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Cardiology Flashcards

1
Q

How is an MI defined?

A

Rise and/or fall in troponin with at least one value greater than the 99th percentile of the the upper limit + cardiac chest pain OR ECG changes (new ST segment change or new LBBB)

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2
Q

How is the of occlusion in an NSTEMI?

A

At least 70 percent of the luminal space

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3
Q

If over 70 percent of the intraluminal space of the coronary artery is occluded what symptoms will result?

A

Unstable angina or non st elevation MI

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4
Q

Which type of MI has less of the lumen included?

A

STEMI

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5
Q

What is a type 1 MI and how does it happen?

A

Spontaneous MI due to plaque rupture

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6
Q

What is a type 2 MI and how does it happen?

A

Ischaemic imbalance due to coronary spasm, embolism, dissection, hypotension etc

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7
Q

What is a type 3 MI and how does it happen?

A

Cardiac death to due presumed MI

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8
Q

What is a type 4a MI and how does it happen?

A

Related to PCI and shows > 5 times upper limit for troponin

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9
Q

How does a type 4b MI occur and how is it confirmed?

A

Stent thrombosis and confirmed by angiography or autopsy

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10
Q

What is type 5 MI and what is key diagnostic factor?

A

Related to CABG and over 10 times upper limit for troponin

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11
Q

What percentage of those that die due to acute myocardial infarction die before they reach hospital?

A

33 percent

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12
Q

What anatomical factors can determine infarct size?

A

Distribution of occluded artery
Proximity of coronary occlusion
Collateralised blood supply of site of occluded artery

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13
Q

What is the first line treatment in a patient complaining of chest pain in A and E?

A

ECG followed by clinical assessment

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14
Q

After ECG and clinical assessment what investigation should be done?

A

Bio markers such as troponin

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15
Q

What is the emergency treatment for STEMI?

A 
Primary PCI
Aspirin plus ticagrelor
GP IIb/IIIa inhibitor
Unfractionated or low molecular weight heparin
PPCI
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16
Q

Give examples of P2Y12 receptor antagonists?

A

Clopidogrel - slow
Prasugrel - fast
Ticagrelor - fast

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17
Q

Which P2Y12 receptor antagonists are given as pro drugs?

A

Clopidogrel and prasugrel

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18
Q

Which P2Y12 have the greatest anti platelet activities?

A

Prasugrel

Ticagrelor

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19
Q

Does a STEMI or NSTEMI give you a greater probability of dying?

A

NSTEMI

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20
Q

What is the immediate treatment in suspected NSTEMI?

A

Aspirin 300mg, fondaparinux/ UFH, ticagrelor 300mg

+- tirofiban/eptifibatide for intermediate or high risk groups

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21
Q

In low risk NSTEMI what is the second line treatment?

A

Conservative management

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22
Q

How is a low risk NSTEMI defined?

A

Less than 3 percent

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23
Q

How is an intermediate NSTEMI defined?

A

Between 3 and 6 percent

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24
Q

How is a high risk NSTEMI defined?

A

Greater than 6 percent risk

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25
Q

What is the second line treatment in intermediate or high risk STEMI?

A

Coronary angiography within 96 hours and then decide PCI or CABG

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26
Q

What are the complications following MI?

A

Heart failure
Bradyarrhythmias
Tacharrhythmias

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27
Q

What type of Post MI bradyarrhymias may occur?

A

Intermittent AVN block (Mobitz I)

Complete AVN block

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28
Q

How are Mobitz I heart block and complete AVN block treated post MI?

A

Atropine if rate is slow
Pacing rarely needed
Usually spontaneous recovery after 7 days with a good prognosis

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29
Q

How is heart failure post MI treated?

A

IV furosemide - give haemofiltration if diuretic resistant
RAAS inhibition either by ACEI/ARB and then give eplerenone
Ionotropes - noradrenaline and dobutamine
If needed give LV support device such as balloon pump or LVAD

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30
Q

How is intermittent block of both bundle branches (Mobitz II) or complete block of both bundle branches post MI treated?

A

Pacing needed

No spontaneous recovery with a poor prognosis

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31
Q

How is post MI AF treated?

A

Rate control via beta blocker
DC cardio version if haemodynamically compromised
+- cardio version

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32
Q

How is VT or VF post MI treated?

A

DC shock

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33
Q

When do VT or VF after MI occur?

A

In the first 24 hours - little effect on prognosis

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34
Q

How can late presenting VT/VF post MI complicate things?

A

Poor prognostic sign and predictive of sudden cardiac death within a year

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35
Q

How many people die from VF post MI pre hospital?

A

33 percent

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36
Q

How is VF pre hospital treated?

A

Defibrillator as soon as possible

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37
Q

What complication can a large MI cause?

A

Left ventricular failure - initiate reperfusion therapy ASAP

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38
Q

What two things usually cause late death post MI?

A

Recurrent ischaemic deaths - need to implement secondary prevention
Lethal arrhythmia- may need implantable defibrillator

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39
Q

What are the pharmacological agents for secondary prevention of MI?

A 
Aspirin
Station
Beta blocker
ACE I
P2Y12 receptor antagonist (not given for life)
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40
Q

In what age groups in heart failure most diagnosed in?

A

Over 65s

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41
Q

What can cause systolic dysfunction of the heart muscle?

A

Ischaemic heart disease
Pressure or volume overload such as in AS or hypertension
Cardiomyopathy

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42
Q

What does diastolic dysfunction mean?

A

Inability of the heart muscle to relax and refill?

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43
Q

What can cause diastolic dysfunction of the heart muscle?

