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Phase 2 mine > Cardiovascular diseases > Flashcards

Cardiovascular diseases Flashcards

1
Q

What is aortic stenosis?

A

When valve area is smaller than a quater of normal (3-4 cm^2 is normal),`

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2
Q

What are the 3 types of aortic stenosis?

A

Supravalvular, sibvalvular and valvular

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3
Q

What is the Etiology of aortic stenosis?

A

Congenital eg it was not formed correctly in the first place usually preenst in 30-50s, acquired degenerative calcification(comes in 80s), rheumatic heard disease fusions of commisures and cusps, Rare causes like paget disease prostradiation and infections

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4
Q

What is a congenital aortic stenosis?

A

bicuspid aortic valve where two of the leaflets are fused which happens in 0.5% to 2% of people.

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5
Q

What happens as aortic stenosis progresses?

A

The LV can initial compensate due to hypertrophy, later it cannot and LV function declines

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6
Q

What is the physiological evidence of aortic stenosis in terms of pressures?

A

The left ventricular pressure ends up highr than aortic pressure

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7
Q

What are the presentations of aortic senosis?

A

Dysponea on exertion due to heart failure, angina, syncope on exertion and sudden death

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8
Q

What are the pysical signs of aortic stenosis?

A

Slow rising carotid pulse(pulsus tardius) and decreased pulse amplitude (pulsus parvus), heart sounds are soft or absent second heart, S4 gallop due to left ventricular hypertrophy, ejection systolic murmur crecendo-decrescendo,

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9
Q

Can onset of symptoms help prognosis?

A

No as it is very variable

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10
Q

What is the prognosis in Aortic stenosis without treatment?

A

Depends on symptoms, angins 50% survice 5 years syncope 50% for 5 years with heart failure less than 2 years if no intervention is made

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11
Q

What is best treatment for aortic stenosis?

A

Valve replacement for severe classified stenosis

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12
Q

What investigations are needed in aortic stenosis?

A

Echocardiography, left ventricuar size and function, doppler derived gradient and valve area

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13
Q

How are aortic stenosis graded?

A

Mild moderate and seere based on area and velocity

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14
Q

What is ejection fraction?

A

the amount of blood ejected from the ventricle during systole usually between 50 and 70%`

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15
Q

What is mitral regurgitaion?

A

Backflow of blood from the left ventricle to the left atrium during stroke80% have mild which causes no problem

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16
Q

What can cause mitral regurgitation?

A

Myxomatous degeneration (nodules and thickening of valves), Ischemic MR, rheumatic heart disease and infective endocarditis

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17
Q

Which are the main forms of valvular diseases?

A

Mitral regurgitation and aortic stenosis

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18
Q

What should you be careful of with valvular dysfunction?

A

Be careful in dental processes as dont want to get infective endocarditis

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19
Q

What is TAVI?

A

transcatheter aortic valve implantation

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20
Q

What is the pathopysiology of mitral regurgitation?

A

The volume overload on the left ventricle as the regurgitation loses blod in the ventricle

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21
Q

What is the presentation of Mitral regurgitation?

A

A systolic murmur which is pansystolic murmur S3 from overload, intensity of murmer correlates with severity and displaces the apex beat to reflect hypertrophy, exertion dyspnoea, heart failure with increased haemodynamic burden pregnancy infection or atrial fibrilation

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22
Q

How long is compensatory phase for mitral regurgitation?

A

10-15 years

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23
Q

What investigations hould be done in mitral regurgiation?

A

ECG CXR ECHO to look at left atrium and ventricle size and function valve structure assessment trasnsoesophageal echocardiagram usefull for these

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24
Q

How can management of mitral regurgitation?

A

Medication for blood pressure, control of heartrate, anticoagulation in AF and fluid overload
serial echocardigraphy to monitor, IE prophylaxis, replacement with symptoms with severe regurgitation

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25
Q

What is aortic regurgitation?

A

Leakage of blood from aorta in diastole into the left ventricle due to ineffective coactation of the cusps

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26
Q

What is likely to lead to aortic regurgitation?

A

Bicuspid aortic valve, rheumatic, infective endocarditis

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27
Q

What is the pathophysiology of Aortic regurgitation?

A

Pressure and volume overload on the ventiricles, leads to dilaion of ventricle and hypertrophy

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28
Q

What are the physical findings of aortic regurgitaion?

A

Wide pulse pressure most sensitive, hyperdynamic and displasced apical imulse, hear disastolic blowing murmurs at the left sternal border decrecendo, austin flint murmur apex regurgitant jet impinfes on mitral valve causing it to vibrate also systolc ejection murmur due t increased flow across aortic valve

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29
Q

When does aortic regurgitation become symptomatic?

