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Step 1 Pharmacology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the treatment strategies for Diabetes Mellitus Type 1?

A

Low-sugar diet, insulin replacement

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2
Q

What are the treatment strategies for Diabetes Mellitus Type 2?

A

Dietary modification and exercise for weight loss; oral agents, non-insulin injectables, insulin replacement

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3
Q

Diabetes Drugs - What are the treatment strategies for Gestational Diabetes Mellitus?

A

Dietary modifications, exercise, insulin replacement if lifestyle modification fails

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4
Q

Diabetes Drugs - What is the mechanism of the rapid acting Insulin drugs (Lispro, Aspart, Glulisine)?

A

Bind insulin receptor (tyrosine kinase activity).
Liver: ↑ glucose stored as glycogen.
Muscle: ↑ glycogen, protein synthesis; ↑ K+ uptake.
Fat: ↑ TG storage.

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5
Q

Diabetes Drugs - What is the clinical use of the rapid acting Insulin drugs (Lispro, Aspart, Glulisine)?

A

DM1, DM2, GDM (postprandial glucose control)

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6
Q

Diabetes Drugs - What are the toxicities of the rapid acting Insulin drugs (Lispro, Aspart, Glulisine)?

A

Hypoglycemia, rare hypersensitivity reactions

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7
Q

Diabetes Drugs - What is the clinical use of the short acting Insulin drugs (Regular)?

A

DM1, DM2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia

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8
Q

Diabetes Drugs - What is the clinical use of the intermediate acting Insulin drugs (NPH)?

A

DM1, DM2, GDM

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9
Q

Diabetes Drugs - What is the clinical use of the long acting Insulin drugs (Glargine, Detemir)?

A

DM1, DM2, GDM (basal glucose control)

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10
Q

Diabetes Drugs - What is the mechanism of Biguanides (Metformin)?

A

Exact mechanism is unknown. ↓ gluconeogenesis, ↑ glycolysis, ↑ peripheral glucose uptake (insulin sensitivity).

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11
Q

Diabetes Drugs - What is the clinical use of Biguanides (Metformin)?

A

Oral. First-line therapy in type 2 DM.

Can be used in patients without islet function.

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12
Q

Diabetes Drugs - What are the toxicities of Biguanides (Metformin)?

A

GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure)

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13
Q

Diabetes Drugs - What is the mechanism of Sulfonylureas (First generation: Tolbutamide, Chlorpropamide; Second generation: Glyburide, Glimepiride, Glipizide)?

A

Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx

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14
Q

Diabetes Drugs - What is the clinical use of Sulfonylureas (First generation: Tolbutamide, Chlorpropamide; Second generation: Glyburide, Glimepiride, Glipizide)?

A

Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM.

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15
Q

Diabetes Drugs - What are the toxicities of Sulfonylureas (First generation: Tolbutamide, Chlorpropamide; Second generation: Glyburide, Glimepiride, Glipizide)?

A

Risk of hypoglycemia ↑ in renal failure.
First generation: disulfiram-like effects.
Second generation: hypoglycemia.

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16
Q

Diabetes Drugs - What is the mechanism of Glitazones/thiazolidinediones (Pioglitazone, Rosiglitazone)?

A

↑ insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.
Genes activated by PPAR-γ regulate fatty acid storage and glucose metabolism. Activation of PPAR-γ ↑ insulin sensitivity and levels of adiponectin.

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17
Q

Diabetes Drugs - What is the clinical use of Glitazones/thiazolidinediones (Pioglitazone, Rosiglitazone)?

A

Used as monotherapy in type 2 DM or combined with above agents.

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18
Q

Diabetes Drugs - What are the toxicities of Glitazones/thiazolidinediones (Pioglitazone, Rosiglitazone)?

A

Weight gain, edema.

Hepatotoxicity, heart failure.

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19
Q

Diabetes Drugs - What is the mechanism of α-glucosidase inhibitors (Acarbose, Miglitol)?

A

Inhibit intestinal brush-border α-glucosidases.

Delayed sugar hydrolysis and glucose absorption → ↓ postprandial hyperglycemia.

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20
Q

Diabetes Drugs - What is the clinical use of α-glucosidase inhibitors (Acarbose, Miglitol)?

A

Used as monotherapy in type 2 DM or in combination with above agents.

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21
Q

Diabetes Drugs - What are the toxicities of α-glucosidase inhibitors (Acarbose, Miglitol)?

A

GI disturbances

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22
Q

Diabetes Drugs - What is the mechanism of Amylin analogs (Pramlintide)?

A

↓ gastric emptying, ↓ glucagon

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23
Q

Diabetes Drugs - What is the clinical use of Amylin analogs (Pramlintide)?

A

Type 1 and type 2 DM

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24
Q

Diabetes Drugs - What are the toxicities of Amylin analogs (Pramlintide)?

A

Hypoglycemia, nausea, diarrhea

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25
Q

Diabetes Drugs - What is the mechanism of GLP-1 analogs (Exenatide, Liraglutide)?

A

↑ insulin, ↓ glucagon release.

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26
Q

Diabetes Drugs - What is the clinical use of GLP-1 analogs (Exenatide, Liraglutide)?

A

Type 2 DM

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27
Q

Diabetes Drugs - What are the toxicities of GLP-1 analogs (Exenatide, Liraglutide)?

A

Nausea, vomiting; pancreatitis

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28
Q

Diabetes Drugs - What is the mechanism of DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)?

A

↑ insulin, ↓ glucagon release.

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29
Q

Diabetes Drugs - What is the clinical use of DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)?

