Medicine 1 > Week 4 CVS > Flashcards

Week 4 CVS Flashcards

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1
Q

What class of drug is Flecanide ?

A
  • is a sodium channel blocker
  • class IC anti-arrythmic
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2
Q

Flecanide blocks what stage of the non-pacemaker action potential?

A

Flecanide is a sodium channel blocker

it blocks the fast voltage gated Na+ channels (initial rapid depolarisation phase)

decreasing the size of AP/depolarisation

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3
Q

effect of flecanide on AP?

A

class 1C - soidum channel blocker

slows depolarisation of the myocyte (rapid depolarisation phase)

shortens plaque phase

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4
Q

How do cardiac specific beta blockers work (e.g. bisoprolol)

A

block B1 receptors in myocardium

block sympathetic stimulation

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5
Q

How does bisoprolol (cardiac specific beta-blocker) effect the AP of cardiac muscle cells

A

prolongs depolarisation (from resting potential) /discharge of SA/ conduction in AV node

reduces excitability of non-nodal tissue

shortens plaqteau phase (reducing contractility)

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6
Q

First choice for atrial fibrillation

A

Bisoprolol (beta-blocker) cardio specific

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7
Q

how do beta blockers effect the slow plateua phase of cardiac AP?

A
  • shortens the plateu phase

reduces contractility!

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8
Q

how do beta blockers effect the depolarisation of cardiac cells?

A

slows the discharge from SA node and AV node conduction

also reduces excitability of non-nodal cardiac tissue

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9
Q

why are beta-blockers now first line in AF treatment

A
  • slow the AV node down
  • reducing excitability in non-nodal cardiac tissue (potential sources of AF)
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10
Q

flecanide is a sodium channel blocker

a. true
b. false

A

a. true

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11
Q

what is the mechanism of action of Amiodarone

A

class 3 anti-arrhymic

potassium channel blocker

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12
Q

amiodarone is a calcium channel blocker

a. true
b. false

A

b. false

is a potassium channel blocker

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13
Q

What effect does amiodarone have on cardiac AP

(is a potassium channel blocker)

A
  • increases the duration of AP
    by prolonging/delays repolarisation (phase 3)
    *increase effective refractory period
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14
Q

how does amiodarone increase the duration of the AP of cardiac cells?

A

by prolonging the repolarisation (phase 3) -

there is K+ channel blockade (prevents K+ efflux)

(increases refractory period)

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15
Q

Amiodarone is a sodium channel blocker

a. true
b. false

A

b. false

Potassium channel blocker (prevents repolarisation) - prolongs AP

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16
Q

Amiodarone is used to control difficult to treat arrythmias (e.g. life threathening V-Tach or V-Fib)

a. true
b. false

A

a. true

when resistant to other drugs

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17
Q

When is amiodarone most likely to be used

A

VT and occaisonally difficult to treat SVTs (A-fib)

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18
Q

Side effects of amiodarone ( - K+ channel blocker)

A
  • hypo/hyper thyroidism
  • pulmonary fibrosis
  • grey pigmentation
  • corneal deposits
  • LFT abnormalities
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19
Q

a drug that amiodarone interacts badly with (that is also used for anti-arrythmias)

A
  • digoxin
    (competes with digoxin to bind to albumin - digitoxic at lower doses of digoxin)

similar affect with verapamil

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20
Q

What class of drug are verapamil and diltiazem

A

calcium channel blockers

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21
Q

what phase of the AP of cardiac cells do CCBs (verapamil and diltiazem) affect

A

bind to L-type voltage gated channels

  • > depress depolarisation in SA/AV node
    -> shorten plateu phase (reduce contractility)
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22
Q

Verapamil slows the heart rate

a. true
b. false

A

a. true

Calcium channel blocker

reduces contractility and slows AV

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23
Q

Verapamil is more effective for Atrial fibrillation at high HRs

a. true
b.false

A

a. True

CCBs show use dependence
- more effective at higher HR

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24
Q

digoxin properties

A

cardiac glycoside

inhibits sodium potassium ATPase pump

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25
mechanism of action of digoxin
inhibits the sodium potassium ATpase pump leads to accumulation of calcium in the cell
26
digoxin reduces the refractory peirod of the myocardium a. true b. false
a. true as it inhibits the sodium , potassium ATpase pump- Ca2+ accumulates in cell
27
digoxin increases vagal tone a. true b. false
a. true
28
indications for digoxin
AF - second line for difficult (combo with BB or CCB) Atrial flutter SVT heart failure
29
digoxin has a long half life a. true b. false
a. true * monitor K+ levels - especially in elderly/or have diuretics
30
signs of digoxin toxicity
* nausea and vomiting * Xanthopsia (yellow hallow around vision) * bradycardia * tachycardia * arrythmias
31
when can digoxin cause arrythmias
has a positive ionotrophic affect -Ca2+ gets trapped in cells
32
reverse tick sign of ST segments in response to digoxin toxicity a. true b. false
a. true
33
how is digoxin toxicity reversed
digibind - binds to and is excreted in urine
34
Mechanism of action of adenosine
slows/blocks conduction through AV node BLOCKS AV node.
35
what is adenosine used for
* cardioverting SVT to sinus rythmn * diagnose AF/flutter- can see underlying atrial activity by blocking ventricular activity
36
how is adenosine administered
IV push
37
main side effect of adenosine
asystole for a few seconds bronchospasm - asthmatics
38
all anti-arrythmics can cause arrhythmias a. true b. false
a. true
39
atrial fibrillation is a significant risk for stroke a. true b. false
a. true and peripheral embolus
40
virchows triad
* statis * abnormal blood content * abnormal vessels
41
What is the reason for the increased risk of stroke in AF?
STATSIS (Atrial is fibrillating and not properly pumping blood into ventricle) blood gets stuck in** left atrial appendage** leads to formation of thrombus -> embolises -> systemic circulation
42
calculator used to calculate risk of stroke with AF
CHADS-VASC 2+ definitely give anti-coagulants 1+ discuss
43
Anti-coagulants given to reduce the risk of stroke in atrial fibrilation
* Apixaban (DAOC) or rivaroxaban or diabigatran**
44
treatment for AF
Bisoprolol (beta blocker) - anti-arrythmic DOAC - rivaroxaban/apixaban - direct Xa inhibitor - dabigatrain - direct thrombin inhibitor
45
warfarin is a vitamin K anatagonist a. true b. false
a. true
46
Dibigatran mechanism of action
direct thrombin inhibitor (prevents from converting fibrinogen into fibrin)
47
apixaban and rivaroxaban mechanism of action
direct Xa inhibitor- prevents pro-thrombin being converted into thrombin
48
vitamin K is an important co-factor in production of what clotting factors?
2, 7, 9, 10 II , VII, IX, X warfan - reduces level of vitamin K -> cant produce clotting factors
49
when to offer A-fib patient anti-coagulants
when chad-vasc score 2+ foresure 1+ discuss
50
warfarin has a narrow therapeutic index a. true b. false
a. true monitored via (INR) - internationalised ratio actual prothrombin time / standard prothrombin time
51
how is warfarin therapy monitored
INR international normalised ratio actual prothrombin time/standard prothrombin time therapeutic 2.5-4.0 2.5 - patients with AF
52
adverse effects of warfarin
bleeding drug interactions** - cytochrome p450 system teratogenic
53
risk of falling is a good reason not to anti-coagulate a patient a. true b. false
b. false - need to be falling several times a day for a year
54
drugs that increase the action of warfarin
1. aspirin (decrease albunin binding) 2. Erythromycin - inhibits degradation (cytochrome p45 enzymes in liver - decreased activity 3. Anti-biotics (oral) - decrease synthesis of clotting factors/reduced absoprtion of vitamin K
55
300mg + doses of aspirin can displace warfarin from albumin and increase activity a. true b. false
a. true increases INR
56
drugs that decrease warfarin activity
vitamin K - promotes clotting factor synthesis Barbiturates - increases activity of cytochrome p450 enzymes in liver
57
1st line anti-coagulant for A-Fib
apixaban rivaroxaban
58
1st line anti-coagulant for mechanical heart valve
warfarin
59
Excess of blood in vessels or tissue of a tissue or organ describes?
congestion
60
congestion is a primary process a. true b. false
b. false secondary phenonomen - passive process blood increases in volume
61
DVT is an example of congestion a. true b. false
a, True **Local acute congestion** outflow of blood blocked by thrombus reduced pressure gradient across limb - reduced flow (Flow = AP/R) infaraction/iscahemia
62
describe why there is fluid overload in congestive heart failure
* decreased pumping/CO * decreased GFR * activates RAAS system * increased Na+ and H20 retention * fluid overload in veins -> treat with diuretics
