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MBBS - Year 2 > Cardiology - Congenital Heart Disease and HTN > Flashcards

Cardiology - Congenital Heart Disease and HTN Flashcards

1
Q

When is the CDV system first developed

A

By 3rd week - diffusion no longer supplies needs of embryo

Formation of primitive blood vessels

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2
Q

How do primitive blood vessels form

A

In two ways - vasculogenesis and angiogenesis

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3
Q

Vasculogenesis

A

Blood vessels arise from assembly of angioblasts to form blood islands
Vessels fuse together to form vascular network

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4
Q

Where does blood vessel formation start

A

In extraembryonic mesoderm

Mesenchymal cells differentiate into angioblasts

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5
Q

Blood island formation

A

Angioblasts aggregate forming masses and cords

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6
Q

How are the primitive blood vessels formed

A

Cavities form within blood islands and endothelial (angioblast) cells surround these cavities and form endothelium

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7
Q

When are the heart and great vessels formed

A

3rd week in cardiogenic region

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8
Q

Great vessels in embryo

A

Paired longitudinal endothelial lined vessels primordial heart tubes and dorsal aortae

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9
Q

When is the primordial CDV system formed

A

When primitive blood vessels are joined, connecting umbilical vessels

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10
Q

Development of Primary Heart Field

A

Progenitor heart cells migrate to splanchnic mesoderm

Initial forms horseshoe-shaped clusters of cells

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11
Q

What does the PHF become

A

Atria, LV and most of LV - rest of heart comes from 2’ heart field

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12
Q

Formation of primitive heart tube

A

Single tube w/ aortic and venous poles
The heart tube sprouts aortic arch vessels from the (aortic) outflow region
Endocardium w/ mesenchyme around it differentiates into the myoepicardial mantle
Ultimately forms myocardium and epicardium

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13
Q

When does the heart start beating

A

By 22 days

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14
Q

How does blood enter the primitive heart

A

Via 3 main veins into the sinus venosus

Cardinal veins
Vitelline vein
Umbilical vein

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15
Q

How does blood leave the primitive aortic sac

A

Via aortic arches –> brachial arches —> dorsal aortae

Umbilical artery
Vitelline artery

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16
Q

Truncus arteriousus

A

Common arterial trunk - aortic arches

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17
Q

How is the aortic sac formed

A

Distal ends of aortic arches dilate

6 paired aortic arches

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18
Q

In which direction do aortic arches develop

A

Cranial to caudal - ultimately 5 paired, I - VI (not V)

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19
Q

What doe the aortic arches supply

A

Brachial arches

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20
Q

When does septation occur

A

4th week to end of 5th weeks

Heart tube undergoes partitioning into 4 chambers

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21
Q

Process of septation

A

AV partitioning and cuspid valve formation
Atrial partitioning - spetum primum and septum secundum
Ventricular partitioning

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22
Q

When does the interventricuiar septum close

A

End of 7th week

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23
Q

Most common type of birth defects

A

Congenital heart defects

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24
Q

Septal defects

A

Where theres a hole between 2 chambers

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25
Q

Transposition of the great arteries

A

Where the pulmonary and aortic valves and the arteries connected and have swapped positions

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26
Q

Most common cyanotic heart defect

A

Tetrology of Fallots

Cause of blue baby syndrome

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27
Q

Ventricular Septal Defect

A

Defect opening between 2 ventricles on its superior aspect

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28
Q

Pulmonary stenosis

A

Narrowing of RV outflow tract, and or just below the pulmonary valve
The degree of stenosis varies - primary determinant of symptoms and severity

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29
Q

Overriding aorta

A

Biventricular connection of aortic valve above the VSD and connected to both LV and RV
The degree to which the aorta is attached to the RV is referred to as its degree of ‘override’

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30
Q

RVH

A

RV hypertrophy
RV is more muscular than normal to deal w/ increased obstruction to RVOT, results in characteristic boot-shaped appearance on CXR

