How do antiplatelet medications work?

Choice A rationale

Magnesium plays a role in muscle relaxation but is not primarily responsible for muscle contraction. It helps in stabilizing the muscle membrane by acting as a natural calcium blocker. Deficiency in magnesium can lead to muscle cramps and spasms, but it does not directly cause muscle contraction and relaxation processes.

Choice B rationale

Chloride is an essential electrolyte involved in maintaining fluid balance and acid-base balance, but it does not directly influence muscle contraction and relaxation. It works in conjunction with sodium to regulate osmotic pressure and acid-base balance.

Choice C rationale

Calcium is crucial for muscle contraction. It is released from the sarcoplasmic reticulum within the muscle cells and binds to troponin, causing a conformational change that allows actin and myosin to interact and generate contraction. During relaxation, calcium ions are pumped back into the sarcoplasmic reticulum.

Choice D rationale

Hydrogen ions are involved in pH balance and acid-base regulation but do not directly affect muscle contraction and relaxation. Excess hydrogen ions (acidosis) can impair muscle function, but they are not the primary factor in muscle contraction processes.

Choice A rationale

Thiazide diuretics do not block the sodium pump. They act primarily on the distal convoluted tubule in the kidneys.

Choice B rationale

Thiazide diuretics block the chloride pump in the distal convoluted tubule, preventing the reabsorption of sodium and chloride, leading to increased urine output and decreased blood pressure.

Choice C rationale

Thiazide diuretics do not block the carbonic anhydrase pump. This action is associated with carbonic anhydrase inhibitors.

Choice D rationale

Thiazide diuretics do not block the potassium pump. They can cause potassium loss as a side effect, but this is not their primary mechanism of action.