63
left sided HF is associated with blood accumulating in the systemic circulation a. true b. false
b. false blood dams back into the lungs -> pulmonary oedema
64
right sided HF is associated with blood accumulating in the lungs a. true b .false
b. false accumulates in systemic circulation increased JVP, hepatomegaly and peripheral oedema
65
3 main components that affect the net flux and filtration within microciruclation
1, hydrostatic pressure 2. oncotic pressue 3. permeability characteristics and area of endoethelium that divides the the vascular channel from interstitium
66
accumulation of abnormal amounts of FLUID in the extravascular compartment
oedema - fluid within body cavities or intercellular tissue compartment - ECF
67
peripheral oedema
increased interstitual fluid in tissues
68
effusion in adominal cavity
ascites
69
cause of transudate oedema
alterations in the haemodynamic forces that act across capillary wall
70
transudate is low in protein/albumin a. true b. false
a. true few cells lots of water and electrolytes
71
cause of exudate oedema
part of inflammatory process - is increased vascular permeability higher protein/albumin/cells level
72
how do low protein states cause oedema
* reduce oncotic pressure * there is increased filtration
73
how does endothelial damage cause oedema
* increases the permeability to the endothelial lining * proteins and larger molecules leak out - pores - + water * (acute inflammation/burns)
74
Echocardiogram is a useful investigation in heart failure. a. true b. false
True - It may be used to look at the structure of the heart and assess for potential causes.
75
Echocardiogram is a useful investigation in heart failure. a. true b. false
True - It may be used to look at the structure of the heart and assess for potential causes.
76
Wolff- Parkinson White syndrome is due to an accessory conduction pathway also known as the bundle of Kent. a. true b. false
True - In Wolff- Parkinson White syndrome there is an accessory pathway between the atria and ventricles by which conduction can occur. Electrical signals can pass directly to the ventricle via this pathway and can cause the ventricles to contract prematurely. This can result in a type of supraventricular tachycardia.
77
The pulse in atrial fibrillation is classically described as regularly irregular. a. true b. false
False - The pulse is described as irregularly irregular. This means the rhythm has no repeating or predictable pattern.
78
A patient is started on a new medication for heart failure. They are now complaining of a dry cough. This new medication is likely to be an ACE inhibitor. a. true b. false
True - A dry cough is a common side effect of ACE inhibitors.
79
Prolongation of the QRS complex may be seen in Bundle Branch Block. a. true b. false
True - Delay in conduction to the ventricles via the left or right bundle branch may cause prolongation of the QRS complex on ECG.
80
Calcium channel blockers can be used for rate control in atrial fibrillation. a. true b. false
True – examples include verapamil and diltiazem.
81
Digoxin is a negative inotrope and is therefore useful in the management of heart failure. a. true b. false
False - Digoxin is a positive inotrope. It acts to increase the availability of calcium in the myocyte and can therefore increase the contractility of the heart.
82
The classic ECG findings in Wolff-Parkinson-White Syndrome are shortening of the PR interval and delta waves. a. true b. false
True - A delta wave is a slurred upstroke in the QRS complex. This occurs as the electrical impulse travels via the Bundle of Kent to the ventricles without the usual delay of passing through the AV node. There can also be shortening of the PR interval.
83
In systolic dysfunction, cardiac output is usually increased. a. true b. false
False - in systolic dysfunction, cardiac output is reduced, usually due to reduced stroke volume. Heart rate is often increased to attempt to compensate for this (remember that CO = HR x SV)
84
Pericardial disease can cause heart failure. a. true b. false
True – particularly constrictive pericardial disease, where scarring of the pericardium limits the contractility of the heart.
85
In Mobitz type I (2nd degree heart block) there is progressive PR prolongation until a p wave fails to conduct to the ventricle. a. true b. false
True - This is also known as the Wenckebach phenomenon. Quizmaster may be showing their age with this, but I always found this video genuinely helpful! (And horribly catchy…)
86
The Renin-angiotensin-aldosterone system is activated in heart failure. Its end-result is fluid loss and vasodilatation. a. true b. false
False - There is inadequate kidney perfusion in heart failure leading to the activation of the RAAS system, causing fluid retention. Angiotensin II is a potent vasoconstrictor NOT vasodilator.
87
Loop diuretics are used in the management of heart failure a. true b. false
Loop diuretics are the mainstay of symptomatic therapy. These act to inhibit Na-K-Cl transporters in the Loop of Henle and therefore reduce the fluid overload by inducing diuresis.
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