PHARM; Lecture 11, 12 and 13 - Autumn Term Quiz; Drugs and the cardiovascular system: the heart; Drugs and the vasculature Flashcards Preview

Y2 LCRS 1 - Pharm, Endo, Reproduction > PHARM; Lecture 11, 12 and 13 - Autumn Term Quiz; Drugs and the cardiovascular system: the heart; Drugs and the vasculature > Flashcards

Flashcards in PHARM; Lecture 11, 12 and 13 - Autumn Term Quiz; Drugs and the cardiovascular system: the heart; Drugs and the vasculature Deck (46)
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1

Which of the following pharmacodynamic properties is a competitive receptor antagonist most likely to display? 1) High efficacy and zero affinity 2) High potency and moderate affinity 3) Zero efficacy and moderate affinity 4) Zero potency and zero affinity 5) Moderate efficacy and moderate affinity

Zero efficacy and moderate affinity

2

Which of the following forms of drug antagonism describes the ability of adrenaline to reduce the effects of mast cell derived histamine during an anaphylactic response. !) Receptor blockade 2) Physiological antagonism 3) Chemical antagonism 4) Pharmacokinetic antagonism 5) Irreversible antagonism

Physiological antagonism

3

A section of vascular smooth muscle is placed in an organ bath and stimulated with increasing doses of noradrenaline. A graph of the relationship between dose and response (effect) wherein all possible degrees of response between minimum detectable response and a maximum response is produced. From the list below, please select which possibility could NEVER induce a maximal response. 1) Noradrenaline plus Phentolamine (non selective alpha receptor antagonist) 2) Adrenaline (agonist with lower affinity for alpha receptors) 3) Clonidine (partial agonist) 4) Noradrenaline plus Propranolol (non-selective beta receptor antagonist) 5) Phenylephrine (1-selective agonist)

Clonidine

4

With respect to the distribution of a drug around the body; 1) Regional blood flow is an important factor 2) The distribution profile of a drug is determined by its carbon content 3) Capillary structure is unimportant 4) If a drug is highly plasma-protein bound it is not free to be distributed from the blood stream 5) Active transport into tissues does not influence this process

Regional blood flow is an important factor

5

Drug metabolism often reduces the lipid solubility of drugs and thus makes the drug easier to excrete. Why is this so? 1) Reduces distribution to the body fat 2) Reduces reabsorption in the kidney 3) Increases plasma protein binding 4) Reduces the potency of the drug 5) Enhances enterohepatic recycling

Reduces reabsorption in the kidney

6

Which of the following neurones is associated with noradrenaline neurosecretion? 1) Preganglionic sympathetic neurone innervating the sympathetic trunk 2) Postganglionic sympathetic neurone innervating the kidney 3) Sympathetic neurone innervating the adrenal medulla 4) Postganglionic parasymapthetic neurone innervating the heart 5) Postganglionic sympathetic neurone innervating the sweat gland

Postganglionic sympathetic neurone innervating the kidney

7

Which one of the following effects can be attributed to anti-cholinesterase poisoning? 1) Bronchodilation 2) Reduced gut motility 3) Increased secretions 4) Tachycardia 5) Mydriasis

Increased secretions. All others are SNS responses.

8

Why might a patient be prescribed a muscarinic receptor agonist following abdominal surgery? 1) To stimulate gastrointestinal activity 2) To reduce gastric acid production 3) To inhibit bladder emptying 4) To increase gastrointestinal blood flow 5) To increase wound healing

To stimulate GI activity

9

How do muscarinic receptor antagonists influence function within the striatum and thus improve the symptoms of Parkinson’s? 1) Reduced GABA receptor activation 2) Increased dopamine receptor activation 3) Inhibition of DOPA decarboxylase 4) Increased monoamine reuptake transporter function 5) Increased dopamine secretion from nigrostriatal neurones

Increased dopamine receptor activation. Blocks M4 receptor, blocking inhibition of DA receptor, so enhances the receptor activation not the increase of DA

10

A 54-year-old man is admitted to Accident & Emergency suffering an anaphylactic reaction after being stung by a wasp whilst out rambling. The registrar finds a bottle of beta-blocker tablets in his pocket. Which of the following clinical features of anaphylaxis could be worsened by these tablets? 1) Bronchospasm and Hypertension 2) Bronchospasm alone 3) Hypertension alone 4) Bronchospasm + Hyperglycaemia 5) Hypertension + Hyperglycaemia

Bronchospasm alone. Hypotension, bronchospasm are features of anaphylaxis, so beta blocker would exacerbate both, not causing HTN

11

A 75-year-old man is diagnosed with glaucoma and is treated with a α1 selective adrenoceptor agonist. The therapeutic effects of the drug are partly due to which of the following functions? 1) Dilation of the pupil 2) Activation of carbonic anhydrase 3) Accomodation for near vision 4) Opening of scleral spur 5) Ocular vasoconstriction

