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STEP > Endo pharm > Flashcards

Endo pharm Flashcards

1
Q

Rapid acting insulins

A

Lispro, aspart, glulisine

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2
Q

Short acting insulin

A

Regular

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3
Q

Intermediate acting insulin

A

NPH

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4
Q

Long acting insulin

A

Detemir, glargine

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5
Q

Effects of insulin

A

Liver – increase glucose stored as glycogen
Muscle – increase glycogen, protein synth, K uptake
Fat – increase trig storage

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6
Q

Risks w/ insulin

A

Hypoglycemia, lipodystrophy

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7
Q

Biguanides example

A

Metformin

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8
Q

Clinical use of biguanides

A

T2DM (can cause some wt loss)

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9
Q

MOA of biguanides

A

Inhibit hepatic gluconeogenesis and action of glucagon via mitochondrial glycerophosphate DHase –> less gluconeogenesis, increased glycolysis, increased peripheral glc uptake, increased insulin sensitivity

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10
Q

ADE w/ biguanides

A

GI upset, lactic acidosis (rare – but cautin in renal insufficiency)

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11
Q

Sulfonylureas 1st gen examples

A

Chlorpropamide, tolbutamide

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12
Q

Sulfonylureas 2nd gen examples

A

Glimepiride, glipizide, glyburide

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13
Q

Shortest half life of SU 2nd gen

A

Glipizide

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14
Q

Clinical use of SUs

A

Stimulate release of endogenous insulin in T2DM (req some islet fxn)

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15
Q

MOA of SUs

A

Close K channel in B cell membrane –> depolarization –> insulin release due to Ca influx

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16
Q

ADE in SUs

A

Hypoglycemia (worse in renal failure), wt gain
1st gen: disulfiram life rxn
2nd gen: hypoglycemia

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17
Q

Thiazolidinediones examples

A

Pioglitazone, rosiglitazone

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18
Q

Clinical use of TZDs

A

Monotherapy in T2DM or combined

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19
Q

Pro to TZDs

A

Safe in renal impairment

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20
Q

TZD MOA

A

Regulates PPAR-gamma –> Increased insulin sensitivity in peripheral tissue (upreg of Glut4)

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21
Q

ADE of TZDs

A

Wt gain (adipocyte maturation), edema, HF, increased risk of fractures

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22
Q

Meglitinides examples

A

Nateglinide, repaglinide

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23
Q

Clinical use of meglinitides

A

T2DM

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24
Q

MOA of meglinitides

A

Stimulate postprandial insulin release by binding K channels on B cell membranes (diff site from SUs)

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25
Q

ADEs of meglinities

A

Hypoglycemia (worse risk w/ renal failure), wt gain

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26
Q

GLP1 analog examples

A

Exanatide, liraglutide (SQ)

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27
Q

Clinical use of GLP1 analogs

A

T2DM

28
Q

MOA of GLP1 analogs

A

Increases glucose dependent insulin release, less glucagon release, less gastric emptying, increased satiety (can cause wt loss)

29
Q

ADE in GLP1 analogs

A

NV, pancreatitis

30
Q

DPP4 inhibitors examples

A

Linagliptin, saxagliptin, sitagliptin

31
Q

Clinical use of DPP4 inhib

A

T2DM

32
Q

DPP4 inhib MOA

A

Inhibits DPP4 that deactivates GLP1 –> increased glucose dependent insulin release, lower glucagon release, less gastric emptying, increase satiety

33
Q

ADE in DPP4 inhib

A

Mild urinary or respiratory infxns

34
Q

Amylin analog example

A

Pramlintide (SQ)

35
Q

Amylin analog clinical use

A

T1/T2DM

36
Q

Amylin analog MOA

A

Less gastric emptying, less glucagon

37
Q

Amylin analog ADE

A

Hypoglycemia (mistime prandial insulin), nausea

38
Q

SGLT2 inhibitor examples

A

Canagliflozin, dapagliflozin, empaglifozin

39
Q

SGLT2 inhibitor clinical use

A

T2DM

40
Q

SGLT2 inhibitor MOA

A

Blocks resorption of glc in PCT

41
Q

ADE of SGLT2 inhibs

A

Glocusria, UTIs, vaginal yeast infxns, hyperkalemia, dehydration (–>othostatic hypotension), wt loss

42
Q

alpha glucosidase inhib exmaples

A

Acarbose, miglitol

43
Q

alpha glucosidase clinical use

A

T2DM

44
Q

alpha glucosidase MOA

A

Inhibit intestinal brush border alpha glucosidases – delated carb hydrolysis and glc absorption –> lower post prandial hyperglycemia

45
Q

ADE w/ alpha glucosidase

A

GI disturbances (short chain carbs fermented by bacteria in colon)

46
Q

Thioamide examples

A

PTU, MMI

47
Q

MOA of thioamides

A

Block TPO –> no oxidation/organification/coupling in thyroid hormone synth
PTU also blocks peripheral 5’ deiodinase T4–>T3

48
Q

Clinical use of thioamides

A

Hyperthyroidism
PTU in 1st tri of pregnancy
MMI in 2-3rd (risk of PTU hepatotox)

49
Q

ADE w/ thioamides

A

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotox (PTU), MMI is a possible teratogen (aplasia cutis), drug induced lupus/ANCA vasculitis (PTU)

50
Q

Levothyroxine, triiodothyronine MOA

A

thyroid hormone replacement

51
Q

Clinical use of thyroid hormones

A

Hypothyroidism, myxedema (beware people using as wt loss supplements)

52
Q

ADE of thyroid hormones

A

tachycardia, heat intolerance, tremors, arrhythmias

53
Q

ADH antagonist exmaples

A

Conivaptan, tolvaptan

54
Q

Clinical use of ADH antagonists

A

SIADH, block actin of ADH at V2

55
Q

Desmopressin acetate clinical use

A

Central (NOT NEPHRO) DI, von Willebrand disease (extra renal V2 receptors regulate clotting factors), sleep enuresis

56
Q

GH clinical use

A

GH deficiency, Turner

57
Q

Oxytocin clinical use

A

Stimulates labor, uterine contractions, mile let-down, controls uterine hemorrhage

58
Q

Somatostatin (octreotide) clinical uses

A

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices, somatostatinoma

59
Q

Demeclocycline MOA

A

ADH antagonist (member of tetracyclines)

60
Q

Demeclocyline clinical use

A

SIADH

61
Q

Demeclocycline adverse effects

A

Nephrogenic DI, photosens, abnormalities of bone/teeth

62
Q

Fludrocortisone MOA

A

synthetic analog of aldo w/ some glucocorticoid effects

63
Q

CLinical use of fludrocortisone

A

Mineralocorticoid replacement in 1o adrenal insuff

64
Q

Adverse effects of fludrocortisone

A

Similar to glucocorticoids but also edema, exacerbation of heart failure, hyperpigmentation

65
Q

Cinacalcet MOA

A

Sensitizes Ca sensing receptor (CaSR) in parathyroid to circulating Ca –> lower PTH

66
Q

Clinical use of cinacalcet

A

1o or 2o hyperparathyroidism

67
Q

ADE of cinacalcet

A

Hypocalcemia

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