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5033 > Week 6 & 7 Flashcards > Flashcards

Week 6 & 7 Flashcards

1
Q

Prednisone - Mechanism of Action

A

Prednisone binds to glucocorticoid receptors, influencing gene transcription to increase anti-inflammatory proteins and suppress pro-inflammatory mediators.

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2
Q

Dexamethasone - Mechanism of Action

A

Dexamethasone binds to glucocorticoid receptors, modifying gene transcription and exerting potent anti-inflammatory and immunosuppressive effects.

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3
Q

Hydrocortisone - Mechanism of Action

A

Hydrocortisone binds to glucocorticoid receptors, altering gene transcription to suppress inflammation and immune responses.

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4
Q

Prednisone - Pharmacokinetics

A

Prednisone is a prodrug, converted to active prednisolone in the liver; it has a moderate mineralocorticoid effect and a biological half-life of 18-36 hours.

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5
Q

Dexamethasone - Pharmacokinetics

A

Dexamethasone has a long half-life of 36-54 hours with high glucocorticoid and negligible mineralocorticoid activity; cleared primarily by hepatic metabolism.

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6
Q

Hydrocortisone - Pharmacokinetics

A

Hydrocortisone has a biological half-life of 8-12 hours, significant mineralocorticoid activity, and moderate glucocorticoid potency; cleared hepatically.

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7
Q

Prednisone - Drug Interactions

A

Prednisone can cause hypokalemia, especially with potassium-depleting diuretics and digoxin. It increases hyperglycemia risk and interacts with NSAIDs and vaccines.

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8
Q

Dexamethasone - Drug Interactions

A

Dexamethasone interacts with potassium-depleting drugs, NSAIDs (GI bleeding), hypoglycemics (hyperglycemia), and vaccines (reduced response).

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9
Q

Hydrocortisone - Drug Interactions

A

Hydrocortisone interacts similarly with NSAIDs, diuretics, and digoxin; risk for adrenal suppression with abrupt discontinuation.

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10
Q

Prednisone - Adverse Effects

A

Prednisone’s adverse effects include osteoporosis, hyperglycemia, infection susceptibility, delayed wound healing, and adrenal suppression with prolonged use.

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11
Q

Dexamethasone - Adverse Effects

A

Dexamethasone can cause muscle weakness, hyperglycemia, mood changes, immune suppression, cataracts, and peptic ulcers with prolonged use.

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12
Q

Hydrocortisone - Adverse Effects

A

Hydrocortisone’s adverse effects include significant sodium retention, potassium loss, hypertension, and GI disturbances.

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13
Q

Prednisone - Therapeutic Use

A

Prednisone is used for inflammatory, autoimmune, and allergic conditions; also in transplant rejection prevention and as part of cancer therapy.

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14
Q

Dexamethasone - Therapeutic Use

A

Dexamethasone is used for severe inflammation, cerebral edema, respiratory distress syndrome, and diagnostic testing for Cushing syndrome.

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15
Q

Hydrocortisone - Therapeutic Use

A

Hydrocortisone is used for adrenal insufficiency, allergic reactions, and inflammatory conditions with balanced glucocorticoid and mineralocorticoid effects.

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16
Q

Prednisone - Contraindications

A

Prednisone is contraindicated in systemic fungal infections and live virus vaccination; caution in diabetes, osteoporosis, and infections.

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17
Q

Dexamethasone - Contraindications

A

Dexamethasone is contraindicated in systemic fungal infections and live vaccines; use caution in hypertension, diabetes, and pediatric patients.

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18
Q

Hydrocortisone - Contraindications

A

Hydrocortisone is contraindicated in systemic fungal infections; caution in patients with renal or cardiac impairments.

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19
Q

Prednisone - Monitoring

A

Monitor blood glucose, bone density, potassium levels, and signs of infection during long-term prednisone use.

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20
Q

Dexamethasone - Monitoring

A

Monitor glucose levels, signs of adrenal suppression, infection, and psychologic disturbances with dexamethasone.

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21
Q

Hydrocortisone - Monitoring

A

Monitor electrolyte balance, fluid retention, glucose levels, and adrenal function during hydrocortisone therapy.

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22
Q

Prednisone - Black Box Warning

A

Prednisone carries no black box warning but risks adrenal insufficiency, especially if discontinued abruptly after long-term use.

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23
Q

Dexamethasone - Black Box Warning

A

Dexamethasone carries no black box warning but requires tapering after prolonged use to prevent adrenal crisis.

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24
Q

Hydrocortisone - Black Box Warning

A

Hydrocortisone carries no black box warning but long-term use can cause adrenal insufficiency and significant fluid retention.