Ocular vasoconstriction. PSNS: angle of lens, opening of scleral spur (+ve glaucoma effect but not SNS). SNS: carbonic anhydrase (important to produce aqueous humour and beta-mediated); Dilation of pupil (alpha mediated but as lens pulls back it block the drainage of aqueous humour so -ve impact)

12

Neuromuscular blockade by tubocurarine is used as an adjunct to anaesthesia in surgery. How does tubocurarine bring about its effects at the motor end plate? 1) Inhibition of acetylcholine release from nerve endings. 2) Antagonism of the actions of acetylcholine at nicotinic receptors 3) Causes persistent depolarisation 4) Increases the rate of acetylcholine breakdown 5) Prevents opening of the voltage sensitive Na+ channels

Antagonism of actions of ACh at nAChR

13

How is HR regulated?

Na enters through channels; then Ca enters through the VGCS, activating the transient channels then the long acting ones. K channels cause the repolarisation of the heart.

14

What are the effects of the SNS and PSNS on the heart rate regulation?

B1 upregulate cAMP which has an effect on If chnnels, which speeds up depolarisation of the heart and on PKA which acts on Ica channels. PSNS: work the other way round, by downregulating cAMP and increasing the Ik channels

15

Which mechanisms regulate contractility?

  1. Electrical excitation of the cell from action potentials arising from the sino-atrial node induce membrane depolarization that promotes gating of Ca2+ channels, which open and cause a small release of Ca2+ into the cytoplasm.
  2. The small Ca2+ current induces a release of Ca2+ from the SR by a process called Ca-induced Ca-release, occurs through Ca2+ release channels (RyR).
  3. Depolarization-induced influx of Ca2+ current (ICa) through the L-type channels contributes approximately 20–25% of the free Ca2+ in a cardiac twitch.
  4. The release of Ca2+ through the RyRs contributes the remaining 75–80% of Ca2+ necessary for cardiac contraction.
  5. 20-25% of Ca come from outside via dihydropiridine receptor and the rest from the sarcoplasmic reticulum.
  6. Na/Ca exchange protein and Ca ATPase channel which are there to remove Ca from the cell after the contraction has taken place.

16

Which mechanisms regulate myocardial O2 supply and demand?

The balance needs to occur between the demand and supply to the myocardial O2 supply

17

Which drugs influence HR?

  • Beta-blockers (decrease cAMP production, leaving the If channels decreased and the Ica are decreased)
  • Ca channel antagonists (block Ca long receptors which decreases the Ca intake)
  •  Ivabradine (decrease If).

Prolong rate of depolarisation

18

Which drugs influence contractility?

B blockers reduce cross-bridge formation; Ca antagonists reduce Ca entry into cell

19

What are the 2 classes of Ca antagonists?

20

Which drugs influence myocardial O2 supply?

Organic nitrates, deliver NO to coronary vessels, involved in cGMP, which is involved in relaxation of coronary vessels; K channel opener: leading to hyperpolarization of coronary cells, which impair ability to contract. Overall, increase coronary blood flow

21

What two different effects of nitrates/potassium channel openers influence preload and afterload?

Indirectly decrease preload (decrease preload by venodilation in peripheral tissues) and afterload (vasodilation of arterioles to cause the decrease – reduce force the heart needs to put, reducing TPR)

22

Summarise the drugs which can affect the HR, contractility nd myocardial O2 supply.

23

Which drugs would you use in angina treatment?

Angina = Myocardial Ischaemia. Beta blocker or calcium antagonist as background anti-angina treatment. Ivabradine is a newer treatment (only affects HR as only affects If channels - may be useful to reduce risk of problems which are related to elevated HR). Nitrate as symptomatic treatment (short acting) Other agents e.g. potassium channel opener if intolerant to other drugs.

24

What are the side effect of beta blockers?

The red ones are the questioned for validity by RCTs

25

What are the side effects of Ca channel blockers?

Effects can be so substantial that they can affect compliance with these drugs

26

What are rhythm disturbances and what are the aims of treatment of these?

  • May be associated with decreased HR or increased HR.
  • Classifications based on site of origin:
    • Supraventricular arrhythmias (e.g. amiodarone, verapamil)
    •  Ventricular arrhythmias (e.g. flecainide, lidocaine)
    •  Complex (supraventricular + ventricular arrhythmias) (e.g. disopyramide).

27

What is the Vaughan-Williams classification of anti-arrhythmic drugs?

Can have drugs which don't fall into just one class

28

What is adenosine?

Has its own sub-type as it doesn't fall into any class; increases If channels. Prolonging HR increases chances of arrhythmia decreasing and sorting itself out

29

What is Verapamil?

Class IV

30

What is Amiodarone?

Reentry rhythms cause arrhythmia, where the hyperpolarisation should occurs; prolong action potential and hyperpolarisation to reduce the action of reentry AP

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