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Year 2 > Case 15 > Flashcards

Case 15 Flashcards

1
Q

Diastasis

A

Middle phase of diastole when initial phase of passive filling has slowed down.
Absent during exercise.

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2
Q

Mitral annulus

A

Fibrous ring attached to mitral valve leaflets

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3
Q

Arrangement of cardiac muscle fibres

A 
Subepicardial = left handed helix (clockwise)
Subendocardial = right handed helix (anticlockwise)
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4
Q

Factors which increase systolic pressure:

A

Anything which increases afterload.

Aortic stenosis, hypertension, ventricular dilatation

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5
Q

Factors which increase diastolic pressure:

A

Anything which increases preload +/- increased diastolic pressure

Hypervolaemia, increased atrial contractility, decreased HR, increased ventricular compliance

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6
Q

End diastolic pressure volume relationship

A

Passive filling curve for the ventricle

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7
Q

Steep end diastolic pressure volume relationship suggests

A

A less compliant ventricle

Pressure increasing more with every unit increase in volume

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8
Q

Steep end systolic pressure volume relationship

A

Increased contractility

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9
Q

Causes of systolic heart failure

A

Dilated cardiomyopathy
Coronary artery disease (reduced blood supply to heart)
Valve disease - regurgitation/stenosis
Arrhythmias

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10
Q

Mechanism for systolic heart failure

A

Underlying disease causing death of cardiomyocytes.
Walls become thin, ventricles are large.
Weakened heart muscle has decreased inotropy.
Stroke volume reduced.

Reduced ejection fraction

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11
Q

Mechanism for diastolic heart failure

A

Hypertrophy and stiffening of cardiac muscle due to underlying disease.
More space taken up by muscle - less space for filling.
Large muscle requires greater O2 supply which cannot be reached - fibrotic scar tissue
Increased stiffness of muscle - reduced ejection.

Preserved ejection fraction

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12
Q

Causes of diastolic heart failure

A

Chronic hypertension
Aortic stenosis
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy

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13
Q

Left Ventricular Dysfunction

A

Decreased longitudinal function.
Increased radial function.
(Heart becomes more spherical)

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14
Q

How do we increase rate of ventricular filling during exercise?

A

Increased untwisting of left ventricle causes pressure in left ventricle to fall.
Pressure gradient across mitral valve between LA and LV
Suction of blood from LA into LV

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15
Q

Why does reduced relaxation affect cardiac output?

A

Less untwisting of ventricle - Reduced suction from LA into LV during ventricular filling = Reduced stroke volume

Tension causes compression of coronary arteries - ischaemia of cardiac myocytes.

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16
Q

First-pass Gadolinium MRI

A

Used to assess myoardial perfusion

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17
Q

Symptoms of right sided heart failure

A 
Fatigue
Palpitations
Peripheral oedema
Weight gain
Raised JVP
Frequent urination at night
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18
Q

Symptoms of left sided heart failure

A 
Fatigue 
Palpitations 
Decreased urination 
Dyspnoea and coughing (worse when lying down)
Weight gain
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19
Q

Heart Failure Functional Class I

A

Breathless only on marked exercise

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20
Q

Heart Failure Functional Class II

A

Breathless on moderate exercise

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21
Q

Heart Failure Functional Class III

A

Breathless on mild exercise

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22
Q

Heart Failure Functional Class IV

A

Breathless on minimal exercise

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23
Q

Heart Failure Functional Class V

A

Breathless at rest

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24
Q

How useful is breathlessness as a symptoms in diagnosis of heart failure?

A

87% sensitive i.e. seen in a lot of patients with heart failure

51% specific i.e. seen in a lot of other conditions as well

(Orthopnoea is less sensitive but more specific)

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25
Q

First line imaging technique for suspected heart failure

A

Echocardiogram

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26
Q

Kerley lines

A

Seen when interlobular septa in the pulmonary interstitium become prominent
A sign of pulmonary oedema

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27
Q

BNP is released in response to…

A

End diastolic wall stress (excessive stretching of ventricular wall)

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28
Q

Effects of BNP

A

Decreases Na+ reabsorption, therefore decreasing H2O reabsorption.

Overall, decrease in total blood volume.

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29
Q

How useful is BNP in diagnosis of heart failure?

A

90% sensitive

65% specific

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30
Q

Clinical measurement of BNP

A

N-terminal pro-BNP

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31
Q

Most common cause of restrictive cardiomyopathy in older people

A

Amyloid

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32
Q

Biplane Simpson Technique

A

Assesses volumes i.e. determines ejection fraction

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33
Q

L wave in mitral doppler velocity graph

A

Seen in impaired relaxation, between E and A waves.

Represents continued pulmonary vein mid diastolic flow through LA into LV after EARLY (passive) filling.

(i.e. Blood travelling from pulmonary vein to LV directly since mitral valve is open)

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34
Q

Mitral Doppler Velocity : E/A < 1

A

Impaired relaxation

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35
Q

Normal mitral valve inflow pattern

A

Rapid early (passive) phase of filling, slower late phase of filling generated by atrial contraction

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36
Q

Late ventricular filling may be faster than early filling due to…

A

Impaired relaxation.

Early filling is slow due to reduced gradient between LA and LV.
Late filling higher since it is generated by atrial contraction

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37
Q

Mitral Doppler Velocity :

Features of impaired relaxation

A

Late filling greater than early filling since it is generated by contraction.
Prolonged isovolumetric relaxation time
Decreased blood velocity out of heart
Change in heart shape longitudinally
Pronounced L wave (continued mid diastolic flow between E and A)

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38
Q

Mitral Doppler Velocity :

How does a pseudonormal diastolic heart failure occur?

A

Early and late filling have increased in velocity due to higher LA and LV pressures.
Ratio of E:A appears normal

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39
Q

Mitral Doppler Velocity :

Features of restrictive diastolic heart failure?

A

Decreased mitral inflow (due to reduced press. gradient)
Short duration of ventricular filling (due to high press. in LV)
End diastolic mitral regurgitation (due to high pressure at end of diastole)
Retrograde flow from atria into pulmonary vein (not all blood can enter less compliant ventricle)

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40
Q

Secondary mitral regurgitation

A

Mitral valve is intact

Change in geometry and dysfunction of LV is causing regurgitation.

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41
Q

S2 Heart sound

A

Closure of aortic valve

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42
Q

Heaves

A

Parasternal impulse

Due to hypertrophy of right ventricle

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43
Q

Signs of tricuspid regurgitation

A

Pan systolic murmur
Raised JVP
Enlarged pulsatile liver

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44
Q

Systolic murmur

A

Starts at S1 and ends at S2

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45
Q

Causes of midsystolic murmur

A

Aortic or pulmonary valve stenosis

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46
Q

What does a midsystolic murmur sound like?

A

From S1 to S2

Starts softly, increases in intensity then decreases in intensity.

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47
Q

Causes of pansystolic murmur

A

Mitral/tricuspid regurgitation

Ventricular septal defect

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48
Q

What does a pansystolic murmur sound like?

A

From S1 to S2

Intensity is high throughout

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49
Q

Causes of diastolic murmurs

A

Aortic/Pulmonary valve regurgitation

Mitral/tricuspid valve stenosis

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50
Q

What does a diastolic murmur caused by Aortic/Pulmonary valve regurgitation sound like?

A

Begins immediately after S2 and quickly reaches maximal intensity.
Intensity then diminishes throughout diastole.

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51
Q

What does a diastolic murmur caused by Mitral/Tricuspid valve stenosis sound like?

A

Delayed beyond S2 (i.e. until AV valves open)
More intense early during diastole then decreases in intensity
Atrial contraction near the end of diastole can cause a brief increase in intensity just before S1

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52
Q

Normal Blood pressure

A

120/80

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53
Q

Blood pressure in premenopausal women

A

5-10mmHg lower than normal

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54
Q

Blood pressure at which antihypertensive treatment should be initiated

A

160/100mmHg

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55
Q

Blood pressure 140-150/90-99

A

Take into account other factors (heart and kidney problems, diabetes) prior to starting antihypertensive treatment

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56
Q

Conn’s Syndrome

A

Hyperaldosterone state

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57
Q

How does hypertension cause left ventricular hypertrophy?

A

HTN causes increased afterload.

Hypertrophy of myocytes since they must work harder during systole.

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58
Q

How does hypertension affect atherosclerosis?

A

Accelerates atherosclerosis due to wall stress

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59
Q

How does hypertension affect vascular walls?

A

Increases thickness of tunica media in muscular arteries

Hyperplasia of muscle and collagen deposition (increased stiffness).

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60
Q

How does hypertension cause renal failure?

A

Proliferation of small blood vessels in kidney.
Hypertrophic and hyaline changes in arterioles.
Sclerosis of glomeruli causes nephron to become ischaemic - undergo atrophy and fibrosis.
Eventually, kidney contracts with a finely scarred surface (Nephrosclerosis)

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61
Q

How does hypertension cause intracerebral haemorrhage?

A

Pathological changes in intracerebral vessels:

Microaneurysms of perforating arteries
Accelerated atherosclerosis
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis

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62
Q

Pathological consequences of hypertension

A 
LV hypertrophy 
Athersclerosis 
Changes in vascular walls 
Renal failure 
Intracerebral haemorrhage 
Subarachnoid haemorrhage 
Dissecting aneurysm of aorta
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63
Q

Renal Factors which increase cardiac output

A

Decrease GFR
Increase Na+ reabsorption
Activation of RAAS
Sympathetic drive

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64
Q

Renal Factors which decrease cardiac output

A

Renal production of prostaglandins (enhance GFR)

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65
Q

Renal factors which increase total peripheral resistance (vasoconstriction)

A

Sympathetic drive
Activation of RAAS
Endothelin

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66
Q

Renal factors which decrease total peripheral resistance (vasodilation)

A

Renal PGs
Renal kinins
NO
Platelet activating factor

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67
Q

How do natriuretic peptides lead to hypertension?

A

Inhibit Na+/K+ ATPase in smooth muscle cells of blood vessel walls.
Increased Na+
Inhibits Na+/Ca2+ exchanger
Increased Ca2+ in smooth muscle cell = VASOCONSTRICTION

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68
Q

Liddle’s Syndrome

A

Overexpression of Na+ channel in apical membrane of CD
Elevated Na+ reabsorption in nephron
Therefore, elevated blood pressure early in life

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69
Q

How does metabolic syndrome increase risk of hypertension?

A

Increased Na+/H+ exchanged in PCT.
(H+ excreted, Na+ reabsorbed)

i.e. abnormally high Na+ reabsorption

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70
Q

How does obesity cause hypertension?

A

High insulin, activates Na+/K+ ATPase

Increased Na+ reabsorption in PCT

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71
Q

Medications which increase risk of hypertension

A

NSAIDs
Oestrogen
Corticosteroids

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72
Q

Stage 1 Hypertension

A

Clinic BP > 140/90

Daytime BP > 135/85

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73
Q

Stage 2 Hypertension

A

Clinic BP > 160/100

Daytime BP > 150/95

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74
Q

Stage 3 Hypertension

A

Clinic BP
Systolic > 180
Diastolic > 110

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75
Q

Investigations using urinalysis in hypertension

A

Protein
Albumin:Creatinine ratio
Haematuria

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76
Q

Blood tests used in investigation of hypertension

A 
Glucose
Electrolytes 
Creatinine 
estimated GFR
Total and HDL cholesterol
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77
Q

Grade 1 Hypertensive retinopathy

A

Tortuosity of retinal veins (silver wiring)

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78
Q

Grade 2 Hypertensive retinopathy

A 
Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
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79
Q

Grade 3 Hypertensive retinopathy

A

Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
Flame haemorrhages
Cotton wool exudates

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80
Q

Grade 4 Hypertensive retinopathy

A

Tortuosity of retinal veins (silver wiring)
Arteriovenous nipping (thickened arteries passing over veins)
Flame haemorrhages
Cotton wool exudates
Papilloedema

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81
Q

Why is a 12 lead ECG performed in investigation of hypertension?

A

To detect LV hypertrophy

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82
Q

Conn’s Syndrome

A

Primary Hyperaldosteronism

XS K+ secretion and Na+ reabsorption

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83
Q

How would you distinguish between primary and secondary hyperaldosteronism?

A

Primary - renin is low

Secondary - renin is high

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84
Q

Causes of secondary hyperaldosteronism

A

Coronary heart failure
Renal artery stenosis
Cirrhosis
Nephrotic syndrome

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85
Q

Adrenal causes of secondary hypertension

A

Conn’s Syndrome
Secondary Hyperaldosteronism - coronary heart failure, RAS, cirrhosis and nephrotic syndrome
Phaeochromocytoma

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86
Q

Phaeochromocytoma

A

Adrenal medullary tumor secreting catecholamines

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87
Q

Labile hypertension

A

Spasms of vasoconstriction and organ ischaemia.

Associated with phaeochromocytoma (XS catecholamines)

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88
Q

Renal causes of secondary hypertension

A 
Renal ischaemia (Renal vascular disease)
Renal parenchymal disease
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89
Q

When do we suspect renal artery stenosis?

A

Sudden appearance of HTN in an older person.
Resistant to usual HTN medication
Abrupt deterioration in BP control (previously stable)
Deterioration of renal function.

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90
Q

How does renal parenchymal disease cause hypertension?

A

Loss of renal vasodilator substances

Reduced GFR = salt and water retention = increased ECF volume and cardiac output

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91
Q

Macula Densa Cells release…

A

Adenosine

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92
Q

Macula densa cells are activated by…

A

Increased [Na+] in distal tubule

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93
Q

Effect of adenosine

A

Vasodilator

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94
Q

Most common cause of secondary hypertension

A

Renal parenchymal disease

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95
Q

Compensated Heart Failure

A

Stroke volume can be maintained as a result of increased preload

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96
Q

Decompensated Heart Failure

A

Volume expansion and increased preload does not bring stroke volume back up to normal

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97
Q

Why does left sided heart failure cause pulmonary hypertension ?

A

Right ventricle pumps blood into the pulmonary circulation until left ventricular preload is increased sufficiently.

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98
Q

Organ responsible for EPO production

A

Kidney

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99
Q

EPO and renal dysfunction

A

Less EPO produced by dysfunctional kidney.

Exacerbates free radical production and poor O2 supply

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100
Q

Direct effect of Angiotensin II on the heart

A

Positive inotrope

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101
Q

Most common cause of cardiomyopathy

A

Ischaemic heart disease

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102
Q

Definition of hypertrophic cardiomyopathy

A

A condition causing increased wall thickness that is not explained solely by loading conditions.

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103
Q

Epidemiology of Hypertrophic cardiomyopathy

A

Prevalence ~ 0.1%

Males affected more than females

Seen in athletes

Leading cause of death in young adults

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104
Q

Features of hypertrophic cardiomyopathy

A 
Wall thickness >15mm (normally <12mm)
Myocardial fibrosis 
Disarray (loss of uniform architecture)
Abnormal mitral valve apparatus 
Abnormal microcirculation 
Abnormal ECG
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105
Q

Most common cause of hypertrophic cardiomyopathy

A

40-60% are caused by sarcomeric protein gene mutations

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106
Q

Most sarcomeric protein mutations causing hypertrophic cardiomyopathy

A

Myosin Heavy Chain 7 (MYH7)

Myosin binding protein C3 (MYBPC3)

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107
Q

Pathophysiology of hypertrophic cardiomyopathy

A

Disarray
Myocyte hypertrophy
Abnormal coronary arteries (hypertrophy decreases luminal area) - ischaemic episodes leading to fibrosis

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108
Q

How does hypertrophic cardiomyopathy cause mitral regurgitation?

A

Septal hypertrophy causes narrowing of outflow tract.
Narrow outflow tract has a suction effect (Venturi Effect).
Pulls mitral valve leaflet towards septum - opening of mitral valve

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Perfectly
109
Q

How does hypertrophic cardiomyopathy cause atrial fibrillation?

A

Results in mitral regurgitation.
Increased pressure in right atrium.
Dilatation of atrium - a cause of AF

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110
Q

Why does hypertrophic cardiomyopathy cause angina?

A

Hypertrophic myocardium has a higher O2 demand.

Hypertrophy also compresses coronary vessels - microvascular diease

O2 supply:demand mismatch

111
Q

Symptoms of hypertrophic cardiomyopathy

A 
Angina 
Syncope 
Dyspnoea 
Sudden death
(May be asymptomatic prior to sudden death)
112
Q

Examination findings in hypertrophic cardiomyopathy

A

Pulse has a rapid upstroke/downstroke

Ejection systolic murmur (between S1 and S2)

113
Q

Sokolov-Lyon equation

A

(S wave in V2) + (R wave in V5) > 35mm

More than 35mm in left ventricular hypertrophy

114
Q

ECG changes in hypertrophic cardiomyopathy

A

LV Hypertrophy - deep S wave in V2 and tall R wave in V5

May show atrial fibrillation

ST segment changes
T wave inversion

115
Q

Cardiac MRI in hypertrophic cardiomyopathy would show:

A

Fibrotic changes - patchy, midwall
Ventricular hypertrophy
Abnormal papillary muscle insertion
Elongated anterior mitral valve leaflet (due to venturi effect)

116
Q

Ideal echocardiogram view for viewing hypertrophic cardiomyopathy

A

Parasternal short axis

117
Q

When is LV myomectomy indicated?

A

HCM
Outflow gradient > 50mmHg
NYHA III/IV
Syncope despite optimal medical therapy

118
Q

What is LV mymectomy?

A

Removal of left ventricular wall

Used in treatment of HCM

119
Q

Complications of myomectomy

A

AV block
Aortic regurgitation
Mortality (3-4% with mitral valve surgery)

120
Q

Advantage of myomectomy over Alcohol septal ablation

A

Lower risk of AV block

Septal ablation is dependent on septal branch anatomy.

Can treat mitral valve pathology at the same time

121
Q

Advantages of alcohol septal ablation over myomectomy

A

Less invasive (percutaneous)

Better recovery - better for elderly px with many comorbidities

No risk of aortic regurgitation

122
Q

When is alcohol septal ablation indicated?

A

HCM
Outflow gradient > 50mmHg
NYHA III/IV
Syncope despite optimal medical therapy

123
Q

Procedure for Alcohol Septal Ablation

A

Percutaneous route.

Small amount of pure alcohol infused into septal artery to produce a small heart attack

124
Q

Alcohol septal ablation is not recommended in cases with…

A

Concurrent mitral valve/apparatus pathology

125
Q

First line surgery for asymmetrical septal hypertrophy

A

Left ventricular myomectomy

126
Q

Second line surgery for asymmetrical septal hypertrophy

A

Pacing of RV apex - to maintain AV synchrony

127
Q

Risk Factors for Sudden Cardiac Death:

A 
Family History of SCD
Syncope 
Non sustained ventricular tachycardia 
Blood pressure response to exercise 
Septum > 30mm
128
Q

High risk of Sudden Cardiac Death:

A

> 2/5 of the following:

Family History of SCD
Syncope 
Non sustained ventricular tachycardia 
Blood pressure response to exercise 
Septum > 30mm
129
Q

Management of individuals at high risk of sudden cardiac death

A

ICD - terminates life threatening ventricular tachycardias in HCM

130
Q

Definition of Dilated Cardiomyopathy

A

A condition characterised by cardiac enlargement with reduced systolic function, absence of primary valve disease, and non significant coronary artery disease.

131
Q

Epidemiology of Dilated cardiomyopathy

A

Prevalence ~ 0.5%
Males > females
Blacks > whites (2:1)

Accounts for 1/3 of all heart failure and a majority of heart transplantation

132
Q

Myotonic Dystrophy is a cause of which cardiomyopathy?