A

Amyloid
Myocardial fibrosis
Constrictive pericarditis

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44
Q

What are the compensatory mechanisms the heart has to deal with heart failure.

A

Frank Starling - increased stretching leads to increased contraction
Hypertrophy with possible chamber dilatation
Activation of noradrenaline, RAAS, ANP

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45
Q

What type of hypertrophy does pressure overload lead to?

A

Concentric hypertrophy

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46
Q

Which type of heart remodelling does volume overload lead to?

A

Cavitary dilation that may be without thickening

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47
Q

How does hypertrophy affect the perfusion of the heart muscle?

A

Decreased capillaries leading to an increase in fibrotic tissue but there are already increased metabolic needs leading to worsening HF

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48
Q

How does pulmonary congestion and oedema occur in left sided heart failure?

A

Decreased peripheral pressure and damming of blood in pulmonary circulation causes the lungs to be congested, oedema to develop and accumulation of haemosiderin laden macrophages. These lead to dyspnoea, orthopnoea and PND

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49
Q

What is right sided heart failure usually secondary to?

A

Left ventricular failure

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50
Q

Which complications can arise from right sided heart failure?

A

Pulmonary hypertension that can cause the liver to become congested creating nutmeg liver. Portal vein pressure will also increase leading to splenomegaly and ascites.

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51
Q

What is nutmeg liver and how does it occur?

A

Blood backing up in the liver due to right sided heart failure causing pulmonary hypertension. This leads to centrilobular necrosis and fibrosis.

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52
Q

How is hypertension defined?

A

Diastolic > 90 or systolic > 140

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53
Q

What percentage of hypertension is primary?

A

95 percent

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54
Q

What percentage of hypertension is malignant?

A

5 percent

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55
Q

How is blood pressure worked out?

A

BP=COxPeriperal Resistance

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56
Q

What can affect cardiac output?

A

Blood volume
Heart rate
Contractility

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57
Q

What can alter blood volume?

A

Sodium
Mineralocorticoids
Atriopeptin

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58
Q

What can increase peripheral resistance?

A

Constrictors e.g. Angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin
Dilators e.g. Prostaglandins, kinins, NO
Local factors e.g. Autoregulation, pH, hypoxia
Neural factors, constrictors are alpha adrenergic and dilatory are beta adrenergic

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59
Q

What genetic influences may raise blood pressure?

A 
Defects in renal homeostasis
Functional vasoconstriction (may lead to increased vascular reactivity)
Defects in vascular smooth muscle growth and structure
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60
Q

How does hypertension affect small vessels?

A

Hyaline ateriosclerosis (especially kidneys)
Hyper plastic ateriosclerosis (onion skinning)
Fibrinoid necrosis in accelerated disease

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61
Q

What is cor pulmonale?

A

Right ventricular hypertrophy with right atrial hypertrophy and dilation

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62
Q

What are clinical features of cor pulmonale?

A

Thickened right ventricle (normally greater than 0.5cm)
Possibly tricuspid regurgitation
Acute or chronic

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63
Q

What is vasculitis?

A

Inflammation of the vessel walls

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64
Q

Can vasculitis be caused by infection?

A

Yes

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65
Q

How is non infectious vasculitis mediated?

A

By immune complexes such as ANCA mediated, direct antibody mediated, cell mediated, paraneoplastic or idiopathic

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66
Q

What is common to all forms of vasculitis?

A

Vessel injury with mural necrosis and haemorrhage

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67
Q

How can vasculitis be classified?

A 
On pathogenesis
Vessel size
Localised, systemic or organ restricted
Can be granulomatous
Secondary ischaemia of downstream tissue
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68
Q

What is the clinical picture of polyarteritis nordosa?

A

Systemic vasculitis
Small and medium sized arteries affected
Often spares lungs
Segmental necrosing inflammation of the GI tract/renal/cardiac arteries especially
Branching sites
Leads to aneurysms, infarcts and haemorrhage
Fibrinosis becomes nodular later on in the disease
Lesions of different ages

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69
Q

What is seen on histology with polyarteritis nodosa?

A

Transmural inflammation and fibrinoid necrosis

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70
Q

What is found in 30 percent of polyarteritis nodosa cases?

A

Hep B antigen positive

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71
Q

What further clues may point to a diagnosis of polyarteritis nodosa?

A 
Young adults
Acute/subacute/chronic
Episodic
Gangrene
Vague aches and pains
Infarcts
Hep b or c
No haematuria
No glomerular involvement
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72
Q

How is polyarteritis nodosa treated?

A

Steroids and cyclophosphamide

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73
Q

What are the features of ANCA related vasculitis?

A

Systemic/renal limited/other
85 percent of cases ANCA positive
Flu like illness
Fever, athralgia, myalgia, purpura, peripheral neuropathy, GI involvement
Possibly provoked by drugs - propylthyrouracil, penicillamine, hydrasalazine)

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74
Q

Which drugs can trigger ANCA associated vasculitis?

A

Propylthyrouracil, penicillamine, hydrasalazine

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75
Q

What are the features of Wegeners granulomatous?

A

Upper and lower respiratory tract
Ocular/ ear involvement
Necrotising granulomas
Vasculitis

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76
Q

Which antibody is present in Wegners granulomatosis?

A

cANCA usually against proteinase 3 (PR3)

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77
Q

What are clinical signs and symptoms of Wegeners granulomatosis?

A 
Sore joints
Destruction of the face
Trace of blood in the urine
Gangrene
Permanent kidney failure
Sore eyes and ears
Lung cavities and bleeds
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78
Q

Which test is positive in Wegeners granulomatosis?

