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mpharm year 3 sem 2 > week 4 > Flashcards

week 4 Flashcards

1
Q

what does LVSD stand for and cause?

A

Left Ventricular Systolic Dysfunction

it causes the symptoms associated with heart failure

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2
Q

heart failure is caused by dysfunction of one or both of which 2 things ?

A

structure or function of the heart

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3
Q

what are the aims of heart failure treatments?

A

prolong life and manage symptoms
not going to cure just make patient more comfortable

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4
Q

name 7 common presenting symptoms associated with heart failure

A
  • breathlessness
  • not being able to lie flat at night (should ask patient about how many pillows they sleep with)
  • waking through the night gasping for air
  • fatigue
  • ankle oedema
  • pulmonary oedema
  • poor exercise tolerance
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5
Q

name 8 investigation we should do when a suspected heart failure patient presents at hospital

A
  • chest x-ray
  • echo (only way to diagnose really)
  • ejection fraction
  • ECG
  • BNP (protein measure)
  • listen for 3rd heart sound (gallop rhythm)
  • JVP (Jugular venous pressure)
  • full blood count
  • Us & Es
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6
Q

what is BNP used for?

A

a measure of a protein used to diagnose heart failure- mostly used to screen high risk patients

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7
Q

describe New York classification of heart failure stage I

A

asymptomatic- even with exercise

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8
Q

describe New York classification of heart failure stage II

A

heart failure symptoms only with exercise

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9
Q

describe New York classification of heart failure stage III

A

heart failure symptoms on very light exercise

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10
Q

describe New York classification of heart failure stage IV

A

heart failure symptoms at rest

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11
Q

name 7 non pharmacological management strategies for heart failure patients

A
  • reduce salt intake
  • fluid restriction (1.5-2L/ day)
  • moderate alcohol intake
  • self monitoring of weight - of gain 2kg in 3 days need to seek medical advice- patient needs higher dose of diuretic
  • weight reduction of obese/ overweight
  • smoking cessation
  • exercise (best rest in acute heart failure, exercise training programs encouraged for stable patients)
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12
Q

name 7 drug options for heart failure

A
  • ACE I’s
  • ARB’s
  • beta blockers
  • aldosterone antagonist
  • digoxin
  • vasodilators (hydralazine or isosorbide dinitrate-used in severe renal impairment)
  • entresto (sacubitril/ valsartan)
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13
Q

what treatment option would you offer in a heart failure patient with severe renal impairment?

A
  • where ACE or ARB cannot be used- we would use hydralazine or isosorbide dinitrate
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14
Q

why are loop diuretics used in heart failure patients?

A

used to manage symptoms and make patient more comfortable - get rid of excess fluid around heart and in lungs

to treat pulmonary oedema - very common symptom in HF

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15
Q

name a counselling point for loop diuretics

A
  • flexible dosing time- advise patient that they can take their dose at a time convenient for them ie not before bed to not disrupt sleep or just before they’re going out and won’t have access to a toilet
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16
Q

what would we do in a situation where the loop diuretic a heart failure patient is on has caused gout?

A

treat gout but don’t stop diuretic

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17
Q

in what circumstance would we use an ARB in heart failure?

A
  • in those who cannot tolerate an ACE I
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18
Q

when are beta blockers indicated in heart failure?

A

stable patients (class I to IV)
can be given in addition to ACE I or ARB

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19
Q

in what circumstance would u choose carvedilol over bisoprolol for heart failure management ?

A

if the patient is also hypertensive- carvedilol is non selective and so is better at targeting both conditions

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20
Q

which drug can be used in patients who are intolerant to beta blockers, in heart failure ?

A

ivabradine

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21
Q

what drug can be added to a beta blocker in heart failure when heart rate is over 75bpm?

A

ivabradine

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22
Q

what does ivabradine interact with?

A

grapefruit

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23
Q

when is digoxin indicated in patients with heart failure?

A

when they also have atrial fibrillation

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24
Q

what is first line aldosterone antagonist for heart failure?

A

spironolactone

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25
Q

which classes of heart failure is aldosterone antagonists such as spironolactone or eplerenone indicated in?

A

class III and IV

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26
Q

what would u give a heart failure patient who is intolerant to both ACE I’s and ARB’s?

A

hydralazine and isosorbide dinitrate

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27
Q

how long do u need to stop ACE I before starting entresto? why?

