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Integrated Physiology and Pharmacology > Cardiac Channelopathies > Flashcards

Cardiac Channelopathies Flashcards

1
Q

How many people per year die of sudden cardiac arrest in the UK?

A

70,000

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2
Q

How many sudden cardiac arrest cases are caused by ischaemic heart disease?

A

60% - in the other 40% there is no detectable cause

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3
Q

Long and Short QT syndrome generally affect what?

A

Ventricular myocyte action potentials

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4
Q

What are the normal segments of an ECG and what do the show?

A

P wave -atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarisation
PR interval - start of atrial depolarisation to the start of ventricular depolarisation
Q-T interval - Start of ventricular depolarisation to the end of ventricular repolarisation
The T-P interval -Time between the end of ventricular repolarisation and the start of a new cardiac cycle

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5
Q

Which interval changes in long/ short QT syndrome?

A

The QT interval changes - shorter or longer

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6
Q

What are the stages of a ventricular action potential?

A

1) Large increase in sodium permeability occurs as well as a small increase in potassium permeability
2) Voltage gated calcium channels open = plateau
3) Potassium channels drive repolarisation

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7
Q

What is the normal QT time interval at rest?

A

0.36s

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8
Q

In patients with long QT syndrome what is their QT time interval?

A

0.45s or longer

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9
Q

In patients with short QT syndrome what is their QT time interval?

A

0.34s or less

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10
Q

Why can beats be skipped in long QT syndrome?

A

The SAN is firing normally but the ventricles have not fully repolarised so a beat is missed

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11
Q

What is triggered activity?

A

Where after depolarisation occurs in the ventricles myocytes reach threshold. The sodium channels may get to a closed state and ready to respond before repolarisation is finished so the sodium channels may reactivate again

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12
Q

What is an addition ectopic beat?

A

Extra contraction of the myocytes which can cause ventricular tachycardia -> ventricular fibriliation -> sudden cardiac arrest

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13
Q

What is ventricular fibrilation?

A

A complete lack of coordination of the contraction of cells

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14
Q

What is Re-entrant excitation?

A

Not seen across all layers of the myocytes - triggering of extra activity only in some parts of the muscle

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15
Q

What is spatial dispersion?

A

Only certain parts of the myocytes are impacted

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16
Q

What is temporal dispersion?

A

Extra electical acvitivty of the heart but only at certain times

17
Q

What are the possible symptoms felt by a patient with long QT syndrome?

A

Syncope (fainting)
Palpitations
Some patients have no ‘warning signs’

18
Q

In long QT syndrome, what increases the chances of sudden cardiac arrest?

A

Exercise

Diving into cold water

19
Q

What is torsades de pointes?

A

Specific form of polymorphic ventricular tachycardia in patients with a long QT interval
Characterized by rapid, irregular QRS complexes, which appear to be twisting around the ECG baseline
Arrhythmia may cease spontaneously or degenerate into ventricular fibrillation.

20
Q

What is the incidence of long QT synrdrome?

A

1:10,000 - 1:15,000

21
Q

How many forms of long QT syndrome are there?

A

12

22
Q

Which gene is mutated in long QT type 1 and what is its incidence?

A

KCNQ1
Mutation in Kv7.1a
Loss of function = no IKs current
Incidence is 30-35%

23
Q

Which gene is mutated in long QT type 2 and what is its incidence?

A

KCNH2
Mutation in Kv11.1a
Loss of function = no Ikr current
Incidence is 25 - 30%

24
Q

Which gene is mutated in long QT type 3 and what is its incidence?

A

Gain of function in voltage gated sodium channel

Incidence is 5-10%

25
Q

Which gene is mutated in long QT type 4 and what is its incidence?

A

Loss of function in ankyrin B

Incidence is 1-2%

26
Q

Which gene is mutated in long QT type 5 and what is its incidence?

A

Loss of function in Mink - contributes to IKs
Mink is a B subunit which regulates Kv7.1 by forming a complex
Incidence is 1%

27
Q

Long QT1 and 5 are also associated with what and why?

A

Deafness
The stria vascularis secretes potassium into the endolymph
The endolymph is bordered by hair cells and Reissner’s membrane
If potassium is not secreted Reissner’s membrane collapses = no endolymph = deafness

28
Q

Gain in function of sodium or calcium channels prolongs what?

A

The plateau phase (depolarisation)

29
Q

How can long QT syndrome be treated?

A

B blockers
Atenolol
Negative chronotrophic and ionotrophic actions

30
Q

How many types of short QT syndrome are there?

A

5

31
Q

Males make up for how much of short QT syndrome cases?

A

75%

32
Q

Which gene is mutated in short QT type 1?

A

Kv.11.1a - gain of function mutation
Affects IKr
KCNH2

33
Q

Which gene is mutated in short QT type 2?

A

KCNQ1
KV7.1a - gain of function
Affects IKs

34
Q

Which gene is mutated in short QT type 3?

A

KCNV2
Kir2.1 gain of function
Affects IKi

35
Q

Which gene is mutated in short QT type 4?

A

CACNAIC
CaV1.2a - loss of function
Affects ICa

36
Q

Which gene is mutated in short QT type 5?

A

CACNB2
CaV1.2B2 - loss of function
Affects ICa

37
Q

What is the treatment for short QT syndrome?

A

Implant a defibrillator

Quinide - potassium channel blocker slows down repolarisation

Integrated Physiology and Pharmacology (17 decks)

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