A

Positive anti neutrophil cytoplasm test (cANCA)

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79
Q

How is Wegeners granulomatosis treated?

A

Aggressive immunosuppression with cyclophosphamide and steroids.

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80
Q

What is cardiomyopathy?

A

Cardiac disease resulting from a primary intrinsic myocardial abnormality - other causes, such as ischaemia, need to be excluded

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81
Q

What types of cardiomyopathy are there?

A

Idiopathic or secondary to a known cause
Dilated - ventricles enlarge
Hypertrophic - ventricles thicken and become stiff
Restrictive - walls of the ventricle become stiff but do not thicken

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82
Q

What are features of dilated cardiomyopathy?

A

Progressive cardiac dilatation and contractile dysfunction
Large heart with four chamber dilation
Valves are arteries are not significantly abnormal
Micro myocardial hypertrophy/fibrosis
May be thrombi

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83
Q

What are the causes of dilated cardiomyopathy?

A 
Idiopathic
30 percent genetic
Past myocarditis
Alcohol or other drug toxicity e.g. Doxorubicin
Pregnancy associated
Haemochromatosis
Sarcoidosis
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84
Q

What are the clinical signs of dilated cardiomyopathy?

A

Occurs at any age but especially 20-50
Progressive congestive cardiac failure
Signs of LVF and RVF
Death from heart failure or sudden cardiac death via arrhythmia

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85
Q

What is the treatment for dilated cardiomyopathy?

A

Heart transplant

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86
Q

What are the features of hypertrophic cardiomyopathy?

A

Poor diastolic filling
Often outflow obstruction
Little to no dilation
Classical disproportionate thickening of septa, especially sub aortic
Micro hypertrophy p, disarray and fibrosis

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87
Q

What is the aetiology of hypertrophic cardiomyopathy?

A

Mutation of muscle protein especially beta myosin heavy chain, this leads to poor compliance and reduced left ventricular chamber size with possible outflow obstruction
Mostly familial
Many different mutations found

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88
Q

What do people die from in dilated or hypertrophic cardiomyopathy?

A

Heart failure
Stroke
Atrial fibrillation
Sudden death from arrhythmia

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89
Q

What are the features of restrictive cardiomyopathy?

A

Primary decrease in vascular compliance
Idiopathic
Firm normal sized ventricles with dilated atria
Secondary to irradiation fibrosis, amyloid, sarcoidosis, tumour metastasis (cause found with LM)

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90
Q

What is myocarditis?

A

Inflammation causing myocardial injury

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91
Q

Which viruses can cause myocarditis?

A

Cocksackie
Enteroviruses
HIV

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92
Q

Which bacteria typically cause myocarditis?

A

Chlamidya

Rickettsiae

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93
Q

Other than viruses and bacteria, which pathogens may cause myocarditis?

A

Fungi
Protozoa
Helminths

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94
Q

What are the immunological causes of myocarditis?

A 
Post viral infection
SLE
Drug reactions
Transplant reaction
Sarcoidosis and giant cell myocarditis (more rare)
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95
Q

What is the aetiology of myocarditis?

A

Direct damage or T cell mediated injury to antigens on myocyte surface causing inflammation and myocyte necrosis

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96
Q

How might myocarditis present clinically?

A

May mimic acute infarct clinically
May lead to dilated cardiomyopathy
Arrhythmia, sudden death, fatigue, fever, chest discomfort, heart failure

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97
Q

What is the aetiology of ischaemic heart disease?

A

95 percent of cases are coronary artery atheroma
Coronary artery vasculitis
Coronary artery vasospasm

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98
Q

What is the aetiology of ischaemic heart disease due to thrombus?

A

Encrustation (rokitansky) - platelets thrombi over injured endothelium
Imbibition (Virchow) - low grade inflammation leads to increased plasma filtration
Reaction to injury (Ross and glomset) - endothelial injury with increased permeability and macrophage and smooth muscle accumulation
Monoclonal hypothesis - smooth muscle cells

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99
Q

What are the complications of ischaemic heart disease?

A 
Ulceration
Fissuring
Haemorrhage
Thrombosis
Aneurysm
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100
Q

What are the throw types of acute myocardial infarct?

A

Transmural and subendocardial

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101
Q

What is a transmutation infarct?

A

Involves whole of the ventricular wall

The underlying lesion is an atheromatous plaque that undergone fissuring and occlusive thrombosis

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102
Q

What is a subendocardial infarct?

A

Confined to the inner third or half of the myocardium and results from generalised under perfusion of the myocardium

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103
Q

If the main left coronary artery is occluded, where would the sit of the MI be?

A

Massive anterolateral MI

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104
Q

If there was an occlusion in the left anterior descending artery where would the MI be?

A

Anteroseptal MI

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105
Q

If there was an occlusion in the left circumflex artery, where the MI be?

A

Lateral MI

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106
Q

If there was an occlusion in the right coronary artery where would the MI be?

A

Posterior inferior MI

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107
Q

How does a MI appear macroscopically and on histology if it has lasted 0-12 hours?

A

No changes

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108
Q

How does an MI appear visually aft 12-24 hours?

A

Pale with blotchy discolouration

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109
Q

How does the histology appear with a MI that has lasted 12-24 hours?

A

Bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis
Intracellular oedema

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110
Q

How does a MI appear macroscopically if it has lasted 24-72hr?

A

Soft, pale and yellow

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111
Q

What is the histological appearance of an infarct lasting 24-72 hours?

A

Coagulation necrosis with loss of nuclei and strait ions, beginning of acute inflammatory response with neutrophil infiltrate

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112
Q

How does an MI macroscopically after 3-10 days

A

Soft, yellow - brown border with hyperaemic border

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113
Q

How does an MI appear histologically after 3-10 days?

