A) selective beta 1 blocker
B) selective alpha 1 blocker
C) calcium channel blocker
D) selective serotonin reuptake inhibitor
The correct answer is C) calcium channel blocker.
Amlodipine is one of the most commonly prescribed medications for high blood pressure.
How Amlodipine Works
To understand why it's effective for hypertension, it helps to look at how it interacts with your vascular system:
Mechanism of Action: Amlodipine inhibits the movement of calcium ions into the smooth muscle cells of the heart and blood vessel walls.
Since calcium is required for muscles to contract, blocking it causes the muscles to stay relaxed. Vasodilation: By relaxing the smooth muscles in the arterial walls, the blood vessels widen (dilate).
Pressure Reduction: When blood vessels are wider, there is less resistance to blood flow, which directly lowers the systemic blood pressure.
Why the other options are incorrect:
A) Selective beta-1 blocker: These (like Atenolol or Metoprolol) primarily target the heart to slow the heart rate and reduce the force of contraction.
B) Selective alpha-1 blocker: These (like Doxazosin) work by blocking norepinephrine from tightening the muscles in the walls of smaller arteries and veins.
D) Selective serotonin reuptake inhibitor (SSRI): These (like Sertraline or Fluoxetine) are antidepressants used to treat mental health conditions, not hypertension.
The correct answer is C) Decrease in serum olanzapine levels.
The Science Behind It
The interaction between smoking and olanzapine is a classic example of enzyme induction.
Enzyme Induction: Polycyclic aromatic hydrocarbons (PAHs) found in tobacco smoke induce the hepatic enzyme CYP1A2.
Metabolism Boost: Olanzapine is primarily metabolized by this specific enzyme.
When the enzyme is "turned up" by smoking, the body clears the medication much faster than usual. The Result: This leads to a significant decrease (often by 30-40%) in the steady-state serum concentration of the drug compared to non-smokers.
Clinical Significance
This interaction is highly relevant in clinical settings for two main reasons:
Higher Dosing: Smokers often require higher doses of olanzapine to achieve the same therapeutic effect as non-smokers.
Toxicity Risk upon Quitting: If a patient who smokes heavily suddenly stops (e.g., during a hospital admission where smoking is prohibited), their CYP1A2 activity slows down. This can cause olanzapine levels to rise sharply, potentially leading to toxicity or increased side effects.
Important Note: It is the tobacco smoke (hydrocarbons), not the nicotine itself, that causes this effect.
Therefore, nicotine replacement therapy (patches or gum) does not cause this metabolic shift.
A) low TSH and a low free T4
B) low TSH and elevated free T4
C) elevated TSH and low free T4
D) elevated TSH and elevated T4
The correct answer is B) low TSH and elevated free T4.
Understanding Primary Hyperthyroidism
In medical terms, "primary" means the issue originates within the gland itself—in this case, the thyroid gland.
The Thyroid's Role: The thyroid gland becomes overactive and pumps out excessive amounts of thyroid hormones (Free T4 and T3).
The Feedback Loop: Your pituitary gland monitors these levels. When it senses there is already too much T4 in the bloodstream, it shuts down the production of Thyroid-Stimulating Hormone (TSH) to try and stop the thyroid from making more.
The Result: High "output" (T4) but very low "signal" (TSH).
Comparison of Lab Results
To help you keep these straight for exams or clinical practice, here is how the different options translate to thyroid status:
| Condition | TSH Level | Free T4 Level | Mechanism |
| Primary Hyperthyroidism | Low | High | The thyroid is overproducing; the pituitary is inhibited. |
| Primary Hypothyroidism | High | Low | The thyroid is failing; the pituitary is screaming (high TSH) for more. |
| Secondary Hyperthyroidism | High | High | A pituitary tumor is pumping out TSH, forcing T4 up. |
| Secondary Hypothyroidism | Low | Low | The pituitary is failing to send the signal (TSH) to the thyroid. |
Clinical Context
Common causes of the "Low TSH, High T4" pattern include Graves' disease, toxic multinodular goiter, or thyroiditis.
The correct answer is A) permethrin.
Why Permethrin?
Permethrin (typically as a 1% cream rinse) is widely considered the first-line gold standard for treating head lice (Pediculus humanus capitis).
Mechanism of Action: It is a neurotoxin that disrupts the sodium channel currents in the neurons of the lice, leading to paralysis and death.
Safety Profile: It has been used for decades and is FDA-approved for children as young as 2 months old.
Application: It is usually applied to damp hair (after washing with a non-conditioning shampoo), left for 10 minutes, and then rinsed.
A second treatment is typically required 7–9 days later to kill any lice that hatched from surviving eggs (nits).
Evaluating the Other Options
B) Magic Mouthwash: This is a compounded liquid used for oral mucositis or mouth sores; it has no role in treating external parasites.
C) Ketoconazole Shampoo: This is an antifungal medication.
It is excellent for dandruff (seborrheic dermatitis) or tinea capitis (fungal scalp infection), but it does nothing to kill lice. D) Dimethicone Lotion: While dimethicone is a very effective physical occlusive (it suffocates the lice) and is gaining popularity due to increasing permethrin resistance in some areas, permethrin remains the classic "best" or first-line answer in most medical examinations and standard guidelines.
Non-Pharmacological Tips
Even with the best medication, management is more successful when you:
Nit-pick: Use a fine-toothed comb to manually remove eggs.
Wash bedding: Clean sheets, pillowcases, and hats in hot water (60°C or 140°F).
Check contacts: Screen family members or close playmates to prevent "ping-pong" re-infections.
The correct answer is B) indomethacin.
How Indomethacin Works
In a developing fetus, the ductus arteriosus is a necessary blood vessel that allows blood to bypass the fluid-filled lungs. Normally, this vessel closes shortly after birth. When it stays open (Patent Ductus Arteriosus, or PDA), it can lead to heart strain and lung congestion.
The Role of Prostaglandins: Prostaglandins (specifically PGE2) are responsible for keeping the ductus arteriosus open.
Mechanism of Indomethacin: Indomethacin is a potent NSAID (Non-Steroidal Anti-Inflammatory Drug). It works by inhibiting the enzyme cyclooxygenase (COX), which in turn decreases the synthesis of prostaglandins.
The Result: Without prostaglandins to keep it relaxed, the smooth muscle of the ductus arteriosus constricts, leading to its closure without the need for an invasive surgical procedure.
Evaluating the Other Options
The other choices are not used in neonatal cardiac care:
A) Allopurinol: A xanthine oxidase inhibitor used to treat gout or high uric acid levels.
C) Pseudoephedrine: A decongestant used for nasal congestion.
D) Brompheniramine: An antihistamine used for allergy symptoms.
Important Clinical Note
While Indomethacin (or its "cousin" Ibuprofen) is the standard for closure, there are some cases where a doctor actually wants to keep the ductus open—specifically in "cyanotic heart defects" where the PDA is the only way for oxygenated blood to reach the body. In those opposite cases, doctors would administer Alprostadil (synthetic PGE1).
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