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C. Year 3: Core Drugs > Antiarrhythmics - Class II (B-blockers) > Flashcards

Antiarrhythmics - Class II (B-blockers) Flashcards

1
Q

The cardiac electrophysiology in a pacemaker cell has only 3 phases, which ultimately lead to an action potential (as seen in the image). What is occurring at stage 4?

1 - pacemaker potential phase
2 - depolarisation phase
3 - Leaky K+ phase
4 - Ca2+ leaking into cell phase

A

1 - pacemaker potential phase

  • similar to resting membrane potential
  • around -65 mV
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2
Q

The cardiac electrophysiology in a pacemaker cell has only 3 phases, which ultimately lead to an action potential (as seen in the image).To move between phase 4 and 0, there is a special type of channel located on the pacemaker cells that allows Na+ to flow into the pacemaker cells, raising the action potential to -50 mV. What is the channel called?

1 - Na+ channel
2 - Na+/K+ ATPase channel
3 - hyperpolarization-activated cyclic nucleotide-gated channels (HCN)
4 - Na+/Ca2+ co-transport

A

3 - hyperpolarization-activated cyclic nucleotide-gated channels (HCN)

  • important when cells hyperpolarise following an action potential, these channels help the pacemaker cell get close to action potential and fir again
  • called the funny current
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3
Q

The cardiac electrophysiology in a pacemaker cell has only 3 phases, which ultimately lead to an action potential (as seen in the image). The funny current (Na+ entering the pacemaker cells) then enters phase 0. What is this phase called?

1 - pacemaker potential phase
2 - depolarisation phase
3 - Leaky K+ phase
4 - Ca2+ leaking into cell phase

A

2 - depolarisation phase

  • Na+ enters cell through HCN
  • Ca2+ enters the cell through Ca2+ channels
  • pacemaker cells membrane potential becomes + (around 10mV
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4
Q

The cardiac electrophysiology in a pacemaker cell has only 3 phases, which ultimately lead to an action potential (as seen in the image). In phase 0 Na+ and Ca2+ enter pacemaker cells causing depolarisation (aprox 10 mV). The pacemaker cell then enters phase 3. What of the following then happens here?

1 - Ca2+ channels close
2 - Na+ channels remain open
3 - K+ channels open and K+ leaves the cell
4 - all of the above

A

4 - all of the above

  • lots of K+ channels
  • overall this causes the membrane potential to drop called repolarisation
  • phase 4 begins again
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5
Q

In a myocyte cell the cardiac electrophysiology has 5 phases (0-4), which ultimately lead to an action potential (as seen in the image). Phase 0 is the resting phase (-90mV). What then enters the myocyte through gap junctions that raises the resting membrane potential (-90mV) to the threshold potential (-70mV)?

1 - Na+
2 - K+
3 - Ca2+
4 - Mg+

A

3 - Ca2+

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6
Q

In a myocyte cell the cardiac electrophysiology has 5 phases (0-4), which ultimately lead to an action potential (as seen in the image). Phase 0 occurs when the the membrane potential reaches -70mV. Which channels then open causing depolarisation, reaching around 20mV?

1 - Na+
2 - K+
3 - Ca2+
4 - Mg+

A

1 - Na+

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7
Q

In a myocyte cell the cardiac electrophysiology has 5 phases (0-4), which ultimately lead to an action potential (as seen in the image). Following depolarisation, we reach phase 1, called initial repolarisation. Which 2 of the following occurs here?

1 - Na+ channels close
2 - K+ channels open and K+ leaves the cell
3 - Ca2+
4 - Mg+

A

1 - Na+ channels close
2 - K+ channels open and K+ leaves the cell

  • causes a drop in membrane potential
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8
Q

In a myocyte cell the cardiac electrophysiology has 5 phases (0-4), which ultimately lead to an action potential (as seen in the image). Following initial repolarisation (phase 1), to stop the myocyte going into full repolarisation, another channel opens and the membrane potential plateaus, called the plateau phase. Which channel opens to maintain this plateau phase (phase 2)?

1 - Na+ channels
2 - K+ channels
3 - Ca2+ channels
4 - Mg+ channels

A

3 - Ca2+

  • Ca2+ flows into the cell
  • membrane charge is maintained
  • responsible for heart contraction
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9
Q

In a myocyte cell the cardiac electrophysiology has 5 phases (0-4), which ultimately lead to an action potential (as seen in the image). Following the plateau phase (phase 2) which is when the heart contracts, which of the following occurs in phase 3, called repolarisation?