A

Replacement of infarct end area with granulation tissue

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114
Q

How does an MI appear after weeks to months?

A

White fibrous scar

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115
Q

How does an MI appear histologically after weeks to months?

A

Collagenous scar tissue

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116
Q

What are the long term complications of MI?

A

Intractable heart failure
Ventricular aneurysm
Dressler’s syndrome
Recurrent MI

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117
Q

What factors may influence the severity of a PE?

A

Size of occluded vessel
No. Emboli
Adequacy of bronchial blood supply

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118
Q

What is a saddle emboli?

A

Embolus in the pulmonary trunk leading to circulatory collapse

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119
Q

Why is a small to medium sized PE not life threatening?

A

Dual blood supply protects lungs from effects of pulmonary artery obstruction

120
Q

What is angina?

A

Clinical syndrome characterised by discomfort in the chest, jaw, shoulder, back or arm. Typically aggravated by exertion or emotional stress and relieved by GTN. Angina normally occurs in patients with coronary artery disease involving at least epicardium artery.

121
Q

What is unstable angina?

A

Angina that is either severe new onset, worsening or occurring at rest

122
Q

How is unstable angina treated?

A

Combination antiplatelet therapy

PCI or CABG carries prognostic benefit

123
Q

How is stable angina treated?

A

Medically with PCI or CABG for symptom releif

124
Q

Why does chest pain occur on exertion in angina?

A

Increased myocardial oxygen demand that cannot be met as coronary blood flow cannot increase

125
Q

What can cause decreased oxygen supply to the heart?

A

Coronary artery disease
Anaemia
Hypoxia

126
Q

What can cause increase oxygen demand in ischaemic heart disease?

A

Left ventricular hypertrophy

Thyrotoxicosis

127
Q

What are modifiable risk factors relevant to angina?

A

Smoking
Blood pressure target of 130/80 or less
Hypercholesterolaemia - give statins anyway
Diabetes - importance for good glycemic control

128
Q

What clinical sign indicates hypercholesterolaemia and may point to ischaemic heart disease?

A

Xanthalasma - fatty deposits around the eyes

129
Q

How should angina be investigated?

A

Taking the clinical history and ECG into account
If estimated coronary artery disease is 61-90 percent offer invasive coronary angiograph
If estimated coronary artery disease is 30-60 percent off nuclear perfusion scan
If estimated coronary artery disease is 10-29 percent off CT calcium scoring as first line diagnostic investigation
DO NOT USE EXERCISE ECG TO DIAGNOSE OR EXCLUDE STABLE ANGINA FOR PEOPLE WITHOUT KNOWN CORONARY ARTERY DISEASE

130
Q

How should stable angina be treated?

A

Improve symptoms with sublingual GTN and beta blocker
Improve prognosis with addressing lifestyle, aspirin, statins and ACEI
IF they cannot tolerate beta blocker due to wheeze give second line therapy of CCB/nitrate/potassium channel opener/ IF channel blocker (ivabradine)

131
Q

What treatment should be considered in stable angina persists?

A

PCI or CABG after angiogram

132
Q

How is a coronary artery stent designed?

A

Metallic lattice structure

Balloon mounted scaffold

133
Q

What are physiological role of lipids?

A 
Important part of cell membranes
Helps to absorb fat soluble vitamins
Maintains membrane fluidity 
Acts as a thermal insulator and cellular metabolic regulator
Hormone synthesis 
Organ padding
134
Q

What are the sizes of cholesterol containing particles from largest to smallest?

A

Chylomicron
VLDL
LDL
HDL

135
Q

What is the role of chylomicrons?

A

To transport fats from the intestinal mucosa to the liver. In the liver the chylomicrons release triglycerides and some cholesterol becomes LDLs and free cholesterol

136
Q

What is the role of LDLs?

A

To carry fat into the body’s cells

137
Q

What is the role of HDLs?

A

HDLs carry fat and cholesterol back to the liver for excretion
HDLs can remove cholesterol from an atheroma

138
Q

What happens when oxidised LDLs get too high?

A

Atheromatous formation

139
Q

Which transport molecules are atherogenic?

A

VLDL, LDL and IDL

140
Q

Is primary or secondary hyperlidaemia more common?

141
Q

What is familial hypercholesterolaemia?

A

Autosomal dominant genetic condition caused by gene mutations in the pathway that clears LDL from the bloodstream, present from birth and may lead to early atherosclerosis and coronary artery disease. Mutation is in LDL receptor.

142
Q

What is the epidemiology around familial hypercholesterolaemia?

A

Occurs in 1 in 500 individuals
Mortality from CHD is 10x the normal population
High risk premature CHD

143
Q

What is dysbetalipoproteinaemia?

A

Results in apoE2, a binding defect form of apoE (this is normally vital in catabolism of chylomicrons and VLDLs)
Increased risk of atherosclerosis and peripheral vascular disease

144
Q

How many people does dysbetalipoproteinaemia affect?

A

1 in 10,000

145
Q

What signs can be seen in dysbetalipoproteinaemia?

A

Tuberous xanthomas and striae palmaris

146
Q

What cholesterol level is usually present in those with FH?

A

Greater than 7.5mmol/l

147
Q

What clinical signs are present in many patients with FH?

A

Tendon xanthomas
Tuberous xanthomas
Xanthaelasma of the eyes

148
Q

How is definite FH diagnosed with the Simon Boome criteria?

