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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)

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1
Q

What is the treatment strategy for a type I diabetic?

A

Low sugar diet and insulin replacement

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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

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3
Q

What are the rapid acting insulins?

A

Lispro
Aspart
Glulisine

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4
Q

What is the intermediate acting insulin?

A

NPH

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5
Q

What are the long acting insulins?

A

Glargine

Detemir

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6
Q

What are the toxicities of insulin?

A

Hypoglycemia

Hypersensitivity

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7
Q

What is the action of biguanides?

A

Decrease gluconeogenesis
Increase glycolysis
Increase peripheral glucose uptake

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8
Q

What are biguanides used for?

A

First line for Type II

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9
Q

What is the tox of biguanides?

A 
GI upset
Lactic acidosis (CI in renal failure)
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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

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11
Q

What are sulfonylureas used for?

A

Stimulate release of insulin in Type II

Requires some islet fxn

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12
Q

What are the side effects of first gen sulfonylureas?

A

Disulfiram-like effects

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13
Q

What are the first gen sulfonylureas?

A

Tolbutamide

Chlorpropamide

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14
Q

What are the second gen sulfonylureas?

A

Glyburide
Glimepiride
Glipizide

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15
Q

What is the tox in second gen sulfonylureas?

A

Hypoglycemia

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16
Q

What is the MOA of glitazones?

A

Increase insulin sensitivity in peripheral tissue

Binds PPAR-gamma nuclear transcription regulator

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17
Q

What are glitazones used for?

A

Used as monotherapy in type II

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18
Q

What is the tox in glitazones?

A

Weight gain
Edema
Hepatotoxicity
Heart failure

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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.

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20
Q

What are the alpha glucosidases?

A

Acarbose

Miglitol

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21
Q

What are alpha glycosidase inhibitors used for?

A

Monotherapy type II

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22
Q

What is the tox of alpha glucosidase inhibitors?

A

GI disturbances

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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?

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

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