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Questions and Answers
What is the predicted decrease in blood pressure if salt intake is decreased to 0.4g/100g food?
What is the predicted decrease in blood pressure if salt intake is decreased to 0.4g/100g food?
- 15mmHg
- 5mmHg (correct)
- 10mmHg
- 3mmHg
What is the clinical definition of hypertension in individuals over 80 years old?
What is the clinical definition of hypertension in individuals over 80 years old?
- 150/90 mmHg (correct)
- 170/110 mmHg
- 140/90 mmHg
- 160/100 mmHg
What is the formula for blood pressure?
What is the formula for blood pressure?
- BP = CO - TPR
- BP = CO x TPR (correct)
- BP = CO + TPR
- BP = CO / TPR
Which of the following is NOT a key contributor to the maintenance of blood pressure?
Which of the following is NOT a key contributor to the maintenance of blood pressure?
What is the equivalent of 1 pharmacotherapy in terms of blood pressure reduction?
What is the equivalent of 1 pharmacotherapy in terms of blood pressure reduction?
Which hormone is responsible for increasing blood volume by promoting sodium reabsorption in the DCT?
Which hormone is responsible for increasing blood volume by promoting sodium reabsorption in the DCT?
What is the effect of acetylcholine on blood vessels?
What is the effect of acetylcholine on blood vessels?
Which receptor is involved in the vasodilatory effect of nitric oxide?
Which receptor is involved in the vasodilatory effect of nitric oxide?
What is the effect of β-blockers on the renin-angiotensin system?
What is the effect of β-blockers on the renin-angiotensin system?
Which type of diuretic inhibits Na+ reabsorption in the DCT?
Which type of diuretic inhibits Na+ reabsorption in the DCT?
What is the effect of angiotensin II on blood pressure?
What is the effect of angiotensin II on blood pressure?
What is the primary effect of positive inotropes in heart failure?
What is the primary effect of positive inotropes in heart failure?
What is the mechanism of action of nitrates in heart failure?
What is the mechanism of action of nitrates in heart failure?
What is the primary effect of beta blockers in heart failure?
What is the primary effect of beta blockers in heart failure?
What is the primary effect of diuretics in heart failure?
What is the primary effect of diuretics in heart failure?
What is the primary effect of angiotensin-converting enzyme inhibitors (ACEi) in heart failure?
What is the primary effect of angiotensin-converting enzyme inhibitors (ACEi) in heart failure?
What is the primary cause of death in 50% of worst-case heart failure patients within 6 months of diagnosis?
What is the primary cause of death in 50% of worst-case heart failure patients within 6 months of diagnosis?
Which type of diuretics inhibit Na+/K+ exchange in the collecting duct and distal convoluted tubule?
Which type of diuretics inhibit Na+/K+ exchange in the collecting duct and distal convoluted tubule?
What is the effect of Ca2+ channel blockers on smooth muscle cells?
What is the effect of Ca2+ channel blockers on smooth muscle cells?
What is the mechanism of action of K+ channel activators?
What is the mechanism of action of K+ channel activators?
Which type of diuretic is most likely to cause hyperkalaemia, particularly in renal impairment?
Which type of diuretic is most likely to cause hyperkalaemia, particularly in renal impairment?
What is the primary effect of loop diuretics on blood volume?
What is the primary effect of loop diuretics on blood volume?
What is the primary effect of vasodilators on blood pressure?
What is the primary effect of vasodilators on blood pressure?
Noradrenaline increases blood pressure by stimulating β1 receptors.
Noradrenaline increases blood pressure by stimulating β1 receptors.
Atrial natriuretic peptide decreases blood volume by stimulating the release of aldosterone.
Atrial natriuretic peptide decreases blood volume by stimulating the release of aldosterone.
Angiotensin-converting enzyme inhibitors increase blood pressure by converting angiotensin I to angiotensin II.
Angiotensin-converting enzyme inhibitors increase blood pressure by converting angiotensin I to angiotensin II.
β-blockers increase heart rate by stimulating β2 receptors.
β-blockers increase heart rate by stimulating β2 receptors.
Thiazide diuretics inhibit potassium reabsorption in the distal convoluted tubule.
Thiazide diuretics inhibit potassium reabsorption in the distal convoluted tubule.
Vasodilators decrease blood pressure by increasing systemic vascular resistance.
Vasodilators decrease blood pressure by increasing systemic vascular resistance.
Diuretics are primarily used to treat heart failure by reducing blood volume, which in turn decreases cardiac output.
Diuretics are primarily used to treat heart failure by reducing blood volume, which in turn decreases cardiac output.
The equivalent of 1 pharmacotherapy in terms of blood pressure reduction is a 5 mmHg decrease in blood pressure.
The equivalent of 1 pharmacotherapy in terms of blood pressure reduction is a 5 mmHg decrease in blood pressure.
Β-adrenoceptor antagonists (β-blockers) increase heart rate, which in turn increases blood pressure.
Β-adrenoceptor antagonists (β-blockers) increase heart rate, which in turn increases blood pressure.
Vasodilators primarily act by increasing cardiac output, which in turn decreases blood pressure.
Vasodilators primarily act by increasing cardiac output, which in turn decreases blood pressure.
Angiotensin-converting enzyme inhibitors (ACEI) are primarily used to treat hypertension by increasing cardiac output.
Angiotensin-converting enzyme inhibitors (ACEI) are primarily used to treat hypertension by increasing cardiac output.
The primary effect of positive inotropes in heart failure is to decrease sympathetic activity.