A

4th 5th decade often is progressive with palpitation, and dyspnoea

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30
Q

What can you do to investigate aortit regurgiation?

A

CXR enlarged cardiac silhouette and aortic rout enlargement, echocardiagram to assess the level of regurgitation

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31
Q

What are the management options for aortic rgurgitation?

A

IE prophylaxis, replacements of the valve when has symptoms or echocardiagram shows dilation of chambers

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32
Q

What is mitral stenosis?

A

quite rare, rheumatic heart disease problems, obstruction of LV inflow that prevents proper filling of diastole

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33
Q

what causes mitral stenosis?

A

Rheumatic heart disease almost all and infective endocarditis and mitral annular calcification

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34
Q

What are pathophysiological symptomes of mitral stenosis?

A

LA dilatiion and pulmonary congestion and breathlessnes, LA hypertropy and atrial fibulation and Rich heart failyre syymptoms and can get blood in lugs

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35
Q

What causes the problem with mitral stenosis?

A

lung problems embolysism

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36
Q

What are physical signsof mitral stenosis?

A

peripheral oedema, right heart fialur signs, low pitched diastolic rumble heart best lying on left side, A1 snap heard when ape are still mobile,

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37
Q

What investigations are needed for mitral stenosis

A

ECG shows LA enlarge and AF CXR LA enlargment and pulmonary congestion sometiems calcification of valve, Echo gold standard for looking at pressure and area of valve aperture

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38
Q

What is management of mitral stenosis?

A

serial endocardiography, medications dont do much just symptoms, need anticoagulation. replace the valve IE prophylaxis

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39
Q

What is the most indicative risk factor for atherosclerosis?

A

Age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history(strongest predictor)

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40
Q

Where is atherosclerosis usually?

A

Disrupted flow, peripheral and coronary arteries, focal distribution like bifurcations

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41
Q

What are the constituents of an atherosclerotic plaque?

A

Lipid, necrotic, connective tissue and a fibrous cap

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42
Q

What is the problem with astherosclerosis?

A

it can rupture the blood and cause a thrombus to form

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43
Q

What is the underlying cause of atheroclerosis?

A

Inflamation, low density lipoprotein can pass through the wall and can be oxidation and glycation and endothelial dysfunction

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44
Q

What allows leukocytes to get into the artery wall?

A

the endothelium becomes sticky and attracts white blood cells and allows entrance of the cells

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45
Q

What is c reactive protein?

A

cells produce it during inflammation of MI

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46
Q

What happens in intermediat lesions?

A

They have lots of macrophages with lipids accumulation foam cells and vascular smooth muscle cells, get adhesion of platelets

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47
Q

What forms a fatty streak?

A

The macrophages entering the walls

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48
Q

What is the final stage of atherosclerosis?

A

Fibrous plaques or advanced lesions that impede blood flow covered by dense fibrous cap

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49
Q

What causes plaque ruptures?

A

the fibrous cap is dissolved away, usually caused by infection or other inflamatory events

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50
Q

What is plaque erosion?

A

second most cause of coronary thrombosis, tend to be early lesions collagen triggers thrombosis rather thantissue factor

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51
Q

What is intervention for coronary artery disease?

A

PCI percutaneous coronary intervention usually stenting

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52
Q

Which drug is usually used on stents?

A

Siroluus, anti inflamatory and stops prolieration

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53
Q

What drugs are used in PCI?

A

Asprin and clopidogrel or ticagrelor and statins

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54
Q

What is angina?

A

A sympotom of restricted oronary blood flow usually secondary to atherosclerosis mismatch between supply and demand of oxygen

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55
Q

When do you get symptoms of angina?

A

When diameter has fallen 75%

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56
Q

Why might coronary heart disease not cause problems at rest but will when eerted?

A

The increased resistance in arteries at rest can be compensated by reduced resistance in microvasculature but cannot be done enuough for exercise

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57
Q

What are other anginas not coronary artery disease reated?

A

Prinzmetal’s angina form coronary spasm, microvascullar angina syndrome X and crecendo angina and unstable angina

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58
Q

What is presentation for angina?

A

Chest pain or discomfort, very subjectiv, heavy central tight rdiating to arms jaw and neck, precipitated by exertion and relieved by rest ot GTN spray

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59
Q

What are differential diagnosis for patients with angina presentation?

A

Pericarditis/myocarditis, pulmonary embolism pleurisy, chest infection, dissection of aorta, GORD. MSK psychological

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60
Q

What are the basic investigations for Angina?

A

12-lead ecg no abnormalites expected but look for IHD, Echo no markers but could be previous infarcts

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61
Q

What is SCAD?

