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The cardiovascular system > pharmacology > Flashcards

pharmacology Flashcards

1
Q

describe phase 4 of the ventricular AP

A
  • Resting potential

- the outward flux of K+ is dominant

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2
Q

describe phase 0 of the ventricular AP

A
  • Upstroke

- the inward fluff Na+ is dominant

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3
Q

describe phase 1 of the ventricular AP

A
  • early repolarisation

- outward flux of K+ is dominant

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4
Q

describe phase 2 of the ventricular AP

A
  • plateau

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

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5
Q

describe phase 3 of the ventricular AP

A
  • final repolarisation

- the outward flux of K+ I dominant

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6
Q

What is the difference between the ventricular AP and the atrial AP?

A
  • an additional ultra rapid delayed rectifier means that is absent in ventricular cells means that the plateu phase is less evident in atrial cells
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7
Q

how is the pacemaker potential generated in pacemaker cells?

A

the outward flux of K+ is reduced and the inward flux of Ca 2+ and Na+ is increased which generates the pacemaker potential

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8
Q

adrenaline activates …… receptors coupled to …… to …… HR in sympathetic stimulation

A
  • B1
  • Gs
  • increase
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9
Q

sympathetic stimulation causes decreased contractility T/F?

A

False

increased contractility

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10
Q

sympathetic stimulation …….. conduction velocity to the AV node

A

increases

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11
Q

sympathetic stimulation increases automaticity, what does this mean?

A
  • the tendency for non nodal regions to acquire spontaneous activity
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12
Q

sympathetic stimulation decreases the duration of systole T/F?

A

True

due to increased uptake of Ca2+ into the SR

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13
Q

sympathetic stimulation decreases activity of the Na+/K+ ATPase T/F

A

false

increases

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14
Q

sympathetic stimulation causes an increased mass of cardiac muscle T/F

A

true

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15
Q

in parasympathetic stimulation acetylcholine actives …… receptor coupling through …… causes …… HR

A
  • M2
  • Gi
  • Decreased
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16
Q

What does parasympathetic stimulation cause?

A
  • decreased contractility
  • decreased conduction in AV node
  • may cause arrhythmias to occur in atria
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17
Q

what effect does blocking HCN channels have?

A
  • decreases the slope of the pacemaker potential

- reduces HR

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18
Q

Name a drug that selectively blocks HCN channels and what it is used for?

A
  • ivabradine

- used to slow HR in angina

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19
Q

Name some beta adrenoreceptor agonists that act on the heart?

A
  • dobutamine, adrenaline and noradrenaline
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20
Q

Describe the effect of beta adrenoceptor agonists on the heart?

A
  • increase force, rate and cardiac output

- decrease cardiac efficiency (O2 consumption increased more than cardiac work) can cause disturbances in cardiac rhythm

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21
Q

Name a B1 adrenoceptor agonist that is given as an IV infusion for the treatment of acute Heart failure?

A

Dobutamine

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22
Q

propanolol is a selective blocker of beta adrenoceptors T/F

A

False

It is non selective

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23
Q

name some selective blockers of beta 1 adrenoceptors?

A

atenolol
bisoprolol
metoprolol

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24
Q

Name an antagonist that is non selective and a partial agonist?

A

alprenolol

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25
Q

describe the pharmacodynamic effects of non selective blockers?

A
  • at rest, little effect on rate, force, CO or MABP
  • during exercise or stress, rate, force and CO are slightly depressed - reduction in max exercise tolerance
  • coronary vessel diameter marginally reduced but myocardial O2 requirement falls, thus better for oxygenation of the myocardium
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26
Q

how can beta adrenoceptor antagonists be used clinically?

A

For the treatment of:

  • arrhythmias
  • atrial fibrillation
  • supra ventricular tachycardia
  • angina
  • heart failure (low dose in compensated cardiac failure)
  • hypertension
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27
Q

describe some adverse effects of beta blockers?

A
  • bronchospasm (in asthmatics)
  • aggravation of cardiac failure
  • bradycardia (in patients with coronary disease)
  • hypoglycaemia (in patients with poorly controlled diabetes)
  • fatigue
  • cold extremities
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28
Q

What is atropine?

A

non selective muscarinic ACh competitive antagonist

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29
Q

describe the pharmacodynamic effects of atropine?

A
  • increase HR
  • no effect on arterial BP
  • no effect on response to exercise
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30
Q

describe the clinical uses of atropine in relation to the heart?

A
  • first line management of severe or symptomatic bradycardia - following MI
  • also used in anti cholinesterase poisoning
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31
Q

Describe the effect of digoxin?

A
  • Na+/K+ ATPase inhibited
  • increased [Na} and reduced Vm
  • decreased Na+/Ca2+ exchanged and increased [Ca2+]
  • increased storage of Ca2+ in SR
  • increased CICR: increased contractility
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32
Q

What do inotropic drugs do?

A

enhance contractility

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33
Q

describe the pharmacodynamics of digoxin?

A
  • Binds to the alpha subunit Na+/K+ ATPase in competition with K+ - effects can be dangerously enhanced by low plasma [K+]
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34
Q

describe the indirect action of digoxin on electrical activity?

A
  • increased vagal activity
  • slows SA node discharge
  • slows AV node conduction - increases refractory period
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35
Q

describe the direct action of digoxin on electrical activity?

A
  • shortens the AP and refractory period in atrial and ventricular myocytes
  • toxic concentration cause membrane depolarisation and oscillatory afxterpotentials likely due to Ca2+ overload
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36
Q

what are the clinical uses of digoxin?

A
  • IV in acute HF
  • oral in chronic HF (in patients remaining symptomatic despite other treatment)
  • HF with atrial fibrillation
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37
Q

describe the side effects of digoxin?

A
  • excessive depression of AV ode conduction
  • propensity to cause arrhythmias
  • nausea
  • vomiting
  • diarrhoea
  • disturbances of colour vision
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38
Q

name an inotropic drug that is a calcium sensitiser?

A

Levosimendan

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39
Q

describe the mechanism of levosimendan?

A
  • makes troponin C more sensitive to calcium

- opens KATP channels in vascular smooth muscle causing vasodilation

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40
Q

What is levosimendan used for?

A
  • treatment of acute decompensated HF
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41
Q

name some inodilators?

A

amrinone and milrinone

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42
Q

What do inodilators do?

A
  • inhibit phosphodiesterase in cardiac and smooth muscle cell and hence increase [CAMP] I - increase myocardial contractility, decrease peripheral resistance
  • use limited to IV administration in acute HF
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43
Q

describe the clinical use of adrenaline?

A

given in cardiac arrest and the immediate management of anaphylactic shock

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44
Q

adrenaline has a ….. plasma t1/2 due to uptake/metabolism

A

short

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45
Q

Describe the mechanism of adrenaline in cardiac arrest?

A
  • positive inotropic and chronotropic effects via B1
  • redistribution of blood flow to the heart from ‘non-essential tissues’
  • dilates coronary arteries via activation of B2
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46
Q

Name 3 types of common anti cholesterol drugs

A
  • statins
  • fibrates
  • PCSK 9 inhibitors
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47
Q

Name 3 common types of hypertensive drugs

A
  • thiazide diuretics
  • beta blockers
  • vasodilators (calcium antagonists, alpha blockers, ACE inhibitors, ARBs)
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48
Q

describe the mechanism of simvastatin and when it is used?

A
  • statin that blocks HMG coA reductase
  • used in: hypercholesterolaemia
    diabetes
    angina/MI
    CVA/TIA
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49
Q

Describe the side effects of simvastatin?

A
  • myopathy

- rhabdomyolysis (renal failure)

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50
Q

what is bezafibrate and what is it used for?

A
  • it is a fibrate used in hypertriglyceridaemia and low HDL cholesterol
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51
Q

Name 2 PCSK 9 inhibitors and describe their use?

A
  • alirocumab, evolocumab

- used in the treatment of familial hypercholesterolaemia

52
Q

How do PCSK 9 inhibitors work?

A
  • they inhibit the binding of PCSK 9 to LDLR, PCSK9 inhibitor increase the number of LDLRs available to clear LDL thereby lowering LDLC levels
53
Q

What do diuretics do?

A

block Na reabsorption in kidneys

54
Q

Give an example of a thiazide diuretic and its use?

A
  • bendrofluazide

- used in Hypertension

55
Q

Give an example of loop diuretics and its use?

A
  • furosemide

- used in HF

56
Q

Give the side effects of diuretics?

A
  • hypokalaemia - tired
  • arrhythmias
  • hyperglycaemia - diabetes
  • increased uric acid - gout
  • impotence
57
Q

give examples of cardioselective beta blockers and their use?

A
  • atenolol, bisoprolol
  • only block beta 1 receptors
  • used in angina, acute coronary syndrome, MI, hypertension, HF
58
Q

give examples of non selective beta blockers and their use?

A
  • propanolol, carvedilol
  • block beta 1 and beta 2 receptors
  • used in thyrotoxicosis, migraine
59
Q

what are the side effects of beta blockers?

A
  • asthma - contraindicated in brittle/severe asthma
  • tired
  • HF
  • cold peripheries
  • can worsen HF
60
Q

Give examples of dihydropyridine calcium antagonists and their use and SE?

A
  • amlodipine
  • used in hypertension and angina
  • SE: ankle oedema
61
Q

give examples of rate limiting calcium antagonists and their use and SE?

