Endocrine Pharm

Front 1

Type 1 diabetics require Insulin injections. What two types of insulin are most patients on?

Back 1

Rapid acting and Long acting

(one to take everyday and other before meals to keep sugar low)

Front 2

What are the rapid-acting insulin?

Back 2

Lispro
Aspart
Glulisine

(LAG) - Take before MEALS

Front 3

What are the other Insulin types?

Back 3

Regular (short acting)
NPH (intermediate)

Glargine (long-acting)
Detemir (long-acting)

Front 4

What are some effects of insulin (biochemistry)?

Back 4

Bind insulin receptor (tyrosine kinase activity)

Increases glycogen storage in Liver
Increases Fat storage in Adipose
Increases Protein+glycogen storage in muscle

Front 5

What are some clinical uses of Insulin?

Back 5

Mainly for Type 1 DM

Severe Type 2 DM

Gestational Diabetes* (only option for this)

Front 6

What are the main side effects of Insulin?

Back 6

Weight gain

Hypoglycemia

Lipodystrophy - abnormal fat degernation in site of injection

Front 7

How to avoid Lipodystrophy for Type 1 diabetics?

Back 7

Change your injection sites!

Front 8

Metformin

MOA?

Back 8

Unknown. Similar functions to insulin (decrease gluconeogensis, increase glycolysis, incrase glucose uptake)

FIRST LINE THERAPY FOR DM Type II**

Front 9

What is the first line treatment for Type II DM?

Back 9

Metformin

Can work w/o Islet functioning

Front 10

Metformin

Side effects

Back 10

GI upset, WEIGHT loss

Lactic acidosis

Front 11

What are the contraindications to Metformin

Back 11

Hepatic/Renal disease (those organs help deal with acidosis)

Hx of acidosis

Acute MI, acute LVF, Chronic hypoxic lung disease (all have hypoxemia which increases likelyhood of acidosis)

Front 12

What are the advantages of Metformin?

Back 12

Weight loss?

No chances of Hypoglycemia

Front 13

1st Generation:
-Tolbutamide, Chlorpropamide

2nd Generation:
-Glyburide, Glimepiride, Glipizide

What kinds of drugs are these?

Back 13

Sulfonylureas

1st generation not used as much but BOARDS use it :(

Front 14

Sulfonylureas

MOA

Back 14

Close K channels in beta cells so cell depolarizes triggering increase in Ca. MORE INSULIN RELEASE

Require some Islet cell function (thus useless in type I DM)

Front 15

Sulfonylureas

Clinical use

Back 15

Used for Type II DM

Early on only b/c most ppl become resistant in couple of years

Front 16

Side effects of 1st generation drugs

(Tolbutamide and Chlorpropamide)

What is one specific Se of Chlorpropamide?

Back 16

Both cause disuliram-like side effects (N, V, makes you feel like crap; like a bad hangover)

Chloro -- might cause SIADH!

Front 17

What drug is known to cause ectopic SIADH?

Back 17

Chloropropamide

Front 18

What are the side effects of the second generation drugs?

(Glyburide, Glimepiride, Glipizide)

Back 18

Nothing special; typical insulin stuff

Weight gain, hypoglycemia

Front 19

Glitazones/Thiazolidinediones

Name the two drugs

Back 19

Pioglitazone

Rosiglitazone (not used)

Front 20

MOA of Glitazones

Back 20

Stimulates PPAR-Gamma which will increases insulin sensitivity in other tissues

Front 21

Clinical use of Glitazones

Back 21

Type II DM

(monotherapy or combined with other agents)

Front 22

Pioglitazone
Rosiglitazone

Why do you not use Rosiglitazone?

Back 22

Increased risk of MI

(not sure why; but straight up fact from clinical trials)

Front 23

Glitazones Side effects

Back 23

Heart failure, Edema, Weight gain --> all b/c of its effects on kidney (increased reabsorption)

Hepatotoxcity

Front 24

Which enzyme in the intestine breaks down disaccharides into glucose, which now can be absorbed.

Back 24

Alpha-glucosidase

Front 25

Alpha glucosidase inhibitors

(Acarbose and Miglitol)

MOA

Back 25

They inhibit that enzyme. Thus you get delayed sugar hydrolysis and thus DELAYED glucose absorption.

Decreases postprandial hyperglycemia

Front 26

Side effects of alpha-glucosidase inhibitors

Back 26

Bloating, gas, GI upset

Front 27

What is Amylin?

