia and weight gain.Sulfanyl ureas lile chloropropramide can cause disulfram like effect with ingestion of alcohol

21
Q

Name GLP 1 agonists.

A

exenatide, liraglutide - tide suffix

22
Q

Explain MOA of GLP1 agonists

A

GLP-1 agonists (exenatide, liraglutide) activate the Glucagon Like Peptide Receptor (GLP-1), this leads to increased insulin release and satiety, decreasing glucagon release and gastric emptying

23
Q

Name DPP4 inhibitors.

A

“-gliptin” suffix of the DPP-4 inhibitors (stigaliptin, saxagliptin, linagliptin

24
Q

MOA of DPP4 inhibitors.

A

Dipeptidyl peptidases inhibit the breakdown of GLP1, DPP-4 inhibitors (gliptins) increase levels of endogenously secreted GLP-1 (increased insulin release and satiety, decreased glucagon release and gastric emptying). All of this helps in decreasing glucose serum levels.

25
Q

What are the effects of GLP1 and DPP4 inhibitors in terms of weight loss?

A

Decrease gastric emptying and allows the development of feeling of early satiety

26
Q

What are the benefits of using GLP1 agonists and DPP4 inhibitors? What are the adverse effects?

A

Does not cause hypoglycemia, GLP1 can cause acute pancreatitis, DPP4 increase risk for upper respiratory infections an nasopharangyitis

27
Q

What is the first line agent for treating diabetes?

A

Lifestyle changes, then have to prescribe metformin if lifestyle changes fail

28
Q

Explain MOA of metformin

A
  1. Inhibits hepatic gluconeogenesis, inhibits mitochondrial enzyme glycerophosphate dehydrogenase (mGPD)2. Increases insulin sensitivity by activating activated protein kinase (AMP)3. Rest of the effects have poorly understood MOA.
29
Q

What are the adverse effects of Metformin

A

It can cause lactic acidosis, especially in ischemic tissue, metformin is not metabolized and excreted by the kidney so renal insufficiency can increase lactic acidosis, also metformin also inhibit lactic acid from entering the liver so it cannot participate in gluconeogenic pathways.Common side effects are GI side effects

30
Q

What benefit does metformin have over sulfonyl ureas and other diabetes drugs?

A

Causes modest weight reduction, does not cause weight gain

31
Q

Name thiazolidinediones

A

“-glitazone” suffixglitazones, rosiglitazone, pioglitazone

32
Q

Thiazolidinediones MOA

A

Thiazolidinedione are ligands of peroxisome proliferator activated receptor gamma (PPARy) an intracellular nuclear receptor that regulates gene transcription causing increased insulin sensitivity, found in muscle, fat, and the liverUpregulate GLUT4 in peripheral tissues

33
Q

How does PPAR gamma increase insulin sensitivity

A

PPAR-y upregulates adiponectin (increased insulin sensitivity and fatty acid oxidation)Also increase the differentiation and number of adipocytes

34
Q

What are the adverse effects of thiazolidinedione

A

Increase triglyceride storage and fatty acid oxidation, lead to decreased serum triglycerides.Cause significant weight gain, fluid retention, edema and decompensated CHF due to the fact that there is increased Na absorption in PCT

35
Q

What is the effect of thiazolidinedione on bones?

A

Increase the risk of atypical extremity fractures especially in women since thiazolidinedione cause loss of bone density

36
Q

What is the duration of time thiazolidinedione exert its effect? and why?

A

Since it modulates gene transcription through a nuclear receptor it can take days to weeks before patients get a better glycemic control

37
Q

Function of amylin

A

Amylin is a polypeptide which released together with insulin, it inhibits the release of glucagon, delays gastric emptying and induces satiety

38
Q

Name a drug that is an amylin analogue

A

Pramlintide

39
Q

When are amylin analogues used?

A

They delay gastric emptying and inhibit glucagon secretions so they are used for both type 1 and 2 diabetes

40
Q

When exactly are amylin analogues used during the course of the day?What are their side effects?

A

Post prandial, GI disturbances and can cause hypoglycemia

41
Q

What is the function of alpha glucosidase?

A

Found in the brush border of intestinal cells, breaks down disaccharides to absorbable monosaccharides

42
Q

Name alpha glucosidase inhibitors

A

Acarbose and Miglitol

43
Q

When can glucosidase inhibitors be used?

A

Post prandial

44
Q

What are the side effects of glucosidase inhibitors?

A

Cause GI side effects (diarrhea, flatulence, abdominal pain) due to fermentation of the undigested carbs by the gut flora so they are not frequently prescribed

45
Q

What is the function of SGLT2?

A

Reabsorption of glucose from tubules in PCT

46
Q

Name SGLT2 inhibitors.

A

“-flozin” suffix Canigflozin, Dapagflozin

47
Q

AE of SGLT2 inhibitors.When are they contraindicated?

A

UTI’s, increased risk of vaginal candidiasis due to increase glucose in urine.Also they can lead to hypotension as they act as osmotic diureticContraindicated in renal insufficiency

Sketchy Pharmacology Notecards (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions