Cardiovascular ( 20% ) Flashcards
(71 cards)
1
Q
- Muscarinic agonists may produce
- a. Mydriasis
- b. Vasodilatation
- c. Uterine contraction.
- d. Bronchodilatation
- e. B and C
A
e) B and C
(vasodilation + uterine contraction)
M3 contracts the pregnant uterus
M3 causes NO release from vascular endothelial cells->vasodilation
Mydriasis = anticholinergics (eg atropine)
Bronchodilation is caused by beta 2 stimulation
(Muscarinic agonists cause bronchoconstriction)
2
Q
- Effects of isoprenaline include:
- a. Reflex bradycardia
- b. Decreased peripheral resistance.
- c. Marked hypertension
- d. Reduced pulse pressure
- e. A and C
A
b) decreasd PVR
Due to beta 2 stimulation causing vasodilation
Is also a positive inotrope and chronotrope->increased CO but also increase myocardial O2 demand
Increases pulse pressure by reducing diastolic BP and increasing systolic BP
Used in bradycardia and heart block
Beta agonist only -> vasodilation through beta-2 effects and baroreceptor response to increased cardiac output
3
Q
- In the eye
- a. Alpha adrenoceptors cause contraction of the circular papillary muscle
- b. Cyclospasm is a feature of organophosphate poisoning
- c. Beta agonist will reduce intraocular pressure
- d. Antipsychotic agents such as chlorpromazine have no effect on the eye
- e. Diuretics have no use in glaucoma
A
b. Cyclospasm is a feature of organophosphate poisoning
Causes mydriasis (dilation) and cycloplegia
Beta blockers reduced IOP
4
Q
- Which agonist is not correctly paired with its adrenoceptor?
- a. Phenylephrine – alpha 1
- b. Clonidine – alpha 2
- c. Dobutamine – beta 1
- d. Procaterol – beta 2
- e. Prazosin – alpha 2.
A
e. Prazosin
Is a alpha-1 selective antagonist
5
Q
- Regarding beta-receptor antagonist drugs the following has no local anaesthetic action:
- a. Labetalol
- b. Atenolol
- c. Metoprolol
- d. Propranolol
- e. Pindolol
A
b) atenolol
Metoprolol, labetalol, propranolol do
Timolol, atenolol do not.
6
Q
- regarding isoprenaline
- a. it is a potent bronchodilator
- b. it is a selective beta1 agonist.
- c. it can be used in tachyarrythmias to decrease AV conduction
- d. it has negative inotropic effects.
- e. it causes peripheral vasoconstriction
A
a) is a potent bronchodilator
Non-selective beta agonist
Positive inotrope and chronotrope
Causes peripheral vasodilation through B2 agonism
7
Q
- regarding beta blockers
- a. inhibits renin release via beta2 receptors.
- b. metoprolol has intrinsic sympathomimetic effects.
- c. all are well absorbed
- d. beta1 selective antagonists don’t cause bronchoconstriction.
- e. can treat ventricular tachycardias
A
Nick thinks e) can treat ventricular tachycardias
Not sure about this - dont use betablockers for VT/VF or torsades etc, only for SVTs as they slow AV conduction.
I think it is C) all well absorbed
Inhibit renin release via beta 1 receptors
Celiprolol and labetalol have intrinsic sympathomimetic effects (ie partial agonism - avoids bradycardia, bronchospasm, and change in lipids)
beta 1 selective can still cause some bronchoconstriction
8
Q
- IV drug that causes tachycardia, decreases diastolic BP, dilates pupil, doesn’t affect ejaculation, decreases sweating:
- a. Beta agonist
- b. Alpha antagonist
- c. Muscarinic antagonist
- d. Nicotinic antagonist.
- e. Nicotinic agonist
A
c. Muscarinic antagonist
Picture of anticholinergic syndrome
Tachycardia = Must be a beta agonist / parasympathetic antagonist
Reduces diastolic BP, dilates pupil (alpha antagonist or muscarinic antagonist)
Doesnt affect ejaculation, decreases sweating (not an alpha blocker / muscarinic antagonist)
Nicotinic antagonists dont affect ejaculation or dilate pupil
9
Q
- Which has pure beta agonist effects in the circulation?
- a. Adrenaline
- b. Noradrenaline
- c. Isoprenaline
A
c. isoprenaline
A and NA both have alpha effects
10
Q
- Choose the odd one out:
- a. Muscarine
- b. Acetylcholine
- c. Hyoscine.
- d. Bethanachol
A
c. Hyoscine.
Anticholinergic, others are cholinomimetics
11
Q
- A young patient is given a normal dose of a drug in the emergency department. He develops tachycardia, increased BP and dilated pupils. The drug is most likely to be:
a. Adrenaline
b. Atropine.
A
b. Atropine.
Children notoriously sensitive to atropine but it has does not affect BP
12
Q
- dobutamine
a. results in ATP -> AMP
b. can decrease systemic vascular resistance/afterload
A
b. can decrease systemic vascular resistance/afterload
Selective beta 1 agonist
Causes increased CO and decreased PVR
13
Q
- regarding propranolol
- a. is a highly selective beta receptor antagonist
- b. is poorly lipid soluble
- c. has sodium channel blocking activity
A
c. has sodium channel blocking activity
Non-selective beta blockade
Lipophilic so it can cross the BBB
(and is thus used to treat anxiety and tremor)
14
Q
- A young man presents with dilated pupils, confusion and hyperpyrexia. Which of the following could not account for these effects
- a. Atropine
- b. Datura
- c. Morphine
A
c. Morphine
Constricts pupils, does not cause hyperpyrexia
Datura and atropine are anticholinergics
‘Red as a beet, dry as a bone, blind as a bat, mad as a hatter’
15
Q
- pralidoxime acts to
- a. inhibit presynaptic acetylcholine release
- b. cleave organophosphates from acetylcholinesterase
- c. regenerate acetylcholine
A
b. cleave organophosphates from acetylcholinesterase
Regenerates AChE in cases of organophosphate poisoning by removing the phosphate molecule that is blocking the receptor
16
Q
- A patient comes in staggering, agitated and hyperthermic with dilated pupils. Which is LEAST likely to be the cause?
- a. Atropine overdose
- b. Amphetamines
- c. Angels trumpet
- d. Tricyclic overdose
- e. Aspirin overdose
A
e) aspirin OD
Aspirin blocks the krebs cycle->anaerobic metabolism-> lactic acidosis
Atropine + Angels trumpet - anticholinergic
Amphetamine - sympathomimetic
TCA - anticholinergic, indirect NA stimulation, alpha blockade
17
Q
- benztropine causes:
- a. miosis
- b. diarrhoea
- c. confusion
- d. bronchorrhoea
- e. GIT haemorrhage
A
c. confusion
Benztropine = antimuscarinic
Drys secretions, hyperthermia, confusion, seizures, mydriasis, tachycardia, vasoconstriction, bronchial SM relaxing and reduced secretions.
18
Q
- All of the following are characteristics of propranolol EXCEPT:
- a. Lipid soluble
- b. Local anaesthetic action
- c. Half life 3-6 hours
- d. Beta sympathetic selectivity
- e. 30% bioavailability
A
d. Beta sympathetic selectivity
Propranolol is a non-selective beta blocker
19
Q
- regarding prazosin, which is NOT true?
- a. It is a selective alpha 1 blocker
- b. It dilates arterioles only, not veins
- c. It undergoes extensive first pass metabolism
- d. Recipients may develop a positive test for anti-nuclear factor
- e. With negative feedback of noradrenaline on its own, release can still occur
A
b. It dilates arterioles only, not veins
Alpha-1 specific blocker
relax arterial + venous smooth muscle, improve lipids, no reflex tachy, decrease afterload/preload(CHF)
All alpha-1 and beta blockers are well absorped but have high first pass metabolism
Phentolamine is a non-selective alpha blocker and causes a reduced TPR and a rebound tachycardia. Poor oral absorption.
20
Q
- dopamine
- a. has less alpha agonist effect than dobutamine.
- b. dilates the renal vascular bed by its action of beta 1 receptors.
- c. causes a profound rise in peripheral vascular resistance
- d. is inactivated by sodium bicarbonate
- e. causes vasoconstriction at all doses.
A
d. is inactivated by sodium bicarbonate
(inactivated in akaline solution)
-
a. Dobutamine has alpha 1 and beta 1 activity. Dopamine also has alpha agonist activity
- Dopamine D1=D2>>B>>a
- Dobutamine B1>B2>>>>a
- b. dilates the renal vascular bed by its action of D1 receptors
- c. causes a rise in peripheral vascular resistance at high doses
- e. causes Vasodilation at lower doses but starts to act on alpha receptors at higher doses (alpha agonism -> vasoconstriction)
21
Q
- propranolol
- a. has no central effects
- b. can be used safely in type I respiratory failure because of its reliable beta 1 selectivity
- c. in overdose may be effectively treated by administering glucagon
- d. needs to be given in relatively large oral doses because of its poor absorption
- e. does not produce withdrawal symptoms on abrupt cessation because beta receptors do not up regulate
A
c) Glucagon can be used in the OD of betablockers
- a) is lipophilic and crosses the BBB so has central effects (anxiety, tremor medication)
- b) Non-selective beta blockade, but even then you cannot safely use B1 selective agents in asthmatics.
- d) like all beta blockers is well-absorbed, but has high first pass metabolism
- e) beta receptors can upregulate
22
Q
- hyoscine
- a. may potentiate the anticholinergic effects of phenothiazines
- b. is well absorbed from the gastrointestinal tract
- c. readily crosses the blood brain barrier
- d. has its main effect at nicotinic receptors.
- e. produces pronounced tachycardia in therapeutic doses
A
b) Atropine and Hyoscine are naturally-occuring alkaloid esters and are well absorped orally
- a. Phenothiazines do not appear to have much in the way of anticholinergic effects (do have extrapyamidal, sedative, and antihistamine/antinausea effects)
- c. hyoscine (used for nausea) does cross the BBB, hyoscine butylbromide (Buscopan) does not cross the BBB
- d. Has its effect at muscarinic receptors
- e. Can cause tachycardia in overdose
23
Q
- beta blockers
- a. are class III antiarrythmic drugs.
- b. are selective for beta 1 adrenoreceptors.
- c. are useful agents in acute heart failure
- d. may mask the symptoms of hypoglycaemia
- e. are particularly safe and effective in combination with verapamil
A
d. may mask the symptoms of hypoglycaemia
(beta stimulation gives typical warning signs of tremor and palpitations etc)
- a. are Class II antiarrhythmics
- b. Can be beta-1 or non-selective
- c. Are dangerous in acute HF due to reduced inotropy
- e. have additive effects with verapamil and cause cariodepression
24
Q
- atropine
- a. causes ureter and bladder wall contraction
- b. acts by blocking adrenoceptors
- c. is an example of a surmountable blockade
- d. results in miosis
- e. causes bradycardia in a moderate to high therapeutic dose
A
c. is an example of a surmountable blockade
- reversible blockade of muscarinic receptors and competitive antagonist of cholinomimetics*
- Causes ureter and bladder relaxation*
- Blocks muscarinic receptors*
- Causes mydriasis*
- Brady at low doses, tachy at high doses*
25
25. noradrenaline
* a. is more potent than salbutamol at beta 1 receptors
* b. is less potent than isoprenaline at alpha receptors
* c. antagonizes the effects of dopamine
* d. has similar potency to adrenaline at beta 1 receptors
* e. is less potent than adrenaline at alpha receptors
d. has similar potency to adrenaline at beta 1 receptors
Norad: a1=a2; B1\>\>B2
Adrenaline: a1=a2; B1=B2
Isoprenaline B1=B2\>\>\>\>a
Salbutamol B2\>B1
Is less potent than adrenaline at *B2 receptors (hence why noradrenaline is a better pressor, as less vasodilation)*
26
26. which of the following drugs utilises camp as a second messenger?
* a. Adrenaline
* b. Dopamine
* c. Milrinone
* d. Glucagons
* e. All of the above
a) all of the above
Adrenergic and dopamine receptors are GPCRs
(D1 = Gs; D2 = Gi)
Milrinone inhibits Phosphodiesterase 3, which breaks down cAMP
Glucagon receptor has 3 subunits (a, B, y) and -\> adenylyl cyclase -\> cAMP
27
27. which of the following statements is incorrect?
* a. Noradrenaline and adrenaline exert beta effects at low doses and alpha effects at high doses
* b. Dobutamine exerts its actions via alpha effects
* c. Inotropic agents act ultimately by increasing intracellular calcium
* d. Dopamine exerts different effects at different doses
* e. Theophylline is a positive inotrope
b. Dobutamine exerts its actions via *beta* effects
B1\>B2\>\>\>\>a
Increase CO, reduce TPR
28
28. milrinone
* a. has a short half life because of rapid reuptake and breakdown intravascularly by COMT
* b. is extensively metabolized by the liver.
* c. is in the same class of drugs as dobutamine
* d. is a competitive inhibitor of phosphodiesterase.
* e. is one of the most commonly used inotropes in the intensive care setting
d. is a competitive inhibitor of phosphodiesterase.
Prevents cAMP degradation
Has 12% liver metabolism
29
29. alpha-adrenoceptors utilise
* a. camp as a second messenger
* b. cGMP as a second messenger
* c. phosphodiesterase inhibition to achieve positive inotropic effects
* d. phospholipase C to achieve positive inotropic effects
* e. a second messenger system that is yet to be discovered
d. phospholipase C to achieve positive inotropic effects
a1 -\> Gq-\> PLC -\> IP3 + DAG -\> Ca2+
a2 -\> Gi -\>reduce adenylyl cyclase-\>reduce cAMP
beta receptors utilise cAMP as a second messenger
Milrinone utilises phosphopdiesterase inhibition
30
30. beta 1 effects include
* a. positive inotropy
* b. peripheral vasoconstriction
* c. bronchodilation
* d. peripheral vasodilation
* e. a and b only
a. positive inotropy
beta 2 causes skeletal muscle vasodilation
alpha causes skin and splanchnic vasoconstriction
B2 causes bronchodilation
31
31. the following statements are true for catecholamines, EXCEPT:
* a. they all have a very short half life
* b. noradrenaline is used mainly when peripheral vasoconstriction is desirable
* c. dopamine in doses of \<2mcg/kg/min has been proven to directly improve renal perfusion
* d. dobutamine is a synthetic derivative of isoprenaline
* e. they increase myocardial contractility at the expense of increased oxygen consumption
c. Despite improving renal blood flow, dopamine has not been shown to improve renal function in AKI
Dobutamine is a synthetic analogue of isoprenaline (which is itself synthetic)
All broken down rapidly by COMT and MAO
Norad causes more vasoconstriction than adrenaline and dopamine as it has less beta-2 agonism
32
. Digoxin
* a. Causes a decrease in intracellular sodium.
* b. Causes hypokalaemia in overdose.
* c. Has a half-life of 40 hours in a normal patient
* d. Decreases cardiac output.
* e. Has no role in the treatment of heart failure.
* a. Causes a *increase* in intracellular sodium
* b. Causes *hyper*kalaemia in overdose.
* **c. Has a half-life of 40 hours in a normal patient**
* d. *increases* cardiac output.
* e. Has *a small and dated* role in the treatment of heart failure.
33
2. Digoxin
* a. Does not cross the blood brain barrier.
* b. Hypokalaemia decreases efficacy of digoxin.
* c. Hypomagnesaemia decreases efficacy of digoxin.
* d. Antibiotics have effects on digoxin.
* a. _Does_ cross the blood brain barrier.
* b. Hypokalaemia *increases* efficacy of digoxin.
* c. Hypomagnesaemia *increases* efficacy of digoxin.
* **d. Antibiotics have effects on digoxin.**
* **Erythromycin inhibits PGP**
34
3. Digoxin
* a. Is not very lipid soluble and has a low volume of distribution.
* b. Is extensively metabolized prior to its excretion.
* c. Is highly protein bound.
* d. Has a half-life of 100 hours, thus allowing for once daily dosing.
* e. None of the above are correct
* a. _Is_ lipid soluble and has a *high* volume of distribution.
* b. Is *33%* metabolized prior to its excretion.
* Oral bioavailabilty and amount excreted unchanged in urine both 66%
* c. Is *_25%_* protein bound.
* d. Has a half-life of *36* hours, thus allowing for once daily dosing.
* Steady state in 7 days
* **e. None of the above are correct**
35
4. The electrical effects of digoxin in therapeutic concentrations include:
* a. The ability to revert atrial fibrillation to normal sinus rhythm in \>60% of patients \<12 hours
* b. No indirect effect (ie. Vagal) upon the Purkinje fibres in the ventricles.
* c. Increased refractory period at the atrioventricular node.
* d. Increased rate of firing of the sinoatrial node.
* e. ST segment elevation in the inferolateral segments of the ECG
* a. The ability to revert atrial fibrillation to normal sinus rhythm in \>60% of patients \<12 hours.
* Less effective and takes time
* b. *Stimulates cholinergic transmission and has* indirect effect (ie. Vagal) upon the Purkinje fibres in the ventricles, *slowing conduction*
* **c. Increased refractory period at the atrioventricular node.**
* But reduces the RP in the atria, and also the AVN at toxic doses
* d. *Decreased* rate of firing of the sinoatrial node.
* e. ST segment elevation in the inferolateral segments of the ECG
* ?? likely not, havent seen this
36
Which of the following drugs has no significant interaction with digoxin?
* a. Quinidine.
* b. Amlodipine
* c. Verapamil.
* d. Warfarin.
* e. Thiazide diuretics.
* a. Quinidine.
* Increase plasma levels of digoxin by displacing tissue binding sites and depressing renal digoxin clearance
* **b. Amlodipine**
* c. Verapamil - *Same as quinidine (as is amiodarone)*
* d. Warfarin - *99% protein bound, so may displace digoxin*
* e. Thiazide diuretics - *Cause hypokalaemia -\> increase toxicity risk*
37
6. Digoxin exerts its effects upon myocardial muscle at a cellular level by
* a. Increasing intracellular calcium
* b. Inducing Na+/K+/ATPase at the cell membrane
* c. Acting as a second messenger for G proteins
* d. Acting directly upon actin and myosin filaments to promote contractility
* **a. Increasing intracellular calcium**
* b. *Inhibiting* Na+/K+/ATPase at the cell membrane
38
7. Digoxin Fab antibodies
* a. Are used routinely in the management of digoxin toxicity
* b. Decreases the serum digoxin level in the circulation
* c. Are commonly associated with tachyarrythmias after administration
* d. Take approximately 12 hours to have an effect
* e. Are metabolized in the liver
Nick has no answer
* a. Are used routinely in the management of digoxin toxicity
* Only if hypotensive/shocked, very high levels (eg \>10ng/ml for acute ingestions), end-organ damage, symptomatic K+ \>5.0
* **b. Decreases the serum digoxin level in the circulation**
* Maybe? binds to digoxin, rendering it inert, then the complexes are renally excreted
* c. Are commonly associated with *anaphylaxis to sheep protein* after administration
* d. Take approximately 12 hours to have an effect
* Rapid onset effect I think
* e. Are metabolized in the liver
* Excreted in the kidneys
39
9. The primary mechanism of action of digoxin involves:
* a. An increase in action potential amplitude
* b. An increase in ATP synthesis
* c. Modification of the actin molecule
* d. An increase in intracellular Ca2+ levels
* e. Block of the Na+/Ca2+ exchange
d. An increase in intracellular Ca2+ levels
40
10. Regarding pharmacokinetics of digoxin
* a. It is poorly absorbed with oral administration.
* b. Its renal clearance is increased with renal disease.
* c. 40% of individuals have enteric bacteria inactivating it
* d. two thirds of digoxin is excreted by the kidneys
* e. the enterohepatic circulation contributes to the short half-life
* a. It is *well-absorbed (66% bioavail)* with oral administration.
* Reduced by antacids, increased by PPI
* b. Its renal clearance is *decreased* with renal disease.
* c. 40% of individuals have enteric bacteria inactivating it
* Dont think this is a thing
* **d. two thirds of digoxin is excreted by the kidneys**
* e. the enterohepatic circulation contributes to the short half-life
* t1/2 = 36 hours. Thats hardly short, is it?
41
1. All of the following may increase the effect of digoxin EXCEPT:
* a. Amiodarone
* b. Frusemide.
* c. Carbamazepine
* d. verapamil
* e. quinidine
**c. Carbamazepine**
Amiodarone, verapamil, quinidine all increase plasma levels by displacing tissue binding sites and reducing renal excretion
Frusemide -\> hypokalaemia, which increases the potential for ADRs
42
1. Antiarrythmic drugs may work in any of the following ways EXCEPT:
* a. Reducing ectopic pacemaker activity
* b. Modifying conduction in re-entrant circuits
* c. Sodium channel blockade
* d. Calcium channel blockade
* e. Reducing the effective refractory period.
e. Reducing the effective refractory period.
They *prolong the refractory period*
Shortening it is pro-arrhythmogenic
Reduce ectopic activity- eg flecainide
Modify conduction - eg amiodarone
43
. Lignocaine
* a. Has poor oral bioavailability
* b. Blocks sodium channels not inactivated channels.
