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STEP 1 > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

1
Q

Name the rapid acting insulins

A

aspart, glulisine, lispro

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2
Q

Mechanism of rapid acting insulins

A

binds insulin receptor (tyrosine kinase activity)

liver: increases glucose stored as glycogen
mucles: increases glycogen, protein synthesis; increases K+ uptake into cells
fat: increases TG storage

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3
Q

Use of rapid acting insulins

A 
type 1 and 2 DM
gestational diabetes (postprandial glucose control)
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4
Q

Toxicity of rapid acting insulins

A

hypoglycemia

rare hypersensitivity reactions

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5
Q

Treatment strategy for type 1 DM

A

low-carbohydrate diet

insulin replacement

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6
Q

Treatment strategy for type 2 DM

A

dietary modification and exercise for weight loss
oral agents
non-insulin injectables
insulin replacement

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7
Q

Treatment strategy for gestational diabetes

A

dietary modifications
exercise
insulin replacement if lifestyle modification fails

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8
Q

Name the insulin short acting agent

A

INSULIN

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9
Q

Use of short acting insulin

A 
type 1 DM
type 2 DM
GDM
DKA (IV)
hyperkalemia (+ glucose)
stress hyperglycemia
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10
Q

Name the intermediate acting insulin

A

NPH

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11
Q

Use of intermediate acting insulin

A

type 1 DM
type 2 DM
GDM

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12
Q

Name the long acting insulins

A

detemir

glargine

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13
Q

Use of long acting insulins

A

type 1 DM
type 2 DM
GDM (basal glucose control)

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14
Q

Action of detemir vs. glargine

A

detemir binds albumin tightly and is slowly offloaded throughout the day
glargine stays at constant level throughout the day, resembles basal insulin secretion

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15
Q

Name the biguanides

A

metformin

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16
Q

Mechanism of metformin

A

exact mechanism unknown

- decrease gluconeogenesis, increase glycolysis, inrease peripheral glucose uptake (increase insulin sensitivity)

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17
Q

Use of metformin

A

ORAL
first line therapy in type 2 DM - causes modest weight loss
can be used in pts without islet function

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18
Q

Toxicity of metformin

A

GI upset

MOST SERIOUS IS LACTIC ACIDOSIS

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19
Q

Contraindication of metformin

A

pts with renal insufficiency due to risk for lactic acidosis

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20
Q

Name the sulfonylureas

A

first generation:

  • chlorpropamide
  • tolbutamide

second generation:

  • glimepridie
  • glipizide
  • glyburide
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21
Q

Mechanism of the sulfonylureas

A

close K+ channels in the beta-cells –> depolarization –> insulin release via increased Ca2+ influx

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22
Q

Use of sulfonylureas

A

stimulate release of endogenous insulin in type 2 DM
requires some islet function so useless in type 1 DM

UNLESS HAVE CHILDHOOD MUTATION in ATP-K+ channel

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23
Q

Toxicity of sulfonylureas general

A

risk of hypoglycemia is increased in renal failure

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24
Q

Toxicity of 1st generation sulfonylureas

A

disulfiram-like effects

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25
Q

Toxicity of 2nd generation sulfonylureas

A

hypoglycemia

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26
Q

What is disulfiram-like effects?

A

immediate hangover effect caused by a build up of acetylaldehyde due to inhibition of aldehyde dehydrogenase

ethanol –> acetaldehyde via alcohol dehydrogenase
acetaldeyhyde –> acetic acid via acetaldehyde dehydrogenase

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27
Q

Other drugs causing a disulfiram like toxicity?

A

metronidazole (some abx)
1st generation sulfonylureas
some cephalosporins
griseofulvin

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28
Q

Name the glitazones/thiazolidinediones

A

“-glitazones”