A

Dilated cardiomyopathy

133
Q

Infective causes of dilated cardiomyopathy

A

HIV

Lyme disease

134
Q

Medical treatment of dilated cardiomyopathy

A

Diuretics
B-blockers (reduce HR)
ACE-I/ARB (reduce afterload)
Aldosterone antagonists (reduce ECF volume)

135
Q

Protein affected in Duchenne Muscular dystrophy

A

Dystrophin

136
Q

Prevention of Cardiomyopathy in Duchenne Muscular Dystrophy

A

ACE-I (perindopril)

137
Q

Anthracyclines are used in…

A

Cancers (>50% of cancers use this treatment)

138
Q

Common long term cardiac effects of Anthracyclines

A

Left ventricular systolic dysfunction occurs in 40% of patients more than a year after treatment

139
Q

How does anthracycline induce cardiomyopathy?

A

Produces potent reactive oxygen species

140
Q

Cancer drugs associated with cardiomyopathy

A

Anthracycline

Trastuzumab

141
Q

Cardiac effect of Trastuzumab

A

Reduced LV ejection fraction

142
Q

Trastuzumab (cancer treatment) must be stopped if…

A

Ejection fraction falls by more than 10% and EF is less than 50%

143
Q

Arrhythmogenic RV Cardiomyopathy

A

A condition mainly affecting the right ventricle (15% involve LV) characterised by fibro fatty infiltration, ventricular dilatation and hypertrabeculation.

144
Q

ECG for Arrhythmogenic RV Cardiomyopathy

A 
T wave inversion in V1-V3
Epsilon wave (small positive deflection buried in the end of the QRS complex)
145
Q

Ventricular trabeculation

A

Two layered myocardium, with a non compacted inner layer and a compacted outer layer
Deep recesses in communication with ventricular chamber.

146
Q

Echocardiogram for Arrhythmogenic RV Cardiomyopathy

A

RV dilatation and aneurysm

RV hypertrabeculation

147
Q

Definition of restrictive cardiomyopathy

A

Normal cardiac size
Reduced systolic function
Biatrial dilatation

Usually resulting from myocardial infiltration

148
Q

Most common cause of restrictive cardiomyopathy

A

Amyloid

149
Q

Causes of restrictive cardiomyopathy

A 
Amyloid 
Haemachromatosis
Sarcoidosis 
Radiation fibrosis
Endomyocardial fibrosis
150
Q

ECG changes in restrictive cardiomyopathy

A 
ECG may show:
Low voltage QRS
Bundle branch block
AV block
Pathological Q waves 
Atrial and ventricular dysrhythmias
151
Q

How does increased Ca2+ in cardiomyocytes cause contraction?

A

Binds to troponin, allowing tropomyosin to move away from myosin binding sites on actin.
Myosin and actin can bind - cross bridge formation

152
Q

MLCK is found in..

A

Smooth muscle cells

153
Q

How does Angiotensin II cause vasoconstriction?

A

Binds to AT1R (GPCR)
Activation of PLC which converts PIP2 to IP3 and DAG.
IP3 binds to its receptor on SR.
SR releases Ca2+
Ca2+ binds to calmodulin forming a complex which activates MLCK.
MLCK phosphorylates myosin, allowing actin and myosin to interact.

154
Q

Effects of Angiotensin II

A 
Dipsogenic (increased thirst)
Vasoconstriction
Cardiac hypertrophy 
Aldosterone secretion (Na+ reabsorption)
ADH secretion
155
Q

MOA of ramipril

A

ACE-I

156
Q

Indication for ramipril

A 
Hypertension
Cardiac failure (with LV dysfunction)
157
Q

Common ADRs of Ramipril

A 
Cough and dyspnoea 
Hyperkalaemia 
Headache/drowsiness
Weakness/fatigue
Chest pain
Sun sensitivity
158
Q

Serious ADRs of ramipril

A 
Renal Failure 
Liver dysfunction 
Allergic reaction 
Increased WBCs
Angioedema 
Pancreatitis
159
Q

Contraindications for ramipril

A

Renal Artery Stenosis
Afro-Caribbean Px (may respond less well)
Previous angioedema associated with ACE-I

160
Q

Indication for Candesartan/Losartan

A

Hypertension
Cardiac Failure

In patients intolerant to ACE-I e.g. Afro-Caribbean background

161
Q

Common ADRs of Losartan/Candesartan

A 
Cough and dyspnoea 
Hyperkalaemia 
Headache/drowsiness
Weakness/fatigue
Indigestion 
Upper respiratory tract infection
Abnormal taste
162
Q

Serious ADRs of Candesartan/Losartan

A 
Kidney/Liver failure 
Allergic reaction 
Angioedema 
Arthralgia and myalgia (joint and muscle pain)
Hyponatraemia
163
Q

Contraindications of Candesartan/Losartan

A 
Pregnancy
Renal Artery Stenosis 
Mitral/Aortic valve stenosis 
Elderly 
HCM
Hx of angioedema 
Primary aldosteronism
164
Q

Why is bisoprolol used in heart failure?

A

Reduces work load of the heart.
Decreased sympathetic activity.

