Usmle Step 1 High Yield Systems Endocrine Pharmacology 2013

Front 1

Endocrine

Back 1

[MOA/Clinical Use/TOX]

Front 2

Insulin--Rapid acting

Back 2

Lispro, Aspart, Glulisine

Front 3

Insulin--short acting

Back 3

Regular

Front 4

Insulin--intermediate acting

Back 4

NPH

Front 5

Insulin--long acting

Back 5

Glargine, Detemir

Front 6

Insulin MOA

Back 6

Bind insulin receptor (tyrosine kinase activity)

Liver: INC glucose stored as glycogen
MM: INC glycogen and protein synthesis, K uptake
Fat: aids TG storage

Front 7

Insulin clinical use

Back 7

Type 1 and 2 DM
Gestational diabetes
Life threatening HYPERkalemia
stress-induced HYPERglycemia

Front 8

Insulin Tox

Back 8

Hypoglycemia

Very rarely--Hypersensitivity

Front 9

Biguanides

Back 9

Metformin

Front 10

Metformin MOA

Back 10

Exact MOA unknown

DEC gluconeogensis
INC glycolysis
INC peripheral glucose uptake (insulin sensitivity)

Front 11

Metformin clinical use

Back 11

First line therapy Type 2 DM

Oral

Can be used in patients without islet cell function

Front 12

Metformin TOX

Back 12

LACTIC ACIDOSIS!

-->Contraindicated in renal failure

Front 13

Sulfonylureas (1st gen)

Back 13

Tolbutamide and Chlorpropamide

Front 14

Sulfonylureas (2nd gen)

Back 14

Glyburide, Glimepiride, Glipizide

Front 15

Sulfonylureas MOA

Back 15

Close K channel in Beta cell membrane-->depolarization-->Ca influx-->triggering insulin release

Front 16

Sulfonylureas clinical use

Back 16

Stimulate release of endogenous insulin in Type 2 DM

Requires some islet cell function (useless in Type 1)

Front 17

Sulfonylureas TOX

Back 17

1st gen: Disulfiram like effects (drowsiness, headache, metallic/garlic taste)

2nd gen: hypoglycemia

Front 18

Glitazones/thiazolidinediones

Back 18

Pioglitazone, Rosiglitazone

Front 19

Glitazone MOA

Back 19

INC insulin sensitivity in peripheral tissue

Binds to PPAR-gamma nuclear transcription regulator

(PPAR-gamma regulates FA storage and glucose metabolism. Activation INC insulin sensitivity and levels of adiponection)

Front 20

Glitazone clinical use

Back 20

used as monotherapy in Type 2

Front 21

Glitazone TOX

Back 21

Weight gain
Edema
Hepatotox
HEART FAILURE

Front 22

a-glucosidase inhibitors

Back 22

Acarbose, Miglitol

Front 23

a-glucosidase inhibitors MOA

Back 23

Inhibit intestinal brush border a-glucosidases=

Delayed sugar hydrolysis and glucose absorption-->DEC postprandial HYPERglycemia

Front 24

a-glucosidase inhibitor clinical use

Back 24

Monotherapy in Type 2

Front 25

a-glucosidase inhibitor TOX

Back 25

GI disturbances

Front 26

Amylin analogs

Pramlinitde

MOA/clinical use/TOX

Back 26

DEC glucagon

Type I and 2 DM

HYPOglycemia, N/D

Front 27

GLP-1 analogs (Incretins)

Back 27

Exenatide, Liraglutide

Front 28

GLP-1 MOA

Back 28

INC insulin, DEC glucagon release

Front 29

GLP-1 clinical use

Back 29

Type 2 DM

Front 30

GLP-1 TOX

Back 30

N/V
Pancreatitis

Front 31

DPP-4 inhibitors

Back 31

Linagliptin
Saxagliptin
Sitagliptin

Front 32

DPP-4 inhibitor MOA

Back 32

INC insulin, DEC glucagon release

Front 33

DPP-4 inhibitor clinical use

Back 33

Type 2 DM

Front 34

DPP-4 inhibitor TOX

Back 34

Mild urinary or respiratory infections

Front 35

Propylthiouracil, Methimazole MOA

Back 35

Block peroxidase thereby inhibiting organification of iodie and coupling of thyroid hormone synthesis

PPU also blocks 5-deiodinase (DEC peripheral conversion)

Front 36

PPU, MMU clinical use

Back 36

Hyperthyroidism

Front 37

PPU, MMU TOX

Back 37

Skin rash
AGRANULOCYTOSIS (discontinue MMU and give Filgastrim and G-CSF)
Aplastic anemia
Hepatotox (PPU)

MMU=teratogen

Front 38

Levothyroxine (T4), Tiiodothyronine (T3) MOA

Back 38

Thyroxine replacement

Front 39

Levo, Triiodo clinical use

Back 39

HYPOthyroidism
Myxedema

Front 40

Levo,Triiodo TOX

Back 40

Tachy
heat intolerance
tremors
arrythmias

Front 41

GH clinical use

Back 41

GH deficiency
TURNER'S SYNDROME

Front 42

Somatostatin/Octreotide clinical use

Back 42

Acromegaly
Carcinoid
Gastrinoma
Glucagonoma
Esophageal varices

Front 43

Oxytocin clinical use

Back 43

Stimulates labor
Uterine contractions
milk let-down
Control uterine hemorrhage

Front 44

ADH (desmopression) clinical use

Back 44

Central DI

Front 45

Demeclocycline MOA

Back 45

ADH antagonist

Front 46

Demeclocycline clinical use

Back 46

SIADH (caused by small cell carcinoma of lung)

Front 47

Demeclocycline TOX

Back 47

Nephrogenic DI
Photosensitivity
Bone and teeth abnormalities (member of tetracyclines)

Front 48

Gluccocorticoids MOA

Back 48

DEC production of LT and PG by inhibiting phospholipase A2 and expression of COX-2

Front 49

Gluccocorticoids clinical use

Back 49

Addison's disease (DEC steroid production due to primary insufficiency)
inflammation
immune suppression
asthma

Front 50

Gluccocorticoid TOX

Back 50

Iatorgenic Cushing's Syndrome

Adrenal insufficiency when drug stopped abruptly after chronic use

(severe abdominal pains, vomiting, profound muscle weakness and fatigue, depression, extremely low blood pressure (hypotension), weight loss, kidney failure, changes in mood and personality, and shock)