Endo Drugs Step 1

Front 1

What are the 3 rapid acting insulins?

Back 1

LAG:
Lispro, Aspart, Glulisine.

Front 2

Is regular insulin short acting or long acting?

Back 2

Short acting.

Front 3

Name an intermediate-acting insulin.

Back 3

NPH.

Front 4

Name two long-acting insulin drugs.

Back 4

Glargine and determir.

Front 5

What are the clinical uses of insulin drugs?

Back 5

DM 1 and 2, gestational diabetes, life-threatening hyperkalemia, and stress-induced hyperglycemia. 

Front 6

Name a biguanide drug.

Back 6

Metformin.

Front 7

What is the MOA for metformin?

Back 7

Exact mechanism unknown.

Decreases gluconeogenesis,

increases glycolysis,

increases peripheral glucose uptake (insulin sensitivity). 

Front 8

What are the clinical uses of metformin?

Back 8

First line therapy for DM 2. 

Can be used in pts w/o islet function! (unlike sulfonylureas)

Front 9

What are the toxicities of metformin?

Back 9

GI upset, most serious AE is lactic acidosis (therefore contraindicated in renal failure!). 

Front 10

Name some sulfonylurea drugs.

Back 10

1st generation: tolbutamide, chlorpropamide.

2nd generation: glyburide, glimepiride, glipizide.

Front 11

What is the MOA for sulfonylurea drugs?

Back 11

Close K channels in beta cells --> cell depolarizes --> insulin release via increased Ca influx.

Front 12

What are the clinical uses of sulfonylurea drugs?

Back 12

Stimulate release of insulin in DM 2.

Requires some functional islet cells (unlike metformin) so useless in DM 1.

Front 13

What are the toxicities of sulfonylureas?

Back 13

1st generation: disulfiram-like effects.

2nd generation: hypoglycemia.

Front 14

Name some glitazones/thiazolidinediones.

Back 14

Pioglitazone, rosiglitazone.

Front 15

What is the MOA for glitazone/thioglitazidione?

Back 15

Increases insulin sensitivity in peripheral tissue. 

Binds to PPAR-gamma nuclear transcription regulator. (PPAR-gamma regulates fatty acid storage and glucose metabolism. Results in increased insulin sensitivity and levels of adiponectin).

Front 16

What are some clinical uses of glitazones/thiazolidinedione?

Back 16

MONOtherapy for DM 2, or in combination with the above drugs.

Front 17

What are the toxicities of glitazones/thialidinediones?

Back 17

Weight gain.

Hepatotoxicity.

Edema.

Heart failure.

Front 18

Name some alpha-glucosidase inhibitors.

Back 18

Acarbose, and miglitol.

Front 19

What is the MOA for alpha-glucosidase inhibitors?

Back 19

Inhibits intestinal brush-border alpha-glucosidase. 

Delayed sugar hydrolysis and glucose absorption --> decreases post-prandial hyperglycemia. 

Front 20

What are the indications for alpha-glucosidase inhibitors?

Back 20

MONOtherapy for DM 2, or in combination w/the above drugs.

Front 21

What are the toxicities of alpha-glucosidase inhibitors?

Back 21

GI disturbances (unabsorbed sugars cause osmotic diuresis).

Front 22

Name an amylin analog.

Back 22

Pramlintide.

Front 23

What is the MOA of pramlintide? 

Back 23

Decreases glucagone.

Front 24

What are the clinical uses of pramlintide?

Back 24

**Used for DM 1 AND 2. 

Front 25

What are the toxicities of pramlintide?

Back 25

Hypoglycemia,

nausea,

diarrhea.

Front 26

Name some GLP-1 analogs.

Back 26

Exenatide, liraglutin.

Front 27

What is the MOA of exenatide and liraglutin?

What are the clinical uses?

Back 27

Increases insulin, and decreases glucagone.

Used in DM 2.

Front 28

What are the toxicities of exenatide and liraglutin?

Back 28

N/V, and PANCREATITIS.

Front 29

Name some DPP-4 inhibitors. What is the MOA?

What are the clinical uses?

Back 29

Linagliptin, sexagliptin, sitagliptin.

MOA: increases insulin and decreases glucagone (just like GLP-1 analogs).

Used in DM 2 (just like GLP-1 analogs).

Front 30

What are the toxicities of DPP-4 inhibitors?

Back 30

Mild urinary or respiratory infxn. 

Front 31

What are some drugs used to tx hyperthyroidism?

What is the MOA?

Back 31

Propylthiouracil (PTU), and methimazole.

 

MOA: block peroxidase --> inhibits organification and coupling.

PTU also blocks 5`-deiodinase --> decreases peripheral conversion of T4 to T3.

Front 32

What are the toxicities of PTU and methimazole?

Back 32

Skin rash,

agranulocytosis (rare),

aplastic anemia,

hepatotoxicity (PTU only).

 

Methimazole is a possible teratogen. 

Front 33

What drugs are used in myxedema and hypothyroidism?

Back 33

Levothyroxine, triiodothyronine.

(thyroxine replacement)

Front 34

What are the toxicities of levothyroxine and T3?

Back 34

Sx of hyperthyroidism: tachycardia, heat intolerance, tremors, arrhythmia. 

Front 35

What is demeclocycline? What is it used for?

Back 35

ADH antagonist (member of tetracycline family)

 

Used in SIADH.

Front 36

What are the toxicities of demeclocycline?

Back 36

Nephrogenic DI,

photosensitivity,

abnormalities of bone and teeth.

Front 37

What happens when you abruptly stop glucocorticoids?

Back 37

Adrenal insufficiency.