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Pharmacology > Week 5 > Flashcards

Week 5 Flashcards

1
Q

When should labs be re-checked after starting levothyroxine?

A

6-8 weeks

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2
Q

What are normal values for TSH?


A

0.3-6

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3
Q

What are normal values for free T3?


A

230-620

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4
Q

What are normal values for free T4?


A

0.9-2

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5
Q

How is thyroid storm treated?

A

propylthiouracil (PTU) is the preferred medication for treatment of thyroid storm
additionally, corticosteroids, beta-blockers, iodine solution, and supportive measures are warranted

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6
Q

What is the black box warning for propylthiouracil (PTU)?


A

severe liver injury and acute liver failure

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7
Q

What could happen if hypothyroidism is not treated during pregnancy?

A

maternal hypothyroidism can result in neuropsychological deficits and cause decreased IQ in the child

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8
Q

What drugs interact with levothyroxine?

A

drugs that reduce absorption — PPIs, H2 blockers, sucralfate, antacids, calcium supplements, iron supplements, magnesium supplements
drugs that accelerate metabolization of leveothyroxine — phenatoin, carmazepine, rifampin, sertraline, phenobarbital

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9
Q

How should levothyroxine dosing be adjusted in pregnancy?

A

during pregnancy, increased dosage requirements usually begin at 4-8 weeks of gestation and can be increased by as much as 50%; increased dosage begins between weeks 4 and 8 and levels off at week 16

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10
Q

What is the mechanism of action for GLP-1s?

A

Glucagon-like peptide-1s (GLP-1s) such as exenatide (Byetta), semaglutide (Ozempic), dulaglutide (Trulicity), and liraglutide (Victoza) are incretin mimetic that delay gastric emptying, stimulate glucose dependent insulin release, suppress postprandial glucagon release, and reduce appetite.

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11
Q

What is the mechanism of action for DPP-4Is?

A

Dipeptidyl peptidase-4 inhibitors (DPP04Is) such as sitagliptin, linagliptin, saxagliptin, and alogliptin inhibit dipeptidyl peptidase-4 which is the enzyme that breaks down incretins thus delaying gastric emptying, stimulating glucose dependent insulin release, suppressing postprandial glucagon release, and reducing appetite.

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12
Q

What is the mechanism of action for TZDs?

A

Thiazolidinediones (TZDs) such as rosiglitazone, and pioglitazone increase glucose uptake in muscle and adipose tissue and decrease hepatic glycogenolysis.

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13
Q

What are contraindications to pioglitazone?

A

Thiazolidinedione (TZDs) such as rosiglitazone or pioglitazone should be avoided in heart failure as TZDs have been shown to cause dose-related fluid retention in up to 20% of patients, history of bladder cancer, active liver disease

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14
Q

What are adverse effects of TZDs?

A

HF, bladder cancer, fractures, increased LDL & HDL, increased ovulation and teratogenic effects

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15
Q

What are adverse effect of sulfonylureas?

A

photosensitivity (use sunscreen), blood dyscrasias, weight gain, hypoglycemia

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16
Q

For what conditions should sulfonylureas should be avoided?

A

pregnancy, impaired hepatic or renal function

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17
Q

What is the mechanism of action for glinides?

A

Glinides such as nateglinide and repaglinide promote insulin secretion from the pancreas.

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18
Q

What are adverse effect of glinides?

A

weight gain, hypoglycemia

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19
Q

How do you calculate the carbohydrate-to insulin ratio when calculating basal insulin?

A

insulin-to-carb ratio is 500/TDD for rapid acting insulin and 450/TDD for short acting insulin

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20
Q

What is the insulin sensitivity factor ratio when calculating insulin dosage?

A

insulin sensitivity factor is 1800/TDD for rapid acting insulin and 1500/TDD for short acting insulin; the insulin sensitivity factor tells how much one unit of insulin will reduce blood glucose

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21
Q

What causes hypothyroidism?

A

Hasshimotos thyroiditis (autoimmune disorder in which thyroid producing cells are destroyed)
idoine deficiency
insufficient TRH or TSH

22
Q

What causes hyperthyroidism?

A

Grave’s Disease (autoimmune in which thyroid-stimulating immunoglobulin stimulates release of T3 and T4
Toxic goiter

23
Q

What is the first-line pharmacological treatment for hyperthyroidism or Grave’s disease?

A

methimazole

24
Q

What is the mechanism of action of methimazole?

A

Methimazole inhibits thyroid hormone synthesis but does not destroy existing thyroid hormone so it may take 3-12 weeks to produce a euthyroid state

25
Q

What is the most dangerous adverse effect of methimazole?

A

agranulocytosis

26
Q

What baseline monitoring in needed with methimazole?


A

TSH, T3, T4, CBC, and LFTs

27
Q

Is methimaozle safe in pregnancy?

A

Methimazole should be avoided by women who are pregnancy especially in the first trimester

28
Q

What is the preferred medication of choice for hyperthyroidism in pregnancy?

