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MBBS - Year 2 > Cardiology - Heart Failure and CM > Flashcards

Cardiology - Heart Failure and CM Flashcards

1
Q

What is heart failure

A

A syndrome characterised by fatigue, breathlessness and fluid retention
Caused by impaired cardiac function leading to circulatory insufficiency

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2
Q

What does dx of heart failure rely on

A

Clinical judgement based on several factors e..g symptoms and signs, severity, underlying cardiac abnormality, co-morbidities

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3
Q

Classification of heart failure based on LVEF

A

HF w/ reduced LVEF (HFrEF) - <40%
HF w/ mid-range LVEF (HFmrEF) - 40-49%
HF w/ preserved LVEF (HFpEF) - >50%

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4
Q

LVEF

A

LV ejection fraction

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5
Q

Calculating Ejection fraction

A

End diastolic volume - end systolic volume / end-diastolic volume

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6
Q

How can we measure EF

A

Echo
MRI
Myocardial perfusion scan

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7
Q

What is a lower ejection fraction associated with

A

Higher risk of mortality

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8
Q

What is a lower ejection fraction associated with

A

Higher risk of mortality

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9
Q

What does EF look at

A

How much blood is pumped out of the heart vs the volume in ventricles before

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10
Q

Normal EF

A

55%

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11
Q

What are causes of systolic heart failure

A

IHD
DCM
Myocarditis

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12
Q

Causes of diastolic heart failure

A

HCM/ HOCM
Restrictive CM
Cardiac tamponade

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13
Q

Main causes of high-output cardiac failure

A

Anaemia and pregnancy

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14
Q

Pathophysiology of heart failure

A

Initial event causing myocardial damage –> increase in wall stress –> activates multiple neuroendocrine systems causing further damage to myocardium

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15
Q

Epidemiology of heart failure

A

CAD is leading cause of HF in UK

Incidence increases w/ age - age at first px is 76 yrs, M > F

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16
Q

Prognosis of HF

A

Usually poor - 3yrs survival from dx, 40% die within 1 yr

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17
Q

Presentation of HF

A 
SOB 
Fatigue 
Orthopnoea
PND 
Swollen ankles 
Palpitations
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18
Q

NYHA clinical classification of HF

A

Class I - no limitations on activity
Class II - symptoms brought on by ordinary physical activity (mild HF)
Class III - Marked limitation of physical activity (moderate HF)
Class IV - pts have symptoms at rest (severe HF)

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19
Q

Ix in HF

A 
Standard bloods 
Other bloods
Urinalysis 
BNP & N-terminal pro BNP 
ECG 
Echo 
CXR
Cardiac imaging
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20
Q

Standard bloods for HF ix

A

FBC

Renal function

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21
Q

Extra bloods for HF ix

A

LFT
TFT
Glucose
Cholesterol

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22
Q

Urinalysis for HF ix

A

Looking for protein and glucose

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23
Q

What happens if BNP is normal in suspected HF

A

Normal BNP generally rules out HF

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24
Q

When does BNP increase

A

In ventricular stretch/ LVEDP (preload)

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25
Q

CXR in a/c HF

A

Cardiomegaly - cardiothoracic ratio > 0.5
Pulmonary oedema
Bilateral blunting of costophrenic angles

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26
Q

Mx of a/c pulmonary oedema

A

Oxygen
Diuretics
Nitrates
Morphine

Weight pt daily and take daily U&Es

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27
Q

Key imaging method for pts w/ suspected heart failure

A

Echo

Provides info on structure and function of cardiac chambers, valves and pericardium

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28
Q

When can you not do an echo

A

If the ‘window’ is poor

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29
Q

What do stress echos look for

A

Reversible ischaemia

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30
Q

What does a cardiac MR provide info about

A

Extent of fibrosis and perfusion abnormalities

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31
Q

When is a cardiac MR particularly useful

A

When echo images are poor due to obesity or COPD

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32
Q

What is usually required for cardiac MR

A

Specialist referral

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33
Q

Ddx of HF

A 
Chest diseases 
Venous insufficiency in LL 
Drug-induced ankle swelling/ fluid retention 
Angina 
Hypoalumineamia 
Intrinsic renal/ hepatic failure 
Severe thyroid disease 
Bilateral renal artery stenosis
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34
Q

General measures for managing HF

A 
Pt education 
Wt control 
Reducing salt and fluid
Smoking cessation 
Mx of co-morbidities
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35
Q

Poor prognostic factors in HF

A 
Low EF (<30%) - most important 
Low systolic BP
Coronary disease 
Raised creatine/ eGFR
Hyponatremia
DM 
Anaemia 
Arrhythmia
AF
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36
Q

Aims of therapy in HF

A

Improve life expectancy

Improve QoL

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37
Q

Aims of treatment of a/c HF

A

Improve haemodynamic & symptomatic profile

Prevent myocardial & renal damage

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38
Q

A/c HF mx

A

PODMAN

Positioning - sit up (high Fowler's position)
Oxygen 
Diuretics (loop)
Morphine 
Antiemetics 
Nitrates (IV)

May also give IV dobutamine and non-invasive ventilation (CPAP, BiPAP)

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39
Q

Diuretics therapy for HF

A

Rapid relief of congestive symptoms and fluid retention w/ loop diuretics e.g. furosemide, bumetanide
May be titrated according to need after adding new meds

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40
Q

Which HF symptoms do loop diuretics improve

A

Breathlessness

Exercise performance

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41
Q

Drugs for c/c HFrEF

A

ACEi/ ARB
BB - reduce HR
Aldosterone receptor blockers (spironolactone, eplerenone)
Sacubitril/ valsartan

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42
Q

When would you use sacubitril/valsartan in c/c HF

A

Replaces ACEi/ ARB when EF <35%

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43
Q

Other potential treatments for c/c HF

A

Ivabradine (similar to BB)
Digoxin (esp w/ AF)
Amiodarone (pts w/ arrhythmias)
Anticoags

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44
Q

Why does ACE cough develop

A

ACE inactivates bradykinin

ACE inhibition therefore leads to increase in bradykinin levels —> cough and angiodema

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45
Q

Mx of pts w/ HF due to LV systolic dysfunction

A

ACEi (titrated up to correct dose)

Treatment should be initiated before BB introduced

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46
Q

MOA of sacubutril/ valsartan

A

Neprilysin inhibits naturietic peptides and sacubutril is a neprilysin inhibitor (prevents breakdown)
Also inhibits angiotensin pathway

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47
Q

Treating HF and AF

A

Anticoag - consider for those w/ hx of thromboembolism, LV aneurysm or intracellular cardiac thrombus
Amiodarone - effective against most ventricular arrhythmias

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48
Q

Side effects of amiodarone

A

Thyroid dysfunction
Pulmonary fibrosis
Liver damage
Neuropathy

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49
Q

Surgery and devices for c/c HF

A 
Coronary revascularisation 
Transplantation 
LVAD
CRT - biventricular pacing 
Ablation for AF 
ICD 
Valve repairs if indicated
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50
Q

LVAD

A

LV Assist Device

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51
Q

Revascularisation for HF

A

PCI/ CABG may relieve ischaemic symptoms and improve mortality in heart failure pts w/ multi-vessel disease and stable angina

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52
Q

CRT for HF

A

~30% of HF pts have dyssynchronous ventricular contraction (LBBB)

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53
Q

When should CRT be considered in HF pts

A

LVSD (EF < 35%) on medical therapy and a QRS duration > 120msec

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54
Q

Heart transplant for HF

A

Limited availability of donor organs
Few UK centres
c/c immunotherapy required

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55
Q

Mechanical support for HF pts

A

Implanted mechanical pumps can provide circulatory support for short/medium term

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56
Q

When should mechanical support be considered for HF pts

A

Specialists consider this in pts w/ severe refractory symptoms, or refractory symptoms or refractory cardiogenic shock

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57
Q

What is HFpEF associated with

A

Older age and HTN/ LV hypertrophy, obesity, DM

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58
Q

Mutation seen in Marfan syndrome

A

FBN1 gene –> less functional fibrillin-1 produced

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59
Q

Inheritance pattern for Marfan syndrome

A

Autosomal dominant

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60
Q

Mutations seen in Long QT syndrome

A

KCNQ1, KCNH2 and SCN5A genes

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61
Q

Inheritance pattern for long QT syndrome

A

Autosomal dominant

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62
Q

Fabry disease

A

Results from build up of fat, globotriaosylceramide

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63
Q

What mutations cause Fabry disease

A

GLA –> absence of alpha-galactosidase A –> globotriaosylceramide isn’t broken down

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64
Q

Inheritance pattern of Fabry disease

A

X-linked

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65
Q

Mutations causing familiaal hypercholesterolaemia

A

Mutations in APO8, LDLR, LDLRAP1 or PCSK9

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66
Q

Most common cause of familial hypercholesterolaemia

A

Changes in LDLR –> less LDL receptors made –> less LDLs removed from blood stream

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67
Q

Inheritance pattern of familial hypercholesteolaemia

A

Autosomal dominant pattern

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68
Q

Genetic variation affecting mx of pts w/ CVD

A

Some pts treated w/ statins have bad ADRs e.g. myopathy associated w/ simva and a variant of gene SLCO1B1
Some pts treated w/ clopi don’t benefit as variants of cytochrome P450 can alter conversion of inactive prodrug to its active metabolite

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69
Q

Cardiomyopathy

A

Disorder in which heart muscle is structurally and functionally abnormal (in absence of other heart condns severe enough to cause the heart muscle abnormality)

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70
Q

Commonest types of cardiomyopathies

A

Hypertrophic
Dilated
Arrhythmogenic

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71
Q

What type of impairment is seen in HCM

A

Diastolic

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72
Q

What type of impairment is seen in DCM

A

Systolic

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73
Q

Commonest CM

A

HCM

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74
Q

HCM

A

Unexplained LV hypertrophy - Pattern is usually asymmetric septal hypertrophy
Most common inherited cardiac disease (autosomal dominant)
Commonest cause of sudden death in young (<35yrs) and in athletes

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75
Q

What % of HCM pts have Fhx

A

50%

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76
Q

Usual px of HCM

A

HCM can px at any age - birth to >90

Most cases are asymtpmatic

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77
Q

What % of HCM pts have an obstructive form

A

25%

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78
Q

What is HCM a disease of

A

Sarcomere

Mutated peptides incorporated into sarcomere –> impaired contractile function –> increased myocyte stress –> compensatory hypertrophy and increased fibrosis

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79
Q

Which proteins in the sarcomere are affected by HCM

A

Myosin binding protein c

B myosin heavy chain

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80
Q

Hypertrophy vs hyperplasia

A

Hypertrophy is increase in muscle cell SIZE

Hyperplasia is increase inn cell no.