1 - Ca2+ channels close
2 - K+ channels remain open
3 - Ca2+ is pumped out of the cell
4 - all of the above

A

4 - all of the above

  • myocyte returns to resting membrane potential of around -90mV
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10
Q

When looking at an ECG, what does the P wave represent in relation to an an action potential?

1 - sum of depolarisation in all atrial myocytes
2 - sum of depolarisation in all ventricle myocytes
3 - sum of repolarisation in all atrial myocytes
4 - sum of repolarisation in all ventricle myocytes

A

1 - sum of depolarisation in all atrial myocytes

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11
Q

When looking at an ECG, what does the QRS wave represent in relation to an an action potential?

1 - sum of depolarisation in all atrial myocytes
2 - sum of depolarisation in all ventricle myocytes
3 - sum of repolarisation in all atrial myocytes
4 - sum of repolarisation in all ventricle myocytes

A

2 - sum of depolarisation in all ventricle myocytes

  • atrial myocytes also repolarise here as well, but this is masked by the QRS
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12
Q

When looking at an ECG, what does the ST segment represent in relation to an an action potential?

1 - sum of depolarisation in all atrial myocytes
2 - sum of depolarisation in all ventricle myocytes
3 - sum of repolarisation in all atrial myocytes
4 - plateau phase

A

4 - plateau phase

  • this is when the ventricle contract and pump blood
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13
Q

When looking at an ECG, what does the T wave represent in relation to an an action potential?

1 - sum of depolarisation in all atrial myocytes
2 - sum of depolarisation in all ventricle myocytes
3 - sum of repolarisation in all ventricle myocytes
4 - plateau phase

A

3 - sum of repolarisation in all ventricle myocytes

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14
Q

Of the list below, which drug is NOT one of the core B-blocker drug we need to be aware of?

1 - Doxazosin
2 - Bisoprolol
3 - Propranolol
4 - Carvedilol
5 - Atenolol

A

1 - Doxazosin

  • this is an alpha blocker
  • Bisoprolol most commonly used drug
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15
Q

B-blockers atenolol selectively binds with beta 1 receptors located on cardiac tissue. Which of the GPCRs pathways does this activate?

1- Gq
2 - Gs
3 - Gi
4 - Gd

A

2 - Gs
- all beta receptors are Gas

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16
Q

Once catecholamines bind with B receptors they initiate the GPCR Gs. Organised the labels below to show what happens intraceulluarly:

1 - pKA can then phosphorylate inside cell
2 - AC takes 2 phosphates and becomes cyclic adenosine monophosphate (cAMP)
3 - adenylate cyclase (AC) is activate
4 - cAMP activates protein kinase A (pKA)

A

1 - adenylate cyclase (AC) is activate
2 - AC takes 2 phosphates and becomes cyclic adenosine monophosphate (cAMP).
3 - cAMP activates protein kinase A (pKA)
4 - pKA can then phosphorylate inside cell

17
Q

Of the 4 core B-blockers we need to be aware, which drug is commonly used to treat ectopic beats on an as you need it basis?

1 - Bisoprolol
2 - Propranolol
3 - Carvedilol
4 - Atenolol

A

2 - Propranolol

18
Q

Due to their safety profile (although not always tolerated well by patients) which of the following drugs is often the 1st line medication for most tachyarrhythmias?

1 - Flecainide
2 - Atenolol
3 - Amiodarone
4 - Dronedarone

A

2 - Atenolol

19
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. The use of B-blockers is indicated in ischaemic heart disease (IHD), by improving prognosis in angina and acute coronary syndrome. How do B-blockers improve prognosis in IHD?

1 - increase HR and reduce contractility
2 - reduces HR and increase contractility
3 - increase HR and contractility
4 - decrease HR and contractility

A

4 - decrease HR and contractility

  • this reduces the oxygen demand and cardiac workload, whilst increasing perfusion
20
Q

What is the mechanism of action of B-blockers?