A

Propylthiouracil (PTU)

29
Q

What are contraindications to methimaozle?

A

pregnancy (especially in the first trimester), hepatitis, myelosuppression, agranulocytosis, or hepatic impairment

30
Q

How should hypothyroidism be managed in infancy?

A

Hormone replacement therapy should last 3 years and then stop for 4 weeks to allow for follow-up testing.

31
Q

When should TSH be rechecked after levothyroxine is initiated?

A

in 6-8 weeks after dose changes then yearly after a euthyroid state is reached

32
Q

What drug-drug interactions can occur with levothyroxine?


A

H2 blockers (cimetidine) PPIs (lansoprazole), Sucralfate, Aluminum-containing antacids (Maalox), Calcium supplements (Tums), Iron supplements (ferrous sulfate), Magnesium salts, Orlistat can all reduce absorption of levothyroxine

Phenytoin (Dilantin), Carbamazepine (Tegretol), Rifampin (Rifadin), Sertraline (Zoloft), and Phenobarbital can all inhibit metabolization of levothyroxine
Levothyroxine will affect the metabolization of Warfarin, Catecholamines, Insulin, Digoxin

33
Q

What pharmacological therapy is indicated for patients with an HgbA1C > 9%?

A

dual therapy is recommended (i.e., start at step 2).

34
Q

What are the preferred oral antidiabetic medication classes for in the setting of ASCVD, HF, or CKD?

A

SGLT-2 inhibitors

35
Q

What are the preferred oral antidiabetic medication classes for weight loss?

A

GLP-1s or SGLT-2 inhibitors

36
Q

What is the typical initiation dose for insulin?

A

10 IU a day OR 0.1-0.2 IU/kg

37
Q

What is the onset of action and duration for rapid acting insulin?

A

Rapid acting insulins such as lispro (humalog), apart (novolog), or glulisine (apidra) have an onset of action between 15-30 minutes with a duration of 3-6 hours.

38
Q

What is the onset of action and duration for short acting insulin?

A

Short acting insulin such as regular insulin (Humulin R or Novolin R) has an onset of action between 30-60 minutes with a duration of 6-10 hours with a duration of 6-10 hours.

39
Q

What is the onset of action for intermediate acting insulin?

A

Intermediate acting insulin such as neutral protamine Hagedom (NPH) insulin (Humulin N or Novolin N) has an onset of action between 60-120 minutes with a duration of 16-24 hours.

40
Q

What is the onset of action for long acting insulin?

A

Long acting insulin such as insulin glargine (lantus) or determir (levemir) has an onset of action between 60-120 minutes with a duration of 18-24 hours.

41
Q

What are the rapid acting insulins?

A

Rapid acting insulins such as lispro (humalog), apart (novolog), or glulisine (apidra) have an onset of action between 15-30 minutes with a duration of 3-6 hours.

42
Q

What are the short acting insulins?

A

Short acting insulin such as regular insulin (Humulin R or Novolin R) has an onset of action between 30-60 minutes with a duration of 6-10 hours with a duration of 6-10 hours.

43
Q

What are the intermediate acting insulins?

A

Intermediate acting insulin such as neutral protamine Hagedom insulin (Humulin N or Novolin N) has an onset of action between 60-120 minutes with a duration of 16-24 hours.

44
Q

What are the long acting insulins?

A

Long acting insulin such as insulin glargine (lantus) or determir (levemir) has an onset of action between 60-120 minutes with a duration of 18-24 hours.

45
Q

For what condition is metformin contraindicated?

A

renal insufficiency as the drug can accumulate to toxic levels and heart failure as there is an increased risk for acidosis

46
Q

What is an example of an alpha-glucosidase inhibitor?

A

acarbose

47
Q

What is the mechanism of action of alpha-glucosidase inhibitors such as acarbose?

A

they act in the intestine to delay absorption of carbohydrates to decrease the postprandial rise in glucose

48
Q

What are adverse reactions of acarbose?


A

alpha glucosidase inhibitors act in the intestine to delay absorption of carbohydrates and can cause flatulence, cramps, abdominal distention, borborygmus (rumbling bowel sounds), and diarrhea as a result of bacterial fermentation of unabsorbed carbohydrates in the colon. It can also decrease absorption of iron, posing a risk for anemia.

49
Q

DPP4 inhibitors (gliptins) should be used cautiously in patients with which condition?

A

pancreatitis

50
Q

What are adverse effects of DPP4s?


A

disabling joint pain that can occur at any point in time during treatment, angioedema, acute pancreatitis

51
Q

What is the most common side effect of Exenatide (Byetta)?

A

GLP-1s may cause pancreatitis; therefore, monitoring of amylase and lipase is warranted; other adverse effects include renal insufficiency and thyroid cancer

52
Q

What are contraindications to GLP1s?

A

pancreatitis, personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2

Pharmacology (5 decks)

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