The primary effect of positive inotropes in heart failure is to decrease sympathetic activity.
Beta blockers are used to increase the volume of the circulatory system in heart failure.
Beta blockers are used to increase the volume of the circulatory system in heart failure.
The renin-angiotensin system is activated in response to increased blood volume.
The renin-angiotensin system is activated in response to increased blood volume.
Vasodilators, such as nitrates, increase the force of contractions in heart failure.
Vasodilators, such as nitrates, increase the force of contractions in heart failure.
The mechanism of action of cardiac glycosides, such as digoxin, involves the inhibition of sGC and the production of cGMP.
The mechanism of action of cardiac glycosides, such as digoxin, involves the inhibition of sGC and the production of cGMP.
The primary effect of diuretics in heart failure is to decrease sympathetic activity.
The primary effect of diuretics in heart failure is to decrease sympathetic activity.
Furosemide decreases blood pressure by inhibiting Na+ reabsorption in the distal convoluted tubule.
Furosemide decreases blood pressure by inhibiting Na+ reabsorption in the distal convoluted tubule.
K+ sparing diuretics, such as amiloride, prevent hypokalaemia by inhibiting Na+/K+ exchange in the collecting duct and distal convoluted tubule.
K+ sparing diuretics, such as amiloride, prevent hypokalaemia by inhibiting Na+/K+ exchange in the collecting duct and distal convoluted tubule.
Ca2+ channel blockers, such as nifedipine, decrease blood pressure by activating K+ATP channels.
Ca2+ channel blockers, such as nifedipine, decrease blood pressure by activating K+ATP channels.
Heart failure is defined as a cardiac output that is inadequate to meet the metabolic demands only during exercise.
Heart failure is defined as a cardiac output that is inadequate to meet the metabolic demands only during exercise.
VASODILATORS, such as minoxidil, decrease blood pressure by inhibiting Ca2+ influx.
VASODILATORS, such as minoxidil, decrease blood pressure by inhibiting Ca2+ influx.
Bendroflumethiazide is a type of K+ sparing diuretic.
Bendroflumethiazide is a type of K+ sparing diuretic.
Study Notes
Nervous Control of Blood Pressure
- Blood pressure is regulated by the nervous system through the autonomic nervous system, which controls heart rate, contractility, and vasodilation or vasoconstriction.
- Noradrenaline (NA) and adrenaline (A) increase blood pressure, while acetylcholine (ACh) decreases it.
- NA and A work through α1, β1, and β2 receptors, while ACh works through mAChR2 and mAChR3 receptors.
Blood Volume
- Blood volume is regulated by hormones, including aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP).
- Aldosterone and ADH increase blood volume, while ANP decreases it.
Autonomic Control of Blood Pressure
- The autonomic nervous system controls blood pressure through the sympathetic and parasympathetic nervous systems.
- The sympathetic nervous system increases blood pressure, while the parasympathetic nervous system decreases it.
- Agonists and antagonists of these systems can be used to regulate blood pressure.
Anti-Hypertensive Drug Classes
- Diuretics decrease blood volume and blood pressure.
- Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) decrease blood pressure by inhibiting the renin-angiotensin system.
- Β-adrenoceptor antagonists (β-blockers) decrease blood pressure by inhibiting the sympathetic nervous system.
- Vasodilators decrease blood pressure by increasing blood vessel diameter.
Anti-Hypertensive Drugs
- Vasodilators: calcium channel blockers, potassium channel openers, and β-blockers.
- ACEI: captopril, enalopril.
- ARB: losartan, eprosartan.
- Î’-blockers: atenolol, propranolol.
- Diuretics: thiazide diuretics, loop diuretics, potassium-sparing diuretics.
Heart Failure
- Heart failure is defined as the inability of the heart to pump enough blood to meet the body's metabolic demands.
- It can be caused by coronary artery disease, volume overload, pressure overload, and hyperthyroidism.
- Symptoms include oedema, breathlessness, fatigue, and cardiac hypertrophy.
- Treatment options include diuretics, vasodilators, β-blockers, and positive inotropes.
Treatment of Heart Failure
- Diuretics: decrease blood volume and relieve peripheral oedema.
- Vasodilators: decrease blood pressure and peripheral resistance.
- β-blockers: decrease sympathetic activity and cardiac hypertrophy.
- Positive inotropes: increase the force of contractions and decrease cardiac hypertrophy.
Feedback Loops
- Feedback loops regulate blood pressure and cardiovascular function.
Vasodilators
- Vasodilators increase blood vessel diameter and decrease blood pressure.
- Nitrates release nitric oxide, which binds to soluble guanylyl cyclase and produces cGMP, leading to vasodilation.
Beta Blockers
- Beta blockers inhibit β1 receptors on the heart, decreasing heart contractility and rate.
- They also inhibit renin release from the kidney and decrease blood pressure.
Heart Failure – Positive Inotropes
- Cardiac glycosides (e.g., digoxin) inhibit Na+/K+-ATPase, increasing the force of contractions.
- Side effects include arrhythmia, disturbed vision, and GI disturbances.
Learning Outcomes
- Describe the mechanism of action in heart failure and hypertension for ACEI, ARBs, aldosterone antagonists, diuretics, vasodilators, beta-blockers, and positive inotropes.
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Description
This quiz covers the basics of pharmacology, focusing on hypertension, diuretics, ACE inhibitors, beta-blockers, and vasodilators. Test your knowledge of these cardiovascular drugs and their effects on the body.