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25
Rapid-Acting Insulin - Mechanism of Action
Mimics natural insulin release, rapidly lowering blood glucose by promoting glucose uptake in muscle and fat tissues.
26
Short-Acting Insulin - Mechanism of Action
Promotes glucose uptake into tissues; regular insulin is used for mealtime glucose control and emergencies.
27
Intermediate-Acting Insulin - Mechanism of Action
NPH insulin provides prolonged basal glucose control by delaying absorption.
28
Long-Acting Insulin - Mechanism of Action
Degludec, detemir, and glargine provide steady, long-term glucose regulation with minimal peaks.
29
Metformin - Mechanism of Action
Reduces hepatic gluconeogenesis, improves peripheral insulin sensitivity, and slows intestinal glucose absorption.
30
GLP-1 Receptor Agonists - Mechanism of Action
Enhances insulin secretion, slows gastric emptying, increases satiety, and suppresses glucagon secretion.
31
SGLT-2 Inhibitors - Mechanism of Action
Inhibits renal glucose reabsorption, increasing urinary glucose excretion to lower blood glucose.
32
DPP-4 Inhibitors - Mechanism of Action
Inhibits DPP-4 enzyme, prolonging incretin hormone activity, enhancing insulin release, and suppressing glucagon.
33
Sulfonylureas - Mechanism of Action
Stimulates pancreatic beta cells to release insulin by blocking ATP-sensitive K+ channels, reducing glucose levels.
34
Thiazolidinediones (TZDs) - Mechanism of Action
Activates PPAR-y receptors, improving insulin sensitivity in adipose tissue, liver, and skeletal muscle.
35
Rapid-Acting Insulin - Pharmacokinetics
Onset: 10-30 min; peak: 1-3 hr; duration: 3-5 hr. Examples: insulin lispro, aspart, glulisine.
36
Long-Acting Insulin - Pharmacokinetics
Long duration (up to 24-42 hours), no pronounced peak, providing steady glucose control.
37
Metformin - Pharmacokinetics
Well absorbed orally, not metabolized, excreted via kidneys as unchanged drug.
38
GLP-1 Receptor Agonists - Pharmacokinetics
Subcutaneous injection; long-acting forms (dulaglutide, semaglutide) dosed weekly; short-acting daily.
39
SGLT-2 Inhibitors - Pharmacokinetics
Metabolized via glucuronidation; contraindicated in severe renal dysfunction.
40
DPP-4 Inhibitors - Pharmacokinetics
Well absorbed; saxagliptin metabolized via CYP3A4; linagliptin excreted via enterohepatic system.
41
Sulfonylureas - Pharmacokinetics
Oral absorption, metabolized in liver, excreted in urine/feces. Duration: 12-24 hours.
42
TZDs - Pharmacokinetics
Extensive metabolism via CYP2C8; pioglitazone excreted via bile; rosiglitazone excreted renally.
43
Metformin - Adverse Effects
GI issues (nausea, diarrhea); risk of lactic acidosis in renal impairment. Monitor renal function.
44
GLP-1 Receptor Agonists - Adverse Effects
GI effects (nausea, vomiting); risk of pancreatitis; contraindicated in medullary thyroid cancer.
45
SGLT-2 Inhibitors - Adverse Effects
UTIs, genital mycotic infections, hypotension due to osmotic diuresis; rare: ketoacidosis, fractures.
46
Sulfonylureas - Adverse Effects
Hypoglycemia, weight gain, increased risk in renal/hepatic impairment.
47
TZDs - Adverse Effects
Weight gain, fluid retention, risk of fractures; contraindicated in symptomatic heart failure.
48
GLP-1 Receptor Agonists - Therapeutic Use
Type 2 diabetes management; cardiovascular benefits; some forms approved for obesity.
49
SGLT-2 Inhibitors - Contraindications
Severe renal impairment; therapy depends on adequate kidney function.
50
Metformin - Contraindications
Contraindicated in severe renal dysfunction (eGFR <30 mL/min); risk of lactic acidosis.
51
Combination Oral Contraceptives (COCs) - Mechanism of Action
Estrogen inhibits FSH release, preventing follicular development. Progestin suppresses LH, preventing ovulation, and thickens cervical mucus to hinder sperm movement.
52
Progestin-Only Pills - Mechanism of Action
Progestin thickens cervical mucus to prevent sperm penetration and suppresses LH secretion, inhibiting ovulation.
53
Medroxyprogesterone Injection - Mechanism of Action
Progestin suppresses ovulation, thickens cervical mucus, and alters the endometrium to prevent implantation.
54
Etonogestrel Implant - Mechanism of Action
A subdermal progestin implant prevents ovulation and thickens cervical mucus, providing contraception for up to 3 years.
55
Levonorgestrel IUD - Mechanism of Action
Releases progestin locally, thickening cervical mucus, thinning the endometrium, and inhibiting sperm mobility.
56
Combination Oral Contraceptives - Pharmacokinetics
Ethinyl estradiol and progestin undergo hepatic metabolism; synthetic forms resist first-pass metabolism for prolonged action.
57
Progestin-Only Pills - Pharmacokinetics
Rapidly metabolized in the liver, requiring daily administration for effectiveness.
58
Medroxyprogesterone Injection - Pharmacokinetics
Provides high sustained progestin levels with a long half-life (40-50 days), ensuring efficacy for 3 months per injection.
59