A

minimum 36h
risk of bradykinin accumulation

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28
Q

name 3 requirements for starting entresto

A
  • at least 1 hospitalisation in the last year
  • grade II-IV
  • still symptomatic- despite optimise drug therapy
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29
Q

what 2 checks need to be done 2 weeks after staring entresto?

A

serum creatinine and potassium levels

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30
Q

name 7 drugs which can exacerbate heart failure symptoms

A
  • NSAIDs
  • rate limiting CCB (verapamil, diltiazem)
  • chemotherapy drugs (doxorubicin)
  • glitazones
  • corticosteroids (prednisolone)
  • soluble tabs (high sodium content)
  • some antacids (high sodium content)
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31
Q

name 6 signs of digoxin toxicity

A
  • nausea, vomiting, diarrhoea
  • confusion, headache, fatigue
  • bradycardia, AV block
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32
Q

what are the 2 treatment options for digoxin toxicity?

A
  • withhold and treat symptomatically
  • digoxin antibodies (only if life threatening)
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33
Q

describe the volume of distribution of digoxin

A

very large
6-7L/kg

blinds to skeletal muscle and cardiac muscle

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34
Q

how long after dosing digoxin should a sample be taken ?why?

A

6 hours
because of large volume of distribution it takes longer to get into tissues

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35
Q

what cannot be administered via central line for IV? (2)

A

without emulsion (fat embolism)
suspension (particles block capillaries)

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36
Q

name 2 inconvenient things about intracardiac or intraarterial injections

A
  • arteries are difficult to access
  • greater risk of procedure, more invasive
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37
Q

what is max intramuscular injection volume?

A

4ml

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38
Q

what is max subcutaneous injection volume?

A

1ml

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39
Q

what is max intradermal injection volume?

A

0.2ml

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40
Q

what is max intraspinal injection volume?

A

10ml

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41
Q

what is max subcinjunctival injection volume?

A

1ml

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42
Q

what is max intracameral injection volume?

A

0.1 or 1ml in open eye surgery

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43
Q

name 6 pharmacopeial requirements of injections

A
  • sterility
  • excipients (pH, isotonic, stability of drug)
  • containers (transparent to permit inspection of contents)
  • free from endotoxin and pyrogens
  • free from particulates
  • for emulsions for IV injection droplets less than 3um (to prevent oil embolism)
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44
Q

how long does an intramuscular injected suspension work for?

A

1-7 days

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45
Q

how long does intramuscular injected oily vehicle act for?

A

up to 4 weeks

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46
Q

what pHs are suitable for injection ?

A

3-9

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47
Q

what pHs are suitable for injection ?

A

3-9

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48
Q

which state of an enzymatic reaction is highly unstable, energetically unfavourable and reaction is intermediate?

A

transition state

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49
Q

how do intermolecular bonds and susceptible bonds change after induced fit?

A
  • intermolecular bond lengths optimised
  • susceptible bonds in substrate strained
  • susceptible bonds in substrate more easily broken
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50
Q

name 2 catalysis mechanisms

A
  • acid/ base catalysis
  • nucleophilic residues
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51
Q

mechanism for chymotrypsin

A
  • His working with Sir and Asp in triad
  • His accepting and donating protons
  • serine forming E-S intermediate
  • many serine and cysteine proteases as drug targets
52
Q

what kind of inhibitor resembles substrate and binds at active site?

A

competitive inhibitor

53
Q

what kind of inhibitor only binds to enzyme-substrate complex?

A

uncompetitive inhibitor

54
Q

what kind of inhibitor changes the shape of the enzyme and thus changes the shape of the active site?

A

non - competitive inhibitor

55
Q

what kind of inhibitor can bind in the absence of substrate?

A

non- competitive inhibitor

56
Q

define EC50

A

concentration of a drug that gives 50% inhibition
- measure of drug potency
- lower EC50- more potent

57
Q

define IC50

A

the concentration of a drug that gives 50% of its maximum effect
- measures drug efficacy

58
Q

give 2 examples of what primary + secondary prevention prevent and 2 examples of what they don’t prevent

A

prevent
- MI and stroke

don’t prevent
- heart failure or rhythm disorders

59
Q

name 5 causes of heart failure

A
  • Myocardial infarction
  • Hypertension
  • Coronary heart disease
  • Coronary artery disease
  • Chronic kidney disease
  • Liver disease
  • Atrial fibrillation/ arrhythmias
  • Alcohol/ drugs (Cocaine, Verapamil, Diltiazem, Anti-inflammatory’s (increase fluid retention))
  • Valve disease
  • Viral infection
  • Hypothyroidism
  • Anaemia
  • Cardiomyopathy (genetic- born with it, cant do much to prevent)
60
Q

what time of day is the latest time u would recommend taking a loop diuretic?

