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Phase 2 > Cardio > Flashcards

Cardio Flashcards

1
Q

What can Atherogenesis cause?

A

Heart attack
Stroke
Gangrene of the extremeties

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2
Q

What are the risk factors for atherogenesis?

A

Age
Tobacco smoking
High serum cholesterol
Obesity
Diabetes
Hypertension
Family history

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3
Q

Where are atherosclerotic plaques commonly found?

A

Within peripheral and coronary arteries

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4
Q

What can the distribution of atherosclerotic plaques be effected by?

A

By haemodynamic factors -
Changes in blood flow/turbulence at bifurcations cause the artery to adjust its wall thickness ∴ develop neointima (new growth)

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5
Q

What can occur if an atherosclerosis plaque occludes the vessel lumen?

A

A restriction of blood flow (angina) OR a rupture

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6
Q

What are some negative outcomes of inflammation?

A

Artherosclerosis
Rheumatoid arthritis
Ischaemic Heart Disease
Excessive wound healing

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7
Q

What are some positive outcomes of inflammation?

A

Deals with : Pathogens, Parasites, Tumours
Wound Healing

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8
Q

How are leukocytes guided to the arterial wall?

A

Chemoattractants are released from the endothelium and send signals to leukocytes. They are released from the site of injury, and a concentration-gradient is produced -> ∴ leukocytes move toward arterial wall

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9
Q

How do leukocytes transmigrate into the vessel?

A

Selectins on the vessel wall capture the leukocyte and roll it along the vessel wall. Integrins and chemoattractants are responsible for firm adhesion of the leukocytes, and the transmigration into the vessel.

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10
Q

What are the 4 stages of the progression of atherosclerosis?

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaques of advanced lesions
  4. Plaque rupture
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11
Q

Describe stage 1 of the progression of atherosclerosis

A
  1. Fatty streaks
    - Appears at a v early age (<10 years)
    - Consists of aggregations of lipid-laden macrophages within intimal layer of vessel wall
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12
Q

Describe stage 2 of the progression of atherosclerosis

A
  1. Intermediate lesions
    - Composed layers of vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall, isolated pools of extracellular lipid
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13
Q

Describe stage 3 of the progression of atherosclerosis

A
  1. Fibrous plaques OR advanced lesions
    - Impedes blood flow
    - Prone to rupture
    - Covered by dense fibrous cap, made by ECM proteins incl. collagen and elastin
    - Laid down by SMC that overlies lipid core and necrotic debris
    - May be calcified
    - Contains smooth muscle cells, macrophages and foam cells and and T lymphocytes
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14
Q

Describe stage 4 of the progression of atherosclerosis

A
  1. Plaque rupture
    - Fibrous cap has to be reabsorbed and redeposited for it to be maintained -> if balance shifts (e.g. in favour of inflammatory conditions), cap becomes weak and plaque ruptures
    - Thrombus formation and vessel occlusion
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15
Q

What’s another cause of coronary thrombosis?

A

Plaque erosion

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16
Q

What are the differences between Plaque rupture and Plaque erosion?

A

Plaque erosion :
- Lesions tend to be small lesions
- Collagen triggers the thrombosis
- White thrombus
- Small lipid core

Plaque rupture :
- Big lesion (rupture)
- Tissue factor triggers the thrombosis
- Red thrombus
- Large lipid core

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17
Q

When there’s inflammation in the arterial wall, what occurs?

A

LDLs can pass in and out of the wall in XS ∴ accumulation in arterial wall and undergoes oxidation and glycation
∴ Endothelial dysfunction (response to injury hypothesis**)

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18
Q

What’s a method to treat coronary artery disease?

A

PCI - percutaneous coronary intervention

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19
Q

Describe PCI

A

Percutaneous Coronary Intervention - a family of minimally invasive procedures used to open clogged coronary arteries e.g. stent

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20
Q

What’s a major limitation of PCI?

