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
2
Q
heart failure is caused by dysfunction of one or both of which 2 things ?
A
structure or function of the heart
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
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
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
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
7
Q
describe New York classification of heart failure stage I
A
asymptomatic- even with exercise
8
Q
describe New York classification of heart failure stage II
A
heart failure symptoms only with exercise
9
Q
describe New York classification of heart failure stage III
A
heart failure symptoms on very light exercise
10
Q
describe New York classification of heart failure stage IV
A
heart failure symptoms at rest
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)
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)
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
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
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
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
17
Q
in what circumstance would we use an ARB in heart failure?
A
- in those who cannot tolerate an ACE I
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
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
20
Q
which drug can be used in patients who are intolerant to beta blockers, in heart failure ?
A
ivabradine
21
Q
what drug can be added to a beta blocker in heart failure when heart rate is over 75bpm?
A
ivabradine
22
Q
what does ivabradine interact with?
A
grapefruit
23
Q
when is digoxin indicated in patients with heart failure?
A
when they also have atrial fibrillation
24
Q
what is first line aldosterone antagonist for heart failure?
A
spironolactone
25
which classes of heart failure is aldosterone antagonists such as spironolactone or eplerenone indicated in?
class III and IV
26
what would u give a heart failure patient who is intolerant to both ACE I's and ARB's?
hydralazine and isosorbide dinitrate
27
how long do u need to stop ACE I before starting entresto? why?
minimum 36h
risk of bradykinin accumulation
28
name 3 requirements for starting entresto
- at least 1 hospitalisation in the last year
- grade II-IV
- still symptomatic- despite optimise drug therapy
29
what 2 checks need to be done 2 weeks after staring entresto?
serum creatinine and potassium levels
30
name 7 drugs which can exacerbate heart failure symptoms
- NSAIDs
- rate limiting CCB (verapamil, diltiazem)
- chemotherapy drugs (doxorubicin)
- glitazones
- corticosteroids (prednisolone)
- soluble tabs (high sodium content)
- some antacids (high sodium content)
31
name 6 signs of digoxin toxicity
- nausea, vomiting, diarrhoea
- confusion, headache, fatigue
- bradycardia, AV block
32
what are the 2 treatment options for digoxin toxicity?
- withhold and treat symptomatically
- digoxin antibodies (only if life threatening)
33
describe the volume of distribution of digoxin
very large
6-7L/kg
blinds to skeletal muscle and cardiac muscle
34
how long after dosing digoxin should a sample be taken ?why?
6 hours
because of large volume of distribution it takes longer to get into tissues
35
what cannot be administered via central line for IV? (2)
without emulsion (fat embolism)
suspension (particles block capillaries)
36
name 2 inconvenient things about intracardiac or intraarterial injections
- arteries are difficult to access
- greater risk of procedure, more invasive
37
what is max intramuscular injection volume?
4ml
38
what is max subcutaneous injection volume?
1ml
39
what is max intradermal injection volume?
0.2ml
40
what is max intraspinal injection volume?
10ml
41
what is max subcinjunctival injection volume?
1ml
42
what is max intracameral injection volume?
0.1 or 1ml in open eye surgery
43
name 6 pharmacopeial requirements of injections
- 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)
44
how long does an intramuscular injected suspension work for?
1-7 days
45
how long does intramuscular injected oily vehicle act for?
up to 4 weeks
46
what pHs are suitable for injection ?
3-9
47
what pHs are suitable for injection ?
3-9
48
which state of an enzymatic reaction is highly unstable, energetically unfavourable and reaction is intermediate?
transition state
49
how do intermolecular bonds and susceptible bonds change after induced fit?
- intermolecular bond lengths optimised
- susceptible bonds in substrate strained
- susceptible bonds in substrate more easily broken
50
name 2 catalysis mechanisms
- acid/ base catalysis
- nucleophilic residues
51
mechanism for chymotrypsin
- 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
what kind of inhibitor resembles substrate and binds at active site?
competitive inhibitor
53
what kind of inhibitor only binds to enzyme-substrate complex?
uncompetitive inhibitor
54
what kind of inhibitor changes the shape of the enzyme and thus changes the shape of the active site?
non - competitive inhibitor
55
what kind of inhibitor can bind in the absence of substrate?
non- competitive inhibitor
56
define EC50
concentration of a drug that gives 50% inhibition
- measure of drug potency
- lower EC50- more potent
57
define IC50
the concentration of a drug that gives 50% of its maximum effect
- measures drug efficacy
58
give 2 examples of what primary + secondary prevention prevent and 2 examples of what they don't prevent
prevent
- MI and stroke
don't prevent
- heart failure or rhythm disorders
59
name 5 causes of heart failure
- 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
what time of day is the latest time u would recommend taking a loop diuretic?
~2pm- anytime after that is likely to disturb sleep
61
what is the maximum fluid intake for a heart failure patient?
1.5-2L per day
this includes all fluid not just water
62
why is bisoprolol better in heart failure than other beta blockers?
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
what ACE inhibitor is 1st line in heart failure?
enalapril
64
what type of drugs can cause first dose hypotension?
ACE and ARB
65
why is amlodipine not a great choice for heart failure?
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
why is diclofenac contraindicated in patients with heart failure?
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
how long does ACE inhibitor need to be stopped before entresto can be started? why?
36h
to ensure ACEi is gone and bradykinin doesn't accumulate
68
in what classes of heart failure is spironolactone licensed?
III +IV
69
in what classes of heart failure is epleronone licensed?