A

Sever coronary artery disease

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62
Q

What does Pretest probablilty help wiht?

A

Deciding to investigate other causes in heart disease

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63
Q

What is the treadmill test for?

A

Induce ischaemia whille walking up hill look for ST depression, often cant be done by patients,not on guidlines anymore

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64
Q

What are the test statistics for CT angiogram and who is is useful for?

A

High negative predict good for ruling out, low positive predict good for excluding CAD in younger low risk candidates

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65
Q

What is a stess echo used for?

A

good all round functional test depends on local expetse looing at the heart for abnormal behaviour

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66
Q

What is SPECT/myoview?

A

Radiolabelled tracer to kok at perfusio of heart

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67
Q

What is the management of SCAD?

A

primary prevention reducing the risk of CAD complications, secondary prevention symptomatic and prognostic therapy

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68
Q

what are aspects of primary prevention of CAD?

A

correct hypertension, lower cholesterol, improv diabetic control, smoking cessation, exercise

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69
Q

What 1st line medications can be used for angina?

A

beta blockers, Beta 1 specific to reduces heart rate and contractility to reduce the workload of the heart,
nitrates to venodilate
calcium channel antagonists to dilate arteries

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70
Q

What are contraindications for betablockers?

A

severe bronchospasm in asthma, prinzmetals angina, sever heart block and bradycardia

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71
Q

What are 2nd line antianginals?

A

Nicorandil dilates vessels and Ivabridine, funy sodium channes to slow pacemaker currents

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72
Q

What clotting mesaures can be used in CAD?

A

aspririn, Gastric ulceration issues, or clopidogrel ticagrelor

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73
Q

When are revascularisation interventions done?

A

When medication fails and new risks identified

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74
Q

What is cardiogenic shock?

A

severe heart failure

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75
Q

What are are natural hypertorphies?

A

Pregnant females and athletes

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76
Q

Which diseases are related to atherosclerosis?

A

Ischaemic heart disease, myocardial infarction, stroke, peripheral vascular disease

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77
Q

What are complications of plaque rupture?

A

Ischemia, occlusion, chronic narrowing, dissection, aneurisms

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78
Q

What is chronic congestive heart failure?

A

Dilated failing heart reflects ischeamic heart disease

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79
Q

What are the patterns of infarction in the tissue?

A

Subendocardial, patchy infarction and transmural

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80
Q

What happens to ischaemic heart tissues?

A

replacement and revascularisation, deposition of fibrosis all take place over time

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81
Q

What is the problem with ischaemic reprofusion?

A

Reprofusion can sometimes cause dammage due to too much inflammation reprofusion disease

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82
Q

What can happen with complications of ischaemia

A

arrrhythmias, left ventricua failure extension of infarction and rupture of myocardium

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83
Q

What is an aneurysm?

A

Diation of part of the mycocardial wall associated with fibrosis and atrohy of myocytes

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84
Q

What is acute rheumatic fever?

A

Grou A betahaemolytic streptocoocus, upper respiratory tract but usually effect young, the antibodies for the bacteria cause autoimmune attack of the heart

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85
Q

What are clinical features of rheumatic fever complications?

A

dammage of valve architecture, leading to stenosis or regurgittation, can cause succeptibiligt to infective endocarditis,

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86
Q

What disorders can effect heart valves?

A

SLE rheumatoid arthritis, ankylosing spondylitis and connective tissue disorders

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87
Q

Who is likely to get infcctive endocarditis?

A

rheumatic fever, mitral valve prolapse, intravenous drug use, prosthetic valves diabetes and old

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88
Q

What is non-bacterial thrombotic endocarditis?

A

Sterile thrombotic matter deposition on valves

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89
Q

What is myocarditis?

A

inflammation of the myocardium usually associated with necrosis and degeneration

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90
Q

What can often cause myocarditis?

A

Viral infections coxacki adenvirusses, bacteria fungi uaully done by lymphocytic variants

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91
Q

What is cardiomyopathy?

A

death of the myocardium

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92
Q

What are the types of cardiomyopathy?

A

DCM dilated, HCM hypertrophic ARVC arrythmogenic right ventricular there are a lot more rare forms, end secondary

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93
Q

What are dilated cardiomyopathies caused by?

A

Often from chronic ischaemia or myocardial infraction, calcular disease previous myocarditis, often genetic links

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94
Q

What are the causes of hypertrophic cardiomyopathies/

A

Generally from genetic mutations from certain muscular proteins very large hearts very thick hearts can be very young,

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95
Q

What causes the arrhythmogenic right ventricular cardiomyopathy?

A

Mainly genetic linked causes thinning and fatty infiltration

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96
Q

What is restrictive cardiomyopathy?