A

~2pm- anytime after that is likely to disturb sleep

61
Q

what is the maximum fluid intake for a heart failure patient?

A

1.5-2L per day
this includes all fluid not just water

62
Q

why is bisoprolol better in heart failure than other beta blockers?

A

it is cardio selective meaning it doesn’t act in other places and so the patient is much less likely to experience unwanted side effects

63
Q

what ACE inhibitor is 1st line in heart failure?

A

enalapril

64
Q

what type of drugs can cause first dose hypotension?

A

ACE and ARB

65
Q

why is amlodipine not a great choice for heart failure?

A

it too can cause ankle oedema and so it is difficult to tell if the patients heart failure is poorly controlled or if it is an adverse drug reaction

66
Q

why is diclofenac contraindicated in patients with heart failure?

A

it is an NSAID- these can cause water and sodium retention which in turn can cause excess fluid to build up- worsening the symptoms associated with heart failure

67
Q

how long does ACE inhibitor need to be stopped before entresto can be started? why?

A

36h

to ensure ACEi is gone and bradykinin doesn’t accumulate

68
Q

in what classes of heart failure is spironolactone licensed?

A

III +IV

69
Q

in what classes of heart failure is epleronone licensed?

A

I and II- just mild

70
Q

what kind of interaction occurs between digoxin and furosemide?

A

pharmacodynamic- metabolic (severe)
meaning digoxin levels have not changed- yet patient is experiencing digoxin toxicity

70
Q

what kind of interaction occurs between digoxin and furosemide?

A

pharmacodynamic- metabolic (severe)
meaning digoxin levels have not changed- yet patient is experiencing digoxin toxicity

71
Q

what is the maximum dose of simvastatin when taking with amiodarone?

A

20mg daily= max

72
Q

what kind of interaction occurs between simvastatin and amiodarone?

A

pharmacodynamic metabolic

73
Q

what kind of interaction occurs between digoxin and amiodarone ?

A

pharmacokinetic- metabolism

74
Q

what kind of interaction occurs between apixaban and amiodarone?

A

pharmacodynamic - metabolic

75
Q

What causes the upstroke of the action potential?

A

influx of calcium

76
Q

what accounts for the rapid rise in the Na+ current in action potentials?

A

voltage gated sodium channels

77
Q

what explains the sustained phase of the action potential?

A

influx of calcium

78
Q

what accounts for the rapid rise in calcium current in action potentials?

A

voltage gated calcium channels

79
Q

what accounts for the repolarisation phase of the action potential?

A

efflux of potassium and inactivation of sodium and calcium channels

80
Q

what accounts for the potassium current decline at the end of the action potential?

A

voltage dependence of the potassium channel

81
Q

what is the stimulation threshold for the reaction potential?

A

2.6 nA

82
Q

which phase of the action potential does TTX affect most?

A

phase o

83
Q

what effect does TTX have on the stimulus threshold for action potentials?

A

greatly decreases the rate of rise of action potential and the amplitude of the initial peak

stimulus threshold increased from 2.6 to 4.5nA

84
Q

which phase of action potentials does blocking calcium channels affect most ?

A

verapamil affected phase 2 the most- making plateau more hyper polarised and shortening action potential considerably

85
Q

what effect does verapamil have on the stimulus threshold of action potentials?

A

no effect on stimulus threshold or on phase 0 or 1 of the action potential

86
Q

What effect has verapamil had on the action potential waveform and on its rare (dV/dt) during phase 0?

A

Only a slight reduction in the rate of rise of the action potential

87
Q

Which phases of the action potential does blocking K channels affect?

A

No effect on the peak or rise of action potentials- prolongs plateau (phase 2) increasing the duration considerably

88
Q

what do b1 receptors in the kidney control?

A

renin release

89
Q

what receptors control heart rate, force, contractility and cardiac output?

A

b1 adrenoceptors

90
Q

why do we need selectivity over b2 adrenoceptors?

A

vascular smooth muscle has b2 receptors- these are activated by noradrenaline- this can cause unwanted side effects if were using a drug without specificity to which type of b receptor we want to target

91
Q

what type of b receptor is in cardiac?

A

b1

92
Q

what type of b receptor is in respiratory?