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81
Q

Examination findings in HCM

A

May be normal
Double apical impulse
S4
Features of systolic outflow obstruction

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82
Q

Features of systolic outflow obstruction

A

Jerky pulse

Systolic murmur - obstruction –> murmur at LSE (dynamic - changes depending on preload and afterload), MI

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83
Q

Jerky pulse

A

Brisk carotid upstroke which suddenly stops

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84
Q

ECG in HCM

A

Typically, v abnormal showing LVH w/ strain pattern

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85
Q

Imaging tests of choice in suspected HCM

A

Echo or MRI

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86
Q

Mx of HCM

A 
General measure 
Treat symptoms 
Manage AF risk 
Assess risk of sudden death 
Family screening
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87
Q

General measures for HCM

A

Avoid competitive sports
Reassure pt w/out high-risk features
Overall prognosis is good

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88
Q

Treating symptoms of HCM

A

BB (or verapamil)

  • Decreased HR –> increased diastolic filling time
  • Decreased force of contraction —> decreased myocardial oxygen demand

Myomectomy (or septal ablation) if still symptomatic

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89
Q

Myomectomy

A

Surgeon removes small amount of thickened septal wall to widen outflow tracts from LV to aorta

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90
Q

Family screening for HCM

A

Screen by ECG and echo (and genetic testing if mutation known)

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91
Q

What is DCM characterised by

A

Enlargement of one or both ventricles w/ impaired contractile function

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92
Q

What does DCM commonly cause

A

Systolic HF

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93
Q

Pathophysiology of DCM

A

Myocyte injury –> decreased contractility –> decreased SV

This leads to increased ventricular filling pressure, LV dilatation, decreased CO

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94
Q

Types of DCM

A 
Idiopathic 
Familial 
Infl 
Toxic 
Metabolic 
Tachycardia induced 
Neuromuscular
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95
Q

Infl DCM

A

Infectious - post viral

Non-infectious - CTD, peripartum mypoathy, sarcoidosis

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96
Q

When does peripartum myopathy occur

A

Between 6th to 9th month of pregnancy

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97
Q

Toxic DCM

A

Alcohol - may be reversible by stoping alcohol intake

Chemotherapy

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98
Q

Metabolic DCM

A

Caused by hypothyroidism

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99
Q

Tachycardia-induced DCM

A

May recover fully w/ treatment of arrhythmia

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100
Q

Neuromuscular DCM

A

Muscular or myotonic dystrophy

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101
Q

Px of DCM

A

Usually presents w/ signs of CCF

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102
Q

What should you ask a DCM pt when they px

A

Fhx
Alcohol
Exposure to chemotherapeutic drugs

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103
Q

Ix for DCM

A 
Bloods 
ECG 
CXR 
Echo/ MRI 
Angiography
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104
Q

Bloods for DCM

A

U&E’s
Ca
P
TFTs

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105
Q

ECG for DCM

A

No spp features

Finding incl non-spp ST/T wave changes, conduction defects (incl BBB)

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106
Q

CXR findings for DCM

A

Cardiomegaly

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107
Q

Eco/ MRI findings for DCM

A

Enlargement of all 4 chambers w/ decreased systolic function

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108
Q

Angiography for DCM

A

To exclude IHD

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109
Q

Arrhythmogenic CM

A

An inherited heart muscle disorder characterised by replacement of RV myocardium by fibrofatty tissue

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110
Q

What is arrhythmogenic CM a disease of

A

Desmosome

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111
Q

Px of arrhythmogenic CM

A

Presents in young-middle age

May be asymptomatic or present w/ palpitation, syncope or SCD

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112
Q

SCD

A

Sudden cardiac death

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113
Q

CCF

A

Congestive cardiac failure

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114
Q

ECG for arrythmogenic CM

A

Usually abnormal, showing T wave inversion nd localised prolongation of QRS interval in R precordial leads (V1 - V3)

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115
Q

Typical arrhythmia seen in arrhythmogenic CM

A

LBBB morphology VT

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116
Q

Dx of arrhythmogenic CM

A

Combi of ECG, imaging, Fhx, biopsy

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117
Q

ICD for arrhythmogenic CM pts

A

Pts who have survived cardiac aresst
Pts who’ve had haemodynamically unstable ventricular arrhythmias
Pts who have severe cardiac impairment

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118
Q

What do desmosomes do

A

Bind muscle cells together

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119
Q

Restrictive CM

A

Rare
Due to myocardial fibrosis or infiltration (usually amyloid)
Poor prognosis

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120
Q

Pathophsyiology of restrictive CM

A

Rigid myocardium leads to increased diastolic ventricular pressure –> venous congestion

As well as decreased ventricular filling –> decreased CO

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121
Q

Myocarditis

A

Infl of heart muscle

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122
Q

Which groups can the causes of myocarditis be divided into

A

Infection
Immune mediated
Toxic

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123
Q

Infection as a cause of myocarditis

A

Viral (commonest) - coxsackie (enterovirus), adenovirus, others e.g. Chaga disease

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124
Q

What is the commonest infection causing myocarditis worldwide

A

Trypanosoma cruzi

Endemic in Central and South America

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125
Q

Immune-mediated myocarditis

A

Incl giant cell myocarditis, sarcoidosis

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126
Q

Toxic causes of myocarditis

A

Drugs (anthracycline)
Alcohol
Radiation

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127
Q

Which drugs can induce swelling

A

CCB

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128
Q

Which drugs can induce fluid retention

A

NSAIDs

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129
Q

Px of myocarditis

A

Classically presents w/ febrile illness w/ resp/ GI symptoms followed by any cardiac symptoms (fatigue, SOB, chest pain, palpitations, HF)

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130
Q

Spectrum of disease for myocarditis

A

Asymptomatic to cardiogenic shock

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131
Q

Cardiogenic shock

A

Life-threatening condn where heart suddenly cannot pump blood to meet body’s needs