A
  • verapamil, diltiazem
  • used in hypertension, angina and supra ventricular arrhythmias
  • SE: avoid use with beta blocker
62
Q

What do ACE inhibitors do?

A

block angiotensin I becoming angiotensin II

63
Q

give an example of an ACE inhibitor and its uses and SE?

A
  • lisinopril
  • used in hypertension and HF
  • SE: cough, renal disturbance, angioneurmtic oedema
  • cannot be used in pregnancy: hypertension
64
Q

What do ARBs do?

A
  • block angiotensin II receptors
65
Q

Give examples of ARBs and their use and SE?

A
  • losartan
  • used in hypertension and HF
  • SE: renal dysfunctional and no cough
  • never use in pregnancy - hypertension
66
Q

what do alpha blockers do?

A

block alpha adrenoceptors to cause vasodilation

67
Q

Give examples of alpha adrenoceptors and their use and SE?

A
  • doxazosin
  • used in hypertension and prostatic hypertrophy
  • SE: postural hypotension
68
Q

What do mineralocorticoid antagonists do?

A

block aldosterone receptors

69
Q

give examples of mineralocorticoid antagonists and their use and SE?

A
  • spironolactone, eplenerone
  • used in HF and resistant hypertension
  • SE: gynaecomastia, hyperkalaemia, renal impairment
70
Q

Name some common anti anginal drugs?

A
  • vasodilators: nitrates, nicorandil, calcium antagonists
  • slow HR: beta blockers, calcium antagonists, ivabradine
  • metabolic modulator: ranolazine
71
Q

Give an example of a nitrate, its use and SE?

A
  • isosorbide mononitrate
  • ventilators used in angina and acute HF
  • SE: headache, hypotension/collase
  • tolerance common
72
Q

What is Nicorandil?

A
  • vasodilator
  • K ATP channel inhibitor
  • SE: Headache, mouth/GI ulcers
73
Q

What is ivabradine?

A
  • If channel modulator in the sinus node
  • slows HR only in sinus rhythm
  • does not work in atrial fibrillation
  • altered visual disturbance
74
Q

What is ranolazine?

A
  • late sodium channel modulator
  • decrease calcium load on the heart
  • effective in refractory angina
75
Q

what do anti platelet and anti coagulant agents do?

A
  • prevent new thrombosis
76
Q

Give examples of anti platelet agents, their use and SE?

A
  • aspirin, clopidogrel, ticagrelor, prasugrel
  • used in: angina, acute MI, CVA/TIA
  • SE: haemorrhage anywhere, peptic ulcer = haemorrhage, aspirin sensitivity = asthma
77
Q

Give examples of anticoagulants?

A
  • heparin
  • warfarin
  • rivaroxaban
  • dabigatran
78
Q

How is Warfarin used and what are the SE?

A
  • blocks clotting factors (2,7,9,10)
  • used in DVT, PE, NSTEMI, atrial fibrillation
  • SE: haemorrhage anywhere
79
Q

how is streptokinase used and what are the SE?

A
  • tissue plasminogen activator
  • use in STEMI, PE, CVA
  • SE: haemorrhage
80
Q

What do fibrinolytic drugs do?

A

dissolve formed clot

81
Q

Name some common types of drugs used in HF?

A
  • ACE inhibitor
  • ARBS
  • beta blockers
  • mineralocorticoid antagonists
  • neprilysin inhibitors
  • diuretics
  • digoxin
82
Q

What does digoxin do?

A
  • produces delay in AV node conduction (good in AF)

- increases ventricular irritability which produces ventricular arrhythmias (bad)

83
Q

Name some of the side effects of digoxin?

A
  • narrow therapeutic window
  • nausea
  • yellow vision
  • bradycardia, heart block
  • ventricular arrhythmias
84
Q

What is Salcubitril valsartan and what are its SE?

A
  • neprilysin inhibitor

- SE: hypotension, renal impairment, hyperkalaemia, angioneurotic oedema

85
Q

cardiovascular disease is strongly associated with elevated ……. and decreased ………….

A

LDL, HDL

86
Q

What are lipoproteins?

A

microscopic spherical particles of 7-1000 nm diameter consisting of:

  • a hydrophobic core
  • a hydrophilic coat
  • apoproteins
87
Q

What are apoproteins?

A
  • recognised receptors in liver and other tissues allowing lipoproteins to bind to cells
88
Q

What apoproteins do HDL particles contain?

A
  • apo-A-I and apoA-II
89
Q

What apoproteins do LDL particles contain?

A
  • apoB-100
90
Q

What apoproteins do VLDL particles contain?

A

-apoB-100

91
Q

What apoproteins do chylomicrons particles contain?

A
  • apoB-48
92
Q

What do ApoB containing lipoproteins do?

A

Deliver TAGs i) to muscle for ATP biogenesis

ii) to adipocytes for storage

93
Q

where are chylomicrons formed?

