CVR Pharmacology

<p>Provides long-term bronchodilation (A)</p> Signup and view all the answers

<p>B2 receptors (C)</p> Signup and view all the answers

<p>Introduction of oral corticosteroids (A)</p> Signup and view all the answers

<p>Prevent airway tightening (A)</p> Signup and view all the answers

<p>By inhibiting angiotensin converting enzyme (D)</p> Signup and view all the answers

<p>Hydrochlorothiazide (B)</p> Signup and view all the answers

<p>ARBs do not cause a dry cough like ACE inhibitors (B)</p> Signup and view all the answers

<p>Decrease cardiac output and peripheral vascular resistance (A)</p> Signup and view all the answers

<p>They help to prevent hypokalemia caused by other diuretics (B)</p> Signup and view all the answers

<p>Potassium channels open and potassium exits (B)</p> Signup and view all the answers

<p>Phase 4 (Pacemaker Depolarization) (B)</p> Signup and view all the answers

<p>β1/2 adrenergic receptors (B)</p> Signup and view all the answers

<p>Automaticity (C)</p> Signup and view all the answers

<p>Excess calcium inside the cell (A)</p> Signup and view all the answers

<p>Phase 3 (Repolarization) (C)</p> Signup and view all the answers

<p>Vagal stimulation (D)</p> Signup and view all the answers

<p>Electrical signal loop re-exciting already activated heart tissue (C)</p> Signup and view all the answers

<p>Stable negative charge maintained by the sodium potassium pump (B)</p> Signup and view all the answers

<p>Convert angiotensin 1 to angiotensin 2 (B)</p> Signup and view all the answers

<p>Through vasoconstriction of blood vessels (B)</p> Signup and view all the answers

<p>They stimulate aldosterone release to increase sodium retention (B)</p> Signup and view all the answers

<p>It leads to the release of noradrenaline (A)</p> Signup and view all the answers

<p>Negative feedback as blood pressure and fluid levels rise (C)</p> Signup and view all the answers

<p>It increases sodium reabsorption and water retention (C)</p> Signup and view all the answers

<p>In the lungs and kidneys (C)</p> Signup and view all the answers

<p>Antidiuretic hormone (ADH) (D)</p> Signup and view all the answers

<p>Vasodilation of blood vessels (C)</p> Signup and view all the answers

<p>They block L-type voltage-gated calcium channels. (A)</p> Signup and view all the answers

<p>β1-selective β-blockers (C)</p> Signup and view all the answers

<p>Low blood pressure (D)</p> Signup and view all the answers

<p>Sotalol (B)</p> Signup and view all the answers

<p>They may worsen asthma symptoms. (A)</p> Signup and view all the answers

<p>To prevent death and reduce arrhythmias. (D)</p> Signup and view all the answers

<p>They lengthen the action potential duration. (D)</p> Signup and view all the answers

<p>Atrial fibrillation (D)</p> Signup and view all the answers

<p>Atrial fibrillation (B)</p> Signup and view all the answers

<p>They reduce calcium, leading to weaker contractions. (A)</p> Signup and view all the answers

Improve airflow, measured by PEF (Peak Expiratory Flow).

Relaxation of smooth muscles around bronchioles, widening airways and improving airflow.

Reduces inflammation causing airway thickening, edema, and mucus production, preventing narrowing.

Short-acting beta-2 agonist (SABA) inhaler (like salbutamol) for quick relief during attacks.

Low-dose corticosteroid inhaler added daily to reduce inflammation and prevent future symptoms.

Adding a Leukotriene Receptor Antagonist (like montelukast) for persistent symptoms.

Adrenaline causes bronchodilation (opening up of the bronchioles) due to its effect on Beta-2 receptors.

The phase where a cardiac cell returns to its resting state. Potassium exits the cell, making the inside more negative.

A protein that actively pumps sodium out of the cell and potassium into the cell, maintaining the negative resting potential.

The process of electrical signals in pacemaker cells that initiate and regulate heartbeats.

Calcium influx into the pacemaker cell makes the inside more positive, triggering the action potential.

Increases heart rate by accelerating the pacemaker potential, leading to faster action potential generation.

Slows down heart rate by slowing the pacemaker potential, leading to slower action potential generation.

Altering the rate of the heart.

Altering the strength of heart contraction.

The ability of heart cells to generate spontaneous action potentials.

Angiotensin 1 is converted to angiotensin 2 (the active form) by angiotensin-converting enzyme (ACE) in the lungs and kidneys.

Angiotensin 2 regulates blood pressure and fluid balance through its actions on various organs and systems.

Receptors responsible for the major effects of angiotensin 2 on regulating blood pressure and fluid balance.

Angiotensin 2 causes blood vessels to narrow by binding to AT1 receptors, leading to increased blood pressure.

Angiotensin 2 stimulates aldosterone release from the adrenal cortex, causing the kidneys to retain sodium (and water) for increased blood volume.

Angiotensin 2 enhances the sympathetic nervous system, leading to increased heart rate, further vasoconstriction, and higher blood pressure.

Angiotensin 2 promotes ADH release from the hypothalamus, which causes water retention in the kidneys, further contributing to fluid volume increase.

As blood pressure and fluid levels rise, the body reduces the release of renin, which initiates the angiotensin cascade, to maintain balance.

Drugs that block L-type voltage-gated calcium channels, mainly used for atrial tachycardias and post-MI arrhythmias.

β-blockers reduce heart rate by slowing down the electrical signals in the heart's conduction system.

These drugs mainly target the heart, making them safer for most people. Examples: atenolol, bisoprolol, metoprolol.

These β-blockers affect both the heart and other organs, including the lungs. Example: propranolol.

Sotalol is a β-blocker that also has class III effects, meaning it can prolong heart repolarization to control certain arrhythmias.

β-blockers reduce the strength of the action potential (AP) and prolong its duration, increasing the refractory period.

β-blockers reduce calcium entry into heart cells, causing weaker contractions (negative inotropic effect).

Non-selective β-blockers can cause vasoconstriction, narrowing blood vessels and making hands and feet feel cold.

Non-selective β-blockers can worsen asthma symptoms by affecting the lungs, so they should be avoided in patients with asthma.

Sotalol can increase the risk of Torsades de Pointes (TdP), a dangerous heart rhythm problem.

ACE inhibitors block the enzyme ACE, which normally narrows blood vessels, raising blood pressure. Blocking ACE leads to blood vessel relaxation and lower blood pressure.

Common side effects of ACE inhibitors include dry cough, angioedema (swelling around the heart), hyperkalemia (high potassium), and teratogenicity (harmful during pregnancy).

Beta blockers, particularly B1-selective ones, slow down the heart rate and reduce the force of contraction, leading to lower blood pressure.

Diuretics help reduce fluid buildup by promoting water loss. Loop diuretics are powerful but not commonly used for high blood pressure alone. Thiazide diuretics are the most popular for high blood pressure. Potassium-sparing diuretics are weak and often added to prevent potassium loss caused by other diuretics.

Thiazide diuretics work in the distal tubule of the kidney. They inhibit a protein that reabsorbs sodium and chloride back into the bloodstream causing water to follow leading to lower blood pressure.