A

Definite FH with total cholesterol above 7.5mmol/l and LDL-C over 4.9 Plus tendon xanthoma in first or second degree relative OR identified genetic mutation for FH

149
Q

How is possible FH diagnosed with the Simon Boome criteria?

A

Total cholesterol above 7.5 and LDL-C above 4.9 and at least one of
Family history of premature CHD MI under 60 in first degree relative or under 50 in second degree relative
OR
family history of raised cholesterol in first or second degree relative (above 7.5 in an adult, above 6.7 in a child)

150
Q

Which drugs can cause hyperlidaemia?

A

Thiazides
Beta blockers
Antriretrovirals
Anti depressants

151
Q

What are the clinical categories of hyperlipidaemia?

A

Predominant hypercholesterolaemia
Predominant hypertriglyceridaemia
Mixed hyperlipidaemia

152
Q

Describe how fat can accumulate in subcutaneous tissue

A

Eruptive xanthoma - small itchy nodules that are VLDL and chylomicron associated (reversible)
Tuberous xanthomata - yellow plaques over elbows and knees - IDL induced
Xanthalasma- periorbital skin deposits - LDL associated

153
Q

What clinical sign in the eye is indicative of hyperlipidaemia?

A

Cornea arcus (seen in under 40s with FH)

154
Q

Where do tendon xanthomata tend to occur?

A

Extensor tendons

Achilles tendon

155
Q

What is the pathology of familial combined hyperlidaemia?

A

Over production of VLDL and apo B100

156
Q

Give the features of familial combined hyperlipidaemia?

A

Raised LDL and triglyceride
Reduced HDL
Autosomal dominant
No clinical features until premature coronary heart disease

157
Q

What are the features of polygenic hypercholesterolaemia?

A

Modest LDL increase due to impaired LDL clearance
Heterogenous multigene disorder
Continuous cholesterol distribution seen

158
Q

What drug can be given to lower triglycerides?

A

Omega 3 fatty acids (Omacor)

159
Q

What are symptoms of hypertension?

A

Generally asymptomatic
Nosebleeds
Headaches
Signs of end organ damage

160
Q

What are the stages of hypertension?

A

Stage 1: 140/90 and ABPM 135/85
Stage 2: 160/100 and ABPM 150/95
Stage 3: systolic above 180 or diastolic above 110
Malignant: stage 3 with signs of papilloedema and retinal haemorrhage

161
Q

How is postural hypotension diagnosed?

A

Measure BP supine or seated and stand patient for 1min, the BP should not drop by more than 20mm

162
Q

How does ABPM work?

A

Checks BP 3 times per hour in the day and 1 times per hour in the night
Done for 24 hours

163
Q

What are the stages of hypertension treatment?

A
  1. ACE inhibitor or ARB (give both in Afro Carribeans) if under 55
  2. Add CCB if Afro Carribean or over 55
  3. Diuretics
164
Q

What is the target for BP?

A

Under 80 = 140/90
Over 80 = 150/90
If end organ damage, diabetes or renal disease = 130/80

165
Q

Which blood pressure drug should be considered in pregnancy?

166
Q

What is the treatment for acute left ventricular failure?

A

Nitrate infusion
IV loop diuretics
IV diamorphine
Oxygen

167
Q

How does a nitrous infusion work?

A

Causes venous dilation so reduces preload

Does this by being metabolised and releasing nitric oxide which increase cGMP that activates protein kinase G

168
Q

Give examples of lop diuretics

A

Bumetanide

Furosemide

169
Q

How do loop diuretics work?

A

Inhibit transport of NaCl from ascending loop of Henle into interstitial fluid by acting on the Cl binding site
Causes wanted sodium loss but unwanted potassium and magnesium loss

170
Q

What other effects can loop diuretics be useful for?

A

Reno dilator effect when given IV

Calcium loss may be useful in hypercalcaemia

171
Q

What can decrease the absorption of loop diuretics?

A

Gut oedema and ascites

172
Q

Give examples of potassium sparing diuretics?

A

Amiloride

Triameterine

173
Q

Give examples of aldosterone antagonists?

A

Spironolactone

Eplerenone

174
Q

Which drug inhibits angiotensin 1?

A

ACE inhibitors

175
Q

Which drugs act on angiotensin II?

176
Q

Give examples of ACE inhibitors

A

Ramipril
Perindopril
Lisinopril

177
Q

Do ACE inhibitors improve mortality?

178
Q

What are the side effects of ACE inhibitors?

A 
Angioedema
First dose hypotension
High potassium
Improves prognosis
Dry cough
179
Q

How do ARBs work?

A

Blocks the A2 angiotensin receptor

180
Q

Do ARBs improve mortality?

181
Q

Give examples of ARBS

A

Losartan
Irbesartan
Valsartan

182
Q

What are the side effects of ARBs?

A

High potassium

First does hypotension

183
Q

How does spironolactone work?

A

Aldosterone antagonist

184
Q

Does spironolactone improve mortality?

185
Q

What are the side effects of spironolactone?

A

Gyaecomastia due to oestrogen receptor effects
High potassium
Eplerenone has less side effects

186
Q

Do beta blockers improve mortality?

187
Q

When should beta blockers be used?

A

Only if patient is stable as can cause acute left ventricular failure

188
Q

What is the mechanism of action of beta blockers?

A

Blocks actions of catecholamines

Improves diastolic function

189
Q

What treatment should be given in ischaemic heart disease?

A

Statin
Aspirin
Clopidogrel

190
Q

When is digoxin used?

A

Antiarrhymic in AF and atrial flutter

191
Q

What is the mechanism of digoxin?

A

Inhibits Na/K+ pump

192
Q

How is digoxin excreted?

