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Flashcards in Endocrine Drugs Deck (75)
1

Name the rapid acting insulins

aspart, glulisine, lispro

2

Mechanism of rapid acting insulins

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

3

Use of rapid acting insulins

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

4

Toxicity of rapid acting insulins

hypoglycemia
rare hypersensitivity reactions

5

Treatment strategy for type 1 DM

low-carbohydrate diet
insulin replacement

6

Treatment strategy for type 2 DM

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

7

Treatment strategy for gestational diabetes

dietary modifications
exercise
insulin replacement if lifestyle modification fails

8

Name the insulin short acting agent

INSULIN

9

Use of short acting insulin

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

10

Name the intermediate acting insulin

NPH

11

Use of intermediate acting insulin

type 1 DM
type 2 DM
GDM

12

Name the long acting insulins

detemir
glargine

13

Use of long acting insulins

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

14

Action of detemir vs. glargine

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

15

Name the biguanides

metformin

16

Mechanism of metformin

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

17

Use of metformin

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

18

Toxicity of metformin

GI upset
MOST SERIOUS IS LACTIC ACIDOSIS

19

Contraindication of metformin

pts with renal insufficiency due to risk for lactic acidosis

20

Name the sulfonylureas

first generation:
- chlorpropamide
- tolbutamide

second generation:
- glimepridie
- glipizide
- glyburide

21

Mechanism of the sulfonylureas

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

22

Use of sulfonylureas

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

23

Toxicity of sulfonylureas general

risk of hypoglycemia is increased in renal failure

24

Toxicity of 1st generation sulfonylureas

disulfiram-like effects

25

Toxicity of 2nd generation sulfonylureas

hypoglycemia

26

What is disulfiram-like effects?

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

27

Other drugs causing a disulfiram like toxicity?

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

28

Name the glitazones/thiazolidinediones

"-glitazones"

pioglitazone and rosiglitazone

29

Mechanism of glitazones/thiazolidinediones

increase insulin sensitivity in peripheral tissue
binds PPAR-gamma nuclear transcription regulator

30

Use of glitazones/thiazolidinediones

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

31

Toxicity of glitazones/thiazolidinediones

weight gain, edema
hepatotoxicity, HF, increased risk of fractures

32

Name the GLP-1 analogs

Exenatide, liraglutide

33

Mechanism of GLP-1 analogs

increase insulin, decrease glucagon release

34

Use of GLP-1 analogs

Type 2 DM

35

Toxicity of GLP-1 analogs

nausea, vomiting, pancreatitis

36

Name the DPP-4 Inhiubitors

linagliptin, saxagliptin, sitagliptin

37

Mechanism of DPP-4 inhibitors

increase insulin and decrease glucagon release

prevents GLP-1 breakdown

38

Use of DPP-4 inhibitors

type 2 DM

39

Toxicity of DPP-4 inhibitors

mild urinary or respiratory infections

40

Name the amylin analog

pramlintide

41

Mechanism of pramlintide

decrease gastric emptying and decrease glucagon

42

Use of pramlintide

type 1 or 2 DM

43

Toxicity of pramlintide

hypoglycemia, nausea, diarrhea

44

Name the SGLT-2 inhibitors

canagliflozin

45

Mechanism of the SGLT-2 inhibitor

block reabsorption of glucose in PCT

46

Use of SGLT-2 inhibitor

type 2 DM

47

Toxicity of SGLT-2 inhibitor

glucosuria, UTIs, vaginal yeast infections

48

Name the alpha-glucosidase inhibitors

acarbose, miglitol

49

Mechanism of alpha-glucosidase inhibitors

inhibit intestinal brush-border alpha-glucosidases
delayed carbohydrate hydrolysis and glucose absorption --> decreased post-prandial hyperglycemia

50

Use of alpha-glucosidase inhibitors

monotherapy in type 2 DM or in combination with above agents

51

Toxicity of alpha-glucosidase inhibitors

GI disturbances

52

Mechanism of propylthiouracil and methimazole

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

53

Effects of 5'-deiodinase block

via propylthiouracil

prevents peripheral conversion from T4 to T3

54

Use of propylthiouracil and methimazole

hyperthyroidism

55

Special use of propylthiouracil

used in pregnancy because blockers peripheral conversion

56

Toxicity of propylthiouracil and methimazole

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

57

Toxicity of methimazole

possible teratogen that can cause aplasia cutis

58

Levothyroxine (T4) and Triiodothyronine (T3) Use

thyroid hormone replacement
- hypothyroidism
- myxedema
- off label weight loss supplements

59

Toxicity of T4 and T3 as replacement

tachycardia, heat intolerance, tremors, arrhythmias

60

Use and names of ADH antagonists

conivaptan, tolvaptan

SIADH, block action of ADH at V2 receptor

61

Use of desmopressin acetate

central (not nephrogenic) DI
ADH analog

62

Use of GH supplements

GH deficiency, Turner syndrome

63

Use of oxytocin

stimulates labor, uterine contractions and milk let-down
controls uterine hemorrhage

64

Use of somatostatin

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

65

Mechanism of demeclocycline

ADH antagonist (tetracycline family member)

66

Use of demeclocycline

SIADH

67

Toxicity of demeclocycline

nephrogenic DI
photosensitivity
abnormalities of bone and teeth

68

Name some glucocorticoids

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

69

Special attribute of fludrocortisone

mineralocorticoid and glucocorticoid activity

70

Use of glucocorticoids

Addison disease, inflammation, immunosuppression, asthma

71

Toxicity of glucocorticoids

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

Complication of quick discontinuation of glucocorticoids

adrenal insufficiency when stopped after chronic use

73

Mechanism of cinacalcet

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

74

Use of cinacalcet

hypercalcemia due to primary or secondary hyperparathyroidism

75

Toxicity of cinacalcet

hypocalcemia