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132
Q

Px of myocarditis on young pts vs older pts

A

A/c flulike px is commoner in younger pts

Older pts are more likely to px w/ DCM and HF

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133
Q

Ix for myocarditis

A

Bloods
ECG
Imaging
Endomycoardial biopsy

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134
Q

Blood results for myocarditis

A

Increased troponin

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135
Q

ECG changes in myocarditis

A

Non-spp ST/ T wave changes
May mimic MI
Arrhythmias

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136
Q

Imaging of choice for myocarditis

A

CMR

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137
Q

Endomyocardial biopsy

A

Gold standard test for myocarditis
Not performed as is invasive and hit & miss
Generally reserved for sickest pts

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138
Q

Layers of pericardium

A

Parietal pericardium

Visceral pericardium

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139
Q

Functions of pericardium

A

Anchors heart to thorax
Barrier to infection
Limits a/c dilatation of heart

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140
Q

Is the pericardium essential

A

No

Congenital absence or surgical removal aren’t associated w/ adverse effects

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141
Q

What can go wrong w/ the pericardium

A 
Infl (pericarditsi)
Fluid accumulation (effusion --> tamponade)
Fibrosis (constriction)
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142
Q

How can the causes of a/c pericarditis be split up

A

Infectious

Non-infectious

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143
Q

Infectious causes of a/c pericarditis

A 
Idiopathic/ viral - Coxsackie B, influenza, mumps, rubella (80% of cases)
Other infections (bacterial, TB, fungal)
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144
Q

Non-infectious causes of a/c pericarditis

A 
Post MI (Dressler syndrome)
Uraemia 
Malignancy from mediastinal tumours 
CTD (SLE, RhA)
Radiation induced 
Drug induced
145
Q

Examples of mediastinal tumours

A

Lung
Breasts
Lymphoma

146
Q

Clinical features of a/c pericarditis

A

Severe, sharp retrosternal/ left sided chest pain
Low grade fever is common
Sometimes tamponade can occur
Pericardial rub - evanescent

147
Q

Pain in pericarditis

A

May radiate to back and trapezius ridges
Pleuritic
Positional (worse lying down, better leaning forward)

148
Q

Pericardial rub

A

High pitches, scratchy sound heard at LSE

149
Q

Ix for pericarditis

A

Bloods
ECG
CXR
Echo

150
Q

Bloods for pericarditis

A 
Increased infl markers and WCC
Normal troponin (unless concomitant myocarditis)
151
Q

CXR in pericarditis

A

Look at heart size - cardiomegaly suggests effusion, lung lesions?

152
Q

Echo for pericarditis

A

Assessing for pericardial effusion

153
Q

ECG in a/c pericarditis

A

Concave ST elevation - widespread (no pattern)

PR segment depression

154
Q

ECG in MI vs pericarditis

A

MI - ST elevation - dome shaped and regional

Pericarditis - concave and widespread

155
Q

Mx of pericarditis

A

In most pts, idiopathic/ viral pericarditis is self-limiting w/out significant complications
Should be advised to restrict activity

156
Q

Drugs for pericarditis

A

Anti-infl drugs - high dose ibuprofen/ aspirin for 1-2/52 AND colchicine for 3/12
Low dose steroids can be used if necessary

157
Q

When would you give low dose steroids for pericarditis

A

NSAIDs & colchicine have either failed, are contraindicated or there’s an autoimmune cause e.g. SLE

158
Q

How can the causes of pericardial effusions be split up

A

Infl
Non-infl
Haemopericardium

159
Q

Infl causes of pericardial effusion

A

Any cause of pericarditis e.g staph, strep, pneumo

160
Q

Non-infl causes of pericarditis

A

Increased capillary permeability (e.g hypothyroidism)
Increased capillary hydrostatic pressure (HF)
Reduced plasma oncotic pressure (nephrotic syndrome, cirrhosis)

161
Q

Haemopericardium

A

Bleeding into pericardial sac

162
Q

Haemopericardium as a cause of pericarditis

A

Rupture of free wall post MI
Trauma
Cardiac procedure related (e.g. following angioplasty)
Dissecting aortic aneurysm

163
Q

Commonest causes of pericardial tamponade

A

Malignancy

Post-idiopathic/ viral pericarditis

164
Q

What can pericarditis cause

A

Heart failure

165
Q

In which condn is electrical alternans seen

A

In large pericardial effusion

166
Q

Electrical alternans

A

Seen in V1
Height of QRS complex varies from beat to beat due to electrical axis constantly hanging as the heart swings from side to side in pericardial effusion
One large wave then a small one and it continues

167
Q

Pathophysiology of cardiac tamponade

A

Impaired diastolic filling of ventricles leading to elevated venous pressure and impaired SV –> decreased CO

168
Q

Symptoms of cardiac tamponade

A

Medical emergency
Anxiety
SOB
Chest pain

169
Q

Signs seen in cardiac tamponade

A

Tamponade quadrad

Tachycardia
Hypotension
Elevated JVP
Pulsus paradoxus

170
Q

Pulsus paradoxus

A

Abnormally large decrease in SV, systolic bp and pulse during inspiration

171
Q

Pulsus alternans

A

Alternations of one strong beat and one weak beat, without change in cycle length

172
Q

Treatment of pericardial effusion

A

Draining fluid in heart using a large needle between paraxiphoid area and apical area - pericardiocentesis

173
Q

Constrictive pericarditis cause

A

Rare

Most commonly idiopathic (but can be due to any cause of pericarditis)

174
Q

Pathophysiology of constrictive pericarditis

A

Thickened fibrosed pericardium forms a rigid shell around heart –> inhibits normal filling of chambers

175
Q

Clinical features of constrictive pericarditis

A 
Decreased output (fatigue, hypotension, tachycardia)
Increased systemic venous pressure
176
Q