A

Sarcoid disease can cause granulomatous inflammation inflammation also caused by buildup of amyloid

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97
Q

What characteristics of heart tumours?

A

Usually seccondary, can be cardia myxoma commenest rimary, left atrium myxoma, can be non specific.

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98
Q

What is sero-sanguinous effusion?

A

When you get blood in the pericardial fluid

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99
Q

What is haemopericardium?

A

Direct bleeding from casculature wall to the sac

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100
Q

What is cardiac tampnade?

A

Compression of the heart leading to acute cardiac failure from bleeding

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101
Q

What happens to the heart in hypertension/

A

Cardiac enlargement due to hypertrophy and the absence of other cause, also arteriosclerosis and causes hyalin cartilage formed that can calcify

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102
Q

What is vasculitis?

A

Inflammation of the vessels, can involve arteries veins caillaries can be caused by immune disies or viral infection and causes lumina narrowing

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103
Q

What is leukocytoclastic angitis?

A

white blood cells causing a reaction with small blood vessels and a rash

104
Q

What is giant cell arteritis?

A

Thickening of arteries significantly focal chrnic granulomatos inflamation of temporal arteries liked with polymyalgia rheumatica and afffects larer arteries and linke to disection can affect eyes mainly women for this can lead to blinding

105
Q

What is abdorminal aortic aneurism?

A

Often caused by atheroma, casusing a bulge in the vessel often scilent until it ruptures, it is screened later,

106
Q

Where are berry aneurysm/

A

In the circle of Willis it is often silent until but can resolve often with hypertension and atheroma or in connective tissue disorders

107
Q

What is a dissecting aneurism?

A

Blood enters below the endothelium into the layers beneath it is common in marfans syndrome

108
Q

What is embolism?

A

A detachec intravascular solid liqud or gas that moves in the circulation and can cause blockages often from vein thromboses

109
Q

What are systemic arterial embolism?

A

When a clot impacts in the smal vessles, often from atherosclerotic plaques, can come from endocarditis and from brain intestine disal limb and kidney problems

110
Q

What are haemangioma?

A

bening prolifereation of blood vessel tissues can be capillary haemangiouma birth marks rby spots juvanel haemangioma strawberry haemangioma and cavernous haemangioma, port wine stains

111
Q

What is the problem with haemangioma?

A

although benign can casue significant issues with bleeding or mass related ymptoms

112
Q

What is haemangiodnedothelioma?

A

Often low grade malignancy ascular tumour can metastisie but not agressive.

113
Q

What are angiosarcoma?

A

Malignant highly agressive form of cancer than can hapen in skin soft tissue breast bone liver and spleen it can rapidly disseminate to other organs

114
Q

What is Kaposi’s sarcoma?

A

HIV linked and Herpes virus 8 painful nodules on the skin and can disseminate.

115
Q

What are the congenital vascular disease?

A

Ehles-danlos syndrome and marfans they are connective tissue diseases which casuse structural defects.

116
Q

what is another term for stable angina?

A

Chronic coronary syndrome

117
Q

What can exacerbate angina?

A

Anaemia, hypoxemia, polycythemia hypothermia, hypovolemia hypervolaemia, or demand hypertension, tachyarrhythmia valvular heart disease hyperthyroidism hypertrophich cadiomyopathy

118
Q

What environmental factors exacerbate angina?

A

Cold weather, stress or emotion

119
Q

What is microvascular angina?

A

The dd structure of microvasculature often in women that increases resistance in the system

120
Q

What is crescendo angina?

A

angina that just gets worse and worse can feel like a heart attack

121
Q

What do you need for a history of angina?

A

Presenting complaint, history of it Risk factors PMH drug history family history social history and systematic enquirey

122
Q

What is the presenting complaint of angina?

A

Chest pain tightness or discomfort, breathlessness generally may present with heart failure symptoms. On exertion and at rest

123
Q

What makes chest pain more like cardiac chest pain?

A

central heavy pain, provoking factors and relieving factors

124
Q

What are differentials for angina?

A

Myocardial ischemia, pericarditis, myocarditis, pulmonary embolism/pleurisy, chest infection, pleurisy, dissection of aorta, GORD MSK psycological

125
Q

What are treatments for angina?

A

Reassurance lifestyle advice, emergency advice, GTN spray, potential for surgery. calcium channel bloacker beta blockers dilating agents

126
Q

What are the investigations for angina?

A

CT angiography,

127
Q

What are 1st line medical treatment of angina?

A

beta blockers. Reduce contractility and rate reduces demand. Nitrates vaenodilators, reduce bp reduces preload on heart and dilate coronary arteries, calcium channel blockers arteriolar vasodilators, postural hypotension swollen ankles. antiplatelets to stop clotting

128
Q

What are side effects of beta blockers?