* c. Is effective in AF.
* d. Exacerbates VT in 30%
* e. Suppresses electrical activity of normal and arrythmogenic tissue equally.
**a. Has poor oral bioavailability**
* b. Blocks *active and inactive* sodium channels, not *resting* channels.
* c. Is *ineffective* in AF, *due to less effect* on atria. *Hence Used for ventricular arrhythmias*
* d. Exacerbates VT in 30%
* e. *Affects arrhythmogenic tissue more (normal cells depolarise more often and clear the lidocaine)*
44
. Flecainide
* a. Has poor oral bioavailability.
* b. Is safe in ischaemia induced arrhythmias.
* c. May be used in reentry tachycardias
* d. Is a class Ia antiarrythmic.
* e. Reduces mortality in post MI PVCs.
* a. Has *good* oral bioavailability - *so can use as 'pill in the pocket' for SVT*
* b. Is *fuckin dangerous* in ischaemia induced arrhythmias, *and will muder you if you have had an MI in the past or a structurally abnormal heart*
* **c. May be used in reentry tachycardias**
* **eg SVT, AVNRT**
* d. Is a class _Ic_ antiarrythmic.
* Ia is procainamide, TCAs, quinidine
* e. *Increases* mortality in post MI PVCs (see note above re murder)
45
4. adenosine
* a. has a half life of 2 minutes.
* b. increases AV nodal conduction.
* c. predominantly inhibits sinoatrial nodal function.
* d. directly inhibits AV nodal conduction
* e. is more effective in the presence of theophylline or caffeine
* a. has a half life of *10 seconds*
* b. *Slows/stops* AV nodal conduction
* c. predominantly inhibits *Atrioventricular* nodal function (AVN\>SAN)
* **d. directly inhibits AV nodal conduction**
* **By opening K+ channels -\> hyperpolarising the cells and preventing them depolarising**
* e. is *less* effective in the presence of theophylline or caffeine.
46
5. adenosine
* a. has a half life of 30 seconds.
* b. is the drug of choice for ventricular tachyarrythmias.
* c. works by directly inhibiting the sinoatrial node with only mild effect on the atrioventricular node.
* d. causes flushing in over 50% of patients.
* e. is less effective in the presence of caffeine and theophylline
* a. has a half life of *10 seconds*
* b. is the drug of choice for *atrial* tachyarrythmias
* Blocks AV node, hence reduces the rate of impulses propogated, allowing atria time to reset
* c. works by directly inhibiting the *atrioventricular* node with only mild effect on the *sinoatrial* node.
* d. causes flushing in *20%* of patients.
* **e. is less effective in the presence of caffeine and theophylline**
47
6. regarding antiarrythmics
* a. adenosine alters QRS duration
* b. amiodarone has a short half life
* c. lignocaine is also useful in supraventricular arrythmias
* d. flecainide is unsafe in people with ischaemic heart disease
* e. quinidine has no effect on QRS duration
* a. adenosine alters QRS duration - wrong. Prevents AV conduction by hyperpolarising the cell
* b. amiodarone has a *fucking long* half life - 58 days!
* c. lignocaine is also useful in supraventricular arrythmias
* Greater effect on ventricles than atria - good for VT/VF
* **d. flecainide is unsafe in people with ischaemic heart disease**
* **Risk of developing VT**
* e. quinidine has no effect on QRS duration
* Class Ia, so prolongs the AP -\> slowed conduction -\> wide QRS
48
13. amiodarone
* a. is only effective in suppression of ventricular arrythmias
* b. causes peripheral vasodilation via alpha-adrenergic effects
* c. commonly causes corneal opacification
* d. increases warfarin clearance
* e. decreases AV nodal refractory period
* a. is only effective in suppression of ventricular arrythmias
* Wrong - can use for AF
* **b. causes peripheral vasodilation via alpha-adrenergic effects**
* c. commonly causes *pulmonary fibrosis*
* d. *Decreases* warfarin clearance
* As well as statins and digoxin
* e. *increases* AV nodal refractory period (can cause AV nodal block)
49
14. lignocaine displays all of the following EXCEPT:
* a. increased action potential duration
* b. binding to both activated and inactivated sodium channels
* c. predominant metabolism
* d. decreased clearance associated with concomitant propranolol administration
* e. ineffectiveness against arrhythmias in normally polarize tissues
Lignocaine is a Class Ib antiarrhythmic
Therefore it Shortens AP duration with a weak Na block
**a. increased action potential duration**
50
15. which of the following does NOT prolong the effective refractory period in the atrioventricular node?