Symptoms of constrictive pericarditis

A

Increased JVP, hepatomegaly, ascites, peripheral oedema (systemic venous congestion)

177
Q

Treatment of constrictive pericarditis

A

Surgical removal of pericardium

178
Q

How does LV rupture usually present

A

W/ a/c heart failure and signs of cardiac tamponade

179
Q

What is pulsus alternans a sign of

A

LV failure

180
Q

Syncope definition

A 
Rapid onset 
Transient LOC due to global cerebral hypo perfusion 
Short duration (9 secs to 1/2 mins)
181
Q

Usual cause of syncope

A

Usually benign w/ vasovagal syncope by far being commonest cause

182
Q

What is syncope characterised by

A

Rapid onset
Short duration
Spontanoeus, complete recovery

183
Q

Causes of syncope by %

A

60% reflex
15% orthostatic
15% cardiac
10% unknown

184
Q

Types of reflex syncope

A

Situational
Vasovagal
Carotid sinus syndrome

185
Q

Common triggers of vasovagal syncope

A

Pain
Fear
Prolonged standing
Having blood taken

186
Q

Symptoms of vasovagal syncope

A

Dizziness or light-headedness
Blurred or tunnel vision
Sweating
Turning pale

187
Q

Situational syncope

A

Form of reflex syncope caused by spp triggers e.g. defecations, coughing, laughing, swallowing

188
Q

Micturition syncope

A

Fainting occurring shortly after or during urination

189
Q

Who does situational syncope usually occur in

A

Men

190
Q

Situational syncope in younger men

A

Usually benign

May be precipitated by alcohol

191
Q

What is situational syncope in older pts often associated w/

A

Comorbidities and postural hypotension

192
Q

Triggers of situational syncope

A

Genito-urinary
Resp
GI

193
Q

Carotid sinus reflex

A

Dilatation at the base of the internal carotid artery that contains baroreceptor which monitor BP

194
Q

Carotid sinus massage

A

Simple, bedside test to test the carotid sinus reflex

195
Q

Normal response to carotid sinus syndrome

A

Slight drop in HR and/or BP

196
Q

When do we see an exaggerated response to carotid sinus massage

A

Carotid sinus hypertrophy

197
Q

Carotid sinus syndrome

A

Syncope w/out warning and exaggerated CSM response w/ reproduction of syncope

198
Q

When can pacing help w/ carotid sinus syndrome

A

If CSM mainly causes decreased HR

199
Q

Who does carotid sinus syndrome usually occur in

A

Older pts (particularly men)

200
Q

Triggers

A

Head turning
Shaving
Tight collar

201
Q

Orthostatic hypotension explanation

A

Standing from a supine position causes 10-15% of our blood volume to be redistributed to the abdomen and LL thereby reducing venous return and CO
W/out, compensatory mechanisms there would be a fall in BP —> syncope

202
Q

What may orthostatic hypotension cause

A

Syncope
Dizziness on standing
Falls

203
Q

Orthostatic hypotension definition

A

Decreased SBP of >20 mmHg (or >DBP of 10 mmHg) < 3 mins of standing OR
Decreased SBP <90 mmHg on standing

204
Q

Who gets OH

A

Those with autonomic failure, hypovolaemia or taking certain drugs

205
Q

Primary autonomic failure causing OH

A

Parkinsons

206
Q

Secondary autonomic failure causing OH

A

Aging/ DM

207
Q

Hypovoleamia causing OH

A 
Antihypertensives 
Anti-anginals 
Anti-BPH
Anti-depressants 
Anti-psychotics 
Anti-Parkinsonian 
Alcohol
208
Q

Why are elderly pts most susceptible to the hypotensive effects of drugs

A

Reduced baroreceptor sensitivity
Decreased cerebral blood flow
Renal Na wasting
Impaired thirst mechanisms

209
Q

When are OH symptoms worse

A 
On standing 
In the morning 
After meals 
After exercise 
In hot environments
210
Q

When are OH symptoms better

A

When lying down or sitting

OH doesn’t occur when pt is supine

211
Q

Mx of reflex syncope and OH - everyone

A

Reassurance
Education
Lifestyle changes - increase water, decrease salt
Stop/ reduce BP lowering drugs (if possible)

212
Q

Mx of reflex syncope and OH - if still symptomatic

A

Counter pressure manœuvres

213
Q

Mx of reflex syncope and OH - in selected pts

A

Increase BP - fludrocortisone, midodrine

Pacing - selected pts w/ reflex syncope only to increase HR

214
Q

When should pacing be considered for reflex syncope pts

A

Recurrent syncope despite medical therapy
Bradycardia and systolic pauses

Will only benefit pts whose main problem is bradycardia and not low BP

215
Q

Why does pacing help w/ reflex syncope

A

Newer pacemakers can detect when the ventricle is underfilled (happens before the bradycardia has been triggered) and increase HR to try and maintain BP

216
Q

What causes cardiac syncope

A

Arrhythmia

Structural

217
Q

Arrhythmias causing cardiac syncope

A

Brady - sinus node disease, AV block

Tachycardia - VT, SVT

218
Q

Structural causes of cardiac syncope

A

Cardiac - AS, ACS, CM

Vascular - PE, aortic dissection

219
Q

Syncope red flags - symptoms

A

Exertion
Supine
No warning

220
Q

Syncope red flags - PMH

A

Structural heart diseases
CAD
Heart failure

221
Q

Syncope red flags - Fhx

A

SCD

222
Q

Syncope red flags - other symptoms

A 
Chest pain 
Palpitations 
SOB 
Abdo pain 
Headaches
223
Q

Syncope red flags - examination

A

Low BP
Slow HR
Undiagnosed systolic murmur

224
Q

Key points in syncope hx

A

6 P’s

Before - Provoking factors, posture, prodrome, PMH (DH, FH)
During - passer-by account
After - post-event