A

Renally - watch out if patient is renally impaired

193
Q

What are the side effects of digoxin?

A

Does not control exercise induced tachycardia
Narrow therapeutic window
Log half life so may need loading dose
Toxicity increased by low potassium leading to arrhythmias, nausea and vomiting

194
Q

What is amiodarone used for?

A

Ventricular and atrial arrhythmias

195
Q

What are the side effects of amiodarone?

A 
Can cause bradycardia
Very long half life of 6 weeks due to protein binding
Must give loading dose
Contained iodine so hypothyroid and hyperthyroid is a risk
Pulmonary fibrosis
Hepatitis,
Photosensitive skin rashes
Corneal deposits
196
Q

Give examples of dihyropyridine CCBs

A

Amlodipine

Rifedipine

197
Q

Give examples of anti arrhythmic CCBs

A

Dilatizem

Verapamil

198
Q

How do CCBs work?

A

Block calcium channels (3 different sites) for anti anginal and anti hypertensive therapy

199
Q

What are the side effects of calcium channel blockers?

A 
Beta blockers
CCBs
Nitrates
Nicorandil (potassium channel activator)
Ivradibine - acts on sinus node to cause bradycardia
Aspirin
Statins
200
Q

Is flecanide use for rhythm control?

201
Q

In which conditions is flecanide used for?

A

Paroxysmal AF
Paroxysmal SVT
Paroxysmal VT

202
Q

What changes occur in a stenotic mitral valve?

A

Thickening of cusps

Fusion of chordae

203
Q

What can cause mitral stenosis?

A

Rheumatic fever (most common)
Degenerative
Congenital

204
Q

What can cause mitral regurgitation?

A 
Rheumatic fever
Infective endocarditis
Ischaemic heart disease
Functional
Mitral valve prolapse
Congenital
205
Q

What is the time line of right ventricular failure from mitral stenosis?

A

Mitral stenosis leading to raised left atrial pressure so the left atrium enlarges. Cephalisation occurs leading to pulmonary arterial hypertension causing increased pulmonary vessel resisitance so the right ventricle enlarges causing pulmonic regurgitation. This causes the tricuspid annulus to dilate causing tricuspid insufficiency and right ventricular failure.

206
Q

What are the symptoms of mitral valve disease?

A 
Dyspnoea on exertion and rest
Palpitations - predisposed to AF
systemic emboli
Fatigue
Chest pain
Recurrent chest infections
Haemoptysis from bronchial vein rupture, alveolar capillary rupture, PE)
Dysphasia - hoarse voice (dilated left atrium - Ortners syndrome)
Infective endocarditis
207
Q

How should mitral valve disease be assessed?

A

ECG
CXR
Transthoracic or transoesphageal echo

208
Q

What are the characteristics on auscultation of mitral stenosis?

A 
Mid diastolic murmur
Loud S1
Length of murmur indicates severity
Opening snap after S1
Best heard with patient lying on left side
209
Q

What are the characteristics on auscultation of mitral regurgitation?

A

Holosystolic from s1 to s2

Heard best at the apex and radiates to the axilla

210
Q

What may be seen on chest X-ray with tricuspid regurgitation?

A

Right atrial enlargement

211
Q

What might be seen on chest X-ray with mitral stenosis?

A

Enlarged left atrial enlargement

212
Q

How is mitral valve disease graded with echo?

A 
On valve size
Normal 4-6cm
Mild 2-2.5cm
Moderate 1-2cm
Severe is less than 1com
213
Q

What can cause acute mitral regurgitation?

A

Chord rupture and papillary rupture (+-) acute left ventricle failure

214
Q

What interventions can be done for mitral regurgitation?

A

Percutaneous balloon mitral valvotomy for mitral stenosis
Mitral clip for vertical types of mitral regurgitation
Surgical - valve replacement or repair

215
Q

What can cause aortic stenosis?

A

Degenerative
Biscuspid aortic valve
Rheumatic fever
Congenital

216
Q

What can cause aortic regurgitation?

A 
Rheumatic fever
Bicuspid aortic valve
Infective endocarditis
Syphillis aortis
Ankylosing spondylitis
Rheumatoid arthritis
217
Q

What are the symptoms of aortic valve disease?

A 
Shortness of breath due to HF
Chest pain similar to angina
Presyncope or syncope
Palpitation or conduction disease
Infective endocarditis
Sudden death
218
Q

What are the characteristics on auscultation with aortic stenosis?

A

Systolic
Harsh
Crescendo-descrescendo
Character of s2

219
Q

What are the characteristics on auscultation with aortic regurgitation?

A

Early diastolic murmur
Best heard when patient is sitting forward on full expiration
3rd or 4th intercostal space left sterna, edge or 2nd intercostal space on right edge of sternum

220
Q

What intervention can be done in aortic valve disease?

A

Percutaneous balloon valvotomy in aortic stenosis
Percutaneous transcatheter aortic valve implantation
Surgical valve replacement

221
Q

What is the most common form of tricuspid valve disease?

A

Functional tricuspid regurgitation secondary to left heart disease (infective endocarditis, rheumatic fever, carcinoid, congenital)

222
Q

What are the symptoms of tricuspid regurgitation?

A 
Right heart failure (mimics liver disease)
Raised JVP
Hepatic tenderness
Ascites
Pedal oedema
223
Q

What are the characteristics on auscultation with tricuspid regurgitation?

A

Soft inspiratory pansystolic murmur at the left eternal edge

224
Q

How is tricuspid regurgitation managed?

A

Fluid balance
Diuretics
Limited response to surgery

225
Q

What is the leading microorganism for infective endocarditis?

