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Yr3 CLASP > Sudden death > Flashcards

Sudden death Flashcards

1
Q

In the central dogma, which process is most likely to be affected by a mutation changing the first base in an intron

A

Splicing

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2
Q

What is a motif

A

short DNA sequences that indicate where splicing should happen in the RNA strand, the most important parts are the 2 bases in the intron just before and just after the exon

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3
Q

what type of genetic sequence variant is most likely to cause long QT syndrome

A

A premature stop codon in the exon 2 of a gene

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4
Q

what is the effect of deleting a single base in an exon of the gene

A

Frameshift mutation

changes all the following amino acids as the base pairs change

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5
Q

what is a missense mutation

A

single base pair substitution altering genetic code

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6
Q

what is a nonsense mutation?

A

where a stop codon is encoded for, creating short chains

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7
Q

what is next generation sequencing?

A

high throughput method used to determine portion of nucleotide sequence of a genome

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8
Q

what is the most common arrhythmia associated with long QT

A

torsades de pointes

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9
Q

What advice should you give to reduce risk of sudden infant death

A

put baby on their back to go to sleep

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10
Q

what is a feature of an ECG seen in Ventricular tachycardia?

A

The QRS complexes last longer than 120s

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11
Q

what are clinical signs of sepsis

A 
rapid breathing and HR
shortness of breath
low BP
confusion
feverish and clammy
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12
Q

what drug is used to treat a patient with long QT syndrome

A

Atenolol

Avoid QT prolonging drugs
flecainide, haloperidol, furosemide

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13
Q

What are the reversible causes of cardiac arrest

A

4 H’s

  • hypoxia
  • hypovolaemia
  • hypo/hyperkalaemia
  • hypothermia

4 T’s

  • thrombosis (coronary or pul)
  • Tamponade
  • toxins
  • Tension pneumothorax
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14
Q

Name the non - suspicious and suspicious causes of hypoxia

A

Non suspicious

  • asthma
  • pneumothorax
  • respiratory obstruction (epiglottitis, choking)
  • Respiratory depression (drug related, overdose)
  • Aspiration

Suspicious

  • Respiratory obstruction
  • Drug related - overdose, negligence, poisoning
  • Drowning
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15
Q

Name the non - suspicious and suspicious causes of hypovolaemia

A

Non - suspicious

  • upper GI haemorrhage
  • lower GI haemorrhage
  • Haemoperitoneum - liver/spleen laceration
  • Trauma
  • Abdominal aortic aneurysm

Suspicious

  • trauma
  • stabbings
  • shootings
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16
Q

Name the non - suspicious and suspicious causes of hyper/hypokalaemia?

A

Non - suspicious

  • DKA
  • Alcoholic ketoacidosis
  • Toxins

Suspicious
- toxins

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17
Q

Name some non suspicious and suspicious causes of hypothermia

A

Non - suspicious

  • exposure to cold
  • alcoholic
  • drugs
  • underlying medical disease

Suspicious

  • cold exposure
  • water
  • neglect
  • forced outside
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18
Q

Define shock

A

condition of inadequate perfusion to sustain normal organ perfusion

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19
Q

what are the 5 main classes of shock

A

Hypovolaemic - loss of circulating volume, reduced preload and CO

Cardiogenic - myocardial dysfunction causing reduction in systolic function and CO

Obstructive - physical obstruction to filling of the heart, reduced preload and CO

Distributive - significant reduction in SVR

Cytotoxic - uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake

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20
Q

Give examples of causes for the different types of shock

A

Hypovolaemic
- bleeding (most common), third space losses, severe dehydration

Cardiogenic
- MI, myocarditis, acute valve lesion

Obstructive
- Tamponade, PE, Tension pneumothorax

Distributive
- septic shock, anaphylaxis, neurogenic

Cytotoxic
- CO/CN poisoning

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21
Q

Describe hypovolaemic shock

A

where there is insufficient circulating volume to fill the circuit and maintain BP

Leads to hypoperfusion and hypoxia of end organs

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22
Q

Features of hypovolaemic shock

A

Initially people compensate very well and may just have tachycardia

  • sweaty
  • anxious
  • tachycardia
  • narrowing pulse pressure
  • increasing resp rate
  • hypotension is a late sign in haemorrhage
  • confusion
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23
Q

Compensatory mechanisms in hypovolaemia

A

Baroreceptor reflexes - stretch sensitive receptors in carotid sinus and aortic arch, decreased stretch = enhanced symp. output

Sympathetic mediated neurohormonal response - release of adrenergic vasoconstrictors (adrenaline and noradrenaline), redirection of fluids, leads to lactic acidosis driving chemoreceptors, circulating vasodilators also increase

Capillary absorption of interstitial fluid - reduced capillary pressure, net inward filtration

Renal and hypothalamo - pituitary adrenal response - renin release enhancing vasoconstriction and secretion of aldosterone/vasopressin

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24
Q

what are the 3 ways that the heart can increase its cardiac output

A

Increase HR
increase SV (inotropy)
Increase both

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25
Q

In the Frank starling relationship, if the heart is failing what will happen to the curve

A

It will shift down

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26
Q

What does inotropy do to the frank starling curve?