225
Q

Key points in syncope exam

A

Arrhythmia
Lying and standing BP
Carotid sinus hypersensitivity
Systolic murmur - AS, HCM

226
Q

High risk feature on ECG of syncope pts

A 
Arrhythmia 
A/c MI 
Channelopathy - Brugada, LQT1
Structural heart disease - LVH, LBBB
Conduction disease
227
Q

Ix in syncope

A

ECG
Echo - if structural heart disease is suspected
Cardiac rhythm monitoring
Tilt test

228
Q

Cardiac rhythm monitoring

A

Holter

Loop recorder

229
Q

Cardiac rhythm monitoring - Holter

A

Symptoms happening frequently, and arrhythmic cause suspected

230
Q

Cardiac rhythm monitoring - Loop recorder

A

Symptoms happening infrequently by arrhythmic cause suspected

231
Q

When is the tilt test done

A

Syncope of unknown cause where reflex syncope is suspected

232
Q

Implanatable Loop Recorder

A

Useful in dx of recurrent syncope of unknown origin

233
Q

What does implantable loop recorder dx

A

Arrhythmic syncope if it records an arrhythmia when pts has syncope
Suggests arrhythmic syncope when high risk arrhythmias are detected in an asymptomatic pt

234
Q

Tilt table test

A

Provokes reflex syncope in a lab setting
Used to confirm dx of reflex syncope in a pt w/ syncope of unknown cause (where reflex syncope is suspected but not been proven)

235
Q

What is a +ve tilt table test

A

Decrease in SBP

Decrease in HR

236
Q

Hypersensitivity

A

Exaggerated or inappropriate immune response against a foreign or self-antigen

237
Q

Hypersensitivity classification

A

Allergic
Cytotoxic
Immune Compex
Delayed

238
Q

Most common hypersensitivity

A

Allergic/ atopic hypersensitivity

Up to 40% of people in developed countries suffer from Type 1 HS

239
Q

What is allergic HS mediated by

A

IgE
Th2 cells
Mast cells
Eosinophils

240
Q

Associated diseases w/ allergic HS

A

Allergic rhinitis
Asthma
Atopic dermatitis
Anaphylaxis

241
Q

Key phases in Type I HS

A

Sensitisation
Activation
Effectors

242
Q

Sensitisation in Type I HS

A

IgE produced by B cells in response to allergen

IgE binds to FcR on mast cell & basophils

243
Q

Activation in Type 1 HS

A

Re-exposure to allergen (reaction doesn’t happen 1st time)

Allergen cross-link IgE —> immediate degranulation

244
Q

Effectors in Type I HS

A

Tissue damage - vascular permeability, mucus secretion, immune cell infiltration

245
Q

Mediators secreted during Type I HS reaction

A

Histamine
Prostaglandins and leukotrienes
IL-4
IL5

246
Q

Outcomes of mediator secretion in Type I HS reaction

A 
Vascular leak 
Broncho-constriction 
Interstinal hyper motility 
Infl 
Tissue remodelling
247
Q

Typical allergens causing asthma

A

Pollens
Dust mites
Animal dander

248
Q

Asthma allergens route of entry

A

Inhalation

249
Q

Main symptoms of asthma

A

Wheezing, dyspnoea, tachypnoea

250
Q

Allergic rhinitis

A

Hay fever

251
Q

Typical allergens causing allergic rhinitis

A

Pollen spores
Animal dander
House dust mite faeces

252
Q

Main symptoms of allergic rhinitis

A

Runny nose
Redness
Itching of eyes

253
Q

Atopic dermatitis

A

Eczema

254
Q

Typical allergens for atopic dermatitis

A

Dust mites
Pet fur
Pollen
Moulds

255
Q

Main symptoms of eczema

A

Itchy, dry, cracked, sore and red skin

256
Q

Allergic gastroenteropathy

A

Food allergies

257
Q

Main symptoms of allergic gastroenteropathy

A

Vomiting

Diarrhoea

258
Q

Main symptoms. of anaphylaxis

A

Shock
Hypotension
Wheezing

259
Q

How long does early phase of asthma last

A

15-30 mins

260
Q

How long does late phase of asthma last

A

6 - 9 hrs

261
Q

C/c infl in asthma

A

Goblet cell/ smooth muscle hyperplasia
Collagen deposition
Non-spp bronchial hyperactivity

262
Q

Systemic atopy

A

Food allergy

Anaphylaxis shock

263
Q

Urticaria

A

Hives

264
Q

Potentially fatal consequences of an anaphylaxis

A

Laryngeal oedema
Bronchial constriction
Peripheral oedema
2’ mediators cause prolonged effects later - late phase reactions

265
Q

Clinical tests for allergies

A

Skin prick tests
Blood test
Test diet or food challenge

266
Q

Skin prick test for allergies

A

Intradermal injection of antigen

30 min readout for wheal/ flare

267
Q

Blood test for allergies

A

Determine serum IgE levels (total or against spp antigens)

268
Q

Test diet for allergies

A

Pt placed on diet free from common allergen various foods added over time

269
Q

CNS symptoms of anaphylaxis

A 
Lightheadedness 
LOC 
Confusion 
Headache
Anxiety
270
Q

Treatment of Type 1 HS

A

Allergen avoidance
Desensitisation
Drugs

271
Q

Desensitisation for Type I HS

A

Repeated injection of small but increasing doses of purified allergenic over several months —> modification of Th2 response (IgG, allergen binding and less IgE)