Reduced slope of phase 4 of pacemaker action potential - negative chronotrope

Reduced Ca2+ to myocytes - negative inotrope

165
Q

Indications for bisoprolol

A

Cardiac failure
Hypertension
SVT

166
Q

Common ADRs of Bisoprolol

A 
Bronchospasm
Cold extremities 
Loss of libido 
Sleep disturbance 
Dizziness 
Dyspnoea 
GI disturbance
167
Q

Serious ADRs of bisprolol

A

Raynaud’s
Bronchospasm
Serious allergic reaction

(Skin conditions: Toxic epidermal necrosis, Stevens Johnsons Syndrome, Lupus erythema, Erythema multiforme)

168
Q

Contraindications of bisprolol

A 
Asthma/COPD
Cardiogenic shock
Bradycardia
Heart block
Phaeochromocytoma 
Sick sinus syndrome
169
Q

MOA of Digoxin

A

Na+/K+-ATPase inhibitor

Increased Na+ in cells inhibits Na+/Ca2+ exchange, Increased Ca2+ in cells = positive inotropy

170
Q

How does digoxin act as an antiarrhythmic agent?

A

Inhibits Na+/K+-ATPase in brainstem cardiac centre. Increased vagal stimulation of AVN. Therefore, decreased chronotropy.

171
Q

Indication for Digoxin

A

Systolic heart failure
Atrial Fibrillation
Atrial Flutter

172
Q

Age group more likely to be given digoxin for heart failure

A

Elderly

173
Q

Common ADRs of Digoxin

A 
Arrhythmias 
Blurred/Yellow vision
Nausea/Vomiting/Diarrhoea
Dizziness 
Hyperkalaemia
174
Q

Serious ADRs of Digoxin

A 
Confusion
Depression + Psychosis 
Anorexia
Gynaecomastia 
Thrombocytopenia
175
Q

Contraindications of digoxin

A

Constrictive pericarditis
HCM
Heart Block
Arrhythmias (SVT w/ accessory pathway e.g. WPW OR VT)

176
Q

MOA of furosemide/bumetanide

A

Inhibits Na+/K+/2Cl- symporter in thick ascending limb.

High concentration of ions in urine, reduces reabsorption of H2O

177
Q

Why is furosemide the strongest diuretic?

A

Acts in the ascending limb of the loop of Henle (Loop diuretic)
Acts earlier in the tubule than others, therefore more time to prevent reabsorption of water.

178
Q

Indication for furosemide

A

Oedema

Cardiac failure

179
Q

ADRs of furosemide

A

HYPOKALAEMIA

Acute urinary retention
Blood disorders 
Metabolic alkalosis 
GI disturbance 
Pancreatitis 
Postural hypotension
Increased serum cholesterol
180
Q

Contraindications of Furosemide (loop diuretics)

A 
Anuria 
Comatosed/Precomatosed 
Liver cirrhosis 
Renal failure 
Severely hypokalaemic or hyponatraemic
181
Q

Why is bendroflumethiazide a weaker diuretic than furosemide?

A

Furosemide acts in ascending limb, bendroflumethiazide acts in DCT.
Thiazide diuretics act later in the tubule, therefore have less time to inhibit H2O reabsorption.

182
Q

Indication for bendroflumethiazdie

A

Hypertension
Oedema
Cardiac failure

183
Q

Common ADRs of bendroflumethiazide

A 
Hypokalaemia 
Altered plasma lipid concentration 
Gout
Electrolyte disturbance 
GI disturbance
184
Q

Serious ADRs of bendroflumethiazide

A

Blood disorders:
Agranulocytosis and leucopenia (causes low WBCs)
Thrombocytopenia

Pancreatitis
Severe skin reactions
Visual disturbance

185
Q

Contraindications of Bendroflumethiazide

A 
Pregnancy
Addison's - hypocortisolism (Causes dehydration and electrolyte imbalance)
Hypercalcaemia
Hyponatraemia
Refractory hypokalaemia 
Symptomatic hyperuricaemia
186
Q

MOA of spironolactone

A

Competitive inhibitor of aldosterone receptor. Prevents Na+ reabsorption and K+ secretion.
Therefore, K+ sparing diuretic.

187
Q

Indications for spironolactone

A

Hypertension

Cardiac failure

188
Q

Common ADRs of spironolactone

A

Hyperkalaemia

189
Q

Serious ADRs of Spironolactone

A 
Acute renal failure 
Hepatotoxicity 
Hyperkalaemia 
Stevens Johnson Syndrome 
Thrombocytopenia
190
Q

Contraindications of Spironolactone

A

Addison’s
Anuria
Hyperkalaemia

191
Q

ECG changes in hyperkalaemia

A

Peaked T waves
Prolonged QRS (and abnormal morphology)
Eventual loss of P waves
Bradycardia (and even eventual asystole)

192
Q

ECG changes in hypokalaemia

A 
Large P waves 
prolonged PR interval 
ST depression 
T wave flattening/inversion 
U waves
193
Q

Pathogenesis of Anaemia of Chronic Disease

A

Reduced RBC survival
Reduced EPO production
Reduced response to EPO due to apoptosis of RBC precursors
Hepcidin-induced Altered iron metabolism - reduced plasma iron levels

194
Q

Why is EPO production reduced in chronic disease?