* a. Propranolol
* b. Amiodarone
* c. Flecainide
* d. Verapamil
* e. Phenytoin
c. Flecainide
Class 1c - normal ERP and AP duration
51
16. adenosine
* a. is effective in converting atrial flutter
* b. depresses conduction through the AV node
* c. requires reduction of dose in patients with hepatic failure
* d. has a half life of 30-60 seconds
* e. is safe in sick sinus syndrome
b. depresses conduction through the AV node
52
7. amiodarone
* a. has a short half life.
* b. stimulates Na channels.
* c. is only effective against ventricular arrhythmias.
* d. has antianginal effects.
* e. can cause emphysema in 5-15% of people.
* a. has a *looooong* half life - *like, 1 week*
* b. *Blocks* Na channels - Class I activity
* c. is effective against *both atrial and* ventricular arrhythmias.
* **d. has antianginal effects - *Due to calcium and beta-blocking activity (class IV and II)***
* e. can cause *pulmonary fibrosis around 1% of patients*
53
8. In the Vaughan-Williams classification
* a. Class 1 drugs affect potassium channels
* b. Class II drugs affect calcium channels
* c. Class II drugs affect sodium channels
* d. Class III drugs affect potassium channels
* e. Class IV drugs affect chloride channels
* a. Class 1 drugs affect *sodium* channels
* b. Class II drugs affect *beta receptors*
* c. Class II drugs affect *beta receptors*
* **d. Class III drugs affect potassium channels**
* e. Class IV drugs affect *calcium* channels
54
9. In therapeutic doses, adenosine:
* a. Acts by affecting sodium channels
* b. Is administered as a slow IV push.
* c. Is metabolized in the liver
* d. Produces a bradycardia by vagal stimulation
* e. Affects adenosine receptors at the AV node
e. Affects adenosine receptors at the AV node
55
10. adenosine
* a. opens K+ channels
* b. opens Cl- channels
* c. half life of 10min
* d. profoundly blocks SA node
* e. blocks Ca2+ dependent action potential
**a. opens K+ channels**
56
11. regarding adenosine
* a. its receptors are ion channels
* b. it increases AV nodal conduction
* c. it enhances K+ conductance
* d. it is the drug of choice in VF
* e. it has a half life of 2 minutes
c. it enhances K+ conductance
Receptor is a GPCR with caffeine and theophylline as antagonists
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12. which doesn’t prolong the refractory period in normal cells?
* a. Amiodarone
* b. Lignocaine
* c. Sotalol
* d. Quinine
* e. Procainamide
b. Lignocaine
Shortens it as a class Ib
Class Ic has no effect
Class II has no effect.
All others prolong
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17. regarding amiodarone
* a. it has no alpha adrenergic effects
* b. it has no beta adrenergic effects
* c. it has low affinity for activated sodium channels
* d. it increases warfarin clearance
* e. it enhances conduction through accessory pathways
**c. it has low affinity for activated sodium channels**
Has class I, II, III, IV activity
But only acts on inactivated Na channels
Reduces warfarin metabolism -\> increased effect
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18. amiodarone
* a. has a low affinity for activated sodium channels
* b. is associated with thyroid dysfunction in 50% of patients
* c. has a half-life of 8-20 days
* d. increases clearance of warfarin
* e. commonly causes peripheral vasoconstriction
* **a. has a low affinity for activated sodium channels**
* **Works only on inactivated channels**
* b. is associated with thyroid dysfunction in 50% of patients
* c. has a half-life of *56 days*!!!
* d. *decreases metabolism* of warfarin
* e. *occasionally causes peripheral vasodilation due to alpha blockade*
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19. which does not prolong the refractory period of normal cells
* a. amiodarone
* b. lignocaine
* c. quinidine
* d. sotalol
* e. procainamide
**b. lignocaine**
Class Ib - shortens (lidocaine, phenyotoin)
Class Ic - no effect (flecainide)
Class II (beta blockers) - no effect
Others all prolong
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20. the most common adverse effect of procainamide is
* a. bradycardia
* b. pulmonary infiltrates
* c. fever
* d. hypotension
* e. anaphylaxis
d. hypotension
Can also cause QT prolongation -\> torsades, or a lupus-like effect (as does hydralazine) which spares the kidneys, and resolves with stopping the medication
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1. mannitol
* a. inhibits H20 absorption in proximal tubule, loop of Henle and collecting tubule
* b. is metabolized to glycerol
* c. decreases total body water and total body cation content equally.