1 - selectively bind B-1 receptors and compete with binding of noradrenaline and adrenaline
2 - non-selectively binds a1 and B1 receptors, inhibiting Acetylcholine binding
3 - selectively bind a-1 receptors and compete with binding of Acetylcholine
2 - non-selectively binds a1 and B1 receptors, inhibiting noradrenaline and adrenaline binding

A

1 - selectively bind B1 receptors and compete with binding of noradrenaline and adrenaline

  • this is a 2nd generation B-blocker so it is able to selectively bind at the post synapse
  • reduces noradrenaline and adrenaline binding
21
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. The use of B-blockers is indicated in chronic heart failure (CHF). How do B-blockers improve prognosis in CHF?

1 - reduces parasympathetic stimulation
2 - reduces sympathetic stimulation
3 - increases parasympathetic stimulation
4 - increases sympathetic stimulation

A

2 - reduces sympathetic stimulation

22
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. The use of B-blockers is indicated in atrial fibrillation (AF) and supra-ventricular tachycardia (SVT). How to B-blockers improve prognosis in AF and SVT?

1 - prolong refractory period of AV node and terminate SVT
2 - reduce refractory period of AV node and terminate SVT

A

1 - prolong refractory period of AV node and terminate SVT

  • essentially the heart cells cannot repolarise quickly enough to maintain AF
23
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. However, they can also be used as a 4th line treatment in resistive hypertension. Although complex, how is it thought that B-blockers are able to reduce hypertension?

1 - inhibit Ca2+ channels in smooth muscle
2 - inhibits renin release
3 - increases aldosterone release
4 - inhibits Angiotensin-converting enzyme

A

2 - inhibits renin release

  • binds B1 receptors on juxtaglomerular cells
  • less renin is releases, meaning reduced SVR
24
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. However, they can also be used for migraines. How is it thought that they are able to do this?

1 - reduced dopamine release
2 - reduced glutamate release
3 - reduced neuronal activity in noradrenergic excitability

A

3 - reduced neuronal activity in noradrenergic excitability

25
Q

B1 adrenergic receptors typically increase heart rate and contractility in the heart. However, they can also be used in thyroid storm / thyrotoxicosis. How do they help alleviate this?

1 - reduce heart rate
2 - increase heart rate
3 - inhibits pituitary gland

A

1 - reduce heart rate

  • reduces palpitations and tremor
  • reduces B-adrenergic up regulation
26
Q

B-blockers can cause a number of adverse events. Which of the following is NOT a common adverse event?

1 - fatigue
2 - cold extremities
3 - headaches
4 - incontinence
5 - GI upset
6 - sleep disturbance
7 - impotence

A

4 - incontinence

27
Q

Which of the following conditions should B-blockers be avoided?

1 - COPD
2 - asthma
3 - diabetes
4 - crohns

A

2 - asthma

  • can cause life threatening bronchospasm
  • generally safe in COPD
28
Q

In patients taking B-blockers for heart failure, should they be started on the normal dose?

A
  • no
  • should start on a reduced dose, as cardiac function may initially be impaired
29
Q

Which of the following conditions are B-blockers ok to be used in?

1 - heart block
2 - severe hypotension
3 - significant hepatic failure
4 - diabetes

A

4 - diabetes
- contraindication in other conditions

30
Q

Which of the following classes of medications should B-blockers not be prescribed alongside?

1 - cardiac glycosides
2 - class 1 antiarrhythmics
3 - anticoagulants
4 - non-dihydropyridines Ca2+ channel blockers

A

4 - non-dihydropyridines Ca2+ channel blockers

  • this class of drugs work primarily on cardiac Ca2+ channels
  • can cause heart failure, bradycardia and asytole.
  • verapamil and diltiazem
31
Q

When prescribing B-blockers which of the following should you use?

1 - lowest dose and build up as in BNF
2 - lower than the lowest dose in BNF
3 - standard dose patient has had previously

A

1 - lowest dose and build up as in BNF

32
Q

When stoping B-blockers, why should the drugs NOT be stopped immediately?

1 - patient may not want to
2 - heart may fail
3 - hypotension can occur
4 - adrenoreceptors are up regulated and can cause surge in sympathetic stimulation

A

4 - adrenoreceptors are up regulated and can cause surge in sympathetic stimulation

  • adrenoreceptors have increased sensitivity to overcome B-blockers. If B-blockers are then stopped this can cause a massive sympathetic reaction

C. Year 3: Core Drugs (125 decks)

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