A

In intestinal cells and transport dietary triglycerides - the exogenous pathway

94
Q

Where are VLDL particles formed?

A

In liver cells and transport TAGs synthesised by that organ - the endogenous pathway

95
Q

Summaries the life cycle of ApoB containing liposomes?

A
  • assembly: with apoB-100 in the liver and ApoB-48 in the intestine
  • intravascular metabolism: involves hydrolysis of the TAG core
  • receptor mediated clearance
96
Q

How are chylomicrons and VLDL particles activated?

A

by the transfer of ApoC-II from HDL particles

97
Q

What is the role of MTP?

A

lipidates apoB-100 forming nascent VLDL that coalesces with TAG droplets

98
Q

ApoC-II facilitates the binding of ……… and …… to …..

A

chylomicrons/VLDL/LPL

99
Q

What does LPL do?

A

hydrolyses core TAGs to free fatty acids and glycerol which enter tissues

100
Q

What are chylomicron and VLDL remnants?

A

particles depleted of triglycerides (but still containing cholesteryl esters)

101
Q

What is the clearance of LDL particles dependent on?

A
  • LDL receptor expressed by the liver and other tissues
102
Q

How does cellular uptake of LDL particles occur?

A
  • through receptor mediated endocytosis
103
Q

What does released cholesterol do?

A
  • inhibits HMG coA reductase (rate limiting enzyme in cholesterol synthesis)
  • may be stored as cholesterol ester or used as a precursor for bile salt synthesis
104
Q

Why is LDL the ‘bad’ cholesterol?

A
  • triggers the release of inflammatory substances which causes division of smooth muscle cells and deposition of collagen in the TI resulting in an atheromatous plaque
105
Q

Describe the structure of an atheromatous plaque?

A
  • lipid core which is the produce of dead foam cells

- fibrous cap which is made up of smooth muscle cells and connective tissue

106
Q

Why is HDL the ‘good’ cholesterol

A
  • plays a key role in removing excess cholesterol by transporting it in plasma to the liver
107
Q

How do statins work?

A
  • act competitively to inhibit HMG coA reductase which is the rate limiting step in cholesterol synthesis in hepatocytes
108
Q

What does decreased hepatocyte cholesterol cause?

A
  • compensatory increase in LDL receptor expression and enhanced clearance of LDL
109
Q

What do fibres do?

A

act as agonists of a nuclear receptor (PPARalpha) to enhance the transcription of several genes including that encoding LPL

110
Q

Name some drugs that inhibit cholesterol absorption and how do they work?

A
  • bile acid binding resins (colestyramine, colestipol, colsevlam) cause the excretion of bile salts resulting in more cholesterol to be converted to bile salts by interrupting enterohepatic recycling
111
Q

How does ezetimibe work?

A

inhibits NPC1L1 transport protein in enterocytes of the duodenum, reducing the absorption of cholesterol causing a decrease in LDL

112
Q

Describe the use of anticoagulants?

A
  • mainly used in the prevention and treatment of venous thrombosis and embolism
  • carries a risk of haemorrhage
113
Q

How does warfarin work?

A
  • competes for binding to hepatic vitamin K reductase preventing the production of active hydroquinolone
  • renders factors II, VII, IX and X inactive
114
Q

Warfarin has a high therapeutic index T/F?

A

False

It has a low therapeutic index

115
Q

How does heparin work?

A
  • binds to antithrombin III, increasing its affinity for serine protease clotting factors to increase their rate of inactivation
116
Q

Give examples of LMWH and how they work?

A
  • enoxaparin and dalteparin

- inhibit factor Xa

117
Q

The elimination of heparin is first order T/F?

A
  • false

- elimination of LMWH is first order, heparin is 0 order

118
Q

Name an orally active inhibitor that acts as a direct inhibitor of thrombin?

A
  • dabigatran
119
Q

When are anti platelet drugs used?

A
  • in the treatment of arterial thrombosis
120
Q

How does aspirin work?

A
  • irreversibly blocks cycloxygenase in platelets preventing TXA2 synthesis but also COX in endothelial cells inhibiting the production of prostaglandin I2
121
Q

What is the main side effect of aspirin

A

GI bleeding and ulceration

122
Q

How does clopidogrel work?

A

Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition

123
Q

When in Tirofiban used?

A
  • given IV in short term treatment to prevent MI in high risk patients with unstable angina
124
Q

How are fibrinolytic used?

A
  • principally to reopen occluded arteries in acute MI or stroke
  • IV administration ASAP
125
Q

What does streptokinase do?

A
  • reduces mortality in acute MI
126
Q

what do alteplase and duteplase do?

A
  • recombinant tissue plasminogen activators
  • more effective in fibrin bound plasminogen
  • show affinity for clots

The cardiovascular system (6 decks)

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