272
Q

Drugs given for Type I HS

A

Antihistamines
Corticosteroids
Adrenaline (Epipen and Anapen)

273
Q

Which allergic condns have genetic components

A

Hayfever, asthma, and atopic dermatitis

30% chance of allergy w/ one allergic parent and 50% w/ 2 parents

274
Q

Hygiene hypothesis sand risks of allergy

A

Limiting market -life infection impeded natural immune system development and causes predisposition to allergic disease

275
Q

Type II hypersensitivity

A

Cytotoxic HS

Directed against cell surface on extracellular matrix antigens

276
Q

What do most common Type II reactions involve

A

RBCs

277
Q

How are cytotoxic HS reactions activated

A

Via IgM or IgG

278
Q

What does the complement pathway create

A

Membrane attack complex

Creates holes in membrane, cells become leaky and die

279
Q

Associated diseases of cytotoxic HS reactions

A

Autoimmune haemolytic anaemia
Myasthenia gravis
Goodpastures disease

280
Q

Incompatible blood tranfusions as a Type II HS reaction

A

Incompatible donor cells are lysed as they enter the blood stream
Intravascular haemolysis via complement
Leads to renal failure and death

281
Q

How is blood typing done

A

Haemoaggluitination

282
Q

How do we prevent incompatible blood transfusions

A

Cross-matching pt serum w/ donor RBC

283
Q

Haemolytic disease of newborn

A

Occurs in pregnancy - when Rh-ve mother is exposed from Rh+ve foetus it causes sensitisation
Subsequent pregnancies cause mother to create anti-Rh antibodies causing Rh+ve foetus and lysis of their blood cells

284
Q

Drug induced haemolytic anaemia

A

Drugs (or their metabolites) can provoke HS reactions against RBCs and platelets

Drug binds to surface protein on RBC —> Antibody binds to drug and activates complement –> complement causes haemolysis

285
Q

When do we see autoimmunity

A

IgG directed against self Ag on tissues

286
Q

Autoantigen against autoimmune haemolytic anaemia

A

Rh blood group antigens

287
Q

Autoantigen against Goodpasture’s syndrome

A

Collagen type IV (basement membrane)

288
Q

Pathogenesis of Goodpasture’s syndrome

A

Necrosis of glomeruli –> nephritis, lung haemorrhage

289
Q

Autoantigen against Myasthenia graves

A

Ach receptor

290
Q

Pathogenesis of Myasthenia gravis

A

Blocked transmission at neuronal synapses –> muscle weakness

291
Q

Glomerulonephritis

A

Group of kidney disease caused by infl in glomeruli

292
Q

Type III HS

A

Immune complex-mediated HS

Similar to Type II HS but Abs directed against soluble Ags

293
Q

How are immune complexes normally removed from the body

A

RBC binding and phagocytosis by liver/ spleen

294
Q

How do Type III HS reactions cause damage

A

Deposition and build up of complexes in tissues or walls of small blood vessels

295
Q

Examples of infections that can form immune complexes

A 
Hepatitis 
Endocarditis 
Malaria 
Leprosy 
Haemorhagic fever
296
Q

Examples of Type II HS reactions

A 
Rheumatoid disorders (SLE, Henoch-schonlein, 1' Sjorgens)
Arthus reaction 
Inhaled antigens (e.g. Farmers lung)
297
Q

Rheumatoid disorders as Type III HS reaction

A

Continued production of auto-Abs –> immune complex formation and deposition in tissues → cutaneous vasculitis

298
Q

Arthus reaction as Type III HS reaction

A

Formation of Ag/IgG complexes after intradermal Ag injections (e.g. vaccines, sting) into sensitised individuals
Deposition in dermal blood vessels –> local vasculitis

299
Q

Farmer’s lung as a Type III HS reaction

A

Repeated exposure to high Ag quantities (e.g. fungi in mouldy hay) induce IgG –> immune complex formation in lung

300
Q

Type IV HS

A

Delayed

301
Q

What are delayed HS reactions mediated by

A

Ag-spp T cels (mostly Th1)

302
Q

What happens in Type IV HS reactions

A

Ag internalised by dendritic cell —> migration to lymph node and activation of T cells/ memory cell formation (priming phase)
Re-exposure: recruitment of memory T cells causes tissue damage

303
Q

How long does the reaction take in Type IV HS

A

2-3 days

304
Q

Type IV HS - contact HS

A

Small antigens (haptens) penetrate skin and combine with tissue protein and mediate immune reactions

305
Q

Principal APCs in the skin

A

Langerhans cells

306
Q

What can cause localised eczematous skin reactions

A 
Contact with:
o	Nickel salts in jewellery 
o	Drugs 
o	Components in hair dye 
o	Chromates 
o	Chemicals in leather/ rubber 
o	Poison ivy
307
Q

What is the Mantoux test used for

A

Dx of latent TB

308
Q

What is the clinically most important form of DTH

A

Granulomatous Type IV HS

Ag persistence causing c/c T cell and macrophage activation —> granuloma formation

309
Q

When does granulomatous DTH develop

A

After 21-28 days

310
Q

What does DTH cause

A

Caesation and tissue necrosis inside granuloma

311
Q

When are granulomas seen

A

TB
Leprosy
Infection w/ parasites - Leishmaniasis, Schistosomiasis

312
Q

Signs of L side HF

A

Bibasal lung crackles
LV heave (due to hypertrophy)
Dilated LV
Displaced apex beat

