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Cardiovascular RT > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what 2 endogenous substance act on the B1-adrenoceptors in the heart?

A

noradrenaline (sympathetic transmitter)

adrenaline (hormone)

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2
Q

what G protein do B1-adrenoceptors in the heart couple to?

A

Gs proteins

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3
Q

when a B1-adrenoceptor is stimulated, what does the Gs coupled protein do?

A 
acitvates adenylyl cyclase to increase intracellular cAMP concentration
stimulates pKA (within myocytes)
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4
Q

what does increasing intracellular cAMP concentration within the pacemaker cells do?

A

increases slope of pacemaker potential and so increases heart rate
(positive chronotrophic effect)

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5
Q

what endogenous substance acts on M2 muscarinic cholinoreceptors in the heart?

A

ACh

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6
Q

What G protein do M2-adrenoceptors in the heart couple to?

A

Gi

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7
Q

when a M2 muscarinic receptor is stimulated, what does the Gi coupled protein do?

A
  1. decreases activity of adenylyl cyclase to decrease intracellular concentrations of cAMP
  2. opens potassium channels to cause hyperpolarisation of SA node
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8
Q

what does decreasing intracellular concentrations of cAMP and opening potassium channels within pacemaker cells do?

A

decreases slope of pacemaker potential and so decreases heart rate
(negative chronotropic effect)

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9
Q

what are the 3 internodal pathways between the SA node and the AV node? (contained within the right atrium)

A

anterior internodal pathway
middle internodal pathway
poterior internodal pathway

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10
Q

what is pathway goes to the left atrium from the SA node?

apart from cell-cell spread of excitation through gap junctions

A

anterior interatrial myocardial band

Bachmann’s Bundle

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11
Q

what does the bundle of his split up into?

A

right bundle branch

left bundle branch (which splits into anterior division and posterior division)

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12
Q

what is the hierarchy of pacemakers?

A

SA > AV > other cells within the heart

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13
Q

why is it necessary that the AV node can produce an AP?

A

in case the SA node fails

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14
Q

why is it necessary that other cells within the heart can produce an AP? (ie like within the conducting fibres)

A

in case both the SA and AV nodes fail

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15
Q

what is the inwards current of the pacemaker potential also known as?

A

I(f)

funny current

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16
Q

what stimulates the inwards current of the pacemaker potential? (funny current)

A
  1. hyperpolarisation
    (ie turning resting potential negative)
  2. cAMP
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17
Q

what does blocking HCN (hyperpolarisation-activated cycline neucleotide gated) channels do to the pacemaker potential slope?

A

decreases the slope

negative chronotrophic effect

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18
Q

what does ivabradine do?

A

a selective blocker of HCN channels so slows the heart rate down

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19
Q

what medical condition is ivabradine used in and why?

A

angina

because slower rate reduces O2 consumption and so reduces coronary artery supply requirement

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20
Q

what does isoprenaline do?

A

a agonist of B-adrenoceptors and so increases intracellular cAMP concentration and so increases heart rate

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21
Q

what do thyroid hormones do to heart rate?

A

increase heart rate

positive chronotrophic effect

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22
Q

what does adenosine do to the heart rate?

A

decreases heart rate

negative chronotropic effect

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23
Q

what does nitric oxide do to the heart rate?

A

increases heart rate

positive chronotrophic effect

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24
Q

what are the 6 effects of the sympathetic system on the heart?

A
  1. increases heart rate
  2. increases contractility
  3. increases conduction velocity in AV node (decreases delay)
  4. increases automacity (tendancy for non-nodal regions to acquire spontaneous activity)
  5. decreases duration of systole
  6. decreases cardiac efficiency (with respect to O2 consumption)
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25
Q

what are the 4 effects of the parasympathetic system on the heart?

A
  1. decreased heart rate
  2. decreased contractibility
  3. decreased conduction in AV node (increased delay)
  4. overaction may cause dysrhythmias in the atria (not fatal)
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26
Q

what is the Frank-Starling mechanism?

A

the more the myocardium is stretched, the greater force it exerts upon contraction
(despite of autonomic control)
[ie the greater the venous return, the greater the stroke volume]

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27
Q

what autonomic control can tweak the frank-starling curve?

A

sympathetic

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28
Q

what happens to the frank-starling curve in cardiac failure?

A

curve fails as force is not able to match the venous return (stretch)

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29
Q

what 3 factors contribute to increased venous return? (and therefore increased stretch)

A
  1. increased skeletal muscle activity
  2. adrenergic effects on blood vessels (increased venous tone)
  3. respiratory pump (increased depth and freq)
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30
Q

what does increased intracellular calcium cause?

A

contraction

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31
Q

what is excitation coupling?

A

coupling mechanical force to electrical excitation

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32
Q

for the action potential to excite a ventricular muscle cell what must it do when it sweeps across the cell?

A

dive down into the T-tubules

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33
Q

during depolarisation of a ventricular muscle cell (fast Na influx) what happens?

A

voltage-gated L-type Ca channels located in the T tubule membrane are opened by depolarisation and let a small amount of Ca in

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34
Q

what does the small calcium influx within a ventricular muscle cell cause?

A

the activation of RyR (ryanodine) receptors which cause the release of large amounts intracellular calcium from the SR.

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35
Q

what is the process called by which RyR receptors in the ventricular muscle are stimulated cause the release of calcium from the SR?

A

Ca-induced Ca release

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36
Q

for contraction within the ventricular muscle cell to occur what does calcium activate?

A

the myofilaments

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37
Q

once the myofilaments within the muscle cell have been activated what occurs?

A

the Ca is removed from the cytoplasm by the SR CA ATPase (SERCA) and the sarcolemma Na/Ca exchanger

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38
Q

what does the decreased intracellular concentration of calcium after myofilament activation cause?

A

relaxation

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39
Q

what do positive chronotropic drugs/hormones do to the calcium transients within the cardiac myocyte?

A

cause bigger and faster calcium transients

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40
Q

what is the function of the RyR within the myocyte?

A

when stimulated by calcium cause the Ca-induced Ca release from SR

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41
Q

what is the function of SERCA 2a within the myocyte?

A

removal of Ca at the end of a beat (puts Ca++ back into stores

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42
Q

what are the 4 sites of protein kinase A action within the myocyte?

A

RyR (ryanodine receptor)
LTCC (L-type calcium channels on T-tubule membrane)
PLB
Troponin

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43
Q

what does protein kinase A phosphrylation of LTCC cause within the myocyte?

A

increases trigger calcium and so increases Ca-induced Ca release (causing increased force of contraction)

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44
Q

what does protein kinase A phosphorylation of RyR do within the myocyte?

A

increases size of Calcium transient (ie amount leaving SR) and therefore increases force of contraction

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45
Q

what does protein kinase A phosphorylation of PLB do?

A

increases uptake by SERCA and so:

  1. accelerates relaxation (makes contraction shorter)
  2. increases SR calcium content
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46
Q

what is the function of troponin?

A

regulates the actin/myosin interaction using calcium

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47
Q

what does protein kinase A phosphorlation of troponin do?

A

phosphorylation of troponin reduces the affinity for calcium, there is a minor reduction in contraction but this accelerates relaxation

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48
Q

what is the principal determinant of calcium binding to troponin C to cause contraction?

A

the rate calcium diffuses from the SR

ie phosphorylation of RyR

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49
Q

what is the principle determinant of the unbinding of calcium once a contraction has occured?

A

phosphorylation of troponin

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50
Q

what is dobutamines effect on the heart?

A

selective b1-adrenoceptor agonist so increases force and rate

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51
Q

when is exogenous adrenaline used?

A

during cardiac arrest
emergency treatment of asthma
anaphylactic shock

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52
Q

when is dobutamine used?

A

for acute, but potentially reversible, heart failure

eg following cardiac surgery

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53
Q

why are b-1 adrenoceptor agonists regarded as ‘toxic’?

A

because long term stimulation of sympathetic system causes heart failure

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54
Q

what is propanolol?

A

a non-selective b-blocker

antagonist of b1 and b2 adrenoceptors

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55
Q

at rest, what is the effect of b-adrenoceptor antagonists on the heart and why?

A

little effect on rate, force

this is due to the sympathetic system not being too active during rest

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56
Q

during exercise, what is the effect of b-adrenoceptor antagonists on the heart?

A

rate and force are significantly depressed
coronary vessel diameter are marginally vasodilated
(as myocardial O2 requirement falls there is more effective oxygenation of the heart)

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57
Q

what do b2-adrenoceptors stimulation cause on the coronary vessels?

A

vasodilation

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58
Q

what is atenolol?

A

a selective B1-blocker

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59
Q

what is metoprolol?

A

a selective B1- blocker

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60
Q

what are the 4 clinical uses of B-adenoceptor antagonists?

A
  1. dysrhythmias
  2. hypertension
  3. angina
  4. heart failure
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61
Q

what are the 6 adverse effects of b-blockers?

* which have a lesser risk is B1 selective agents are used

A
  1. bronchospasm*
  2. aggravation of cardiac failure
  3. bradycardia (or heart block)
  4. hypoglycaemia* (in patients with poorly controlled diabetes)
  5. fatigue (due to decreased CO and skeletal muscle perfusion)
  6. cold extremities (loss of vasodilation in cutaneous vessels)
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62
Q

why might b-blockers cause aggravation of cardiac failure?

A

patients with heart disease may rely on sympathetic drive to maintain an adequate CO for perfusion of their body tissues

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63
Q

what is atropine?

A

a non selective muscarinic receptor antagonist

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64
Q

what are the effects of atropine on the cardiovascular system?

A
  1. increase in heart rate (modest in normal subjects, pronounced in athletes who have increased vagal tone)
  2. no effect on TPR (no parasympathetic innervation to blood vessels)
  3. no effect upon the respone to exercise
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65
Q

what are the 3 clinical uses of atropine?

A
  1. to reverse bradycardia following an MI (in which vagal tone is elevated)
  2. as an adjunt to anaesthesia
  3. in anticholinesterase poisoning (to reduce excessive parasympathetic activity
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66
Q

what is the pharmocodynamic effect of digoxin?

A

increases contractility of the heart?

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67
Q

what type of drugs are digoxin and dobutamine?

A

inotropic drugs

enhance contractility

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68
Q

what is the clinical use of digoxin?

A

in heart failure

especially in patients with AF- due to effects on AV node

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69
Q

how does digoxin work?

A
  1. blocks the sarcolemma Na/K ATpase which results in calcium unable to leave cell causing more to go into the SR
    (incresed contactility)
  2. increases AV node refractory period
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70
Q

what effect does digoxin have on the autonomic system?

A

none

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71
Q

what happens if you give digoxin to a patient with hypokalaemia?

A

effects of digoxin are dangerously enhanced

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72
Q

what are the 2 most serious effects of digoxin?

A
  1. excessive depression of AV node conduction- heart block

2. dysrhythmias

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73
Q

what is levosimendan?

A

a calcium-sensitiser: inotropic drug

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74
Q

how does levosimendan work?

A
  1. binds to troponin C in cardiac muscle sensitising it to the action of calcium
  2. causes vasodlation
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75
Q

what is the clinical use on levodimendan?

A

treatment of acute decompensated heart failure

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76
Q

what does contraction of vascular smooth muscle depend on?

A

intracellular concetration of calcium

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77
Q

in a vascular smooth muscle cell what are the 2 ways calcium concentration can be increased?

A

influx of Ca across membrane gradient (conc or electrical gradient)

Ca released from intracellular stores (eg SR)

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78
Q

in smooth muscle cell (very different to cardiac and skeletal muscle), how does calcium cause contraction?

A
  1. calcium binds to calmodulin to form a calcium-camodulin complex.
  2. this complex activates myosin light chain kinase (MLCK) which phosphorylates myosin-light chain.
  3. the phosphorylated myosin-LK can form cross bridges and allow myosin and actin to slide over each other and contract.
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79
Q

how does relaxation occur in a vascular smooth muscle cell?

A
  1. cGMP activates myosin-LC-phosphotase
  2. myosin-LC-phosphotase strips a phosphate from the phosphorylated myosin-LC converting it into inactive myosin-LC.
  3. the cross bridges break and relaxation occur
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80
Q

compare the functions of MLCK and MLC-phosphotase

A

MLCK phosphorylates inactive Myosin-LC
MLC-phosphotase strips a phosphate from active mysoin-LC

reverse roles

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81
Q

what 3 vasodilating substances work through NO production?

A

bradykinin
ANP
serotonin (5-HT)

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82
Q

what type of manner does NO signal in?

A

paracrine (induces an effect in cells near by)

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83
Q

what does NO do within a vascular smooth muscle cell?

A
  1. activation of guanylate cyclase

2. activates calcium-dependent potassium channels

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84
Q

what is the role of guanylate cyclase within a vascular smooth muscle cell?
(activated by NO)

A

converted GTP to cGMP

cGMP initiates the relaxation pathway

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85
Q

what happens when calcium-dependent potassium channels are activated?

A

cause potassium to leave the cell causing repolarisation.

this repolarisation closes voltage gated calcium channels and causes relaxation

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86
Q

what 2 ways can calcium-dependent potasssium channels become activated?

A

stimulation by NO

depolarisation

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87
Q

what is the function of organic nitrates?

A

relax all type of smooth muscle

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88
Q

why are organic nitrates a first choice for angina patients?

A
  1. they redirect the blood from unhealthy vessels to healthy vessels to bypass the block
  2. decreased myocardial oxygen requirement
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89
Q

why is there a decreased myocardial oxygen requirement when using organic nitrates?

A 
decreased preload (due to reduced venomotor tone)
decreased afterload (de to reduced vasomotor tone)
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90
Q

how do organic nitrates redirect blood from unhealthy vessels to bypass blockages?

A

dilate collateral vessels

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91
Q

why are arterioles downstream to a blockage already fully dilated?

A

due to local factors such as hypoxia etc

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92
Q

what are the 2 main types of organic nitrates used in practice?

A

glyceryltrinitrate

isosorbide mononitrate

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93
Q

compare glyceryltrinitrate and isosorbide mononitrate in terms of length of acting?

A

GTN- short acting (30 min)

isosorbide mononitrate- long acting (4 hours)

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94
Q

compare glyceryltrinitrate and isosorbide mononitrate in terms of effect of first pass metabolism?

A

GTN- extensive first pass metabolism

isosorbide mononitrate- resistant to first pastt metabolism

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95
Q

how it GTN administered?

A

sublinguial tablet or spray or transdermal patch

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96
Q

how should organic nitrates be used for angina?

A

prophylactically

GTN can also relieve attacks

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97
Q

what can happen with repeated administration of organic nitrates?

A

tolerance- diminished effect

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98
Q

how can you minimise tolerance of organic nitrates?

A

nitrate-low periods

usually at night

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99
Q

what is a common effect of organic nitrates which may occur initially?

A

headaches due to dilation of cranial circulation

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100
Q

what 3 things down regulate the production of endothelin?

A

nitric oxide
natriuretic peptides
shear stress

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101
Q

what are bosentan and ambrisentan?

A

antagonists of the ETa receptor (which endothlin acts on)

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102
Q

when are bosentan and ambrisentan (antagonists of the ETa receptor) used?

A

in treatment of pulmonary hypertension

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103
Q

what is a long term effect of angiotensin II?

A

promotes cell growth

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104
Q

what are the 2 functions of ACE?

A

converts angiotensin I to angiotensin II

inactivated bradykinin

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105
Q

where is ACE found?

A

bound to the membrane of endothelial cells

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106
Q

what is the role of ace inhibitors?

-pril

A

block the conversion of angiotensin I to angiotensin II

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107
Q

compare the effect of ACE inhibitors in normal subjecs and hypertensive patients?

A

small fall in MAP in normal subjects

large fall in MAP in hypertensive patients (since in these patients renin secretion is usually enhanced)

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108
Q

what are the common adverse effects of ACE inhibitors?

A 
initial hypotention (esp in patients on diuretics too)
dry cough (due to bradykinin accumulation)
renal dysfunction
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109
Q

what are the adverse effects of ACE inhibitors?

A 
initial hypotention (esp in patients on diuretics too)
dry cough (due to bradykinin accumulation)
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110
Q

what is the role of AT1 receptor blockers (ARBs)?

-sartan

A

competitevly block the agonist action of angeiotensin I at AT1 receptors

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111
Q

what are ACEIs and ARBs contraindicated in?

A

pregnancy

bilateral renal artery stenosis

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112
Q

if a patient has a intolerable dry cough with ACE inhibitors what drug should they be switched to?

A

ARBs

as there is no increase in bradykinin

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113
Q

what are ACEIs and ARBs contraindicated in?

A

pregnancy

bilateral renal artery stnosis

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114
Q

what are the clinical uses of ACE inhibitors and ARBs? (and explain)

A
  1. hypertension (reduces TRP and MABP)
  2. cardiac failure (reduces TPR to decrease cardiac work load, also causes regression of LVH)
  3. following an MI (same as above)
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115
Q

what are the clinical uses of beta-blockers?

A
  1. angina (only stable and unstable)
    because the decrease myocardial O2 requirement and increase the amount of time spent in diastole which improves perfusion
  2. hypertenstion
    reduce MAP and reduced renin release from the kidneys
  3. heart failure
    decreases cardiac work load
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116
Q

what is the function of calcium antagonists?

A

prevent the opening of L-type channels in response to depolarisation, this limits calcium influx

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117
Q

in the SA node what do calcium antagonists do?

A

reduce heart rate by reducing rate of upstroke of the AP

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118
Q

in the AV node what do calcium antagonists do?

A

reduce rate of conduction

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119
Q

in the ventricles what do calcium antagonists do?

A

reduce force of contraction by reducing Ca in plateau phase

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120
Q

what are the 3 main calcium antagonists?

A

verapamil (cardiac selective)
amlodipine (smooth muscle selective)
diltiazem

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121
Q

what are calcium antagonists clinically used in?

A

hypertension (reduce TPR and MAP)
angina (coronary vasodilation)
dysrhthmias (supression of AV conduction)

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122
Q

which calcium antagonists are preferred for hypertension and why?

A

smooth muscle selective

to minimise unwanted effects on cardiac muscle (important in heart failure or heart block)

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123
Q

what is the length of acting for amlodopine?

A

long acting

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124
Q

what calcium antagonists is used in dysrhthmias?

A

verapamil

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125
Q

what drug combination should be completely avoided in heart failure?

A

beta-blockers and verapamil

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126
Q

why do calcium antagonists work in variant angina? (unlike beta blockers)

A

variant angina is caused by episodic coronary spasms, so calcium antagonists work well by not allowing the cell to obtain the calcium required for a spasm

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127
Q

what are minoxidil and nicorandil?

A

potassium channel openers

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128
Q

how do potassium channel openers work?

A

work on vascular smooth muscle to open calcium-dependent K channels. this causes hyperpolarisation which switches off L-type calcium channels- causing relaxation of vascular smooth muscle

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129
Q

what is nicorandil used in?

A

angina

not used too commonly

130
Q

what is minoxidil used in?

A

hypertension (but only as a last resort)

131
Q

what are the negative effects of minoxidil?

A 
reflex tachycardia (prevented by a beta-blocker)
salt and water retention (alleviated by a diuretic)
132
Q

what are prazosin and doxazosin?

A

a1-adrenoceptor antagonists

133
Q

what is the dunction of a1-adrenoceptor antagonists?

A

cause vasodilation by blocking sympathetic/hormonal effect on a1-adrenoceptors

134
Q

what is the clinical use a1-adrenoceptor antagonists?

A

hypertension (especially if patient has prostatic hyperplasia)

135
Q

what is the function of diuretics?

A

act on kidneys to increase the excretion of Na, Cl and H20

136
Q

where do thiazide diuretics inhibit NaCl reabsorption?

A

distal tubule

137
Q

where do loop diuretics inhibit NaCl reabsorption?``

A

ascending limb of hte loop of Henle

138
Q

what is the main adverse affect of using thiazide or loop diuretics?

A

loss of K+

139
Q

how is the loss of K+ due to thiazide or loop diuretics corrected?

A

co-administration of a potassium sparring diuretic

k+ supplements

140
Q

what are the clinical uses of thiazide diuretics? (eg bendroflumethiazide)

A

mild heart failure

hypertension

141
Q

what are the clinical uses of loop diuretics?

A

acute pulmonary oedema

chronic heart failure

142
Q

name 6 classes of anti-hypertensive drugs?

A 
calcium antagonists
ACE inhibitors
ARBs
alpha blockers
beta blockers
thiazide diuretics
143
Q

name 4 classes of anti-anginal drugs?

A

nitrates
beta blockers
calcium antagonists
nicorandil

144
Q

name 3 classes of antithrombotic drugs?

A

antiplatelets (against platelets)
anticoagulants (against clotting factors)
fibrinolytics (dissolve preformed clots)

145
Q

name 2 classes of anticholesterol drugs?

A

statins

fibrates

146
Q

what is bendroflumethiazide?

A

thiazide diuretic

147
Q

what is furosemide?

A

a loop diuretic

148
Q

what are the 4 side effects of diuretics?

A
  1. hypokalaemia (tiredness, arrhythmias)
  2. hyperglycaemia (diabetes)
  3. hyperuricaemia (gout)
  4. impotence
149
Q

what are cardioselective b-blockers used in?

eg atenolol

A

angina
hypertension
heart failure

150
Q

what are non-selective b-blockers used in?

eg propanolol

A

thyrotoxicosis

151
Q

what type of patients are beta blockers contraindicated in?

