Brainscape's Knowledge GenomeTM

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


See full index

Boards > Endo Pharm > Flashcards

Endo Pharm Flashcards

0
Q

What is the tx strategy for type II diabetic patients?

A

Diet modification
Exercise/ weight loss
Oral hypoglycemics
Insulin replacement (end-stage)

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

What is the treatment strategy for a type I diabetic?

A

Low sugar diet and insulin replacement

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

What is the MOA of insulin?

A

Bind insulin receptor - tyrosine kinase activity
Causes increased glucose storage as glycogen in liver, muscle
Increased protein synthesis
Potassium uptake (forces potassium into the cells)
Aids in TG storage

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

What are the rapid acting insulins?

A

Lispro
Aspart
Glulisine

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

What is the intermediate acting insulin?

A

NPH

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

What are the long acting insulins?

A

Glargine

Detemir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the toxicities of insulin?

A

Hypoglycemia

Hypersensitivity

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

What is the action of biguanides?

A

Decrease gluconeogenesis
Increase glycolysis
Increase peripheral glucose uptake

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

What are biguanides used for?

A

First line for Type II

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

What is the tox of biguanides?

A 
GI upset
Lactic acidosis (CI in renal failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the MOA of sulfonylureas?

A

Close K channel in beta cell membrane so cell depolarizes and insulin is released via calcium influx

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

What are sulfonylureas used for?

A

Stimulate release of insulin in Type II

Requires some islet fxn

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

What are the side effects of first gen sulfonylureas?

A

Disulfiram-like effects

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

What are the first gen sulfonylureas?

A

Tolbutamide

Chlorpropamide

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

What are the second gen sulfonylureas?

A

Glyburide
Glimepiride
Glipizide

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

What is the tox in second gen sulfonylureas?

A

Hypoglycemia

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

What is the MOA of glitazones?

A

Increase insulin sensitivity in peripheral tissue

Binds PPAR-gamma nuclear transcription regulator

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

What are glitazones used for?

A

Used as monotherapy in type II

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

What is the tox in glitazones?

A

Weight gain
Edema
Hepatotoxicity
Heart failure

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

What is the MOA of alpha glucosidase inhibitors?

A

Inhibit intestinal brush border alpha glucosidase

Delay sugar hydrolysis and glucose absorption so it decreases postprandial hyperglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the alpha glucosidases?

A

Acarbose

Miglitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are alpha glycosidase inhibitors used for?

A

Monotherapy type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the tox of alpha glucosidase inhibitors?

A

GI disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the MOA of amylin analog (pramlintide)?

A

Decreases glucagon

24
Q

What is pramlintide used for?

A

Type I and type II DM

25
Q

What are the side effects of pramlintides?

A

Hypoglycemia
Nausea
Diarrhea

26
Q

What is the MOA of GLP-1 analogs?

A

Increase insulin

Decrease glucagon release

27
Q

What are the GLP-1 analogs?

A

Exenatide

Liraglutide

28
Q

What are GLP-1 analogs used for?

A

Type II DM

29
Q

What are the side effects of GLP1 analogs?

A

Nausea
Vomiting
Pancreatitis

30
Q

What is the MOA of Dpp-4 inhibitors?

A

Increase insulin

Decrease glucagon release

31
Q

What are the Dpp 4 inhibitors?

A

The gliptins
Linagliptin
Saxagliptin
Sitagliptin

32
Q

What are Dpp 4 inhibitors used for?

A

Type II DM

33
Q

What are the side effects of Dpp 4 inhibitors?

A

Mild urinary or respiratory infections

34
Q

What does activation of PPAR- gamma cause?

A

Increase insulin sensitivity

Increased levels of adiponectin

35
Q

What is the MOA of propylthiouracil?

A

Blocks peroxidase thereby inhibiting organification of iodide and coupling of thyroid hormone synthesis
Blocks 5’-deiodinase blocking conversion of T4 to T3

36
Q

What is the MOA of methimazole?

A

Blocks peroxidase thereby inhibiting organification of iodide and coupling of thyroid hormone synthesis

37
Q

What are methimazole and propylthiouracil used for?

A

Hyperthyroid

38
Q

What are the toxicities of propylthiouracil and methimazole?

A 
Skin rash
Agranulocytosis 
Aplastic anemia
Hepatotoxicity (propylthiouracil)
Teratogen (methimazole)
Edema
39
Q

What is GH given for?

A

Turner syndrome and GH deficiency

40
Q

What is octreotide given for?

A 
Acromegaly
Carcinoid
Gastrinoma
Glucagonoma
Esophageal varices
41
Q

What is oxytocin given for?

A

To stimulate labor, uterine contractions, milk-let down

Controls uterine hemorrhage

42
Q

What is desmopressin given for?

A

Central diabetes insipidus

43
Q

What is the MOA of demeclocycline?

A

ADH antagonist

44
Q

What is the demeclocycline used for?

A

SIADH

45
Q

What is the tox of demeclocycline?

A

Nephrogenic DI
Photosensitivity
Abnormalities of bone and teeth

46
Q

What are the glucocorticoids?

A 
Hydrocortisone 
Prednisone
Triamcinolone
Dexamethasone 
Beclomethasone
47
Q

What is the MOA of glucocorticoids?

A

Decreased production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2

48
Q

What is the tox of glucocorticoids?

A

Iatrogenic Cushing’s

49
Q

How do the glitazones work?

A

They increase insulin sensitivity in target tissues by increasing the expression of GLUT4 in target tissues and causes differentiation of pre-adipocytes to adipocytes by up regulating transcription of insulin responsive genes

50
Q

What is repaglinide?

A

A meglinitide derivative, short-acting insulins tropic agent used in type II with diet and exercise. MOA is similar to sulfonylureas but doesn’t cause insulin release when extra cellular glucose is low

51
Q

When should executive be used?

A

For type II diabetics with suboptimal glucose control despite adequate levels of metformin and sulfonylureas

52
Q

Which drugs are known to cause SLE-like syndrome?

A 
Hydralazine 
Procainamide 
Isoniazid 
Minocycline
Quinidine
53
Q

Which insulin is best to decrease postprandial glucose level?

A

Lispro
Aspart
Glulisine
Peak at 45-75 minutes

54
Q

Which insulin is best for IV use DKA?

A

Regular insulin - peak 2-4 hours

55
Q

What is the duration of NPH and why?

A

It is a crystalline suspension of protamine and zinc which prolongs the duration of action. It starts working within 2 hours, peaks at 12 and ends at 18

56
Q

What is the duration of glargine and why?

A

It last 24 hours because it precipitates in the subcutaneous tissue allowing for slow absorption

57
Q

What is the duration of action of detemir and how does it work?

A

It has a fatty acid bound to a losing residue that allows it to bind to albumin and slowly dissociate from there.
It lasts 24 hours and peaks between 3-9

Boards (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions