Pharmacology Practice Quiz 8

Adenosine receptors are a type of G protein-coupled receptors (GPCRs). GPCRs are a large family of cell surface receptors that are involved in transmitting signals from the outside of the cell to the inside. Adenosine receptors specifically bind to the molecule adenosine and play a role in regulating various physiological processes such as neurotransmission, inflammation, and cardiovascular function. Therefore, the statement "Adenosine receptors are G coupled protein receptors" is true.

Calcium channel blockers are a class of medications that work by blocking the influx of calcium into the cells of the heart and blood vessels. By doing so, they can slow down the rate at which electrical signals are conducted through the atrioventricular (AV) node in the heart. Atrial fibrillation is a condition characterized by irregular and rapid heartbeats, and slowing down the conduction of electrical signals through the AV node can help to control the heart rate in patients with this condition. Therefore, it is true that calcium channel blockers are used to slow the rate of AV-conduction in patients with atrial fibrillation.

The statement "I can't wait until December 15th" implies that the person is excited and eager for December 15th to arrive. Therefore, the correct answer is True, indicating that the person is looking forward to that date.

This would be true because you would get more sodium influx and you would have more depolarization that you would have to reverse.

Patients with Congestive Heart Failure (CHF) experience a weakened heart muscle and impaired pumping function, which can lead to fluid build-up in the lungs and other parts of the body. This fluid build-up increases the workload on the heart and disrupts the normal electrical signals that regulate the heart's rhythm. As a result, patients with CHF are more susceptible to developing cardiac arrhythmias, such as atrial fibrillation or ventricular tachycardia. Therefore, the statement that patients with CHF are more vulnerable to cardiac arrhythmias is true.

Flecainide showed a 2.5 increase in mortality and this arm of the study was stopped early. Propranolol was shown to have a protective effect.

Loss of function mutations in the hERG gene would result in LONG QT syndrome, while a GAIN in function mutation would result in short QT syndrome.

Depends who you ask. Lexicomp lists the first pronunciation.

Subclass IA: Medium Duration of Blockade
Subclass IB: Short Duration of Blockade
Subclass IC: Long Duration of Blockade

An increased expression of the sodium/calcium exchanger can lead to the occurrence of delayed afterdepolarizations (DADs). DADs are abnormal depolarizations that can occur during the repolarization phase of the cardiac action potential. The sodium/calcium exchanger is responsible for maintaining the balance of sodium and calcium ions within the cardiac cells. When there is an increased expression of this exchanger, it can disrupt this balance and lead to the generation of DADs, which can potentially cause arrhythmias. Therefore, the statement that an increased expression of the sodium/calcium exchanger can produce DADs is true.

The proarrhythmia classes are Class IA and Class III.

Erythromycin is a CYP 3A4 inhibitor, and disopyramide is a hERG channel inhibitor metabolized by CYP 3A4. This combination can fatally prolong the QT interval.

Lidocaine preferentially interacts with INACTIVATED sodium channels.

The three mechanisms of cardiac arrythmias are Enhanced Automaticity, Afterdepolarizations & triggered automatcity, and Re-entry.

Increasing the levels of extracellular potassium will lead to an increase in the resting membrane potential of cells. This is because potassium ions play a crucial role in determining the resting membrane potential. The resting membrane potential is primarily determined by the balance between the concentrations of potassium ions inside and outside the cell. When the extracellular potassium levels increase, the concentration gradient across the cell membrane is disrupted, causing an increase in the resting membrane potential. This, in turn, makes the membrane potential less negative. Therefore, the statement "If you increase the levels of extracellular potassium, you will increase the resting membrane potential (make less negative)" is true.

A non-selective hERG blocker is less likely to have EADs (early afterdepolarizations) as a consequence than a selective hERG blocker. This is because a non-selective hERG blocker affects multiple ion channels, not just the hERG channel. By blocking multiple channels, it can prevent the occurrence of EADs, which are abnormal electrical impulses that can lead to arrhythmias. In contrast, a selective hERG blocker only targets the hERG channel, leaving other channels unaffected and potentially allowing EADs to occur. Therefore, a non-selective hERG blocker is a safer option in terms of reducing the risk of EADs.

Torsades de pointes is a life treatening VENTRICULAR arrhythmia.