A

asthmatic patients

patients with reynaulds

152
Q

what are the effects of beta blockers in short term heart failure vs long term heart failure?

A

beta blockers can worsen heart failure in short term

improve heart failure in long term

153
Q

what are the 2 types of calcium antagonists?

A

dihydropyridines eg amlodipine

rate-limiting calcium antagonists eg verapamil, diltiazem

154
Q

what can be the adverse result of giving beta blockers and rate-limiting calcium antagonists together?

A

full heart block

155
Q

what type of arrhythmias are rate-limiting calcium antagonists useful in treating?

A

superventricular arrthymias (AF, SVT)

156
Q

what is the main side effect of alpha blockers?

A

postural hypotension

157
Q

what is a rare, life threatening adverse reaction of ACE inhibitors?

A

angioneurotic oedema

never give to a patient with previous angioneurotic oedema

158
Q

why should you avoid giving ACEI to women of childbearing ages?

A

they might not know they are pregnant yet, contraindicated in pregnancy

159
Q

what type of drugs can pregnant women use to control pregnancy-induced hypertension?

A

calcium inhibitors and beta blockers

160
Q

what type of heart failure can nitrates be used in?

A

acute heart failure not chronic

161
Q

what is the function of antiplatelet agents?

A

prevent new thrombosis

dont break down clots that have already formed

162
Q

when are antiplatelet agents used?

A

angina
acute MI
CVA/TIA
(patients at risk of MI/CVS)

163
Q

what are the 3 main side effects of antiplatelet agents?

A 
haemorrhage
peptic ulcer (leading to haemorrhage)
aspirin sensitivity (asthma)
164
Q

what is the function of anticoagulants?

A

prevent new thrombosis

165
Q

how is heparin administered?

A

IV

166
Q

how is warfarin administered?

A

oral

167
Q

what clotting factors does warfarin block?

A

2, 7, 9, 10

168
Q

what is warfarin used in?

A

DVT
PE
NSTEMI
AF

169
Q

what are the side effects of anticoagulants?

A

haemorrhage

170
Q

how do you control the dose of warfarin?

A

using INR

171
Q

how do you reverse an overdose of warfrin? (ie if there is a haemorrhage)

A

vitamin K

172
Q

what clotting factor does rivaroxaban inhibit?

A

10a

173
Q

what clotting factor does dabigatran inhibit?

A

2a

174
Q

what does clotting factor Xa do?

A

convert prothrombin (II) into thrombin (IIa)

175
Q

name 2 fibrinolytic drugs?

A

streptokinase

tPA

176
Q

when are fibrinolytic drugs used?

A

STEMI
PE
CVA
(Selected cases only)

177
Q

what is the adverse side effect of fibrinolytic drugs?

A

haemorrhage

178
Q

when must you avoid using fibrinolytic drugs?

A 
recent haemorrhage
trauma
bleeding tendencies (eg haemophilla)
severe diabetic retinopathy
peptic ulcer
179
Q

how do statins work?

A

block HMG CoA reductase

180
Q

when are statins used?

A 
hypercholesterolaemia
diabetes
angina/MI
CVA/TIA
(high risk of MI/CVA)
181
Q

what are the possible side effects of statins?

A

myopathy (muscle ache)

rhabdomyolysis renal failure (renal muscle break down)

182
Q

when are fibrates used?

A

hypertriglyceridaemia

low HDL cholesterol

183
Q

what 2 drugs are anti-arrhythmic drugs?

A 
amiodarone
flecainide
(calcium antagonist
beta blockers
digoxin can also be used in SVAs but arent technically anti-arrhythmic drugs)
184
Q

what drug do you use in the acute phase of an SVT?

A

adenosine

185
Q

what are the 3 side effects of anti-arrhythmic drugs?

A

photoxicity
pulmonary fibrosis
thyroid abnormalities

186
Q

what are the 2 main effects of digoxin?

A
  1. degree of AV node block

2. increased ventricular contraction

187
Q

what are the side effects of digoxin?

A 
bradycardia and heart block
ventricular arrhythmias (fatal)
nausea
vomitting
yellow vision
188
Q

how are non-polar lipids transported in the blood?

A

within lipoproteins

189
Q

what ratio of LDL:HDL is strongly associated with cardiovascular disease? (atherosclerosis)

A

high LDL

low HDL

190
Q

what are the 2 main sections of an lipoprotein?

A

hydrophobic core

hydrophilic coat

191
Q

what does the hydrophobic core of the lipoprotein contain?

A

esterified cholesterol and triglycerides

192
Q

what does the hydrophilic coat of the lipoprotein contatin?

A

a monolayer of amphipathic cholesterol, phospholipids and one or more apoprotein

193
Q

what are the 4 main lipoproteins?

A

HDL
LDL
VLDL
chylomicrons

194
Q

what is the biggest lipoprotein in terms of diameter?

A

chylomicrons

195
Q

cholesterol within the hydrophilic coat of the lipoprotein are amphipathic. where does the hydrophobic part face and where does the hydrophilic part face?

A

hydrophobic part of cholesterol face into the centre of the sphere
hydrophilic part of the cholesterol face the aqeuous component of the blood

196
Q

what apoproteins are associated with HDL?

A

apoA1

apoA2

197
Q

what apoproteins are associated with LDL?

A

apoB-100

198
Q

what apoproteins are associated with VLDL?

A

apoB-100

199
Q

what apoproteins are associated with chyomicrons?