313
Q

Cor pulmonale

A

R HF due to pulmonary HTN

314
Q

Which drug can cause pitting oedema

A

CCB

315
Q

Signs of R HF

A 
Pitting oedema in peripheries 
RV heave 
Raised JVP 
Ascites 
Scrotal oedema
316
Q

Why do we see fluid retention in symptoms of HF

A

RAAS

317
Q

How can AF cause HF

A

Can cause atrial failure which leads to ventricular failure

318
Q

When is S3 heard

A

HF

319
Q

Categories of disease causing HF

A 
Reduced ventricular contraction
Ventricular outflow obstruction 
Ventricular inflow obstruction 
Venticular volume overload 
Arrhythmia 
Diastolic dysfunction
320
Q

Reduced ventricular contraction causing HF

A

IHD

Myocarditis

321
Q

Ventricular outflow obstruction

A

AS

HTN

322
Q

Ventricular inflow obstruction causing HF

A

MS

323
Q

Ventricular volume overload causing HF

A

AR

MR

324
Q

Arrhythmia causing HF

A

AF

325
Q

Diastolic dysfunction causing HF

A

HCM
RCM
Cardiac tamponade

326
Q

Why might oromorph be given for c/c HF

A

Vasodilation

327
Q

Rhabdomyolysis caused by statin

A

Blood in urine but -ve for RBC

328
Q

Cardiorenal syndrome

A

Heart and renal failure together

329
Q

Which drugs can cause angiodema

A

ACEi

330
Q

Pathophysiologic difference between HFrEF and HFpEF

A

Reduced - cardiomyocytes dysfunction

Preserved - due to endothelial dysfunction

331
Q

Why do HF pts experience SOB

A

Increased filling pressure

Low CO

332
Q

What is v suggestive fo SOB being caused by HF

A

Orthopnea and PND

333
Q

Measuring cardiothoracic ratio on Xray

A

Draw midline and mark largest bulge on R and L

Choose the highest number and divide by sternal diameter of thorax

334
Q

Dx algorithm for HF

A

IF pt has risk factors, symptoms& signs and an abnormal ECG –> measure NT-pro BNP –> if elevated do an Echo

335
Q

Does furosemide have an effect on mortality

A

Yes, increases mortality as is a disease-modifying drug

336
Q

Drug therapy for systolic heart failure

A

Diuretics - furosemide 40mg od, Spiro 25mg od
Ramipril 2.5mg note
Bisoprolol 2mg od

337
Q

Class I therapies in HFrEF

A 
Quadruple therapy:
ACEi/ Entrestro 
BB
Spiro - MRA
Dapagliflozin

Add loop diuretic if signs of congestion

338
Q

When is CRT suggested for HF pt

A

After drug therapies failed and if pts has broad QRS

339
Q

When is an ICD suggested for HF pts

A

If pt has narrow QRS w/ LVH

340
Q

Why might c/c HF pts lose wt

A

Impaired absorption due to GI congestion

341
Q

Why might we see skeletal muscle atrophy in c/c HF

A

Immobility

342
Q

CXR for HF

A 
Alveolar oedema (batwing opacity)
Kerly B lines 
Cardiomegaly 
Dilated upper lobe vessels 
Pleural effusion
343
Q

Cardiac MR in HF

A

Ventricular volumes

Mass and evidence of remodelling

344
Q

Physiologic changes seen in a/c Left HF

A

Pulmonary oedema

345
Q

Physiologic changes seen in c/c Left HF

A

Reflex pulmonary vasoconstriction to protect from oedema, increased resistance and pulmonary HTN

346
Q

Physiologic changes seen in Right HF

A

Reduced RV output

Increased RA and systemic venous pressure

347
Q

What should me be done is PODMAN isn’t effective for a/c HF

A

Give inotropic agents e..g IV dobutamine

Insert intra aortic balloon pump

348
Q

When should a HF pt have ventilation

A

Non-invasive - if cardiogenic pulmonary oedema w/ severe dyspnoea
Invasive - resp failure or reduced consciousness

349
Q

Bilateral oedema ddx

A 
Congestive heart failure 
Hepatic failure 
Renal failure 
Neohrotic syndrome 
Malnutrition 
Immobility 
Drugs (NSAIDs or CCBs)
350
Q

Unilateral oedema ddx

A

DVT
Cellulitis
Ruptured Baker’s cyst
Lymphatic obstruction

351
Q

Mx of bilateral oedema

A

Diuretics - monitor renal function
If oedema is resistant, diuretic and thiazide
Spiro or amiloride (K sparing diuretics)

352
Q

When is ivabradien indicated for hF failures

A

NYHA classification ois II to IV w/ systolic dysfunction AND sinus rhythm of 75+bpm
BB contraindicates/ not tolerated
LVEF of 35% or less

353
Q

How do ACEi improve mortality and morbidity in hF

A

Reduce afterload to improve EF
Reduce preload to decrease pulmonary congestion
Improves oxygen supply
Prevents cardiac remodelling

354
Q

What is the best time to give statins

A

Nocte

Except atorva which can be taken any time

355
Q

Interaction between ACEi and ARBs

A

Hyperkalaemia
Hypotension
Renal impairment

356
Q

How doe BBs improve mortality and morbidity in HF pts

A

Reduces HR –> increasing filling time –> increase EF

Reduces cardiac remodelling

357
Q

MOA of aldosterone antagonists

A

Antagonises effects of aldosterone so more Na and water can be excreted, preventing fluid retention

358
Q

Interactions of aldosterone antagonists

A

ACEi and aldosterone antagonists = hyperkalaemia (Monitor K+ levels)

359
Q

In which condn do we see a displaced apex beat

A

LV dilatation - HF

MBBS - Year 2 (20 decks)

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