A

Cold hands and feet erectile dysfunction, bradycardia don’t give with asthma, or peripheral vascular disease

129
Q

`What psychosocial factors affect Coronary heart disease?

A

Stress, Depression, Anxiety, Type A behaviours like anger.

130
Q

What can doctors do for psychosocial factors that lead to cardiovascular risk?

A

Ask about job occupation, asses depression anxiety social Networks for support.

131
Q

What is acute coranry syndromes?

A

Unstable angina and myocardia infarction and vary degrees

132
Q

What are the ways to asses levels of myocardial infarction?

A

ST elevation With Q waves, ST depreession or elevation without q waves and no abnormalities is unstable angina

133
Q

What are diagnoses of unstable angina?

A

No troponin no ecg changes and history of angina

134
Q

How can you retrospectively se MI?

A

Q waves on ECG as pathalogical changes following an event

135
Q

What is Q wave athology?

A

Low or no R wave and deep Q wave

136
Q

What are symptoms of MI?

A

Generaly unremitting, usually severe but can be mild or absent, can have vagal symptoms and breathlessness

137
Q

What are risk factors for not recovering for MI?

A

Diabetes renal failure LVSD

138
Q

What is initial management of MI?

A

Call 999 ST elevation, contact PCI centre asprin

139
Q

What is hospital management of MI?

A

Bed rest oygen pain relief aspirin platelet clocker beta blcokers and angiography

140
Q

What usualyl causes ACS?

A

Rupture of atherosclerotic plaque and consequeent arterial thrombosis, stress induced cardiomyopathy, coronary vasospasm, drug use, dissectoen of coronary artery due to vonnective tisue, thoracic aortic dissection

141
Q

What is troponin what does its presence indicate?

A

Part of the actin myosin contraction and MI causes its release which is higly sensitive for cardiac muscle injury, not MI but does show muscle injury,

142
Q

Why is aspirin used?

A

It inhibits platelet agregation by inhibition of cox enzymes to stop thromboxane a2 release

143
Q

Why is fibrinolysis not used?

A

It casues excess bleeding in unwanted sites as breakdown fibin

144
Q

How is clotting reduced in MI other han aspirin?

A

P2Y12 antagonists clopidogrel, ticagralor and

145
Q

What do GPIIb/IIaa antagonists?

A

stop platelet aggrigation, do use sometimes in PCI, really increase risk of bleeing IV only

146
Q

What are common anticoagulants?

A

heparin low molecularweight heparin,sometimes ue others to target formation of thrombin

147
Q

What is the treatments for STEMI?

A

Primary PCI with stenting

148
Q

What is treatment for NSTEMI?

A

10% CABG but PCI is more used. could be non ACS or thrombus could have changed

149
Q

What is the pharmacology of clopidogrel?

A

Lots broken down in plasma but is converted to nactive form needs to be activated by the liver for functionality.

150
Q

What is better than clopedogrel?

A

Ticagrelor is more effective and prasugrel

151
Q

What is the difference of ticagrelor to clopidogrel?

A

ticagrelor is reversible binding rather than permanent

152
Q

What are adverse effect of ticagrelor and p2y12 inhibitors?

A

bleeding epistaxis GI bleeds, haematuria, rash GI disturbance.( dyspnoea, ventricular pauses ticagrelor specific)

153
Q

How long should dual antiplatelet therapy after MI?

A

Patient specific assessment depends on factors usually used over a year

154
Q

Other than the heart, what lies in the pericardium?

A

the great vessels

155
Q

What is the function of the paricardium?

A

To limi expasion of the heart

156
Q

What happens in chronic pericardial effusion?

A

The paricardium can stretch slowly over time with long term filling. meanign cardiac tamponade is unlikely

157
Q

What is acute pericarditis?

A

inflamation of the pericardium either with or without effusion

158
Q

What is needed to diagnose acute pericarditis?

A

Chest pain, friction rub, ECG changes and pericardial effusion.

159
Q

What can cause acute pericarditis?

A

Viral- enteroviruses, herpese viruses, adenoviruses, parvoviruses, bacterial- TB, autoimmune in R Artheritis, Sjogen syndrome, neoplastic secondart metastatic tumours and metabolic myxoedema. Trauma and iatrogenic after intervention and damage or from thoracic injuries

160
Q

Who is pericarditis likely to afect/

A

Young usually well and a lot is ideopathic

161
Q

What is the presentatin of pericarditis?