A

Cytokines released in chronic disease

195
Q

Why do many patients with heart failure have anaemia/iron deficiency?

A

Absolute iron deficiency i.e. malnourished or malabsorption
Anaemia of chronic disease (low RBCs, low EPO, altered iron metabolism)
ACE-I and ARBs result in reduced EPO synthesis.

196
Q

Obstructive sleep apnoea

A

Collapse of pharyngeal airway

Sleep test shows complete cessation of airflow for >10s, thoracoabdominal movements present

197
Q

Central Sleep Apnoea

A

Unstable feedback of respiratory control system
Sleep test shows complete cessation of airflow for >10s, thoracoabdominal movements absent (brain not stimulating respiratory muscles)

198
Q

Apnoea/Hypopnoea Index

A

Total number of apnoea/hypopnoea events per hour of sleep

199
Q

Mild Sleep Apnoea

A

5-15 apnoea/hypopnoea events per hour of sleep

200
Q

Moderate sleep apnoea

A

16-30 apnoea/hypopnoea events per hour of sleep

201
Q

Severe sleep apnoea

A

> 30 apnoea/hypopnoea events per hour of sleep

202
Q

Why are external jugular veins not used to measure JVP?

A

They become small and barely visible in hypertension.

They are superficial and prone to kinking.

203
Q

Why are left jugular veins not used to measure JVP?

A

They are not in a straight line - transmission of haemodynamic changes in right atrium is disrupted.

204
Q

Features of Jugular Venous Pulses

A

Non palpable
Obliterated by pressure on clavicle
Decreased by inspiration, increased by expiration
Usually 2 pulsations/systole
Prominent descents
More prominent with increased abdo pressure

205
Q

Measuring and calculating JVP

A

Measure vertical distance from sternal angle to vertical ruler at the level of JVP.
Add 5cm

1.3cm = 1mmHg

206
Q

How far does the right atrium lie below the sternal angle?

A

5cm

207
Q

Normal vertical distance from sternal angle to JVP

A

<4cm

208
Q

Normal vertical distance from centre of right atrium to JVP

A

<9cm

209
Q

Normal jugular venous pressure

A

<7mmHg

210
Q

JVP Waveform: A wave

A

Active atrial contraction

Ascent

211
Q

JVP Waveform: X

A

Atrial relaxation

Descent

212
Q

JVP Waveform: C

A

Bulging of tricuspid valve with ventricular contraction

Ascent

213
Q

JVP Waveform: X’

A

Downward movement of tricuspid valve with ventricular contraction
(Descent)

214
Q

JVP Waveform: V

A

Passive atrial filling

Ascent

215
Q

JVP Waveform: Y

A

Atrial emptying with opening of tricuspid valve

216
Q

JVP Waveform: H

A

Relatively slow ventricular filling - diastasis

Between bottom of y descent and beginning of A ascent.

217
Q

JVP waveform which corresponds with S1

A

A (Ascent)

218
Q

JVP waveform which comes after S1

A

X (descent)

219
Q

JVP waveform which corresponds with S2

A

V (ascent)

220
Q

JVP waveform which comes after S2

A

Y (descent)

221
Q

Cause of prominent a waves in JVP waveform

A

Tricuspid stenosis
Aortic stenosis
RV hypertrophy
Tricuspid regurgitation

222
Q

Causes of Cannon Waves in JVP waveform

A

i.e. Very prominent a waves

Caused by atrial contraction against a closed tricuspid valve due to dissociated between atrial and ventricular contraction

223
Q

Causes of absent a waves in JVP waveform

A

Atrial fibrillation Hyperkalaemia

224
Q

Cause of single wave wavepattern in JVP waveform

A

HR > 120/min

Tricuspid regurgitation

225
Q

Absent X wave in JVP waveform

A

Atrial fibrillation
Tricuspid regurgitation
Constrictive pericarditis

(Prevention of relaxation of RA)

226
Q

Prominent X wave in JVP waveform

A

Cardiac tamponade

227
Q

Prominent V wave in JVP waveform

A

RV failure
Tricuspid regurgitation
Atrial septal defect

(Increased passive atrial filling)

228
Q

Diminished V wave in JVP waveform

A

Hypovolaemia
Venodilators

(Decreased passive atrial filling)

229
Q

Rapid Y descent in JVP waveform

A

Constrictive pericarditis

230
Q

Slow Y descent in JVP waveform

A

Tricuspid stenosis
Pericardial tamponade
Tension pneumothorax

(Prevention of atrial emptying)

231
Q

Kussmaul’s sign

A

Paradoxical rise in JVP during inspiration

Caused by constrictive pericarditis, cardiac tamponade, restrictive cardiomyopathy

WHY?
Increased venous return on inspiration

232
Q

Positive test for hepatojugular reflux.

What does this indicate?