A

apoB-48

200
Q

what are apoproteins?

A

markers which say if the lipoprotein is LDL or HDL

201
Q

what is familial hypercholesterolaemia?

A

a genetic condition in which the patient is unable to clear LDL from the blood due to lack of LDL receptors on hepatocytes

202
Q

what type of lipoproteins deliver triglycerides to muscle (for ATP) and adipocytes (for storage)?

A

apoB -containing lipoproteins

203
Q

where are chylomicrons formed?

A

intestinal cells

204
Q

what is the function of chylomicrons?

A

transport dietary triglycerides to muscle and adipocytes

exogenous pathway

205
Q

what is the 3 phase life cycle of an ApoB-containing lipoprotein?

A
  1. assembly
  2. intravascular metabolism
  3. receptor mediated clearance
206
Q

where does assembly of an ApoB-containing lipoprotein occur?

A

apoB100-containing lipoproteins: liver

apoB46-containing lipoproteins: intestine

207
Q

what does intravascular metabolism of an apoB-containing lipoprotein involve?

A

hydrolysis fo the triglyceride core

208
Q

what does receptor mediated clearance of an apoB-containing lipoprotein involve?

A

lipoprotein attaches to a receptor and is endocytsosed into the cell and removed

209
Q

what needs to happen to the triglyceride to be absorbed in the intestine?

A

broken down into monoglyceride and free fatty acids

210
Q

after absorption in the intestine what happens to the monoglyceride and free fatty acids?

A

triglyceride is resynthesised from them

211
Q

how is cholesterol absorbed by an enterocyte?

A

a transport protein:

NPC1L1

212
Q

where within the enterocyte is apoB-48 made?

A

ribosome

213
Q

once the triglycerides have reformed in the enterocyte what happens?

A
  1. they form a droplet with apoB48 incorporated inside
  2. lipidation occurs
  3. cholesteryl esters are added
  4. particle (now called a chylomicron) leave by exocytosis
214
Q

where do chylomicrons go once having left the enterocyte?

A

lymphatic syste,

215
Q

where are VLDL particles assembled?

A

in liver hepatocytes

216
Q

what are VLDL partcles (containing triglycerides) assembled from?

A

from free fatty acids derived from adipose tissue and de novo synthesis

217
Q

to target triglyceride delivery to adipose and muscle tissue, chylomicrons and VLDL particles must become activated. How does this occur?

A

activation of chylomicrons and VLDL occurs by the transfer of apoCII from HDL particles
(apo C2)

218
Q

what does apoCII facilitate once transfered to the VLDL or chylomicron?

A

binding of chylomicrons and VLDL particles to lipoprotein lipase (LPL)

219
Q

what is lipoprotein lipase? (LPL)

A

a lipolytic enzyme associated with the endothelium of capillaries in adipose and muscle tissue

220
Q

what does lipoprotein lipase (LPL) do?

A

LPL hydrolyses the lipoprotein core triglycerides to free fatty acids and glycerol which enter tissues

221
Q

what are chylomicron and VLDL remnants?

A

lipoprotein particles depleted of triglycerides (due to the action of LPL) but still containing cholesteryl esters

222
Q

once LPL has enriched the chylomicrons and VLDL with cholesterol ester by removing triglyceride what happens?

A

chylomicrons and VLDL dissociate from LPL and apoCII is transferred back to HDL particles in exchange for apoE

223
Q

apoE causes the remnants to return where?

A

to the liver

224
Q

once in the liver what happens to the VLDL and chylomicron particles?

A

further metabolised by hepatic lipase and then all apoB48-containing remnants and 50% of apoB100 containing-remnants are cleared by receptor-mediated endocytosis into hepatocytes

225
Q

what happens to the remaining 50% of apoB100-containg remnants which havent been taken into the hepatocytes?

A

they loose further triglycerides through hepatic lipase, so become smalle and more enriched in cholester ester and eventually beome LDL particle
(only have apoB100 now, lost apoE)

226
Q

during triglyceride metabolism by hepatic lipase of the remaining apoB100-containing remnants, what particle forms first before the LDL forms?

A

IDL

227
Q

what is clearance of LDL particles dependent upon?

A

expression of the LDL receptor expressed by the liver (and other tissues)

228
Q

how do hepatocytes uptake the LDL particles?

A

receptor-mediated endocytosis

229
Q

once the LDL has been taken up by the hepatocyte, how is cholesterol released from the cholesterol ester?

A

hydrolysis

230
Q

what 3 things does the cholesterol released from the LDL cause?

A
  1. inhibition of HMG CoA reductase
  2. down regulation of LDL receptor expression
  3. storage of cholesterol as cholesterol ester
231
Q

what is HMG-CoA reductase?

A

the rate limiting enzyme in de novo cholesterol synthesis

232
Q

what does inhibition of HMG-CoA cause?

A

suppression of de novo endogenous cholesterol synthesis

233
Q

when an endothelium lining is damaged, what is it able to do?

A

uptake LDL from blood into the intima of the artery

234
Q

when LDL is within the intima of the artery what occurs?

A

oxidation to OXLDL

arthrogenic oxidised LDL

235
Q

why do monocytes migrate to the intima of the damaged endothelium?
(where they become macrophages)

A

to try mop up the cellular debris

236
Q

what do macrophages turn into when they take up the OXLDL in the damaged endothelium?

A

foam cells that form a fatty streak

237
Q

what starts to lay down on top of this fatty streak?

A

smooth muscle cells and collagen

238
Q

what makes up an atheromatous plaque?