A

shifts the curve up

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27
Q

what is cardiogenic shock

A

where the heart as a pump cannot meet circulatory demands

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28
Q

What are clinical signs of cardiogenic shock?

A

Poor forward flow - hypotension, shock, fatigue, syncope

Back pressure - pulmonary oedema, elevated JVP, hepatic congestion

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29
Q

what is inotropy

A

A measure of the contractile state for any given preload

Positive inotropy is an increase in force of cardiac contraction

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30
Q

How is positive inotropy achieved

A

The sympathetic nervous system
Can be replicated with drugs
- Dopaminergic stimulation using dobutamine, adrenaline

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31
Q

What is obstructive shock

A

Involves a physical obstruction to either the heart or great vessels, mainly affects the cardiac filling rather than cardiac ejection

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32
Q

Treatment of obstructive shock

A

Remove underlying cause:

PE - anticoagulation +/- thrombolysis
Cardiac tamponade - pericardial drainage
Tension pneumothorax - decompression and chest drain

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33
Q

what is distributive shock?

A

The circuit is too big

caused by excessive vasodilation resulting in inadequate oxygen delivery and perfusion to organs

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34
Q

What are the 3 subtypes of distributive shock?

A

Septic - bacterial endotoxin mediated capillary dysfunction

Anaphylactic shock - mast cell release of vasodilators

Neurogenic shock - loss of thoracic sympathetic outflow following spinal injury

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35
Q

what do a rise in lactate levels suggest?

A

a marker of tissue hypoperfusion and shock

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36
Q

What are the 2 shockable cardiac arrest rhythms

A

Ventricular fibrillation

Pulseless Ventricular tachycardia

37
Q

what are the 2 non - shockable cardiac arrest rhythms

A

Pulseless electrical activity

Asystole

38
Q

what two categories can you split inherited cardiac conditions into?

A

Channelopathies

carddiomyopathies

39
Q

Give some examples of channelopathies

A 
Congenital long QT syndrome
Brugada
Catecholaminergic polymorphic ventricular tachycardia
short QT
familial Wolf parkinsons white
Familial AF
40
Q

Give some examples of cardiomyopathies

A

Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy

41
Q

what is a channelopathy and a cardiomyopathy

A

Channelopathy - problem in the conduction system, usually associated with proteins, ion current imbalances

Cardiomyopathy - problem with the heart muscle, can be caused by scarring

42
Q

what are after depolarisations

A

Abnormal depolarisation of cardiac myocytes that interrupt the cardiac action potentials and can lead to triggered activity, occur in phase 2, 3, 4

43
Q

What are early after depolarisations?

What can they result in?

A

Abnormal depolarisations which occur in phase 2 or 3 caused by an increase in frequency of AP

Torsades de pointes

44
Q

what arrhythmia is commonly seen in long QT syndrome

A

Torsades de pointes

45
Q

what are delayed after depolarisations

A

These are depolarisations that begin during phase 4 after repolarisation has completed but before another action potential would normally occur.

46
Q

what can cause delayed after depolarisations

A

elevated calcium concentrations

seen in digoxin toxicity

47
Q

where is calcium ions stored and released from?

A

sarcoplasmic reticulum

48
Q

what is a classic feature of delayed after depolarisations and what condition is it usually seen in?

A

Bidirectional ventricular tachy

Catecholaminergic polymorphic ventricular tachycardia

49
Q

what is the commonest (autosomal dominant) long QT syndrome?

A

Romano ward syndrome

50
Q

Physiology of LQT syndrome

A 
Defect in a channel protein
Reduced or dysfunctional ionic current
Prolonged cardiac repolarisation 
QT interval prolongation
Polymorphic ventricular tachycardia (torsades)
51
Q

what can trigger sudden cardiac death in someone with long QT

A

Exercise
Emotional stress
Sleep

52
Q

what are some examples of QT prolonging drugs

A

amiodarone
erythromycin
haloperidol

53
Q

what are the main arrythmias associated with brugada syndrome

A

polymorphic VT
VF
AF

54
Q

what are ECG findings in brugadas

A

ST elevation
RBBB in V1 - V3

often intermittent ECG findings and so can use provocative testing using flecainide (sodium blocker)