A

Pressure applied to liver for 30s. Rise in JVP for >10s

Early cardiac failure

233
Q

Cause of false positive Hepatojugular reflux test

A

Valsalva - abdominal guarding

Fluid overload

234
Q

Cause of false negative Hepatojugular reflux

A

Budd Chiari

Compression of SVC/IVC

235
Q

Frailty

A

Reduced homeostatic reserve. Small stressors have a massive impact.

236
Q

Sarcopenia

A

Loss of muscle mass with loss of muscle strength and function

237
Q

Delirium

A

Acute disorder of mental processes accompanying organic brain disease.
May be manifested by hallucination, delusions, disorientation.
Can be caused by intoxication, infection, deficiency and metabolic disorders.

238
Q

Barthel Score

A 
Activities of daily living  including:
Continence
Grooming
Feeding 
Transfer 
Dressing
Mobility 
Stairs

Out of 16

(Only useful in hospital)

239
Q

Cranial nerves which carry information on blood pressure to the brain

A

Vagus (X)

Glossopharyngeal (IX)

240
Q

Information on blood pressure from baroceptors in aortic arch are carried to the brain via…

A

Vagus nerve (X)

241
Q

Information on blood pressure from baroreceptors in carotid sinus are carried to the brain via…

A

Glossopharyngeal nerve (IX)

242
Q

NTS is located in…

A

The medulla

243
Q

Bainbridge Reflex

A

Stretch receptors in vana cava and right atrium detect an increase in blood volume.
Generate an increase in heart rate to prevent congestion of venous system

244
Q

Central chemoreceptors detect…

A

Changes in pCO2 ([H+] in CSF)

245
Q

Central chemorecpetors are located in…

A

Ventrolateral surface of medulla

246
Q

Central chemoreceptors respons (quickly/slowly)

A

Slowly

247
Q

Peripheral chemorecepetors detect…

A

low O2, high CO2 and high H+

248
Q

Peripheral chemoreceptors are located in

A

Carotid and aortic bodies

249
Q

Peripheral chemoreceptors respond (quickly/slowly)

A

Quickly

250
Q

Myogenic Mechanism in regulation of GFR

A

Constriction of preglomerular (afferent) resistance vessels.

Rapid - responds in 3-10s

251
Q

Tubuloglomerular feedback mechanism in regulation of GFR

A

Macula densa cells detect an increased [Na+] in DCT when GFR is increased.
Macula densa cells then release adenosine which causes vasoconstriction of afferent arteriole.
Therefore, GFR decreases.

252
Q

Why does adenosine not cause vasoconstriction of efferent arteriole?

A

Efferent arteriole does not have voltage gated Ca2+ channels

253
Q

Effect of SNS on GFR

A

Reduces GFR to normal level (when it has increased during exercise/haemorrhage)
Causes vasoconstriction of renal arterioles (afferent > efferent)

254
Q

Effect on GFR of Vasoconstriction of afferent arteriole

A

Decreased GFR

255
Q

Effect on GFR of Vasoconstriction of efferent arteriole

A

Increased GFR

256
Q

Effect of ANP/BNP on GFR

A

Increased due to relaxation of interglomerular mesangial cells

+ Afferent dilatation

257
Q

Effect of angiotensin II on GFR

A

Low dose = increased GFR (Efferent constriction)

High dose = decreased GFR (afferent constriction

258
Q

Aldosterone is released from

A

Zona glomerulosa of adrenal cortex

259
Q

Effect of aldosterone on sodium reabsorption

A

Increased sodium reabsorption by activation of Na+/K+-ATPase

260
Q

Effect of prostaglandins on the kidney

A

Afferent arteriole dilatation therefore GFR is increased.

Decreased Na+ reabsorption

261
Q

Effect of aldosterone on ion levels in blood

A

Increased Na+

Decreased K+ and H+

262
Q

S3 sound is generated by

A

Sudden deceleration of blood into LV from LA

Due to thin walled, dilated left ventricle with generalised decreased contraction.

263
Q

When in the cardiac cycle is S3 heard?

A

Early in diastole

264
Q

S4 sound is generated by

A

Contraction of atria against a stiffened vessel wall

265
Q

When in the cardiac cycle is S4 heard?

A

Late diastole

266
Q

Pathological causes of S4 additional heart sound

A

Hypertrophy due to: Hypertension, Aortic stenosis etc

Scar tissue formation due to coronary heart disease.

267
Q

Causes of raised JVP

A 
RV failure 
Pericardial compression 
Tricuspid stenosis 
SVC obtruction 
Circulatory overload 
Renal failure 
Atrial septal defect with mitral valve disease
268
Q

Causes of displacement of apex beat

A

Obesity - deviation of heart axis

Change in shape of heart e.g. more spherical in HF

269
Q

Cardiothoracic ratio should normally be:

A

50% (i.e. heart should take up 50% of the width of the thoracic cavity)

270
Q

Causes of poor pulses in lower limb

A

Hypertension - damage to vessel walls due to stress

Diabetes - wall damage due to hyperglycaemia

271
Q

Renal bruit is due to..

A

Turbulent flow in a renal artery

272
Q

Renal bruits are ausculated for at…

A

the periumbilical region

273
Q

Protein ++ in urine suggests

A

Kidney damage

Year 2 (17 decks)

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