A

lipid core (Dead foam cells) and a fibrous cap (smooth muscle and connective tissue)

239
Q

what is the role of HDL?

A

transports excess cholesterol from cells to liver

reverse cholesterol transport

240
Q

how is cholesterol removed from the body?

A

synthesised to make bile salts or secreted in bile

241
Q

what are the 2 mechanisms of reverse cholesterol transport?

A
  1. HDL reaching liver interacts with receptor that allows transfer of cholesterol and cholestryl esters into hepatocytes
  2. in plasma, cholesterol ester transfer protein (CETP) mediates transfer of cholesterol esters from HDL to VLDL and LDL (indirectly returning cholesterol to the liver)
242
Q

what is secondary dislipidaemia?

A

lipidaemia as a consequence of another disease

eg type 2 diabetes, hypothyroidism, alcoholism, liver disease

243
Q

by competitively inhibiting HMG CoA reductase, what effect to statins have?

A

decrease in hepatocyte cholesterol synthesis causes a decreased cholesterol concentration in the hepatocyte which results in a compensatory increased LDL receptor expression and enhanced LDL clearance

244
Q

why are statins ineffective in familial hypercholesterolaemia?

A

LDL receptors are lacking, so increased clearance of LDL doesnt occur

245
Q

when and how are statins administered?

A

orally at night

246
Q

what is the first line drug for patients with very high triglycride levels?

A

fibrates

247
Q

how to fibrates work?

A

act as agonists of a nuclear receptor (PPARalpha) to enhance the transcription of LPL

248
Q

what type of patients should you avoid giving fibrates in and why?

A

alcoholics

because even though they are predisposed to hypertriglyceridaemia they are also exposed to rhabdomyolosis

249
Q

what type of drug are colestyramine, colestipol and colsevelam?

A

bile acid binding resins

250
Q

what is the function of bile acid binding resins?

A

interrupt enterohepatic recycling of cholesterol

non-absorbable so cause the excretion of bile salts thus resulting in more cholesterol to be converted to bile salrs

251
Q

what 2 main effects do bile acid binding resins have?

A
  1. decreased absorption of bile salts and triglycerides

2. increased LDL receptor expression

252
Q

what is the adverse effect of bile acid binding resins?

A

GI irritation

253
Q

how does ezetimibe work?

A

inhibits NPC1L1 to reduce cholesterol absorption

254
Q

when is ezetimibe contraindicated?

A

breast-feeding females

255
Q

in what type of heart condition should calcium antagonists not be used?

A

heart failure

they make it worse as they are negative inotropes

256
Q

what is the process of haemostasis?

A

preventing blood loss from a damaged vessel

257
Q

what are the 3 features of haemostasis?

A
  1. local vasoconstriction
  2. adhesion and activation of platelets at site of injury
  3. formation of fibrin (a insoluble mesh)
258
Q

what is type of haemostasis is thrombosis?

A

pathological

259
Q

what is thrombosis?

A

a haemotological plug formed in the absence of bleeding

260
Q

what are the predisposing factors to thrombus formation?

A

virchows triad:

  1. injury to vessel wall
  2. abnormal blood flow.
  3. increased coaguablity of the blood
261
Q

what is an arterial thrombus?

A

a white thrombus made of mainly platelets in a fibrin mesh

262
Q

what is a venous thrombus?

A

a red thrombus rich in red blood cells and fibrin. has a white head and a jelly-like red tail

263
Q

compare the sites of an embolism formed from an arterial thrombus and a venous thrombus?

A

embolism from an arterial thrombus lodges in an artery in the systemic circulation
embolism from a venous thrombus lodges in an artery in the pulmonary circulation

264
Q

what is the main event in blood coagulation?

A

fibrinogen (a soluble agent) turning into fibrin (an insoluble agent)

265
Q

what activated clotting factor converts fibrinogen to fibrin?

A

thrombin (IIa)

266
Q

how are clotting factors activated?

A

proteolytic cleavage

267
Q

what activated clotting factor activates prothrombin? (II)

A

Xa

268
Q

how is factor X activated?

A

in vivo pathway or contact pathway

269
Q

what are the contact pathway factors?

A

XIa and XIIa

270
Q

what are the in vivo pathway factors?

A

tissue factor and VIIa

271
Q

what activates the in vivo pathway or contact pathway which ultimately ends up in fibrin formation?

A

endothelial damage

272
Q

upon activation of plateltes what aggregation factors do they release?

A

preformed (ADP, 5-HT)

synthesised on demand (TXA2)

273
Q

what do platelets do to help the coagulation cascade?

A

provide surfaces which bring clotting factors together

274
Q

before a clotting factor can attach to the negative phospholipids on the platelet surface what must occur?

A

gamma- carboxylation of glutamate residues of the cloting factor
(clotting factors are still inactive at this point)

275
Q

what co-factor does the carboxylase enzyme that mediates gamma-carboxylation of the glutamate residues of clotting factors require?

A

vitamin K (in it’s reduced form)

276
Q

what happens to the reduced vitamin K co-factor in the process of gamma-carboxylation of the glutamate residues of clotting factors?

A

becomes oxidised

forms oxidised vitamin K

277
Q

what is the job of vitamin K reductase?

A

converts oxidised vitamin K back into reduced vitamin K

278
Q

what enzyme does warfarin block?

and what is the result?

A

blocks vitamin K reductase
prevents formation of reduced vitamin K and therefore gamma-carboxylation of the glutamate residues of clotting factors can’t occur and the coagulationg pathway is interrupted

279
Q

what type of thrombosis are anticoagulants used in the prevention and treatment of?