Combination Oral Contraceptives - Drug Interactions
CYP3A4 inducers like rifampin and carbamazepine reduce efficacy. Antibiotics may interfere with enterohepatic recycling of estrogen.
60
Combination Oral Contraceptives - Adverse Effects
Common effects include nausea, breast fullness, headache, fluid retention, and increased blood pressure. Severe risks: thromboembolism, MI, and stroke.
61
Progestin-Only Pills - Adverse Effects
Irregular bleeding, headache, and reduced efficacy compared to combination oral contraceptives.
62
Medroxyprogesterone Injection - Adverse Effects
Weight gain, bone loss (osteoporosis risk), delayed return to fertility post-discontinuation.
63
Levonorgestrel IUD - Adverse Effects
Irregular bleeding and headaches; efficacy may decrease in women >130% ideal body weight.
64
Combination Oral Contraceptives - Contraindications
Contraindicated in thromboembolic disease, estrogen-dependent cancers, liver disease, and pregnancy.
65
Transdermal Patch - Contraindications
Not recommended in women with BMI ≥ 30 kg/m² due to increased venous thromboembolism risk.
66
Levonorgestrel IUD - Contraindications
Avoid in patients with pelvic inflammatory disease or a history of ectopic pregnancy.
67
Combination Oral Contraceptives - Monitoring
Monitor for adverse effects like thromboembolism, breakthrough bleeding, and blood pressure elevation.
68
Medroxyprogesterone Injection - Monitoring
Monitor bone mineral density for long-term users due to osteoporosis risk.
69
Levonorgestrel IUD - Therapeutic Use
Long-term contraception and treatment for heavy menstrual bleeding.
70
Emergency Contraception - Therapeutic Use
Postcoital contraception: single high dose of levonorgestrel within 72 hours or ulipristal within 5 days. Copper IUD effective within 5 days.
71
Combination Oral Contraceptives - Black Box Warning
Increased risk of thromboembolism, especially in women over 35 who smoke.
72
Medroxyprogesterone Injection - Black Box Warning
Black box warning for significant bone loss with prolonged use beyond 2 years.
73
Levothyroxine - Mechanism of Action
Levothyroxine (T4) is converted into active T3 in tissues, which binds to nuclear receptors, modulating gene expression and restoring normal metabolism.
74
Liothyronine - Mechanism of Action
Liothyronine (T3) directly binds nuclear receptors, stimulating gene transcription and rapidly improving hypothyroid symptoms.
75
Methimazole - Mechanism of Action
Inhibits thyroid peroxidase, blocking iodination and coupling of tyrosines, preventing T3/T4 synthesis.
76
Propylthiouracil (PTU) - Mechanism of Action
Blocks thyroid peroxidase and inhibits peripheral conversion of T4 to T3, reducing thyroid hormone levels.
77
Levothyroxine - Pharmacokinetics
Absorbed orally but reduced by food, calcium, and iron. Metabolized via deiodination; long half-life (7-10 days), allowing once-daily dosing.
78
Methimazole - Pharmacokinetics
Longer half-life than PTU (6-13 hours), enabling once-daily dosing; metabolized hepatically.
79
Propylthiouracil (PTU) - Pharmacokinetics
Shorter half-life than methimazole; metabolized in the liver, requires multiple daily doses.
80
Levothyroxine - Drug Interactions
CYP450 inducers (e.g., rifampin, phenytoin) increase metabolism of levothyroxine, reducing efficacy.
81
Methimazole - Drug Interactions
Minimal drug interactions compared to PTU; fewer effects on CYP450 enzymes.
82
Levothyroxine - Adverse Effects
Overdose mimics hyperthyroidism, causing tachycardia, heat intolerance, weight loss, and nervousness.
83
Methimazole - Adverse Effects
Common: rash, pruritus. Severe: agranulocytosis and hepatotoxicity. Methimazole has a lower risk of hepatotoxicity than PTU.
84
Propylthiouracil (PTU) - Adverse Effects
Severe risk of hepatotoxicity and agranulocytosis; black box warning for liver failure.
85
Levothyroxine - Therapeutic Use
First-line for hypothyroidism; preferred due to its stability, once-daily dosing, and predictable effects.
86
Methimazole - Therapeutic Use
First-line for hyperthyroidism except in pregnancy (first trimester); normalizes thyroid function within weeks.
87
Propylthiouracil (PTU) - Therapeutic Use
Used in hyperthyroidism during the first trimester of pregnancy due to lower teratogenic risk than methimazole.
88
Levothyroxine - Contraindications
Contraindicated in untreated adrenal insufficiency and thyrotoxicosis; caution with cardiac disease.
89
Methimazole - Contraindications
Contraindicated in severe liver dysfunction; caution in pregnancy (except for second/third trimesters).
90
Levothyroxine - Monitoring
Monitor TSH levels 6-8 weeks after initiation or dose changes; assess symptom improvement.
91
Methimazole - Monitoring
Monitor for agranulocytosis (sore throat, fever) and liver function during treatment.
92
Thyroid Storm - Management
Treat with beta-blockers (e.g., propranolol) for sympathetic symptoms, thioamides (high-dose methimazole/PTU), and supportive care.

5033 (20 decks)

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