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31
Q

Anatomical abnormalities seen in Tetralogy of Fallots

A

VSD
Pulmonary stenosis
Overriding aorta
RVH

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32
Q

Why does Tetrology of Fallot result in R to L shunt

A

Mixing of oxygenated & deoxygenated blood in LV due to VSD

Outflow of the mixed low oxygenated blood from both ventricles through aorta because of pulmonary stenosis

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33
Q

What is CHD

A

Any structural heart abnormality that is present from birth

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34
Q

Epidemiology of CHD

A

Approx 1% of live-born infants

Palliated, never cured

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35
Q

Commonest lesions in CHD

A

ASD
VSD
CoA
ToF

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36
Q

What does mx of CHD depend on

A

Physiology at the time

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37
Q

Normal foetal circulation

A

High pulmonary vascular resistance in utero
PVR decreases rapidly at. birth, then progressively over 4-6 wks
Arterial duct closes at birth
Oval foramen flap closes w/ increased LA pressure

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38
Q

What does IV PGE2 do to the arterial duct

A

Keeps it open - given in PDA

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39
Q

What happens with closure of arterial duct and atrial communication at birth

A

Decreased PVR
RV systolic pressure
RA pressure

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40
Q

Features of ASD

A

Pre-tricuspid shunt
High pulmonary flow
R heart dilatation - incl RA, RV and pulmonary artery

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41
Q

Presentation and symptoms of ASD in children

A 
Incidental murmurs 
Recurrent pneumonia 
Poor growth 
FTT
Exercise intolerance 
Fatigue
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42
Q

Presentation and symptoms of ASD in adults

A 
Paroxical embolus 
Stroke 
Exercise intolerance 
Recurrent pneumonia 
Atrial arrhythmia 
Tricuspid regurgitation, HF, pulmonary HTN
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43
Q

ASD - CXR signs

A

Cardiomegaly
Dilation of RA and/or RV
Prominent main pulmonary artery
Increased pulmonary vascular markings

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44
Q

Signs of ASD in adults

A

Prominent RV impulse
Soft, ejection systolic murmur - pulmonary flow murmur
Widely split, soft S2. Fixed in all stages of in/expiration

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45
Q

Indications for closure of ASD

A

Symptomatic
RA and RV enlargement
Systolic PA pressure < 50% systemic pressure
PVR < 1/3 SVR

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46
Q

What does the feasibility of ASD device closure depend on

A

Defect size

Anchoring ‘rims’

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47
Q

Features of VSD

A

Ventricular level shunt
High pulmonary blood flow - pulmonary artery dilatation
L heart dilatation - LA and LV

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48
Q

Presentations and symptoms seems in large VSDs

A 
Frequent chest infections 
Exercise intolerance 
Fatigue 
HF
Pulmonary HTN
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49
Q

Indications of VSD closure

A

Symptomatic
LA & LV enlargement
Systolic PA pressure <50% systemic pressure
PVR < 1/3 SVR

Usually surgical process done early in childhood

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50
Q

Main complication from small VSD

A

IE

Endothelial damage from aberrant jet streams and turbulent flow

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51
Q

Where might IE vegetations appear in small VSD pts

A

At tricuspid valve
Opposite or around defect
On aortic valve

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52
Q

Prevention of endocarditis in VSD pts

A

Good dental hygiene - best
Avoid tattoos and piercings
Prophylactic abx for HIGH-RISK CHD only

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53
Q

High-risk CHD requiring prophylactic abx for IE

A

R to L shunts (cyanosis)
Valve replacements
Previous endocarditis

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54
Q

Main long-term complications of large VSD shunts

A

Pulmonary HTN 2’ to c/c high pulmonary blood flow

Once pulmonary vasc resistance > SVR, shunt across any communication reserves (atrial, ventricular or duct)

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55
Q

Problems seen in Eisenmerger syndrome

A 
Polycythaemia 
Fe deficiency 
Acne, gout, hypertrophic polyarthropy 
High pregnancy risk - mustn't get pregnant 
Paradoxical embolus at IV sites 
Arrhythmia risks
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56
Q

What is CoA associated with

A

Bicuspid aortic valve

VSDs

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56
Q

What is CoA associated with

A

Bicuspid aortic valve

VSDs

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57
Q

Longterm outcome of CoA

A

Residual CoA
Aneurysmal dilatation
Aortopathy

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58
Q

Surgical mx of CoA

A

End to repair (resection)
L subclavian flap repair (neonate)
Coarctation stent in preferred for adults
Balloon angio

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59
Q

Resection for CoA

A

Constricted section of aorta removed

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60
Q

L subclavian flap repair for CoA

A

Subclavian artery is used as a flap to enlarge the constricted parts of the aorta

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61
Q

Definitive surgery for ToF

A

Within 1st year of life - RVOT enlargement, patch closure of VSD, patch enlargement of PA

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62
Q

Residual lesions after surgery for ToF

A

Pulmonary regurgitation
RVOT stenosis
Branch PA stenosis
RV dysfunction

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62
Q

ToF follow up to monitor RV dysfunction

A 
Clinical signs and symptoms 
MRI 
Catheterisation 
CXR 
ECG & Holter 
CT
CPEX 
Echo
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62
Q

Simple predictors of maternal risk of ACHD

A

Prior cardiac event (TIA, stroke, arrhythmia, heart failure)
NYHA > grade II pre-pregnancy
L heart obstruction – mitral or aortic stenosis, CoA
LV EF <40%

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63
Q

Risk scores for pregnancy

A

WHO
ROPAC
CARPREG 2

64
Q

CHD related to Down syndrome

A

ASD
VSD - main one
AVSD
ToF

65
Q

CHD related to Turner syndrome

A

BAV
CoA
VSD
ASD

66
Q

CHD related to Marfans’

A

Dilated Ao

Aortopathy

67
Q

Psychological issues in ACHD

A

Ill health and poor schooling – employment difficulties
Difficulty w/ insurance
Self-image – scar on chest
Lifelong follow-up, tests, spectre of intervention
QoL

68
Q

Why is MAP closer to diastolic pressure than systolic pressure

A

Diastole lasts 2x as long as systole

69
Q

Short term control of MAP - mechanism

A

Neural

70
Q

Long term control of MAP - mechanisms

A

Hormonal

71
Q

What is MAP determined by

A

Blood volume
CO
TPR
Distribution of blood between arterial and venous blood vessels

72
Q

Stimulus for ANP

A

Increased blood volume causes increased atrial stretch

73
Q

Systemic response to ANP

A

Increased GFR
Decreased Renin
Inhibits aldosterone
Decreases BP

74
Q

What is HTN

A

A rise in arterial bp sufficient to raise the incidence of strokes, MI. HF and renal failure

74
Q

What is HTN

A

A rise in arterial bp sufficient to raise the incidence of strokes, MI. HF and renal failure

74
Q

What is HTN

A

A rise in arterial bp sufficient to raise the incidence of strokes, MI. HF and renal failure

74
Q

1’ HTN and 2’ HTN

A

1’ HTN is essential - no obvious predisposing organic cause

2’ - identifiable pathological cause

75
Q

Proposed model for genesis of HTN

A

HTN initially due to increases in HR but normal TPR

Over time CO falls, with TPR increases permenantly

76
Q

Haemodynamic types of HTN

A

Systolic HTN in the young (increased CO)
Diastolic/ combined hTN of middle age (increased TPR +/- CO)
Isolated systolic HTN in older adults (increased TPR & arterial stiffness)

76
Q

Haemodynamic types of HTN

A

Systolic HTN in the young (increased CO)
Diastolic/ combined HTN of middle age (increased TPR +/- CO)
Isolated systolic HTN in older adults (increased TPR & arterial stiffness)

77
Q

Mechanisms of primary HTN

A

Genetic
Kidney and Na handling
Neurogenic & humoral theories
Vascular remodelling

78
Q

Condns causing 2’ HTN

A

Pre-eclamptic toxaemia
2’ Hyperaldosteronism (Conn’s syndrome)
Renal artery stenosis
Phaechromocytoma

79
Q

Pe-eclamptic toxaemia causing HTN

A

Spiral arteries don’t dilate normally, causing placental ischaemia
Toxins released lead to reduction in endothelial NO/ prostacyclin production
Raised endothelin production
Peripheral vasoconstriction and HTN

80
Q

Threshold for pre-eclamptic toxaemia

A

≥140/90 mmHg during pregnancy, w/ proteinuria >0.3g/day

81
Q

Conn’s syndrome causing HTN

A

Adrenal tumour leads to excess aldosterone production

Stimulates Na and water retention by kidney

82
Q

Renal artery stenosis causing HTN

A

Activates RAAS

83
Q

Phaechromocytoma causing HTN

A

Adrenal medulla, catecholamine secreting tumour

α-adrenoreceptor activation (vasoconstriction) leads to hypertension

84
Q

Main types of lipid in our bodies

A

Triglycerides
Phospholipid
Steroid

85
Q

What di we need cholesterol for

A

Used to make steroid hormones and bile salts

Increases cell membrane fluidity

86
Q

Cholesterol structure

A

Hydrohilic heads
4 fused hydrocarbon rings
Hydrophobic tails

87
Q

Why do gats need to eb transported correctly

A

Or else they ppt in blood vessels, forming plaques

88
Q

By how much is cholesterol solubility increased in our bodies

A

600x

89
Q

Major source of cholesterol in the body

A

Diet - eggs, fatty foods, kidney, liver, prawns

90
Q

Cholesterol transport cycle

A

Liver makes bile salts which act as detergents to assist in absorption of insoluble cholesterol from intestine
Cholesterol (complexed w/ bile salts) is taken into intestinal epithelium and packaged into lipoprotein particles
Cholesterol is transferred between lipoproteins for delivery from intestine to cells and back to liver

91
Q

What is LDL a measure of

A

Cholesterol headed to tissue - ‘bad cholesterol’

92
Q

Target range of lDL cholesterol

A

70-130 mg/dL (lower is better)

93
Q

What is HDL a measure of

A

Cholesterol headed to liver for excretion via bile salts

94
Q

Target range of HDL

A

40-60 mg/dL (higher is better)

95
Q

Target range for total cholesterol in blood

A

<200mg/ dL

96
Q

Where do you see xanthomas in people with familial hypercholesterolaemia

A

Around eyelids

Tendons of hands, elbows, knees, and feet

97
Q

How do statins lower blood cholesterol

A

Main mechanisms is increased expression of lDL receptor
Inhibit HMG CoA reductase
Indirectly promote cholesterol uptake into cells via LDLR through -ve feedback
Inhibits cholesterol synthesis inside cells

98
Q

When can statins be ineffective

A

If dietary intake of cholesterols excessive

99
Q

What are we trying to prevent when aiming to lower BP

A 
CVA 
CHD 
HF 
Renal dysfunction 
Aortic dilatation and dissection 
Occular complivcatsions 
Vascular dementia
100
Q

Epidemiology of HTN

A

V common in UK pop
Prevalence influenced by age and lifestyle factors
23% of adult UK pop have hTN, 50% of those 60+ have HTN

101
Q

What may result from untreated HTN

A

CVD and renal damage leading to a treatment resistant state

102
Q

What is each 2mmHg rise in systolic bp associated w/

A

Proportional increased risk of mortality
7% from heart disease
10% from stroke

103
Q

What is stroke prevention in HTN most dependent on

A

The treatments used
The amount of blood pressure lowering
The type of pts treated
Duration of therapy

104
Q

Key priorities for implementing HTN mx

A

Dx
Risk assessment
Initiating and monitoring antihypertensive drug treatment
Choosing antihypertensive drug treatment
Pt knowledge, education and motivation
Treatments are usually life-long

105
Q

Dx of HTN

A

If clinical BP is 140/90 mmHg or higher, offer ABPM to confirm dx - at least 2 measurement/ hr (14 minimum for day)
Take 2nd reading in clinic, if substantial different from the first, take 3rd
While waiting for confirmation of dx, carry out ix for target organ damage

106
Q

Examples of target organ in HTN

A

LVH
CKD
Hypertensive retinopathy

107
Q

Risk assessment for HTN

A

Carried out to guide treatment of spp risk factors
Clinical risk scores
Framingham risk score
QRISK 2/3 - most reliable

108
Q

Associated condns of HTN

A

CDV disease (coronary, peripheral, cerebral)
Renal impairment
DM

109
Q

Organs that may be damaged from HTN

A 
Eye 
Brain 
Kidney 
Heart 
Other
110
Q

Retinal changes in HTN

A

Hard exudates
Cotton wool spots
Flame haemorrhage
Arterio-venous nipping

111
Q

Criteria for LVH on ECG

A

S wave depth in V1 + tallest R wave height in V5/6 > 35 mm
LAD
Lateral ST segment depression w/ T wave flattening/ inversion

112
Q

Stage 1 HTN

A

Clinic BP is 140/90 mmHg or other ABPM/ HBPM is 135/85 mmHg or higher

113
Q

Stage 2 HTN

A

Clinic BP is 160/100 mmHG or higher and ABPM/HBPM is 150/95 mmHg or higher

114
Q

Stage 3 HTN (severe HTN)

A

Clinic BP is 180 mmHg or higher or clinic diastolic is 120 mmHG or higher

115
Q

White-coat HTN

A

A discrepancy of more than 20/10 mmHg between clinic and avg daytime ABPM/ HBPM BP measurement at time of dx

116
Q

Why do we assess hypertensive pts

A

To find out aetiology, target organ damage, risk factors etc

117
Q

What does the assessment of the hypertensive pts require

A 
Full hx - PMH, SH, risk factors
Careful examination - CDV, peripheral pulses, retinal exam 
Formal risk assessment 
Key basic tests 
Spp tests
118
Q

Key basic tests for HTN pts

A 
ECG 
Renal function (incl eGFR)
Na
K 
Cholesterol 
Glucose/ HbA1c
FBC 
Urinalysis for protein 
ABPM/ HBPM
Fundoscopy - looking for hypertensive retinopathy
119
Q

ABPM

A

Ambulatory BP monitoring

120
Q

HBPM

A

Home BP monitoring

121
Q

Spp tets for hypertensive pts

A 
CXR 
Echo 
Renal ultrasounds 
Tests for 2' HTN
Albumin/ creatine ratio
122
Q

General measures for BP lowering

A 
Wt 
Dietary salt 
Alcohol 
Exercise 
Smoking
123
Q

Wt as mx of BP

A

Every Kg reduction is associated w/ 1-2mmHg drop in systolic BP

124
Q

Dietary salt and mx of BP

A

Suggested to reduce daily intake to 6g

125
Q

Alcohol and mx of BP

A

Association between increased alcohol and elevated BP

126
Q

Exercise and mx of BP

A

Heavy physical exercise associated w/ reduced BP

127
Q

Smoking and mx of BP

A

No clear association

General adverse risk factor

128
Q

Summary of antihypertensives

A

Aged <55 yrs or DM - ACEi/ ARB
Aged >55 or Afro/Carribbean - CCB

Step 2 is ACEi/ARB and CCB 
Step 3 is add this=azide-like diuretic e.g. indapamide, bendrofluazide 
Step 4 (resistant HTN) - consider further diuretic e.g. Spiro or BB
129
Q