A

Staphylococcus aureus followed by Strep

226
Q

What are predisposing factors to infective endocarditis?

A

Valve prosthesis
Degenerative valve sclerosis
IV drug abuse
Invasive procedures

227
Q

What causes infective endocarditis with a positive blood culture (85 percent of cases)?

A

Mostly staph
Strep
Enterococci

228
Q

What causes infective endocarditis with negative blood culture due to previous antibiotics?

A

Oral strep or coagulate negative staph

229
Q

What causes an infective endocarditis that is frequently associated with a negative blood culture?

A

Usually fastidious organisms such as nutritionally variant strep, fastidious gram negative bacilli of the HACEK group

230
Q

What causes infective endocarditis with an always negative blood culture

A

Intracellular bacteria such as Coxiella burnetti, Bartunella, Chlamidya, Trophyerma whippelei (Whipples disease)

231
Q

What percentage of infective carditis cases always present with a negative blood culture?

232
Q

What is the pathophysiology of infective endocarditis?

A

Normal valve resistant to colonisation
Predisposing factors such as endothelial damage cause turbulent blood flow, electrodes, catheters, inflammation (rheumatic carditis) and degeneration in the elderly also cause it.

233
Q

What is transient tacteraemia?

A

In infective endocarditis a consequence of invasive procedures, chewing and tooth brushing (usually causes low grade disease though)

234
Q

What are major criteria in the Dukes criteria for diagnosing infective endocarditis?

A
  1. Blood culture positive - typical microorganisms consistent with infective endocarditis from two separate blood cultures (Viridians, strep, staph, HACEK, strep bovis, enterococci)
  2. Microorganisms consistent with infective endocarditis from persistently positive blood cultures either greater than 12 or less than 4 hours apart
  3. Single culture for Coxiella burnetti or phase 1 IgG antibody titre
  4. Echo showing vegetation, abscess, partial dehiscence of prosthetic valve or new valvular regurgitation
235
Q

What are minor Dukes criteria for diagnosing infective endocarditis?

A 
Predisposition
Fever over 38 degrees
Vascular phenomenon 
Immunological phenomenon 
Microbiological evidence that doesn't fit a major criteria
236
Q

How can the Dukes criteria be used to make a diagnosis of infective endocarditis?

A
  1. Pathological diagnosis with microorganisms in the tissue

2. Clinical diagnosis of 2 major/ 1 major +3 minor/5 minor criteria

237
Q

What are the clinical signs of infective endocarditis?

A

Splinter haemorrhages
Oslers nodes - immune complex deposition
Clubbling
Roths spots - retinal haemorrhages with white/pale centre

238
Q

What is a small vegetation?

A

Less than 2mm

239
Q

Is TTE or TOE more sensitive in diagnosing infective endocarditis?

A

TOE (sensitivity 90-100 percent vs 40-63 percent with TTE)

240
Q

What is the role of a cardiac CT in diagnosing infective endocarditis?

A

Look a perivalvular extent of abscess and pseudoaneurysms

241
Q

How should infective endocarditis be treated?

A

Antibiotics
Surgical intervention if haemodynamically compromised, embolisation, large vegetation, prosthetic valve
Surgery in HF, uncontrolled infection or presenting with aneurysm

242
Q

What prophylaxis is recommended for high risk patients regarding infective endocarditis?

A

Dental antibiotics for procedures requiring manipulation of the gingival or peri apical region of the teeth or perforation of the oral mucosa NOTHING ELSE!!!

243
Q

How is uncomplicated flu treated?

A

Send the patient home with supportive advice

244
Q

How is complicated flu treated?

A

If complicated or immunosupressed give oseltamivir (PO or NG) first line or zanamivir second line
Should be given within 48 hours of the onset of symptoms

245
Q

What is pharyngitis?

A

Sore throat

246
Q

How does pharyngitis present?

A

Sore throat, fever, feeling ill, tonsillar exudate, tender cervical lymph nodes
Absence of cough may point to group A strep
Tonsillar exudate and tender cervical lymph nodes may point to group A strep but 20 percent chance

247
Q

Which viruses commonly cause upper respiratory tract infection?

A 
EBV
CMV
HSV
measles
HIV
248
Q

Which bacteria commonly cause upper respiratory tract infection?

A

Group A/B/C strep
Mycoplasma pneumoniae
Nisseria gonorrhoea
Cornyebacterium diptheriae

249
Q

How is pharyngitis treated?

A

Empirically with penicillin V (clarithromycin if allergic)

250
Q

How is group A strep treated?

A

All are pencillin sensitive or erythromycin in those that are allergic

251
Q

What complication is seen when amoxicillin is given to those with EBV infection?

252
Q

How does acute otitis media normally present?

A

Child with unilateral painful ear

253
Q

Which viruses normally cause otitis media?

A

The ones normally indicated in upper respiratory tract infection

254
Q

Which bacteria normally cause otitis media?

A 
Strep pneumoniae
Haemophilus influenza
Moraxella catarrhalis
Mycoplasma pneumoniae
Strep pyogenes
255
Q

How should otitis media be treated?

A

No antibiotics unless under 2 years
Give amoxicillin/ coamoxiclav or clarithromycin if symptoms last more than 48 hours, high fevers, bilateral disease, otorrhoea

256
Q

What are the complications of otitis media?

A

Decreased hearing
Mastoiditis
Brain abscess

257
Q

What is the pathophysiology of sinusitis?

A

Obstruction from tissue swelling leading to mucus and pressure build up in the sinus cavity

258
Q

Which bacteria commonly cause sinusitis?