Back 27

It is a molecule co-secreted with Insulin

Front 28

Pramlintide

what kind of drug is that?

Back 28

Amylin analog

Front 29

How does Pramlintide work?

Back 29

It delays gastric emptying (thus you feel full --- satiety) and it decreases glucagon release

(endogenous one does same things)

Front 30

Clinical use of Pramlintide

Back 30

Type 1 and Type 2 DM

(probably the only drugs for type I DM besides the Insulin)

Front 31

What is the role of Glucagon like peptides (GLP-1) in the body?

Back 31

Don't let the name confuse you. They come from pro-glucagon gene, however thier function is very different.

They increases INsulin release and decrease Glucagon release

Front 32

What enzyme breaks down GLP1?

Back 32

Dipeptidyl-peptidase-IV (DDP4)

Front 33

GLP-1 Analogs and DDP-4 Inhibitors would have what overall effect?

Back 33

INCREASE insulin

DECREASE Glucagon

Front 34

GLP-1 analogs

Exenatide
Liraglutide

Adverse Effects?

Back 34

N, V, pancreatitis

Front 35

DDP-4 inhibitors

Linagliptin
Saxagliptin
Sitagliptin

Adverse Effects

Back 35

Mild urinary or respiratory infections

Front 36

Treatment plan for hyperthyroidism?

Back 36

Beta blocker
Antithyroid agents (thiamides)

(radiation or surgery if severe)

Front 37

Propylthiouracil and Methimazole

Clinical use?

Back 37

Hyperthyroidism

Front 38

Explain thyroid synthesis process

Back 38

Iodine comes into cell and is oxidaized. That is then put onto the tyrosine residue on thyroglobuin by PEROXIDASE. This makes either MIT or DIT.

MIT + DIT combine to form T3. DIT+DIT form T4.

Front 39

T4 is the major thyroid product. However, most is converted to T3 in periphery tissue. What enzyme does this?

Back 39

5'deiodinase

Front 40

MOA of Methimazole and Propylthiouracil (PTU)

Back 40

Both block Peroxidase

PTU also blocks 5'deiodinase

Front 41

Adverse effects of PTU and Methimazole

(note: name the common ones for both and the UNIQUE ones for each)

Back 41

Agranulocytosis and aplastic anemia

PTU: hepatotosicty, liver failure
Methimazole: way MORE teratogenic. Don't use in first trimester

Front 42

Methimazole is the preferred drug over the two.

Name the circumstances you would use PTU?

Back 42

1st trimester of pregnancy (maybe whole time?)

Thyroid storm (emergency) ---> Use PTU

Front 43

Levothyroxine (T4)
Triiodothyronine/Liothyronine (T3)

Clinical use

Back 43

Hypothyroidism, myxedema

T4 usually used.

Front 44

SE of thyroid hormone replacement

Back 44

Tachycardia, heat intolerance, tremors, arrhthmias (basically all hyperthyroid stuff)

Front 45

What is Demeclocycline

Clinical use?

Back 45

ADH antagonist

use it for SIADH

Front 46

AE of Demeclocycline

Back 46

NDI, photosensitive, abnormalities of bone and teeth

Front 47

Octreotide

Back 47

Somatostatin analog

Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

Front 48

ADH (desmopressin)

Back 48

used for central DI

Front 49

Oxytocin

Back 49

Stimulates labor, uterine contractions, milk let down

(controls uterine hemorrhage)

Front 50

Growth hormone

Back 50

GH defiency

Turner Syndrome

Front 51

Hydrocortisone, predinisone, dexamethasone, beclomethasone, etc.

What kind of drugs are these?

Back 51

Glucocorticoids

Front 52

MOA of glucocorticoids

Back 52

Decrease the production of BOTH leukotriences and PGE by inhibiting Phospholipase A2.

(also inhibit COX)

Front 53

Clinical use of glucocorticoids

Back 53

Addison's dz. inflammation, immune suppression, asthma

Front 54

What are the long acting glucocorticoids?

Back 54

Dexamethasone

Beclomethasone

Front 55

SE of glucocorticoids**

Back 55

Iatrogenic Cushing's syndrone (bufalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisablity, osteoporosis, peptic ulcers, diabetes)

Front 56

What is the number 1 cause of cushing syndrome?

Back 56

exogenous steroids (glucocorticoids)

Front 57

What can happen if you abruptly stop glucocorticoids?

Back 57

adrenal insuffiency (ween off)