Week 6_7 reverse cards Flashcards

1
Q

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

A

Prednisone - Mechanism of Action

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2
Q

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

A

Dexamethasone - Mechanism of Action

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3
Q

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

A

Hydrocortisone - Mechanism of Action

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4
Q

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.

A

Prednisone - Pharmacokinetics

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5
Q

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

A

Dexamethasone - Pharmacokinetics

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6
Q

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

A

Hydrocortisone - Pharmacokinetics

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7
Q

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

A

Prednisone - Drug Interactions

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8
Q

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

A

Dexamethasone - Drug Interactions

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9
Q

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

A

Hydrocortisone - Drug Interactions

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10
Q

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

A

Prednisone - Adverse Effects

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11
Q

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

A

Dexamethasone - Adverse Effects

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12
Q

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

A

Hydrocortisone - Adverse Effects

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13
Q

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

A

Prednisone - Therapeutic Use

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14
Q

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

A

Dexamethasone - Therapeutic Use

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15
Q

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

A

Hydrocortisone - Therapeutic Use

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16
Q

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

A

Prednisone - Contraindications

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17
Q

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

A

Dexamethasone - Contraindications

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18
Q

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

A

Hydrocortisone - Contraindications

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19
Q

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

A

Prednisone - Monitoring

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20
Q

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

A

Dexamethasone - Monitoring

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21
Q

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

A

Hydrocortisone - Monitoring

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22
Q

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

A

Prednisone - Black Box Warning

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23
Q

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

A

Dexamethasone - Black Box Warning

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24
Q

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

A

Hydrocortisone - Black Box Warning

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