A

Strep pneumoniae
Haemophilus influenzae (unencapsulated)
Moraxella catarrhalis

259
Q

What treatment is advised in sinusitis?

A

Not usually needed but consider coamoxiclav or clarithromycin

260
Q

How should legionella pneumonia be treated?

A

Quinolones>macrolides>tetracyclines (+rifampicin in severe disease)

261
Q

How should mild CAP be treated?

A

Oral amoxicillin

262
Q

How should moderate CAP be treated?

A

IV benzylpenicillin + clarithromycin

263
Q

How should severe CAP be treated?

A

IV coamoxiclav + clarithromycin

264
Q

How should CAP be treated in a traveller?

A

Ceftriaxone + clarithromycin

265
Q

How is mild to moderate HAP treated?

A

Doxycycline

266
Q

How is severe HAP treated?

A

Piperacillin- tazobactam

267
Q

What are the symptoms of an exacerbation of COPD?

A

Shortness of breath
Cough
Sputum

268
Q

What can trigger an exacerbation of COPD?

A 
CCF
VTE
Aspiration
Pollution
Bacteria 
Viruses
269
Q

Which bacteria commonly cause an infective exacerbation of COPD?

A 
H.influenzae
Moraxella catarrhalis
Strep pneumoniae
Pseudomonas oeurginosa
Chlamidya pneumoniae
270
Q

What viruses can cause IECOPD?

A 
Rhinovirus
Influenza
Parainfluenza
Adenovirus
RSV
Metapneumovirus
Corona virus
271
Q

When are antibiotics effective in treated IECOPD?

A

If two of increased dyspnoea, increased sputum purulence, increased sputum amount

272
Q

What is the empirical treatment for an infective exacerbation of COPD?

A

Doxycycline or clarithromycin for 5 days

If relapse within 3 months treat with alternative

273
Q

What is empyema (complicated parapneumonic effusion)?

A

Effusion into the pleural space adjacent to bacterial pneumonia, bacteria also invade pleural space and empyema develops

274
Q

How is empyema treated?

A

Parapneumonic effusion usually resolves with treatment of pneumonia
If not drainage and give antibiotics for 2-4 weeks

275
Q

Which pathogens normally cause the infection of a normal heart valve?

A

Staph aureus
Strep pneumoniae
(Usually iatrogenic)

276
Q

Can phagocytes penetrate vegetations?

277
Q

What is the empirical treatment of endocarditis?

A

Vancomycin plus gentamicin BUT vancomycin plus meropenem if risk of gram negative sepsis
If prosthetic valve give vancomycin plus gentamycin plus rifampicin (to stop biofilm developing)

278
Q

What directed therapy is given in infective endocarditis with staph?

A

Fluxocillin 4 hourly

279
Q

What directed therapy is given in infective endocarditis with MRSA?

A

Vancomycin

280
Q

What directed therapy is given in infective endocarditis with step?

A

Benzylpenicillin 4 hourly

If resistant give vancomycin plus gentamicin

281
Q

What directed therapy is given in infective endocarditis with enterococci?

A

Amoxicillin 4hourly plus gentamicin

282
Q

What can cause high output heart failure?

A

Anaemia, thyrotoxicosis, pregnancy, thiamine deficiency (beriberi), Paget’s disease, AVM

283
Q

What is heart failure with preserved ejection fraction?

A

Objective evidence of normal systole LV function but usually evidence of diastolic dysfunction causing reduction in heart compliance resulting in compromised ventricular filling and ejection
No evidence that treatment works in the long term

284
Q

Does preload and after load decrease in CCF?

285
Q

Which nutritional deficiencies can lead to heart failure?

A

Selenium

Thiamine (beriberi)

286
Q

What are the signs and symptoms of left heart failure?

A

Pulmonary congestion - tachypnoea, fine basal inspiratory crackles, wheeze
Systemic hypoperfusion - cold clammy peripheries, feeble pulses, tachycardia, pulsus alternans
Hypotension and shock
Faint first heart sound and 3rd and 4th heart sounds

287
Q

What are the signs and symptoms of right heart failure?

A

Systemic congestion - peripheral pitting oedema, raised JVP, ascites, liver congestion, pleural effusion
Pulmonary hypoperfusion

288
Q

What is the target saturation in managing acute heart failure?

A

Above 95 percent (88-92 in chronic lung disease)

289
Q

What are the role of ionotropes in heart failure?

A

Increased force of contraction - indicated in cardiogenic shock

290
Q

Give examples of ionotropes used in heart failure?

A

Dobutamine - non selective beta 1 and 2 adrenergic receptor agonist
Milrinone/enoximone - phosphodiesterase type III inhibitor
Levosimendan - calcium channel sensitiser
Dopamine/dopexamine- DA1 receptor agonist

291
Q

What are the side effects of furosemide?

A

Low potassium/ magnesium/ calcium
Gout
Impaired glucose tolerance
Tinnitus with fast IV bolus

292
Q

What are the side effects of thiazides?

A

Low potassium (especially with metolazone), low magnesium, low sodium
High calcium
Gout
Impaired glucose tolerance

293
Q

What are side effects of ACE inhibitors?

A 
High potassium
First dose postural hypotension
AKI with flash bilateral pulmonary oedema
Cough
Angioedema
294
Q

What are the side effects of spironolactone?

A

High potassium

Gynaecomastia

295
Q

Which medications can be used instead of spironolactone in patients with gynaecomastia as a side effect?

A

Eplerenone

Amigo ride

296
Q

What are the side effects of beta blockers?

A

Nightmares

Cold peripheries

Cardiorespiratory (3 decks)

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