pioglitazone and rosiglitazone

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29
Q

Mechanism of glitazones/thiazolidinediones

A

increase insulin sensitivity in peripheral tissue

binds PPAR-gamma nuclear transcription regulator

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30
Q

Use of glitazones/thiazolidinediones

A

used as monotherapy in type 2 DM or combined with above agents

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31
Q

Toxicity of glitazones/thiazolidinediones

A

weight gain, edema

hepatotoxicity, HF, increased risk of fractures

32
Q

Name the GLP-1 analogs

A

Exenatide, liraglutide

33
Q

Mechanism of GLP-1 analogs

A

increase insulin, decrease glucagon release

34
Q

Use of GLP-1 analogs

A

Type 2 DM

35
Q

Toxicity of GLP-1 analogs

A

nausea, vomiting, pancreatitis

36
Q

Name the DPP-4 Inhiubitors

A

linagliptin, saxagliptin, sitagliptin

37
Q

Mechanism of DPP-4 inhibitors

A

increase insulin and decrease glucagon release

prevents GLP-1 breakdown

38
Q

Use of DPP-4 inhibitors

A

type 2 DM

39
Q

Toxicity of DPP-4 inhibitors

A

mild urinary or respiratory infections

40
Q

Name the amylin analog

A

pramlintide

41
Q

Mechanism of pramlintide

A

decrease gastric emptying and decrease glucagon

42
Q

Use of pramlintide

A

type 1 or 2 DM

43
Q

Toxicity of pramlintide

A

hypoglycemia, nausea, diarrhea

44
Q

Name the SGLT-2 inhibitors

A

canagliflozin

45
Q

Mechanism of the SGLT-2 inhibitor

A

block reabsorption of glucose in PCT

46
Q

Use of SGLT-2 inhibitor

A

type 2 DM

47
Q

Toxicity of SGLT-2 inhibitor

A

glucosuria, UTIs, vaginal yeast infections

48
Q

Name the alpha-glucosidase inhibitors

A

acarbose, miglitol

49
Q

Mechanism of alpha-glucosidase inhibitors

A

inhibit intestinal brush-border alpha-glucosidases

delayed carbohydrate hydrolysis and glucose absorption –> decreased post-prandial hyperglycemia

50
Q

Use of alpha-glucosidase inhibitors

A

monotherapy in type 2 DM or in combination with above agents

51
Q

Toxicity of alpha-glucosidase inhibitors

A

GI disturbances

52
Q

Mechanism of propylthiouracil and methimazole

A

block thyroid peroxidase (propyl- also blocks 5’-deiodinase) –> inhibition of oxidation of iodide and organification (coupling) of iodine –> inhibited thyroid hormone synthesis

53
Q

Effects of 5’-deiodinase block

A

via propylthiouracil

prevents peripheral conversion from T4 to T3

54
Q

Use of propylthiouracil and methimazole

A

hyperthyroidism

55
Q

Special use of propylthiouracil

A

used in pregnancy because blockers peripheral conversion

56
Q

Toxicity of propylthiouracil and methimazole

A

skin rash
agranulocytosis (rare)
aplastic anemia
hepatotoxicity (propylthiouracil)

57
Q

Toxicity of methimazole

A

possible teratogen that can cause aplasia cutis

58
Q

Levothyroxine (T4) and Triiodothyronine (T3) Use

A

thyroid hormone replacement

  • hypothyroidism
  • myxedema
  • off label weight loss supplements
59
Q

Toxicity of T4 and T3 as replacement

A

tachycardia, heat intolerance, tremors, arrhythmias

60
Q

Use and names of ADH antagonists

A

conivaptan, tolvaptan

SIADH, block action of ADH at V2 receptor

61
Q

Use of desmopressin acetate

A

central (not nephrogenic) DI

ADH analog

62
Q

Use of GH supplements

A

GH deficiency, Turner syndrome

63
Q

Use of oxytocin

A

stimulates labor, uterine contractions and milk let-down

controls uterine hemorrhage

64
Q

Use of somatostatin

A

GH excess (acromegaly), carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

65
Q

Mechanism of demeclocycline

A

ADH antagonist (tetracycline family member)

66
Q

Use of demeclocycline

A

SIADH

67
Q

Toxicity of demeclocycline

A

nephrogenic DI
photosensitivity
abnormalities of bone and teeth

68
Q

Name some glucocorticoids

A

beclomethasone, dexamethasone, fludrocortisone, hydrocortisone, methylprednisone, prednisone, triamcinolone

69
Q

Special attribute of fludrocortisone

A

mineralocorticoid and glucocorticoid activity

70
Q

Use of glucocorticoids

A

Addison disease, inflammation, immunosuppression, asthma

71
Q

Toxicity of glucocorticoids

A

Iatrogenic Cushing Syndrome: HTN, immune suppression, central/truncal obesity, buffalo hump, osteoporosis, moon facies, insulin resistance, striae

Adrenocortical atrophy
peptic ulcers
steroid diabetes
steroid psychosis

72
Q

Complication of quick discontinuation of glucocorticoids

A

adrenal insufficiency when stopped after chronic use

73
Q

Mechanism of cinacalcet

A

sensitizies Ca2+-sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ –> decreased PTH

74
Q

Use of cinacalcet

A

hypercalcemia due to primary or secondary hyperparathyroidism

75
Q

Toxicity of cinacalcet

A

hypocalcemia

STEP 1 (26 decks)

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