55
Q

what inheritance pattern does brugada follow

A 
Autosomal dominant
(mainly men)
56
Q

Brugada syndrome VF triggers

A

rest or sleep
fever
excessive alcohol, large meals

57
Q

What drugs should be avoided in brugada

A 
Anti - arrhythmics
- sodium channel blockers
Psychotropics
Analgesics
Anaesthetics
58
Q

what is catecholaminergic polymorphic ventricular tachycardia

A

sensitivity of cardiac muscle to adrenaline which can be triggered by emotional stress or exercise

59
Q

what will an ECG look like in someone with CPVT

A

normal at rest

Can cause bidirectional tachycardia and polymorphic VT

60
Q

Treatment in CPVT

A 
beta blockers
lifestyle changes (avoid competitive sports, stress)
ICD implantation (who have had cardiac arrest)
61
Q

what will be seen on an ECG in wolff parkinson white syndrome

A

Short PR interval
Delta waves
AF (maybe)

62
Q

what causes Hypertrophic cardiomyopathy

A

mutation in sarcomeric genes

63
Q

investigations for hypertrophic cardiomyopathy

A

doppler echo

48hr ambulatory ECG

64
Q

what is dilated cardiomyopathy

A

a type of heart muscle disease that causes the heart chambers to thin and stretch, growing larger

65
Q

treatment of dilated cardiomyopathy

A

lower BP

flecainide - rhythm control drug

66
Q

what is arrhythmogenic right ventricular cardiomyopathy

A

it is where cardiomyocytes is replaced by fibro fatty tissue

67
Q

what inheritance pattern is arrhythmic right ventricular cardiomyopathy

A

Autosomal dominant - for desmosomal proteins

Autosomal recessive - for nondesmosomal proteins

68
Q

Treatment of arrhythmogenic right ventricular cardiomyopathy

A

Avoidance of competitive sports
Beta blockers
ICD implantation
Amiodarone if not beta blockers

69
Q

Diagnosis of inherited cardiac conditions

A

Clinical testing
genetic testing
family screening

70
Q

what is the only known treatment for ventricular fibrillation, how does it work?

A

Defibrillation

Resets all the cardiac myocytes to enable normal electrical activation to recommence
Causes all cardiac myocytes to fully depolarise

71
Q

what is a polymorphism

A

a variant that is prevalent in the general population. Often used to imply benign

72
Q

how do you classify a variant

A 
Class 1: definitely benign
Class 2: probably benign
Class 3: Variant of uncertain significance
Class 4: Probably pathogenic
Class 5: Definitely pathogenic
73
Q

When would you use FISH

A

for translocation mutations

74
Q

When would you use microarray CGH

A

To detect any missing or duplicated pieces of chromosome

This is first line chromosome test

75
Q

what is PCR used for

A

allows you to select one small piece of the human genome and amplify it

76
Q

what is NGS

A

a high throughput method used to determine a portion of the nucleotide sequence of an individual genome

77
Q

what pattern of inheritance causes dissecting aortic aneurysm

A

autosomal dominant

78
Q

what is an aortic dissection

A

a condition in which a tear occurs into he inner layer of the aorta, blood rushes through the tear causing the inner/middle layers of the aorta to split

79
Q

what is marfans syndrome caused by

A

fillibrin mutation

A disorder of the body’s connective tissues

80
Q

what is classed as a stillbirth

A

When a baby dies after 24 weeks of pregnancy and before or during birth

81
Q

what is classed as a miscarriage

A

Loss of a baby before 24 weeks of pregnancy

82
Q

Risk factors for stillbirths

A 
Congenital abnormalities
Cord prolapse
maternal infections
extremes of ages
multiple pregnancies
Medical complications - pre eclampsia ect.
83
Q

What is some advice you should give to women to prevent the likelihood of a stillbirth

A

Sleep on side in third trimester
Quitting smoking
Staying healthy weight
Avoid alcohol and drugs
Take folic acid until end of first trimester
Report any leaking fluid/discharge in pregnancy

84
Q

In what instances should immediate delivery of baby be strongly advised?

A

Sepsis
Eclampsia
Placental abruption
Membrane rupture

85
Q

what is SUDI?

A

All infant deaths which happen suddenly for which there is no apparent reason, are unexpected

86
Q

At what age do SUDI’s mainly occur?

A

2 - 6 months

87
Q

Risk factors for SUDI

A 
Acute illness (URTI/otitis media)
Preterm birth before 37 weeks
Congenital anomaly
Multiple birth
Previous unexplained infant death
Small for gestational age
Male
Sleeping prone or on side
Co - sleeping
sleeping with pillows
Substance misuse in parents
88
Q

What are the 5 stages of grief

A 
Denial
Anger
Depression
Bargaining
Acceptance

Yr3 CLASP (2 decks)

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