A

Restenosis - when a previously clogged artery that was opened with a stent or angioplasty becomes narrowed again

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21
Q

Name some drugs used to treat coronary artery disease and describe their function

A

Aspirin – irreversible inhibitor of platelet cyclo-oxygenase
Clopidogrel / ticagrelor – inhibits of the P2Y12 ADP receptor on platelets
Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis
PCSK9 inhibitors - monoclonal antibodies that inhibit PCSK9 protein in liver -> leads to improved clearance cholesterol from blood

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22
Q

What are some major cell types involved in atherogenesis?

A

Endothelium
Macrophages
Smooth muscle cells
Platelets

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23
Q

Name a method to improve the duration of stents

A

Drug-eluting stents - anti-proliferative and inhibits healing

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24
Q

What is cyclo-oxygenase required for?

A

The synthesis of Thromboxane A2 (TxA2)

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25
Q

What does TxA2 stimulate?

A

Platelet aggregation and vasoconstriction

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26
Q

What drug reduces TxA2?

A

Aspirin

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27
Q

What role does P2Y(12) ADP play?

A

Plays a central role in platelet activation

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28
Q

What can ECGs identify?

A

Arrhythmias
Myocardial ischaemia and infarction
Pericarditis
Chamber hypertrophy
Electrolyte disturbances (hyper/hypokalaemia)
Drug toxicity

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29
Q

What’s the dominant pacemaker of the body and what’s its intrinsic rate?

A

Sinoatrial node (60-100bpm)

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30
Q

What are the backup pacemakers of the body and what are their intrinsic rates?

A

Atrioventricular node (40 - 60bpm)
Ventricular cells (20 - 45bpm)

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31
Q

What is the standard calibration of an ECG machine?

A

25mm/s
0.1mV/mm

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32
Q

Describe the route of impulse conduction through the heart

A

SAN
AVN
Bundle of His
Bundle branches
Pukinje fibres

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33
Q

Describe the sections of an ECG wave

A

P wave – atrial depolarisation

QRS – ventricular depolarisation

T wave – ventricular repolarisation

The PR interval – atrial depolarisation and delay in AV junction (delay allows time for the atria to contract before the ventricles contract)

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34
Q

What are the two types of leads used in ECGs?

A

Bipolar leads & Unipolar leads

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35
Q

Describe bipolar leads

A

Two different points of the body (pos & neg)

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36
Q

Describe the Unipolar leads

A

One point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart (only require a positive electrode for monitoring)

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37
Q

Name the two types of cardiac myocytes

A
  1. Atrio-ventricular conduction system (slightly faster conduction)
  2. General cardiac myocyte
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38
Q

What are some common ECG abnormalities related to the P wave?

A

Right atrial enlargement - talkk > 2.5mm - P pulmonale

Left atrial enlargement - notched (M-shaped) - P mitrale

Long PR interval - first degree heart block

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39
Q

What are some common ECG abnormalities related to the QRS complex?

A

Depth of the S wave should NOT exceed 30mm

Pathological Q wave
= >2mm deep and >1mm wide
= >25% amplitude of the subsequent R wave

QRS axis represents the overall direction of heart’s electrical activity ∴ abnormalities of QRS axis are likely to be ventricular enlargement OR conduction blocks

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40
Q

Describe a regular ST segment

A

ST segment usually flat (isoelectric) ∴ elevation/depression by ≥1mm can be pathological

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41
Q

Describe a regular T wave

A

Should be at least 1/8 but less than 2/3 of amplitude of R

Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted

T wave amplitude RARELY exceeds 10mm

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42
Q

Describe a regular QT interval

A

Regular interval = 0.35 - 0.45s
& interval decreases when heart rate increases

Should NOT be more than half of interval between adjacent R waves

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43
Q

Describe a regular U wave

A

Small, round, symmetrical and positive in lead II w/ amplitude <2mm

U wave should be same direction as T wave

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44
Q

How do you determine heart rate from an ECG?

A

Rule of 300/1500 – regular rhythms
Count the number of big/small boxes between two QRS complexes and divide this into 300/1500 for regular rhythms.

10 second rule – irregular rhythms
Count the number of beats present on the ECG and multiply by 6.

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45
Q

Describe the quadrant approach for the QRS axis

A

The quadrant approach for the QRS axis
QRS complex in leads I and aVF
Determine if they are predominantly positive or negative
The combination should place the axis into one of the 4 quadrants below

                                     **Lead aVF**
           POS    |    Normal axis  |   LAD **Lead 1**| 
           NEG    |   RAD     |  Indeterminate Axis

LAD = left axis deviation
RAD = right axis deviation

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46
Q

finish

A
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47
Q

What is the normal systolic ejection fraction?

A

60 - 65%

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48
Q

Define cardiac failure

A

Failure to transport blood out of the heart

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49
Q

What is cardiogenic shock?

A

Severe failure to transport blood out of the heart

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50
Q

What is required for relaxation of the heart to occur?

A

Removal of calcium (energy dependent)

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51
Q

Myocardial hypertrophy can be ________

A

adaptive / physiological
e.g. athletes and pregnancy

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52
Q

What happens if you stretch capability of sarcomeres?

A

Cardiac contraction force diminishes

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53
Q

What triggers the hypertrophic response?

A

Angiotensin-2
ET-1 and insulin-like growth factor 1
TGF - beta

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54
Q

What does Left-sided cardiac failure cause?

A

Pulmonary Congestion
LV cannot pump efficiently ∴ blood backs up in veins that take blood to lungs
Pressure in these vessels ↑↑
∴ Fluid pushed into alveoli
∴ Overload of RHS of heart

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55
Q

What does Right Sided Cardiac Failure cause?

A

Venous Hypertension
High pressure in veins of legs - caused by venous insufficiency where blood leaks downwards due to effect of gravity through leaky valves
∴ Congestion

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56
Q

What does Diastolic Cardiac Failure cause?

A

Stiffer heart (LV)
This means LV cannot fill with blood fully during diastole ∴ ↓blood pumped to the body

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57
Q

Describe the heart structure up until the 5th week of gestation

A

Single chamber, divided by intra-ventricular and intra-atrial septa from endocardial cushions

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58
Q

How do the further chambers form in the heart after the 5th week of gestation?

A

Muscular intra-ventricular septum grows upwards from apex of the heart - also allows valve development to occur

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59
Q

Define congenital heart disease

A

A general term for a range of birth defects that affect the normal way the heart works

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60
Q

Name the 4 most common congenital heart disease and

A

Ventricular Septal Defect (VSD)

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61
Q

Name the 4 most common congenital heart disease and its % occurence

A

Ventricular Septal Defect (VSD) 25 - 30%
Atrial Septal Defect (ASD) 10 - 15%
Persistent/Patent Ductus Arteriosus (PDA) 10 - 20%
Fallots 4 - 10%

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62
Q

Define multifactorial inheritance

A

One child with the defect increases the probability of second child with another defect

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63
Q

Give some examples of single genes associated with multifactorial inheritance

A

Trisomy 21, Turner Syndrome (XO)

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64
Q

What is Turner Syndrome?

A

When woman only have 1 X chromosome
Results in short stature and underdeveloped ovaries

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65
Q

Give some examples of Homeobox genes associated with multifactorial inheritance

A

Infections e.g. rubella - causes congenital heart disease in baby if pregnant mother develops rubella

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66
Q

Define a cardiac shunt

A

A pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system

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67
Q

What are some causes of a Left-Right cardiac shunt

A

Ventricular septal defect
Atrial septal defect
Persistent ductus arteriosus
Truncus arteriosus (a single blood vessel comes out of the right and left ventricles)

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68
Q

What happens during anomalous pulmonary venous drainage?

A

Blood flow from some pulmonary veins flows into RA instead of LA ∴ some pulmonary venous flow enters into systemic venous circulation

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69
Q

What happens during hypoplastic left heart syndrome?

A

Left side of heart is not formed correctly
∴ underdeveloped LV

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70
Q

What causes a Right-Left cardiac shunt?

A

Tetralogy of Fallot
Tricuspid atresia - absence of tricuspid valve

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71
Q

What are some defects that result in NO shunt. Describe them.

A

Complete transposition of great vessels - an abnormal spatial arrangement of any of the great vessels

Coarctation - congenital narrowing of a short section of the aorta

Pulmonary stenosis - narrowing at a point from the right ventricle to the pulmonary artery causing obstruction of blood flow

Aortic stenosis - narrowing of the aortic valve opening restricting blood flow from the left ventricle to the aorta

Coronary artery origin from pulmonary artery
Ebstein malformation/anomaly - faulty tricuspid valve

Endocardial fibroelastosis - thickening within the muscular lining of the heart chambers due to an increase in the amount of supporting connective tissue, leading to cardiac hypertrophy

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72
Q

Initial Left-Right shunting is ___________

A

Inefficient

73
Q

What happens if Left-Right shunting progresses and is not repaired?

A

If progresses to Eisenmenger’s complex, this will involve right-left shunting
∴ right side cardiac failure AND right side cardiac hypertrophy

74
Q

What is patent foramen ovale?

A

A condition that occurs when the foramen ovale present before birth fails to close

75
Q

What does patent foramen ovale cause?

A

Cardiac Arrythmias
Pulmonary Hypertension
Right ventricular Hypertrophy
Cardiac Failure
Risk of infective endocarditis

76
Q

What is the ductus arteriosus?

A

A blood vessel connecting the pulmonary artery to proximal descending aorta before birth. Should occlude once baby starts breathing

77
Q

What does patent ductus arteriosus cause?

A

Left-right shunt overloads lung circulation w/ pulmonary hypertention ∴ right side cardiac failure
Causes risk of infecting endocarditis

78
Q

How can patent ductus arteriosus be treated?

A

Can be closed surgically, by catheters OR by prostaglandin inhibitors

79
Q

What are the main 4 features of Tetralogy of Fallot?

A
  1. Pulmonary stenosis
  2. Ventricular septal defect
  3. Dextroposition / Over-riding aorta (aorta straddles the VSD)
  4. Right ventricle hypertrophy
80
Q

What is pulmonary stenosis?

A

Narrowing of the valve between RV and lungs
∴ reduced blood flow

81
Q

What is ventricular septal defect?

A

Hole in the ventricular septum, causes increased blood pressure
∴ decreased blood flow

82
Q

//

A
83
Q

What is angina?

A

A symptom which occurs as a result of restricted coronary blood flow, almost exclusively secondary to atheroscelorisis.

84
Q

What are the types of angina?

A

Stable
Unstable
Prinzmetal’s
Microvascular
Crescendo

85
Q

What is Pouisuille’s Law?

A

Very small reduction in blood vessel causes large difference to blood flow

86
Q

Describe the causes of O2 supply demand mismatch

A

Impairment of blood flow by proximal arterial stenosis
Increased distal resistance e.g. LV hypertrophy
Reduced oxygen-carrying capability in blood vessel causes large difference to blood flow

87
Q

What is the flow through the vascular system determined by in a healthy system? Why?

A

Resistance of microvascular vessels
Because the resistance of the epicardial artery is negligible

88
Q

What is the total flow through the vascular system?

A

~ 3ml/s

89
Q

During exercise, in a healthy system, what happens?

A

More flow required to meet metabolic demand
∴ Microvascular resistance ↓
∴ Flow can increase up to 5x (15ml/s)

90
Q

What does epicardial disease due to the resistance of the epicardial vessel? How does the microvascular resistance respond?

A

Increases
∴ Microvascular resistance reduces so flow is maintained at 3ml/s

91
Q

What happens during exercise in a person with epicardial disease?

A

Epicardial resistance is high (due to stenosis)
∴ Microvascular resistance ↓ to increase flow

BUT at a point, microvascular resistance cannot fall any further
∴ Flow CANNOT meet metabolic demand

∴ Myocardium becomes ischaemic & pain is experienced

The only way to reverse this is to rest and reduce the demand for flow.

92
Q

Name the non-modifiable risk factors for stable angina

A

Gender
Family history
Personal history
Age

93
Q

Name the modifiable risk factors for stable angina

A

Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Sedentary lifestyle
Stress

94
Q

What is a precipitant of angina?

A

A precipitant reduces blood supply/ increases demand.

95
Q

Name the precipitants of angina that affect supply

A

Anaemia
Hypoxemia
Hypothermia
Hypovolaemia
Hypervolaemia

96
Q

Name the precipitants of angina that affect demand

A

Hypertension
Hyperthyroidism
Valvular heart disease
Tachyarrhythmia
Cold weather

97
Q

/inherited cardiac conditions

A
98
Q

What is cardiomyopathy?

A

A primary heart muscle disease, often genetic. ALL cardiomyopathies carry an arrhythmic risk.

99
Q

What is Hypertrophic cardiomyopathy (HCM) caused by?

A

Sarcomeric protein gene mutations

100
Q

List some signs and symptoms for HCM

A

Angine
Dyspnoea
Palpitations
Dizzy spells
Syncope

101
Q

What could be a feature of HCM?

A

Left ventricular outflow tract (LVOT) obstruction

102
Q

What is Dilated cardiomyopathy (DCM) caused by?

A

Cytoskeletal gene mutations

103
Q

What symptoms are associted with DCM?

A

Heart failure symptoms

104
Q

What occurs in DCM?

A

LV/RV OR 4 chamber dilation and dysfunction

105
Q

What is Arrhythmia cardiomyopathy (ARVC/ALVC) caused by?

A

Desmosome gene mutations

106
Q

What occurs with ARVC?

A

May be some structural change OR may diffusely involve RV and LV

107
Q

What is the main feature of arrhythmogenic cardiomyopathy?

A

Arrhythmia cardiomyopathy

108
Q

What causes Channelopathy?

A

It’s an inherited arrhythmia caused by ion channel protein gene mutations

109
Q

How is the structure effected in Channelopathy?

A

Structurally normal

110
Q

What are signs of Channelopathy?

A

Long QT / short QT
Brugada (abnormal electrical activity of the heart)

111
Q

What channels does channelopathy usually effect?*

A

Potassium, sodium or calcium channels

112
Q

What symptoms does channelopathy present with?

A

Recurrent syncope

113
Q

What can QT prolonging drugs do to people with long QT symdrome?

A

Kill them

114
Q

What is sudden cardiac death most likely due to?

A

An inherited condition
e.g. cardiomyopathy or ion channelopathy

115
Q

What do sudden arrhythmic death syndromes (SADs) usually refer to?*

A

Normal heart arrhythmia

116
Q

What is Familial hypercholestrolaemia (FH)?

A

An inherited abnormality of cholesterol metabolism (abnormal LDL protein)

117
Q

What can FH lead to?

A

Serious premature coronary and other vascular disease

118
Q

Inherited cardiac conditions are usually _______________

A

Dominantly inherited - offspring have 50% risk of inheritance
∴ family evaluation is essential

119
Q

Name some aortovascular syndromes

A

Marfan
Loeys - Dietz
Vascular Ehler Danlos (EDS)

120
Q

Describe the anatomy of pericarditis

A

2 layers which are continuous

  1. Serous visceral (single cell layer adherent to epicardium)
  2. Fibrous parietal (2mm thick layer, has fibrous attachments to fix heart in thorax)
121
Q

What is the mechanical function of the pericardium?

A

Restrains the filling volume of the heart

122
Q

Describe the properties of the pericardium

A

Similar properties to rubber - initially stretchy but becomes stiff at high tension

Sac has a small reserve volume

123
Q

Define tamponade physiology

A

Small amount of volume added to space has a dramatic effect on filling
But so does removal of a small amount

124
Q

Describe chronic pericardial effusion and its effect of filling

A

Chronic accumulation allows adaptation of the parietal pericardium
This reduces effect of diastolic filling of the chambers
∴ V Slow accumulating effusions rarely cause tamponade

125
Q

What are the main clinical indications for ACE inhibitors?

A

Hypertension
Heart failure
Diabetic nephropathy

126
Q

What are the main adverse effects for ACE inhibitors?

A

1. Related to reduced angiotensin II formation
results in ->
Hypotension, Acute renal failure, Hyperkalaemia, Teratogenic effects in pregnancy

2. Related to increased kinin production
results in ->
Cough, Rash, Anaphylactoid reactions

127
Q

What are the main clinical indications of ARB?

A

Hypertension
Diabetic nephropathy
Heart failure (when ACE - I contracindiated)

128
Q

What are the main adverse effects of ARB?

A

Symptomatic hypotension (esp. vol deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema

Contraindicated in pregnancy
Usually very well tolerated though

129
Q

What are the main clinical indications of CCB?

A

Hypertension
Ischaemic Heart Disease - angina
Arrhythmia (tachycardia)

130
Q

What are the three types of CCB?

A
  1. Dihydropyridines
  2. Phenylalkylamines
  3. Benzothiazepines
131
Q

Give examples of dihydropyridines

A

Nifedipine, amlodopine, felodipine, lacidipine

132
Q

Give an example of phenylalkylamines

A

Verapamil

133
Q

Give an example of Benzothiazepines

A

Diltiazem

134
Q

Give the adverse effects of CCB and what is it due to?

A
  1. Due to peripheral vasodilation (mainly dihydropyridines)
    Flushing
    Headache
    Oedema
    Palpitations
  2. Due to negatively chronotropic effects (mainly verapamil/diltiazem)
    Bradychardia
    Atrioventricular block
  3. Due to negatively inotropic effects (mainly verapamil)
    Worsening of cardiac failure
  4. Verapamil causes constipation
135
Q

What are the main clinical indications?

A

IHD
Heart failure
Arrhythmia
Hypertension

136
Q

What are the main clinical indications of Diuretics?

A

Hypertension
Heart failure

137
Q

What effect does aspirin have when taken for angina?

A

Antiplatelet effect ∴ avoids thrombosis

138
Q

Name a side effect of aspirin

A

Gastric ulceration

139
Q

How does aspirin reduce platelet aggregation?

A

COX inhibitor
∴ ↓prostaglandin synthesis (incl. TxA2)
∴ ↓platelet aggregation

140
Q

What do betablockers do when prescribed for angina?

A

Reduces force of contraction of heart

141
Q

What are the side effects of BB?

A

Fatigue
Trouble sleeping/nightmares
Bradycardia
Erectile dysfunction
Cold hands/feet

Worsens asthma, heart failure, hypotension and bradyarrhythmias !!!

142
Q

Describe how betablockers reduce the force of contractions

A

Act on B1 receptors in heart (adrenergic sympathetic pathway)

∴
↓ Heart rate
↓ LV contractility
↓ Cardiac output

143
Q

How does GTN spray reduce angina symptoms?

A

Dilates systemic veins
∴ ↓ Reduces venous return to right heart
∴ Reduces preload
∴ ↓ Workload of heart and O2 demand
ALSO dilates coronary arteries

144
Q

State the side effects of GTN spray

A

Headache immediately after use

145
Q

GTN spray is a nitrate that is a ______dilator

A

Venodilator

146
Q

CCB is a primary _____dilators

A

Arterodilators

147
Q

How do CCBs work to treat angina?

A

Dilates systemic arteries ∴ ↓ BP drop
∴ ↓ afterload on heart
∴ ↓ Energy req. to produce same cardiac output
∴ ↓ work on heart and O2 demand

148
Q

Describe the physiology of Tetralogy of Fallot

A

Stenosis of RV outflow -> RV is at a higher pressure than LV
∴ Deoxygenated blood passes from RV to LV
∴ Patients are ‘blue’

149
Q

Describe Ventricular septal defect (VSD)

A

Abnormal connection between the 2 ventricles

150
Q

Describe the physiology of Ventricular septal defects

A

↑ Pressure LV
↓ Pressure RV
∴ Blood flows from high pressure -> low pressure (not blue)
∴ Increased blood flow through lungs

151
Q

State some symptoms of VSD

A

↑↑ High pulmonary blood flow in infancy
Breathless
Poor feeding
Failure to thrive

152
Q

State some clinical signs of VSD

A

Small, breathless, skinny baby
↑Resp rate
Tachycardia
Big heart on CXR
Murmur varies in intensity

153
Q

eisenmengers syndrome

A
154
Q

What is Atrial Septal Defect? (ASD)

A

An abnormal connection between two atria

155
Q

Describe the physiology of ASD

A

Slightly higher pressure in LA than RA
∴ Shunt is left to right (∴ not blue)
↑ Flow into R.Heart and lungs

156
Q

State some symptoms of ASD

A

↑↑ Flow through R Heart and lungs in youth
R heart dilation
Shortness of breath on exertion
↑ Chest infections

157
Q

State some clinical signs of ASD

A

Pulmonary flow murmur
Fixed split second heart sound (bc delayed closer of PV bc more blood to get out)
Big heart and pulmonary arteries on CXR

158
Q

Describe a Atrio-ventricular septal defect

A

A hole in the centre of heart
Can be complete of partial
Involved ventricular septum, atrial septum & mitral and tricuspid valves

Instead of 2 AV valves, there is one big malformed valve

159
Q

What occurs with ASD (complete defect)?

A

Poor feeding / poor weight gain
Torrential pulmonary blood flow
Breathless as neonate
Needs repair or PA band in infancy

160
Q

What occurs with ASD (partial defect)?

A

Presents like a small VSD/ASD
Can present in late adulthood
May be left alone if no R heart dilation

161
Q

What occurs with patent ductus arteriousus?

A

Ductus arteriosus fails to close after birth
∴ Vessel formed connecting aorta and pulmonary artery

162
Q

What are some clinical signs of PDA?

A

Continuous murmur
If large - BIG heart, breathless
Eisenmenger’s syndrome - cyanosis

163
Q

What symptoms does PDA present?

A

Breathless
Poor feeding
Failure to thrive
Torrential flow from aorta to pulmonary arteries in infancy

164
Q

What is usually done to treat PDA?

A

Surgical closure under local anaesthetic.
(Has low risk of complications)

165
Q

Define Conn’s syndrome

A

The overproduction of aldosterone due to unilateral adrenal adenoma.

166
Q

What does Conn’s syndrome result in?

A

Sodium and water retention

167
Q

Name the causes of Hypertension and what % of cases they result in

A

85% are primary and aetiology is unknown

10% are due to overproduction of aldosterone (Conn’s syndrome)

5% are due to cases such as renal failure, drugs and rare hormone secreting tumours

168
Q

What are some drugs that cause hypertension?

A

NSAIDs
Combined oral contraceptive
Corticosteroids
Ciclosporin
Cold cures
Antidepressants
Illicit drugs e.g. cocaine, amphetamines

169
Q

Name some lifestyle causes of hypertension

A

Excessive salt and alcohol intake
Obesity

170
Q

What is the Framingham scale?

A

Framingham Coronary Heart Disease Risk Score estimates risk of heart attack in 10 years

171
Q

Name the methods of treatment for hypertension

A

CCBs
ACE inhibitors
ARBs
Thiazide diuretics

172
Q

How do CCBs work?

A

Inhibit the opening of voltage-gated calcium channels in vascular smooth muscle
∴ ↓ Calcium entering muscle
∴ ↓ Calcium available for muscle contraction

173
Q

Give an example of a CCB

A

Dihydropidines

174
Q

Describe how ACE inhibitors work

A

Prevent the generation of Angiotensin II from Angiotensin I

175
Q

Give examples of ACE inhibitors

A

Ramipril
Captopril

176
Q

Describe how ARBs work

A

Block the action of angiotensin II at peripheral angiotensin II receptors

177
Q

Which drug inhibits renin?

A

Aliskiren

178
Q

How do Thiazide diuretics work?

A

They inhibit sodium reabsorption by DCT
∴ ↓ ECF vol (which is elevated in hypertension)

179
Q

Give an example of a thiazide diuretic

A

Bendroflumethiazide

Phase 2 (24 decks)

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