Cardiovascular and renal drugs
Diperkenalkan| English | Makna |
|---|---|
| ACE inhibitors | ACE inhibitors |
| loop diuretics | loop diuretics |
| thiazide diuretics | thiazide diuretics |
| warfarin | warfarin |
| antiplatelet drugs | antiplatelet drugs |
A dry cough that is not an infection
- A man starts a blood pressure tablet and a month later has a dry, nagging cough. Antibiotics will not help: the cough comes from the drug's mechanism.
- Heart, kidney and clotting drugs each turn down one named step, and the step predicts both the effect and the side effects.
Lowering blood pressure
- Diuretics reduce volume. ACE inhibitors ACE抑制剂 block angiotensin II formation; angiotensin receptor blockers (ARBs) block its receptor.
- Calcium-channel blockers relax arteries; β1 blockers lower cardiac output and renin release.
Match each blood pressure drug to how it works.
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Each class turns down one named step.
Diuretics down the nephron
- Loop diuretics 袢利尿剂 block the Na⁺-K⁺-2Cl⁻ carrier in the thick ascending limb, which reabsorbs about 25% of filtered sodium: the strongest effect.
- Thiazide diuretics 噻嗪类利尿剂 act in the distal tubule (weaker); potassium-sparing diuretics act in the collecting duct (mild).
Order the diuretic sites as fluid flows down the nephron.
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The further down, the smaller the share of sodium left to block.
Electrolyte fingerprints
- Loop and thiazide diuretics both lose potassium, because more sodium reaches the collecting duct. Loops lose calcium too; thiazides keep calcium.
- Potassium-sparing diuretics keep potassium, so levels can rise too high, especially with an ACE inhibitor.
Which diuretic lowers potassium but keeps calcium?
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Thiazides lose K⁺ but increase calcium reabsorption.
Potassium-sparing diuretics can push potassium too high, especially with an ACE inhibitor.
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Both keep potassium in the body.
Anticoagulants
- Heparin acts at once and is monitored with the aPTT. Warfarin 华法林 stops the liver making working vitamin K-dependent factors; existing factors must decay first, so it takes days, and the INR is monitored.
- Direct oral anticoagulants block one factor (Xa or thrombin) with predictable effects, so they usually need no routine test.
Match each drug to how its effect is followed.
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The monitoring test follows the mechanism.
Antiplatelets are different
- Antiplatelet drugs 抗血小板药 stop platelets sticking. Aspirin blocks platelet COX-1 for the platelet's whole life, about 7–10 days.
- Anticoagulants treat clots of fibrin (in veins, or the atria in atrial fibrillation); antiplatelets treat platelet plugs in arteries.
Worked example: why warfarin is slow
- (Illustrative) Prothrombin has a half-life of about 60 hours. Warfarin stops new production, but the old prothrombin decays at its own pace.
- After 60 hours, half is left; after 120 hours, a quarter. Full effect takes days, so heparin covers the gap.
(Illustrative) A clotting factor has a half-life of 60 h. Warfarin stops new production. What percentage remains after 180 h?
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180 h is 3 half-lives, 100 → 50 → 25 → 12.5%.
Worked example: the cough
- (Fictional) ACE also breaks down bradykinin. Block ACE, bradykinin builds up in the airway, and a dry cough follows.
- An ARB blocks angiotensin II at its receptor without touching ACE, so switching to an ARB usually ends the cough.
A patient gets a dry cough on an ACE inhibitor. What is the logical switch?
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An ARB does not block ACE, so bradykinin is broken down normally.
Three common slips
- Placing thiazides in the loop. They act in the distal tubule, are weaker and keep calcium.
- Expecting warfarin to act on factors already made. It stops new ones being made.
- Treating anticoagulants and antiplatelets as the same. Fibrin clot against platelet plug, with different tests.
Recap
- Blood pressure: diuretics, ACE inhibitors (cough), ARBs, calcium-channel blockers, β1 blockers.
- Loop (25% of sodium; loses K⁺ and Ca²⁺), thiazide (distal; loses K⁺, keeps Ca²⁺), potassium-sparing (keeps K⁺).
- Heparin: aPTT, immediate. Warfarin: INR, days. DOACs: one factor. Aspirin: platelets for 7–10 days.