A

venous thromosis

280
Q

what are 4 uses of warfarin?

A

DVT
prevention of post-operative thrombosis
patients with artificial heart valves
atrial fibrillation

281
Q

what is the name of the reduced form of vitamin K?

A

hydroquinone

282
Q

what is the name of the oxidised form of vitamin K?

A

epoxide

283
Q

what factors does warfarin render inactive?

A

II, VII, IX, X

284
Q

describe the onset/duration of warfarin?

A

slow onset, long half life (40 hrs)

285
Q

what type of therapeutic index does warfarin have?

A

low therapeutic index

286
Q

what are the 3 main factors that potentiate warfarin action and so increase risk of haemrrhage?

A

liver disease
high metabolic rate
drug interactions

287
Q

why might liver disease potentiate warfarin?

A

decreased clotting factors

288
Q

why might high metabolic rate potentiate warfarin?

A

increased clearance of clotting factors

289
Q

what 3 types of drug interactions might potentiate warfarin?

A
  1. agents that inhibit hepatic metabolism of warfarin
  2. agents that inhibit platelet function (eg some NSAIDS)
  3. agents that inhibit decrease availability of vitamin K
290
Q

what are the 3 main factors which might lessen warfarin action? (risk of thrombosis increased)

A
  1. physiological state
  2. vitamin K consuption
  3. drugs interactions
291
Q

what types of physiological states may lessen warfarin action and increase risk of thrombosis?

A

hypercoaguable states

low metabolic states (decreased degradation of clotting factors)

292
Q

what is antithrombin III? (AT III)

A

clotting factor inhibitor

binds to clotting factors rendering them inactive

293
Q

how does heparin work?

A

binds to antithrombin III and increases its affinity for clotting factors (particularly Xa and IIa) to increase their rate of inactivation

294
Q

compare heparins effect on Xa and IIa

A

heparin must bind to both AT III and IIa to inhibit IIa

heparin only needs to bind to AT III to inhibit Xa

295
Q

what factors do LMWHs inhibit?

A

Xa
(cant inhibit IIa because they cant bind to both AT III and IIa at the same time, for Xa they only need to bind to AT III)

296
Q

what is the order of elimination of herparin?

A

zero order kinetics

297
Q

what is the order of elimination of LMWHs?

A

first order kinetics

298
Q

why is heparin preferred to LMWH in renal failure?

A

LMWH is excreted by renal ecretion

299
Q

why should the inibility of LMWH to inhibit factor IIa not be important?

A

because it inhibits factor Xa which is upstream to IIa, so should indirectly inhibit IIa

300
Q

what are the 4 adverse affects of heparin gnd LMWHs?

A

haemorrhage
osteoporosis (long term)
hypoaldosteronism
hypersensitivity reactions

301
Q

what is the treatment for a patient on heparin or LMWH wo gets a haemorrhage?

A

discontiunue the heparin or LMWH

administer protamine sulfate (inactivated heparin)

302
Q

what is the benefit of dabigatran and rivaroxaban over heparin and LMWHs?

A

orally active agents
(no need for IV)
less haemorhage risk

303
Q

what factor does dabigatran inhibit?

A

IIa (thrombin)

304
Q

what factor does rivaroxaban inhibit?

A

Xa

305
Q

when are rivaroxaban and dabigatran used clinically?

A

to prevent venous thrombosis in patients undergoing hip and knee replacements

306
Q

what is the function of von willebrand factor?

A

allows platelets to adhere to endothelium

307
Q

what do ADP, 5HT and TXA2 do?

A

act on the cell surface receptor of platelets to cause aggregation and cross linking via fibrinogen

308
Q

what enzyme does aspirin block irreversibly?

and what effect does this have?

A

cyclo-oxygenase 1
(COX 1)
in platelets: prevents the synthesis of thromboxane A2 (TXA2) and so prevents stimulation of aggregation and cross-linking (adhesion)

309
Q

what does clopidogrel block irreversibly?

A

P2Y(12) receptor on platelets

prevents ADP binding to receptor and stimulation of aggregation and cross-linking (adhesion)

310
Q

what does tirofiban block?

A

GPIIb/IIa receptor on platelt to prevent the cross-linking by fibrinogen

311
Q

what type of thrombosis are anti-platelet drugs used in?

A

arterial thrombosis

312
Q

how and why is tirofiban administered?

A

IV in short term treatment to prevent MI in high risk patients with unstable angina
(with aspirin and heparin)

313
Q

describe the fibrinolytic cascade?

A

opposes coagulation cascade

plasminogen is converted to plasmin which breaks down the fibrin into fibrin fragments causing clot lysis

314
Q

what type of agents up regulated the conversion of plasminogen to plasmin?

A

fibrinolytic agents eg tPA, strptokinase

315
Q

how are fibrinolytic drugs administered?

A

IV

within as short a period as possible of the event

316
Q

what are fibinolytics used for clinically?

A

reopen occluded arteries eg MI or stroke

less freq: reopen life-threatening venous thrombosis or PE

317
Q

why are fibrinolytics not given to every patient who has had an acute MI?

A

because PCI is superior if aviable promptly

318
Q

why is action of streptokinase blocked after 4 days?

A

generation of antibodies

319
Q

to what patients should you not give streptokinase?

A

to patients with recent streptococcal infections

320
Q

how are tPAs administered?

A

IV (because of short half life)

Cardiovascular RT (12 decks)

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