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STEP 1 > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

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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
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

STEP 1 (26 decks)

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