Who do we offer antihypertensive drug treatment to

A

Anyone w/ stage 2 HTN

Those w/ stage 1 HTN, <80 who meet identified criteria (DM, CDV, renal disease, target organ damage, 10-yr CDV risk > 10%)

130
Q

What should you do if someone has stage 1 HTN but doesn’t meet all the criteria for antihypertensives

A

Do further assessment

131
Q

Monitoring drug treatment for HTN

A

Using clinic BP measurements, aim for 140/90 mmHg in those <80 and 150/90 in 80+
Aim for ABPM/ HBPM target bag of <135/85 mmHg in people aged under 80 and <145/85 mmHg in people 80+

132
Q

Long term mx of HTN

A

Partnership care - pt has greater role
Mx of other health condns (CVD, renal, DM, prior CVA)
Mx of other risk factors e.g. cholesterol, smoking, wt
Appropriate diet and lifestyle measures
HBPM
Med review, compliance and appropriate dosing
Encouragement, support and counselling

133
Q

Monitoring for those on step 4 HTN treatments

A

Serum Na, K and renal function

134
Q

Why should pregnant women be offered alternatives to ACEi and ARBs when pregnant

A

These can cause congenital abnormalities

Alternatives incl methyldopa, labetolol and slow-release nifedipine

135
Q

Using HBPM to confirm dx of HTN

A

For each recording, take 2 consecutive measurements at least 1 min apart w/ pt seated
Record bP 2x/day - morning and night for 4/7 (ideally 7/7)
Discard measurements taken on 1st data and use avg value of all other measurements

136
Q

What 3 ducts are present at birth

A

Ductus venous
Ductus arteriosus
Foramen ovale

137
Q

How does the ductus venous close after birth

A

Physiological sphincter

138
Q

How does the ductus arteriosus close after birth

A

Pulmonary Vascular resistance decreases as SVR increases

139
Q

How does the foramen ovale close after birth

A

Pressure in LA rises

140
Q

Examples of acyanotic CHD

A 
VSD
PDA 
ASD
Pulmonary stenosis 
AS
CoA
141
Q

Examples of cyanotic CHD

A

ToF

Transposition of great arteries (TGA)

142
Q

CHD resulting in L to R shunt

A

VSD
PDA
ASD

All acyanotic

143
Q

CHD resulting in outflow obstruction

A

Pulmonary stenosis
AS
CoA

144
Q

Murmur heard in VSD

A

Pansystolic

145
Q

Murmur heard in PDA

A

Continuous, machinery-like

146
Q

Murmur heard in ASD

A

Ejection systolic

147
Q

Murmur heard in ToF

A

Cresecendo-decresdo systolic

148
Q

What feature is more likely to cause cyanosis

A

Cyanosis is more likely to occur when blood cannot get to lungs vs when cannot circulate around body
More likely in R —> L shunt

149
Q

What is Eisenmenger’s syndrome caused by

A

Complication of untreated L —> R shunt due to pulmonary HTN

150
Q

Features of innocent murmurs

A 
Soft 
Systolic
Short 
LSE 
Asymptomatic
151
Q

Mx of PDA

A

Indamethicin/ ibuprofen

Catheter closure

152
Q

Medical mx of CoA

A

IV infusion of PGE1 - keeps duct open
Dobutamine/ dopamine - improve contractility
Supportive care to correct any consequences of HF

153
Q

Therapeutics for ToF

A

Oxygen
Morphine
BB
Dig & furosemide - HF

154
Q

ECG findings in hypothermia

A

J wave

+ve deflection seen between QRS complex and ST segment

155
Q

When do we see U waves

A

Hypokalemia

Bradycardia

156
Q

Causes of J wave

A

Hypothermia
Hypercalcaemia
SAH

MBBS - Year 2 (20 decks)

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