A

b2

93
Q

which phase of the action potential does sodium enter the cell? (ventricular muscle cell)

A

depolarisation - phase 0

94
Q

which phases of the action potential does potassium exit the cell? (ventricular muscle cell)

A

phases 1 and 3

95
Q

which phase of the action potential does potassium exit the cell? (ventricular muscle cell)

A

phase 1
and also phase 3

96
Q

which phase of the action potential does L-type calcium enter AND potassium exits the cell? (ventricular muscle cell)

A

phase 2- plateau

97
Q

what phase of action potential is the plateau? (ventricular muscle cell)

A

phase 2

98
Q

what phase of action potential is repolarisation and what happens? (ventricular muscle cell)

A

phase 3
potassium exits the cell

99
Q

what happens in phase 0 of action potential (SA nodal cell)?

A

depolarisation L-type calcium enters cell

100
Q

what happens at phase 4 of action potential(SA nodal cell)?

A

pacemaker potential
slow depolarisation
sodium and T-type calcium enters

101
Q

what happens at phase 3 of action potential(SA nodal cell)?

A

repolarisation- potassium exits

102
Q

define refractory period of cardiac excitation

A

Time following excitation which a second action potential can not be elicited and conducted

103
Q

define membrane responsiveness of cardiac excitation

A

relationship between membrane activation voltage and the maximal rate of rise of the action potential

104
Q

how do anti arrhythmic drugs work?

A

increase refractory period or slow upstroke of action potentials OR BOTH

105
Q

how do class IA antiarrhythmics work?

A

decrease membrane responsiveness
moderate inhibition of sodium channels
prolong action potential duration

106
Q

give 3 examples of IA antiarrhythmics

A
  • quinidine
  • procainamide
  • disopyramide
107
Q

how do class IB antiarrhythmics work?

A

minimal inhibition of sodium channels
shorten action potential and reduce ERP

108
Q

give 2 examples of IB antiarrhythmics

A

lidocaine
mexiletine

109
Q

state 2 examples of IC anti arrhythmics

A

flecainide, propafenone

110
Q

how do class IC antiarrhythmics work?

A

decrease membrane responsiveness
no or minimal effect on action potential duration
ERP is unaffected in cardiac pukinje cells and ventricular myocardium

111
Q

what are class II antiarrhythmics ?

A

beta blockers

112
Q

what phase of the AP do class II or beta blockers work at?

A

phase 2- plateau phase

!think class 2, phase 2!

113
Q

what do beta blockers/ class II antiarrhythmics target?

A

SA and AV node conduction and cardiac contractility

block effect of catecholamines at the beta adrenergic receptors- thus reducing calcium influx, decreasing SA and AV node conduction- also HR and cardiac contractility

114
Q

what are class III antiarrhythmics?

A

potassium channel blockers

115
Q

which phase of the AP do class III/ potassium channel blockers target?

A

phase 3
increase repolarisation period

116
Q

name 2 examples of class III anti arrhythmics or potassium channel blockers

A

amiodarone
sotalol

117
Q

how does amiodarone work?

A

inhibits K channels (delays repolarisation), Na channels and Ca channels (slight), blocks beta-receptors non-competitively, and blocks alpha receptors

extremely long half life

118
Q

what are class IV anti arrhythmics?

A

calcium channel blockers

119
Q

which phase of the AP do class IV/ calcium channel blockers target?

A

phase 2 plataeu phase

120
Q

how do class IV anti arrhythmics/ calcium channel blockers work?

A

slows conduction through AV node, increases refractory period of AV node and also reduce cardiac contractility

121
Q

give 2 examples of class IV antiarrhythmics/ calcium channel blockers

A

verapamil
diltiazem

122
Q

name the 3 class V anti arrhythmics

A

digoxin
adenosine
magnesium sulfate

123
Q

what is digoxins MOA?

A

Inhibits the Na+/K+-ATPase, which is responsible for Na+/K+ exchange across the cell membrane
increases [Na+]in  increases [Ca2+]in
increases force of myocardial contraction

124
Q

name 2 direct effects of digoxin

A

Increased [Ca2+]in stimulates K+ channels, and shorten action potential and refractory period (atria & ventricles)
Increased [Ca2+]in may cause depolarization after normal action potential, which may generate another action potential, causing ectopic beat.

125
Q

does a cardex need to be signed and ticked to be a legal document?

A

yes a supply should not be made if this is not complete

126
Q

do vitamins need to go on a cardex?

A

only when clinically required and prescribed- ie not if the patient has bought them on their own

mpharm year 3 sem 2 (11 decks)

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