* d. is of no value when renal haemodynamics are compromised.
**d. is of no value when renal haemodynamics are compromised.**
***As it requires filtration, which wont happen if renal blood flow is compromised. This can lead to oedema and hyponatraemia (contraindicated in anuria)***
**a. inhibits H20 absorption in proximal tubule *and* loop of Henle, *but not the collecting duct***
*Nick says A is right however I cannot find anywhere that lists CD as a site of action of mannitol in addition to PCT/LoH. d) would seem to be the more correct answer.*
* b. is *not metabolised*
* c. decreases total body water *more than* total body cation content equally *(hence can cause hypernatraemia)*
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2. which raises the pH of urine the most
* a. acetazolamide
* b. frusemide.
* c. chlorthiazide.
**a. acetazolamide**
creates urinary alkilisation
Other agents cause H+ loss and so acidify the urine
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3. which is NOT true of diuretics?
* a. Loop diuretics can be used to treat hypercalcaemia
* b. Frusemide is used in the prophylaxis of acute mountain sickness.
* c. Cirrhotic oedema responds to spironolactone
* d. They may enhance the efficiency of ACE inhibitors
* e. Hydrochlorothiazide is useful in diabetes insipidus
**b. *Acetazolamide* is used in the prophylaxis of acute mountain sickness.**
a) frusemide inhibits Na-2CL-K symporter. Due to the potential changes by impacting K+, less Mg and Ca is reabsorbed.
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4. Which is the correct site of action?
* a. Spironolactone = collecting duct.
* b. Triamterene = ascending loop of Henle
* c. Thiazides = proximal part of distal tubule.
* d. Frusemide = proximal tubule
* e. Acetazolamide = collecting tubule
**a. Spironolactone = collecting duct.**
**c. Thiazides = *distal tubule (Na-Cl symporter)***
*Cannot find which part of the DCT is the site of action for thiazides, so i think a) is the more correct answer.*
* b. Triamterene = *Blocks ENaC in CD (potassium sparing diuretic)*
* d. Frusemide = *ascending limb of thick LoH (Na-2Cl-K symporter)*
* e. Acetazolamide = *PCT (Carbonic anhydrase)*
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5. Loop diuretics (eg frusemide) inhibit:
* a. Na+/Cl- channels
* b. K+/H2CO3 channels
* c. Na+/K+/2Cl- channels
* d. Na+/glucose symporter
* e. Na+/K+ channels
**c. Na+/K+/2Cl- channels**
* In the thick part of ascending LoH*
* Thiazides inhibit Na-Cl*
* Spironolactone inhibits basal Na-K channels*
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6. The elimination half-life of frusemide is:
* a. 30min – 1hr
* b. 1-2hr
* c. 1.5-2hr
* d. 2-3hr
* e. 2.5-3hr
**c. 1.5-2hr**
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7. Which of the following is an aldosterone antagonist?
* d. spironolactone
8. An example of an ADH antagonist is
* a. Ethanol
* b. Amiloride
* c. Lithium
* d. Aldosterone
* e. Triamterene
**c. Lithium**
a. Ethanol
* Nick says Lithium (this enters the principal cells and interferes with aquaporin function, causing ADH resistance). This is probably correct*
* Ethanol and water both inhibit ADH secretion.*
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9. Carbonic anhydrase inhibitors
* a. Were developed from early antibiotics
* b. Are closely related to thiazide diuretics
* c. Cause metabolic acidosis
* d. Decrease the pH of CSF
* e. All of the above
e. All of the above
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10. Which is not the correct site of action
* a. Spironolactone and the collecting duct
* b. Triamterene and the collecting duct
* c. Thiazides and the proximal part of the distal tubule
* d. Acetazolamide and the collecting tubule
* e. Frusemide and the ascending loop of Henle
**d. Acetazolamide and the *PCT***
*Triamterene is a potassium-sparing diuretic which directly blocks ENaCs in the CD -\> reduced Na reabsorption -\> diuresis*
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