A

Severe sharp pleuritic pain not crushing rapid onset, left anterior chest or epigastrium radiates to arm and trapezius ridge co-innervation phrenic nerve, relieves by sitting forward worse lying down, Dyspnoea cough, systemic disturbance antecedent fever PMH of cancer rheumatological cardiac procedure

162
Q

What are differentials for pericarditis?

A

Pneumonia pleurisy PE chostocondritis GORD MI, Aortid disection, Pneumothorax, pancreatitis, herpes zoster virus

163
Q

What can you investigate pericarditis for?

A

Pericardial rub crunching snow, sinus tachycardia, fever sign of effusuion like pulsus paradoxus kussmauls sign. ECG Bloods CXR Echocardiogram

164
Q

What are ECG changes for pericarditis?

A

Diffuse ST segement elevation, concave ST segment may resemble acute injury pattern of STEMI nor reciprocal ST depression, Saddle shaped, PR depression Mechanism is epicardial inflammation

165
Q

What might be seen on Bloods and exray for pericarditis?

A

FBC mild lymphocytosis, ESR and CRP, Troponin my be present, CXR is often normal but can show pneumonia with bacteria and can detect cardiac sillhouettte enlargment

166
Q

What is treatment for pericarditis?

A

Not much evidence, sedentary activity until symptoms, NSAIDS Colchicine

167
Q

What is the prognosis for most patients with pericarditis?

A

usuallt fine rare to get cardiac amponade, more likely in viral and bacterial up to 1/3 get recurrance.

168
Q

What are cardiomyopathies?

A

diseases of the heart muscel whcih are often genetic

169
Q

What is hypertropic cardiomyopathy?

A

Otherwise unexplaind primary cardiac hyprtrophy.

170
Q

What is he cause of hypertrophic cardiomyopathy?

A

Sarcomeric protein gene mutation

171
Q

What are the symptoms of Hypertropphic cardiomyopathy?

A

angina, dysponea, palpitations, dizzy spells or syncope

172
Q

What is often causes dilated cardiomyopathy?

A

Cytoskeletal gene mutations

173
Q

Which chambers does dilated cardiomyopathy usually affect?

A

All of the chambers but often just ventricles first

174
Q

What can cause arrhythmogenic cardiomyopathy

A

Desmosome gene mutations

175
Q

What is an inherited arrhythmia (channelopathy)?

A

ion channel protein gene mutations that cause irregularity in transmisssion of signals

176
Q

WHat types of arrhythmias can channelopathies cause?

A

Long QT short QT Brugaga and CPVT

177
Q

What is the most common pathology for sudde cardiac death in the young?

A

Genetic cause

178
Q

What is familial hypercholesterolaemia?

A

Inherited abnormality of cholesterol metabolism leading to hyper cholesterol

179
Q

What are the syndromes that might lead to vasuclar problems?

A

Mafan, Loeyz-Dietz and Ehler danlos syndrome

180
Q

What type of inheritance do most cardiac diseases have?

A

Autosomal dominant

181
Q

When should you consider secondary hypertension?

A

In young pateints, resistance to BP medications and symptoms/signs of underlying cause

182
Q

What are the targets for blood pressure control?

A

Cardiac output and peripheral resistance, Interplay between renin-angiotensin-aldosterone system and sympathetic nervous system and local vascular vasoconstriction and vasodilator mediators

183
Q

What are the drugs for allterng renin angiotensin aldosterone system?

A

ACE inhibitors prils. Angiotensin 2 receptor blockers sartans, direct renin inhibitor Aliskiren

184
Q

What are indications for ACE inhibitor or ARB?

A

Hypertenson, heartfailure, diabetic nephropathy

185
Q

What are the common adverse effects of ACE inhibitors?

A

Hypotension, acute renal failure, hyperkalaemia teratogenic effects during pregnancy, increased kinin prduction leading to cough rash and anphylactoid reactions

186
Q

What are the main adverse effects of ARBs?

A

Symptomatic hypotension, hyperkalaemia, potential renal dysfunction angio-edema rash, not for use in pregnancy

187
Q

What are main indications for calcium channel blockers?

A

Hypertension, Ishaemic heart disease, angina and arrhythmia(tachycardia)

188
Q

What are the three groups of calcium channel blockers?

A

ones tha act on vascular smooth muscles and peripheral arterial vasodilators, then main effect on the heart being negaively chronotropic and negatively ionotropic, also intermediate heart/peripheral vascular effects

189
Q

What are the adverse effects of ccbs.

A

Flushing headach oedema palpitations from peripheral vasodilations, dradycardia atrioventricular block from chronotripic efffects and worsening cardiac falure if it has ionotopic effects verapamil causes constipation

190
Q

When are beta-adrenoreceptor blockers indicated?

A

Ischaeic heart disease, heart failure arrhythmia and hypertension

191
Q

What might cardioselective mean?