I and II- just mild
70
what kind of interaction occurs between digoxin and furosemide?
pharmacodynamic- metabolic (severe)
meaning digoxin levels have not changed- yet patient is experiencing digoxin toxicity
70
what kind of interaction occurs between digoxin and furosemide?
pharmacodynamic- metabolic (severe)
meaning digoxin levels have not changed- yet patient is experiencing digoxin toxicity
71
what is the maximum dose of simvastatin when taking with amiodarone?
20mg daily= max
72
what kind of interaction occurs between simvastatin and amiodarone?
pharmacodynamic metabolic
73
what kind of interaction occurs between digoxin and amiodarone ?
pharmacokinetic- metabolism
74
what kind of interaction occurs between apixaban and amiodarone?
pharmacodynamic - metabolic
75
What causes the upstroke of the action potential?
influx of calcium
76
what accounts for the rapid rise in the Na+ current in action potentials?
voltage gated sodium channels
77
what explains the sustained phase of the action potential?
influx of calcium
78
what accounts for the rapid rise in calcium current in action potentials?
voltage gated calcium channels
79
what accounts for the repolarisation phase of the action potential?
efflux of potassium and inactivation of sodium and calcium channels
80
what accounts for the potassium current decline at the end of the action potential?
voltage dependence of the potassium channel
81
what is the stimulation threshold for the reaction potential?
2.6 nA
82
which phase of the action potential does TTX affect most?
phase o
83
what effect does TTX have on the stimulus threshold for action potentials?
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
which phase of action potentials does blocking calcium channels affect most ?
verapamil affected phase 2 the most- making plateau more hyper polarised and shortening action potential considerably
85
what effect does verapamil have on the stimulus threshold of action potentials?
no effect on stimulus threshold or on phase 0 or 1 of the action potential
86
What effect has verapamil had on the action potential waveform and on its rare (dV/dt) during phase 0?
Only a slight reduction in the rate of rise of the action potential
87
Which phases of the action potential does blocking K channels affect?
No effect on the peak or rise of action potentials- prolongs plateau (phase 2) increasing the duration considerably
88
what do b1 receptors in the kidney control?
renin release
89
what receptors control heart rate, force, contractility and cardiac output?
b1 adrenoceptors
90
why do we need selectivity over b2 adrenoceptors?
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
what type of b receptor is in cardiac?
b1
92
what type of b receptor is in respiratory?
b2
93
which phase of the action potential does sodium enter the cell? (ventricular muscle cell)
depolarisation - phase 0
94
which phases of the action potential does potassium exit the cell? (ventricular muscle cell)
phases 1 and 3
95
which phase of the action potential does potassium exit the cell? (ventricular muscle cell)
phase 1
and also phase 3
96
which phase of the action potential does L-type calcium enter AND potassium exits the cell? (ventricular muscle cell)
phase 2- plateau
97
what phase of action potential is the plateau? (ventricular muscle cell)
phase 2
98
what phase of action potential is repolarisation and what happens? (ventricular muscle cell)
phase 3
potassium exits the cell
99
what happens in phase 0 of action potential (SA nodal cell)?
depolarisation L-type calcium enters cell
100
what happens at phase 4 of action potential(SA nodal cell)?
pacemaker potential
slow depolarisation
sodium and T-type calcium enters
101
what happens at phase 3 of action potential(SA nodal cell)?
repolarisation- potassium exits
102
define refractory period of cardiac excitation
Time following excitation which a second action potential can not be elicited and conducted
103
define membrane responsiveness of cardiac excitation
relationship between membrane activation voltage and the maximal rate of rise of the action potential
104
how do anti arrhythmic drugs work?
increase refractory period or slow upstroke of action potentials OR BOTH
105
how do class IA antiarrhythmics work?
decrease membrane responsiveness
moderate inhibition of sodium channels
prolong action potential duration
106
give 3 examples of IA antiarrhythmics
- quinidine
- procainamide
- disopyramide
107
how do class IB antiarrhythmics work?
minimal inhibition of sodium channels
shorten action potential and reduce ERP
108
give 2 examples of IB antiarrhythmics
lidocaine
mexiletine
109
state 2 examples of IC anti arrhythmics
flecainide, propafenone
110
how do class IC antiarrhythmics work?
decrease membrane responsiveness
no or minimal effect on action potential duration
ERP is unaffected in cardiac pukinje cells and ventricular myocardium
111
what are class II antiarrhythmics ?
beta blockers
112
what phase of the AP do class II or beta blockers work at?
phase 2- plateau phase
!think class 2, phase 2!
113
what do beta blockers/ class II antiarrhythmics target?
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
what are class III antiarrhythmics?
potassium channel blockers
115
which phase of the AP do class III/ potassium channel blockers target?
phase 3
increase repolarisation period
116
name 2 examples of class III anti arrhythmics or potassium channel blockers
amiodarone
sotalol
117
how does amiodarone work?
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
what are class IV anti arrhythmics?
calcium channel blockers
119
which phase of the AP do class IV/ calcium channel blockers target?
phase 2 plataeu phase
120
how do class IV anti arrhythmics/ calcium channel blockers work?
slows conduction through AV node, increases refractory period of AV node and also reduce cardiac contractility
121
give 2 examples of class IV antiarrhythmics/ calcium channel blockers
verapamil
diltiazem
122
name the 3 class V anti arrhythmics
digoxin
adenosine
magnesium sulfate
123
what is digoxins MOA?
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
name 2 direct effects of digoxin
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
does a cardex need to be signed and ticked to be a legal document?
yes a supply should not be made if this is not complete
126
do vitamins need to go on a cardex?
only when clinically required and prescribed- ie not if the patient has bought them on their own