A

Type 2 DM

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30
Q

Diabetes Drugs - What are the toxicities of DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)?

A

Mild urinary or respiratory infections

31
Q

What is the mechanism of Propylthiouracil and methimazole?

A

Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine → inhibition of thyroid hormone synthesis. Propylthiouracil also blocks 5′-deiodinase, which ↓ peripheral conversion of T4 to T3

32
Q

What is the clinical use of Propylthiouracil and methimazole?

A

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy.

33
Q

What is the toxicity of Propylthiouracil and methimazole?

A

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil). Methimazole is a possible teratogen (can cause aplasia cutis).

34
Q

What is the mechanism of Levothyroxine and triiodothyronine?

A

Thyroxine replacement

35
Q

What is the clinical use of Levothyroxine and triiodothyronine?

A

Hypothyroidism, myxedema

36
Q

What is the toxicity of Levothyroxine and triiodothyronine?

A

Tachycardia, heat intolerance, tremors, arrhythmias

37
Q

Hypothalamic/pituitary drugs - What is the clinical use of GH?

A

GH deficiency, Turner syndrome

38
Q

Hypothalamic/pituitary drugs - What is the clinical use of Somatostatin (octreotide)?

A

Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

39
Q

Hypothalamic/pituitary drugs - What is the clinical use of Oxytocin?

A

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

40
Q

Hypothalamic/pituitary drugs - What is the clinical use of ADH (DDAVP)?

A

Pituitary (central, not nephrogenic) DI

41
Q

What is the mechanism of Demeclocycline?

A

ADH antagonist (member of the tetracycline family)

42
Q

What is the clinical use of Demeclocycline?

43
Q

What are the toxicities of Demeclocycline?

A

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

44
Q

What are the glucocorticoids?

A

Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone, fludrocortisone (mineralocorticoid and glucocorticoid activity)

45
Q

What is the mechanism of Glucocorticoids?

A

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB

46
Q

What is the clinical use of Glucocorticoids?

A

Addison disease, inflammation, immune suppression, asthma

47
Q

What are the toxicities of Glucocorticoids?

A

Iatrogenic Cushing syndrome—buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
Adrenal insufficiency when drug stopped abruptly after chronic use.

48
Q

What is the mechanism of Clomiphene?

A

Inhibits the hypothalamus

49
Q

What do oral contraceptives and danazol do?

A

Inhibit the anterior pituitary

50
Q

What do ketoconazole and danzol do?

A

Inhibit P-450c17

51
Q

What do Anastrozole and others do?

A

Inhibit aromatase

52
Q

What does Fulvestrant do?

A

Inhibit estradiol from interacting with the estrogen response element

53
Q

What do ketoconazole and spironolactone do?

A

Inhibit the testis from producing testosterone

54
Q

What does Finasteride do?

A

5α-reductase

55
Q

What do Flutamide, cyproterone, and spironolactone do?

A

Inhibit testosterone and dihydrotestosterone from becoming an androgen-receptor complex

56
Q

What can Dopamine antagonists (e.g., antipsychotics) cause?

A

Galactorrhea

57
Q

What is used in the treatment of prolactinoma?

A

Dopamine agonists (bromocriptine or cabergoline) inhibit prolactin secretoin and thus can be used to treat prolactinoma.

58
Q

What do dopamine antagonists (most antipsychotics) and estrogens (OCPs, pregnancy) do?

A

Stimulate prolactin secretion

59
Q

What is used for the treatment of central Diabetes Insipidus?

A

Desmopressin (ADH analog; intranasal DDAVP)

60
Q

What can exogenous corticosteroids cause?

A

Reactivation of TB and candidiasis (blocked IL-2 production)

61
Q

What is the difference between Propylthiouracil and Methimazole?

A

Propulthiouracil inhibits both peroxidase and 5’-deiodinase. Methimazole inhibits peroxidase only.

62
Q

What can be used to interfere with trapping of Iodide?

A

Anions (perchlorate, pertechnetate, and thiocyanate)

63
Q

What is the treatment for Primary Hyperaldosteronism?

A

Surgery to remove the tumor and/or spironolactone, a K+ sparing diuretic that acts as an aldosterone antagonist

64
Q

What is the treatment for Secondary Hyperaldosteronism?

A

Spironolactone

65
Q

What is used in the treatment of Pheochromocytoma?

A

Irreversible α-antagonists (phenoxybenzamine) and β-blockers followed by tumor resection. α-blockade must be achieved before giving β-blockers to avoid a hypertensive crisis.

66
Q

How do you treat a Thyroid storm?

A

3 P’s: β-blockers (e.g., Propranolol), Propylthiouracil, corticosteroids (e.g., Prednisolone)

67
Q

How do you treat Acromegaly?

A

Octreotide (somatostatin analog) or pegvisomant (growth hormone receptor antagonist)

68
Q

What do you treat Nephrogenic Diabetes Insipidus with?

A

HCTZ, indomethacin, amiloride

Hydration

69
Q

What drugs can cause Nephrogenic Diabetes Insipidus?

A

Lithium, democlocycline (ADH antagonist)

70
Q

What drug can cause SIADH?

A

Cyclophosphamide

71
Q

What is the treatment for SIADH?

A

Conivaptan, tolvaptan, demeclocycline

72
Q

What is the treatment for hypopituitarism?

A

Hormone replacement therapy (corticosteroids, thyroxine, sex steroids, human growth hormone)

73
Q

What is the treatment for Carcinoid syndrome?

A

Resection, somatostatin analog (e.g., octreotide)

Step 1 Pharmacology (18 decks)

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