A

Beta 1 receptor specific but plenty in heart are beta2 some drucs can be beta 1 selective

192
Q

What are the main adverse effects of beta blockers?

A

Fatigue headache sleep sistrubance bradycardia hypotension cold peripheries and erectile dysfunction worsening of astha COPD PVD calaudication or Raynauds

193
Q

What are the indication for diruetics/

A

Hyoertension and heart failure.

194
Q

What are the classes of diuretics?

A 
Thiazides and related drugs(distal tubule),
Loop diuretics (loop of henle), potassium-sparing diuretics and aldosterone antagonists
195
Q

What are thiazide and related diuretics?

A

Bendroflumethiazide, hydrochlorothiazide and chlorthalidone

196
Q

What are loop diuretics?

A

Furosemide, bumetanide

197
Q

What are potassium sparing diuretics?

A

Spironolactone, eplerenone, amiloride tiamterine

198
Q

What are the main adverse effects of diuretics?

A

Hypovolaemia (loops) hypotension, hypokalaemia hyponatraemia hypocalcaemia hypomanesia, gout, erectile dysfunction impared glucose tolerance

199
Q

What are some less common anhihypertensives/

A

Alpha1 adrenoreceptor antagonists, centrally acting antihypertensive ad direct renin inhibitors

200
Q

What is most evidence for heart failure from?

A

Left ventricular dysfunction chronic

201
Q

What are stages if heart failure pharmacolocy?

A

Diuretics for symptomatic treatment of congestion, for disease infuencing, Ace inhibitors and beta blockers titrate up, aldosterone antagonists, hydralazine/nitrates later digoxin or ivabradine

202
Q

What is the effects of nitrates?

A

Arterial and venous dilators, reduction of preload and afterload, lowrs BP

203
Q

What are the classes or antiarrhythmic drugs?

A

Class I: Sodium channel blockers
Class II : Beta afrenoreceptor antagnoists
Class III: prolonging action potential amiodarone stalol
Class IV: calcium channel blockers

204
Q

What is digoxin?

A

Cardiac glycoside, inhibits NA/K pump, bradicardia, form vaus, slows atrioventricular conduction, increased ectopic activiy and increases force of contraction, narrow theraputic range positive ionotrophic.

205
Q

What are Cardia natriuretic peptides?

A

ANB or BNP releases by stretching of cardiac cells as a resut of volume overload. they increase renal excretion of sodium and water relax vascular smooth mscle and increased vascualr permeabilit inhibit aldosterone angiotensinII endothelin and ADH it is counterregulatory to renin angiotensin system

206
Q

What are subclasses of sodium channel blockers?

A

1a lengthens duration of actionpotential, 1b shortens or has no effect on duration of action potential, 1c no effect on action potential but promotes greater sodium curent depresion

207
Q

Why can Class 1 all have different effects despite all action on the sane channel/

A

Bind to a site, voltage dependance ish shifted to more negative, each channel had different kinetic interaction with the drug affinity of rectptor is modulated by membrane potential

208
Q

What do beta receptors do to cardiac cells?

A

They allow ore calcium in which increases heart rate, conduction speed and contraction strength

209
Q

What heart drug causes a lot of interactions?

A

Amiodarone

210
Q

Which calcium antagonists are not anti-arrhythmic?

A

Dihdropyridines like amlodipine

211
Q

What are potential causes of heart failure?

A

Valcular, arrhytmias, hypertension alcohol excesssl cardiomyopathy pericardial causes

212
Q

What amplifies acute heart failure?

A

pulmonary congestion peripheral hypoperfusion respiratory filure, reduced contractility and fluid retention

213
Q

What is the difference between patients with Acute decompenated heart failure and acute heart faiure?

A

decome are yuually ypunger men and reduced ejection fraction, acute comtenated uaully older and women and have Left vertricular ejection fraction grater than 40%

214
Q

What investigations should eb done during heart failure?

A

CXR, blood tests, ECG ECHO perfusion imagin

215
Q

Which systems are involved in heart failure system?

A

Sympathetic nervous system, inflammation and RAAS

216
Q

What does sympathetic system do in the long term heart failure?

A

Reuces reserve and myocardial dysfunction and alters bea receptors and increases

217
Q

What are the main symptoms of heart failure?

A

SOB, fatigue ankle swelling more specifcorthopnoea and PND are insensitive, tiredness, cold peripherise increased weight

218
Q

What are signs of heart failure?

A

Peripheral oedema, pulmonary crackles tachycardia non specific, raised JVP S3 and displaced apex beat are indicative, ascites hepatomegaly sacral oedema

219
Q

What are the classes of heart failure?

