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My Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What cells use the fast response?

A

atrial and ventricular muscle cells and Purkinje fibres

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2
Q

What cells use the slow response?

A

SA node and AV node cells

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3
Q

What ion is the fast response dependent on?

A

sodium

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4
Q

What ion is the slow response dependent on?

A

calcium

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5
Q

What are changes in the duration and phases of action potentials due to?

A

hormones, cardiac disease, pH and drugs

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6
Q

What is resting potential in ventricular cardiac muscle cells?

A

-90mV which is close to potassium’s equilibrium potential due to outward Ik1 but not exactly due to inward Na+ movement

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7
Q

What is dominant movement in Phase 4 in atrial and ventricular myocytes?

A

outward flux of K+

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8
Q

What is dominant movement in Phase 0 in atrial and ventricular myocytes?

A

inwards lux of Na+

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9
Q

What happens in Phase 0 of atrial and ventricular myocytes?

A
  • triggered by impulses from SA node
  • rapid activation of Na+ channels do inward, depolarising, Na+ current
  • inactivation of channels
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10
Q

What is the dominant movement in Phase 1 of atrial and ventricular myocytes?

A

outward movement of K+

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11
Q

What happens in Phase 1 of atrial and ventricular myocytes?

A
  • brief
  • rapid inactivation of Na channels
  • activation of Ito so outward K+ current
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12
Q

What is the dominant movement in Phase 2 of atrial and ventricular myocytes?

A

inward flux of Ca2+ which is roughly balanced by outward flux of K+

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13
Q

What happens in Phase 2 of atrial and ventricular myocytes?

A
  • balance of conductances
  • inward depolarising of Ca2+ and outward depolarising of K+
  • Ca2+ is voltage-activated Ca2+ channels (L-type) which inactivate slowly producing long lasting Ca2+ current crucial to cardiac muscle contraction
  • Ik1 and Ito reduce and delayed rectifier potassium channels open to give Ik
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14
Q

What factor determines how long plateau persists for?

A

as long as inward Ca2+ balances the outward K+

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15
Q

What drugs reduce plateau?

A

drugs that reduce Ica,l (calcium channel blockers)

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16
Q

What drugs increase duration of ventricular action potential and what is this called?

A

drugs that block certain potassium channels

an acquired long QT syndrome

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17
Q

What is the dominant movement in Phase 3 for atrial and ventricular myocytes?

A

outward flux of K+ is dominant

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18
Q

What happens in Phase 3 of atrial and ventricular myocytes?

A
  • outward K+ exceeds inward Ica,l

- Ica,l decreases due to inactivation of L-type Ca2+ channels

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19
Q

What is the difference in conductance between atrial and ventricular myocytes?

A
  • phase 2 is less evident due to extra Ikur channel so final repolarisarion occurs more rapidly
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20
Q

How does the slow response (in SA and AV tissue) differ from the fast response?

A
  • Vm between action potentials gradually shifts up which is the pacemaker potential
  • the upstroke is less steep as Ica,l channels open not voltage-gated ones
  • no distinct plateau phase but a gradual repolarising by delayed rectifier channels
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21
Q

What is the dominant movement of ions in Phase 4 of SA and AV node tissue?

A

outward flux of K+ is reduced and inward flux of Ca2+ and Na+ is increased generating the pacemaker potential

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22
Q

What three conductances does pacemaker potential in SA and AV node tissues rely on?

A
  • decrease in outward Ik causing depolarisation
  • increase in inward Ica,l causing depolarisation
  • HCN channels edit cation conductance in response to hyper polarisation triggering the funny current so Na+ ions move in causing depolarisation
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23
Q

Which cells do sympathetic adrenaline and noradrenaline activate beta 1 adrenoceptors in?

A

nodal cells and myocardial cells

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24
Q

How is cAMP concentration increased?

A

coupling though Gs protein aloha subunit means adenyl cyclase increases the intracellular concentration of cAMP from ATP

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25
Q

What does sympathetic signalling through Gs beta 1 adrenoceptors cause?

A
  • increased SA node action (+ chronotropic effect) with increased slope of Phase 4 and reduced threshold
  • increased contractility (+ inotropic effect)
  • increased conduction velocity in AV node
  • increased automacity
  • decreased duration of systole
  • increased activity of sodium-potassium pump
  • increased mass of cardiac muscle
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26
Q

How does acetylcholine produce a parasympathetic impulse in regulation of cardiac rate and force?

A

ACh acitvate m2 muscarinic cholinoceptors in nodal cells, coupling through a Gi protein
inhibition of adenylyl cyclase and reduction in cAMP
opening of specific potassium channels in the SA node (GIRKs)

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27
Q

What does ACh signalling in the autonomic regulation of rate and force cause?

A
  • decreased SA node frequency (- chronotropic effect) with decreased in Phase 4 slope, increase in threshold and hyperpolarisation during Phase 4 via GIRKs
  • deceased contractility due to decrease in Phase 2 and decreased Ca2+
  • decreased conduction in AV node due to decreased Ca2+ activity
  • possible arrhythmias occurring in the atria
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28
Q

What is the funny current activated by?

A

hyperpolarisation and cAMP

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29
Q

What effect will block of HCN channels have?

A

decreased slope of the pacemaker potential and reduced heart rate

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30
Q

What does ivabradine do?

A

selective blocker of HCN channels that is used to slow heart rate in angina and therefore reduces oxygen consumption

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31
Q

How does a muscle contract?

A
  • ventricular action potential
  • opening of voltage- activated Ca2+ channels during Phase 2
  • Ca2+ influx into cytoplasm
  • Ca2+ release from SR
  • cross bridge formation between A and M
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32
Q

How does a muscle relax?

A
  • repolarisation in phase 3 to 4
  • voltage-activated L-type Ca2+ channels return to closed state
  • Ca2+ influx ceases and Ca2+ efflux occurs by Ca2+/Na+ exchanger
  • Ca2+ release from SR stops and SERCA actively moves Ca2+ from the cytoplasm
  • cross bridges between A and M break
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33
Q

What are examples of beta adrenoceptor agonists and what effect do they have on the heart?

A
  • dobutamine, adrenaline and noradrenaline
  • increased force, rate and CO and O2 consumption
  • decreased cardiac efficiency
  • disturbance in rhythm
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34
Q

What are the clinical uses of adrenaline?

A
  • in cardiac arrest causing positive ionotropic and chronotropic actions, redistribution of blood flow and dilation of coronary arteries
  • anaphylactic shock
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35
Q

What are the clinical uses of dobutamine?

A
  • acute heart failure
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36
Q

What is an example of beta adrenoceptor antagonist that non-selectively blocks beta adrenoceptors?

A

propranolol

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37
Q

What is an example of beta adrenoceptor antagonist that selectively blocks beta adrenoceptors?

A

atenolol, bisoprolol and metoprolol

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38
Q

What are the pharmacodynamic effects of non-selective beta adrenoceptor antagonists?

A
  • little effect on rate force or CO
  • reduction maximal exercise tolerance
  • coronary vessel diameter marginally reduced but myocardial oxygen requirement falls
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39
Q

What are the clinical uses of beta adrenoceptor antagonists?

A
  • treatment of disturbances of cardiac rhythm (tachycardia or a-fib)
  • treatment of angina
  • treatment of heart failure
  • treatment of hypertension
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40
Q

What are the adverse effects of beta-blockers?

A
  • bronchospasm
  • aggravation of cardiac failure (decompensated.. it is still used in compensated)
  • bradycardia
  • hypoglycaemia
  • fatigue
  • cold extremities
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41
Q

What are the pharmacodynamic effects of atropine?

A
  • increase in HR
  • no effect upon arterial BP
  • no effect on response to exercise
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42
Q

What are the clinical uses for atropine?

A
  • first line in treatment of bradycardia, esp following MI

- im anti cholinesterase poisoning

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43
Q

What is digoxin used for?

A
  • heart failure
  • to increase contractility of the heart
  • heart failure with a-fib
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44
Q

What do inotropes do to the ventricular function curve of SV against EDP?

A

upward and leftward shift so SV increases any given EDP

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45
Q

What is the biochemical effect of digoxin?

A
  • inhibits sodium-potassium pump
  • increases Na concentration inside and reduced Vm
  • decreases sodium calcium exchange and increase inside calcium ion concentration
  • increased storage of calcium ions in SR
  • increases CICR and contractility
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46
Q

What are digoxin’s effects on electrical activity?

A

indirect- increased vagal activity so slows SA node discharge and slows AV node conduction to increase refractory period
direct- shortens action potential and refractory period in atrial and ventricular myocytes but a toxic concentration causes oscillatory afterpotentials

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47
Q

What are the most serious cardiac effects of digoxin?

A
  • excessive depressions of AV node conduction (heart block)

- propensity to cause arrythmias

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48
Q

What are some other adverse non-cardiac effects of digoxin?

A
  • nausea
  • vomiting
  • diarrhoea
  • disturbances of colour vision
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49
Q

What is an example of a calcium-sensitiser drug and how does it work?

A

Levosimendan

  • binds to troponin C in cardiac muscle sensitising it to the action of Ca2+
  • opens Katp channels in vascular smooth muscle causing vasodilation
  • used in acute decompensated heart failure
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50
Q

What are examples of inodilators and how do they work?

A

Amrinone and Milrinone

  • inhibit PDE in cardiac and smooth muscle cells and increase cAMP concentration
  • increases contractility, decrease peripheral resistance but worsen survival
  • used for IV administration in acute heart failure
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51
Q

What are organic nitrates used to treat?

A
  • acute angina and chest pain with associated with acute coronary syndrome
  • prevention of angina
  • treatment of pulmonary oedema
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52
Q

What are calcium channel blocker used to treat?

A
  • hypertension
  • treatment of stable angina
  • control HR in patients with supraventricular arrhythmias
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53
Q

What is angina?

A

a pain that occurs when the oxygen supply to the myocardium is insufficient to meet its metabolic demands

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54
Q

What are the three types of angina?

A
  • Stable angina- due to a fixed narrowing of coronary vessels as a consequence of atherosclerosis
  • Unstable angina- due to platelet-fibrin thrombus in association with an atheromatous plaque
  • Variant angina- associated with coronary artery spasm
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55
Q

How does cyclic GMP-dependent PKG cause smooth muscle relaxation?

A
  • stimulating myosin phosphatase
  • stimulating plasma membrane Ca2+ ATPase
  • stimulating sarcoplasmic reticulum Ca2+ ATPase
  • activating K+ channels that cause hyperpolarization
  • inactivating Ca2+ channels
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56
Q

What do small doses of organic nitrates do?

A

cause venorelaxation with a decrease CVP/preload but CO is maintained by the increased heart rate

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57
Q

What do large doses of organic nitrates do?

A

increased arteriolar dilation

58
Q

What is the effect of organic nitrates?

A

decreased myocardial oxygen requirements by…

  • decreased preload
  • decreased afterload
  • improved perfusion of the ischaemic zone
59
Q

How do organic nitrates increase perfusion to the ischaemic zone?

A

they dilate the collateral vessels so the blood flow to ischaemic myocardium is increased so blood can still get to the ischaemic myocardium despite a plaque blocking the main vessel

60
Q

What are the main types of organic nitrates and what are they used to treat?

A

Organic nitrates are used in all types of angina

The main examples are glycerylnitrate (GTN) and isosorbide mononitrate (ISMN) which are both metabolised to nitric oxide

61
Q

How is GTN administered and how long does it act for?

A

Glyceryltrinitrate is short-acting (30 mins), administered sublinguinally or as a spray (stable angina) or IV with aspirin (unstable angina)
GTN never reaches in the veins from the liver because it is so metabolised by the liver (first-pass metabolism). Therefore, GTN is not effective if swallowed.

62
Q

What is first-pass metabolism?

A

First-pass metabolism is that after a drug is swallowed and enters the intestines, it enters the portal circulation between the intestines and the liver

63
Q

What is isosorbide mononitrate used for and how is it administered?

A

Isosorbide mononitrate (ISMN) is resistant to first-pass metabolism and is administered orally for angina prophylaxis and has a more sustained effect than GTN

64
Q

What are the adverse side-effects of organic nitrates?

A

headaches, hypotension/ fainting, reflex tachycardia (prevented by adding a beta blocker) and formation of methaemoglobin (can be used with amyl nitrate to treat cyanide poisoning)

65
Q

How is tolerance of organic nitrates avoided?

A

there can be a diminished effect which can be avoided by only taking the drug at breakfast and lunch

66
Q

How are calcium channel blockers used to treat hypertension?

A

reduced calcium ion entry into vascular smooth muscle which causes arteriolar dilation
reducing total peripheral resistance and mean arterial blood pressure
drugs with selectivity for smooth muscle L-type channels are preferred to minimise effects on cardiac muscle, they can be used for patients with both angina and hypertension and for isolated systolic hypertension

67
Q

How are calcium channel blockers used to treat angina?

A

prophylactic treatment, used with GTN if beta-blockers are contraindicated
they cause peripheral arteriolar dilation decreasing afterload and myocardial oxygen requirement and they produce coronary vasodilation (useful in variant angina)

68
Q

What are some examples of calcium channel blockers used for angina?

A

Examples are amlodipine (little effect on heart and long-acting) and diltiazem and verapamil (negative inotropic effects)

69
Q

How are calcium channel blockers used to treat dysrhythmias and what particular drug is used?

A

suppression of conduction through AV node

verapamil is used but avoid in heart failure particularly with a beta-blocker

70
Q

What are the adverse effects of calcium channel blockers?

A

from excessive vasodilation so hypotension, dizziness and swollen ankles

71
Q

What so calcium channel blockers do?

A

block or prevent the opening of L-type channels in tissues that depolarise and hence limits an increase in intracellular calcium ions

72
Q

Where do calcium channel blockers act?

A

L-type calcium channels in the heart, smooth muscle or in other locations

73
Q

What do L-type calcium channels mediate and how do antagonists affect this?

A

upstroke of AP in SA and AV nodes (calcium ion antagonists can reduce rate and conduction through AVN) and phase 2 of the ventricular AP (calcium ion antagonists can reduce the force of contraction by reducing the amount of calcium)

74
Q

What are the roles of angiotensin 2?

A
  • Increases sympathetic nerve activity causing vasoconstriction and increasing BP
  • Increases ADH release so increases water reabsorption so there is more water in the circulation so increases blood volume
  • Increases thirst
  • Increases sodium ion reabsorption from the kidney
75
Q

What do ACE inhibitors block and what is an example?

A

the conversion of angiotensin 1 to angiotensin 2 eg Lisinopril

76
Q

What do AT1 receptor antagonists block and what is an example?

A

the agonist action of angiotensin 2 at AT1 receptors in a competitive manner eg Losartan

77
Q

What do ACE inhibitors cause?

A
  • venous dilation (decreased preload) and arteriolar dilation (decreased afterload) which decreases ABP and cardiac load
  • no effect on cardiac contractility
  • reduce the release of aldosterone
  • small fall in MAP (larger fall in hypertensive patients)
  • reduce growth action of angiotensin 2 upon the heart and vasculature
78
Q

What are the adverse effects of ACE inhibitors?

A

hypotension, dry cough, hyperkalemia and angioedema

79
Q

What are AT1 receptor blocker useful for?

A

useful for patients who find dry cough by ACE intolerable

80
Q

When should ACE inhibitors and AT1 receptor blockers never be used?

A

pregnancy and bilateral renal artery stenosis

81
Q

What are the uses of ACEIs and AT1 receptor blockers?

A
  • hypertension (reduced TPR and MABP)
  • cardiac failure (improving perfusion, increassing excretion of Na+ and H2O and causing regression of left ventricular hypertrophy)
  • following MI
82
Q

What are the clinical uses of beta-adrenoceptors?

A
  • Angina pectoris- they decrease myocardial oxygen requirement, counter elevated sympathetic activity associated with ischaemic pain and they increase diastole)
  • Hypertension- reducing cardiac output, reducing renin release from the kidney and reducing sympathetic activity
  • Heart failure- suppress adverse effects associated with increased sympathetic activity and RAAS
83
Q

How do Katp channels act?

A
  • antagonising intracellular ATP
  • cause hyperpolarisation which switches off L-type Ca2+ channel
  • act potently and primarily upon arterial smooth muscle
84
Q

What is an example of a Katp channel opener?

A

E.g. Minoxidil used in severe hypertension (causes adverse reflex tachycardia and salt and water retention) or Nicorandil used in angina

85
Q

What effect do alpha blockers have?

A

Alpha 1 adrenoceptor antagonists cause vasodilation and reduced sympathetic transmission resulting in decrease MAP
They can also relieve benign prostatic hyperplasia

86
Q

What is the adverse effect of alpha blockers?

A

postural hypotension

87
Q

What is a cardiac arrhythmia?

A

a disturbance of rate or rhythm that may be caused by changes in impulse formation or impulse conduction

88
Q

How can cardiac arrhythmias be described?

A

in terms of rate so bradycardia and tachycardia or by site of origin so supraventricular (atria and AV node) or ventricular

89
Q

What do alterations in impulse formation involve?

A

changes in automaticity or triggered activity

90
Q

How does automacity usually work in normal cells?

A
  • SA node is the normal pacemaker but all components in the cardiac conduction system demonstrate a slower phase 4 depolarisation and thus possess automaticity
  • SA node pacemaker is normally highest and is dominant over other latent pacemakers such as the AV node and Purkinje fibres which is known as overdrive suppression
  • SA node must discharge APs at a higher, regular frequency than any other structure in the heart
91
Q

What are the two types of altered autemacity?

A

physiological or pathophysiological (when SA node is taken over by another latent pacemaker as a result of loss of overdrive suppression)

92
Q

When does overdrive suppression occur?

A
  • if SA node firing frequency is pathologically lower or if conduction of impulse from SA node is impaired then a latent pacemaker will initiate an escape beat
  • if latent pacemaker fires at an intrinsic rate faster than the SA node rate: latent pacemaker makes ectopic beat
  • in response to tissue damage even non-pacemaker cells may assume spontaneous activity
93
Q

What can an ectopic beat result from?

A

ischemia, hypokalaemia, increased sympathetic activity or fibre stretch

94
Q

What are afterdepolisations?

A

a normal AP may trigger abnormal oscillations in membrane potential termed afterdepolarizations, ADs of amplitude sufficient to reach threshold cause premature AP and beats

95
Q

What are EADs?

A

early afterdepolaisations occur during the inciting of AP within phase 2 (ca2+ channels) and phase 3 (Na+ channels)

96
Q

When are EADs most likely?

A
  • when HR is slow
  • often occur in Purkinje fibres
  • are associated with prolongation of the action potential and drugs prolonging the QT interval
  • when sustained can lead to life-threatening arrhythmia called ‘torsades de pointes’
97
Q

When do DADs occur and what are they caused by?

A
  • occur after complete repolarization
  • caused by large increases in Ca2+ concentration
  • result in release of Ca2+ from SR and a transient inward current of Na+ that occurs in phase 4
98
Q

When are DADs most likely to occur?

A
  • when the heart rate is fast
  • are affected by drugs that change the length of APs
  • may be triggered by drugs that increase Ca2+ influx or release from SR
99
Q

What do abnormalities in impulse conduction arise from?

A
  • re-entry
  • conduction block
  • accessory tracts
100
Q

How does re-entry cause an impulse conduction abnormality?

A
  • self sustaining electrical circuit stimulates an area of myocardium repeatedly
  • requires unidirectional block (anterograde conduction prohibited and retrograde conduction allowed) and slowed retrograde conduction velocity
  • two APs from two columns collide they extinguish each other but when there is unidirectional block then only one AP gets down so it is not extinguished
101
Q

What are the types of partial conduction block (through AV node)?

A
  • slowed conduction (first degree AV block)
  • intermittent block (second degree AV block)
  • complete block
102
Q

What are the types of intermittent AV partial conduction block?

A
  • Mobitz type 1 (PR interval gradually increases until it fails completely an beat is missed); treat with atropine
  • Mobitz type 2 (PR interval is constant but every nth depolarization is missing); don’t treat with atropine
103
Q

What is complete block?

A
  • no impulses are conducted through the affected area eg third degree AV block
  • atria and ventricles beat independently
  • ventricular pacemaker is now purkinje fibres
104
Q

What are the ways that accessory tract pathways can cause arrhythmias?

A

bundle of Kent is another electrical pathway that is in parallel to the AV node and it conducts more quickly than through the AV node so ventricles receive two signals so there can be tachyarrhythmias

105
Q

What do class IA target?

A

Voltage-activated Na+ channels (moderate rate association/dissociation from Na+ channels, they slow rate of rise of AP and prolong refractory period)

106
Q

What do class IB target?

A

Voltage-activated Na+ channels (rapid association and dissociation and prevent premature beats)

107
Q

What do class IC target?

A

Voltage-activated Na+ channels (slow association/dissociation and depress conduction)

108
Q

What do class II target?

A

Beta-adrenoceptor (decrease rate of depolarisation in SA and AV nodes)

109
Q

What do class III target?

A

Voltage-activated K+ channels (prolong AP duration increasing refractory period)

110
Q

What do class IV target?

A

Voltage-activated Ca2+ channels (slow conduction in SA and AV node, decrease force of cardiac contraction)

111
Q

How do Class I agents work?

A

Class I agents bind and target areas of the myocardium where firing frequency is highest so they block the open state and stabilise the inactivated state.
Class I agents dissociate from the Na+ channel when it is at rest so if HR increases there is less time for dissociation so steady state block increases

112
Q

What changes for Class I agents in ischaemic myocaridum?

A
  • the APs are longer so the inactivated state of the Na+ channel is available to the blockers for longer and the rate of recovery is decreased
  • the higher affinity of channel blockers for the open and inactivated states allows them to act on ischaemic tissue and block arrhythmias at the source
113
Q

What are the features of lipids?

A

insoluble
essential for membrane biogenesis and integrity
energy source
precursors for hormones and signalling molecules

114
Q

What are examples of non-polar lipids?

A

cholesterol esters and triglycerides

115
Q

How are non-polar lipids transported?

A

in the blood

116
Q

What are lipoproteins made up of?

A
  • Lipoproteins have a hydrophobic core containing esterified cholesterol and triglyceride
  • They have a hydrophilic coat comprising of a monolayer of amphipathic cholesterol, phospholipids and one or more apoproteins
117
Q

What are the major lipoproteins and what apoproteins are they associated with?

A

HDL (apoA1 and apoA2)
LDL (apoB-100)
VLDL (apoB-100)
chylomicrons (apoB-48)

118
Q

What do apo-B lipoproteins do?

A

deliver triglycerides to muscle for ATP biogenesis and adipocytes for storage

119
Q

What pathway do chylomicrons form?

A

exogenous pathway

120
Q

Where are VLDL particles synthesised and what do they do?

A

synthesised in the liver and transport the TAGs synthesised by that organ which is the endogenous pathway

121
Q

What is the outline of the life-cycle of an app-B containing liposome?

A
  • assembly
  • intravascular metabolism (hydrolysis of TAG core)
  • receptor mediated clearance
122
Q

How are chylomicrons assembled?

A
  • cholesteryl ester and TAGs are in cytoplasm
  • apoprotein is synthesised in the enterocyte
  • vesicle grows and cholesteryl ester is added to make a chylomicron
  • moves out of the enterocyte by exocytosis and enters the lymphatic system
123
Q

How are VLDLs assembled?

A

assembled in liver hepatocytes from free fatty acids and are derived from adipose tissue and de novo synthesis

124
Q

How are chylomicrons and VLDL particles activated?

A

activated by the transfer of apoC2 from HDL particles
once apoC2 has been added to the LDL
it allows the particles to interact with an enzyme of the surface of capillary cells called LPL
the enzyme can then digest the core to give three fatty acids and a glycerol which can use simple diffusion to cross the capillary wall into the tissues

125
Q

How are chylomicrons cleared?

A
  • depleted core
  • triglycerides removes
  • dissociation from LPL
  • apoC2 returned to the HDL particles and poE is given to partially digested particles
  • remnants are sent to the liver and enter by receptor-mediated endocytosis
  • metabolism by hepatic lipase
  • LDL receptor needed to internalise LDL into liver cell
  • released cholesterol causes inhibition of HMG-CoA reductase
  • down regulation of LDL receptor expression
  • storage of cholesterol as cholesterol ester
126
Q

What do stains block?

A

competitively block HMG-CoA reductase so increases cell surface expression of LDL receptor so more LDL into the liver cells so increased LDL clearance from the blood

127
Q

Why is LDL bad?

A
  • Uptake of LDL into intima and is oxidised to oxidised LDL
  • Migration of monocytes into intima where they become macrophages
  • Uptake of OXLDL by macrophages so they become cholesterol-laden foam cells and form a fatty streak
  • Release of inflammatory substances and proliferation of smooth muscle cells into the intima and deposition of collagen
  • Atheromatous plaque formation involving a lipid core and a fibrous cap
128
Q

Why is HDL good?

A
  • HDL removes excess cholesterol by transporting it into the liver
  • HDL is formed in the liver initially as ApoA1
  • Can accept excess cholesterol onto its surface and is stored in the core as esterified cholesterol
  • It then delivers the cholesterol to the liver by reverse cholesterol transport
129
Q

What is primary dyslipidemia?

A

occurs through a combination of diet and genetics

130
Q

What is secondary dyslipidameia?

A

a consequence of other diseases

131
Q

What are the other benefits of statins?

A

decreased inflammation, reversal of endothelial dysfunction, decreased thrombosis and stabilization of atherosclerotic plaques

132
Q

What do fibrates do?

A

Used to decrease TAGs and small decreases in LDL and HD

It increases activity of LPL by binding to PPARalpha as a competitive agonist

133
Q

What do bile acid binding resins do?

A

bile acid binding resins cause excretion of bile salts resulting in more cholesterol to be converted to bile salts by interrupting enterohepatic recycling

134
Q

What does Ezetimibe do?

A

Inhibits NPC1L1 transport protein in enterocytes which reduces the absorption of cholesterol in the duodenum
This causes a decrease in LDL but little change in HD
L

135
Q

What is the treatment for an MI acutely?

A
  • morphine and anti-emetic
  • oxygen (if needed)
  • nitroglycerin
  • aspirin 300mg
  • clopidogrel
136
Q

What is the treatment of a STEMI in hospital?

A
  • beta-blocker orally if no heart failure, no low output state, no increased risk cardiogenic shock and no contraindications
  • anti-coagulation with fondaparinux
137
Q

What is the time limit for PCI before fibrinolytic are used?

A

90 mins

138
Q

What are the contraindications for thrombolysis?

A
  • recent surgery
  • recent trauma or head injury
  • bleeding diatheses
  • coma
  • active peptic ulcer
  • recent stroke
  • suspected aortic dissection
  • traumatic resuscitation attempt
  • allergy to streptokinase
  • severe hypertension – control the blood pressure first eg with GTN then proceed.
139
Q

What are the side-effects of opiates?

A

sedation, hypoventilation and nausea

140
Q

What are the side-effects of beta-blockers?

A

bradycardia, cardiac failure, bronchospasm in asthma & chronic bronchitis, hypotension

141
Q

What drugs reduce the effects of anti-hypertensive ACEIs?

A

NSAIDs so ibuprofen

My Cardiovascular (13 decks)

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