A

Class 1 no limitation class 2 slight limitation class 3 marked limitation class 4 inability to carry out any physical activity without discomfort

220
Q

What can casuse decompensatio of chronic heartfaulure?

A

MI, uncorrected BP obesity, infection arrhythmias, endocrien, necative ionotropes, NSAIDS, excess sodium

221
Q

what are the complications f heart faulure?

A

Renal dysfunction, rhythm disturbances systemic thromboebolsm, DVT E hepatic dysfunction neurological complications

222
Q

what drugs can be used in heart failure?

A

ACEi, ALdosteron antagonists, betablockersVenodlators

223
Q

what is a sign heart failure is less severe?

A

EF is preserved

224
Q

What is hibernating myocardium?

A

Heart muscle that is viable if revascularised

225
Q

What are the features of hypertrophic cardiomyopathy?

A

chaotic growth of the sarcomeres and impared diastolic relaxation by recirculation of currents in the heart

226
Q

What is the problem in dilated cardiomyopathy?

A

impared contraction and often have heart failure presentation

227
Q

What is arrhythmogenic cardiomyopathy pathology?

A

Fibrofatty replacement of muscle

228
Q

IF you have a patient with long QT what do you need to be aware of?

A

Lots of drugs affect it and can cause death

229
Q

What are some conditions that are due to inherited cardiac conditions?

A

Epilepsy from an attack, drowning from heart attack, asthma, lighter fuel causes a defect, car crashes

230
Q

How should inherited diseases be investigated?

A

3 generation pedigree directly investigate first generations for abnormality

231
Q

When are sympathetic stimulants in heart failure?

A

In acute presentation only

232
Q

When does heart failure affect people?

A

After 55 increasing beyond

233
Q

What are the types of heart failure?

A

HF-REF left ventricular systolic imparement were ejction fractionis less than 40HF-PEF ejection fraction normal left atruym dialated
HF-PH pulmonary hypertension
HF-valve

234
Q

What levels are increased in heart falure?

A

Renin, AVP/ADH, norepinephrin and BNP,

235
Q

How is heart failure managed if ejection fraction is preserved?

A

Comorbitities only and other heart conditions and cardiac rehabilitation

236
Q

How are heart failure with reduced ejection fraction treated?

A

ACE inhibitor, ARB, nitrates or other can give ivabradin or digoxin with AF, Diuretics for congestion, beta blockers for reducing load on heart spiralactone

237
Q

Why would you use Digoxin in heart failure despite positive ionotropin?

A

it stops AF from transferring to the ventricles

238
Q

What is Cardiac resynchronising therapy?

A

Pacing both atria and ventricles at the same time

239
Q

What is infetive endocarditis?

A

Infeion of the heart valves and endotherlium of the heart chamber,

240
Q

What are the types of infective endocarditis?

A

Left sided native IE, left sided prosthetic IE, Right sided IE, Device related IE, Prosthetic early or later, can have different presentation, pathogen and outcomes

241
Q

What are the risk factors for endocarditis?

A

Have abnormal valves regurgitant or prosthetic or have infectios material in blood from surgery or have had IE before.

242
Q

Who does IE affect most?

A

rheumatic heart disease sufferers, elderly young IV drug users, congenital heart disease and prosthetic heart valves. males more than females.

243
Q

What can Infective endocarditis present as?

A

Most thigns often new regurgitant heart murmur, demnolic events of unknown origin, sepsis, fever (screen for history of IE congenital disease immunocompromised or recent sugery)

244
Q

What is the clinical presentation of IE?

A

Depends on site and orgamism, signs of systemic infection, embilisation stroke PE bone infections idney dysfunction MI

245
Q

How can IE diagnosis be made?

A

Blood cultures positive, Echo of endocarditis, predisposing factors fever vascualer phenomena immune phenomina, cna be classified as definite or possible based on criteria

246
Q

What is the best investigation for IE?

A

ECHO but needs to be transoesophageal if possible to get best images

247
Q

What are some signs of IE?

A

Splinter haemrages on nails, petechiae oslersnodes roth spots on fundoscopy

248
Q

What might make it lesss likely to fine bactera in blood of suspected IE?

A

Prior antibiotic use

249
Q

What are 1st line investigation in IE?

A

ECG, TTEcho

250
Q

What is teratment of IE?

A

targeted antimicrobials for 6 weeks treat complications, arrhythmia, heart failure, heart block, embolisation stroe rehabe drainage, potentially valve replacement may be nececcary

251
Q

What are some comp;ications of IE?

A

Valve disfuntion, recurrant infection, aortic root abscess severe valve damage, large vegetations

252
Q

Should IE be prevented?

A

Not according to NICE it is not worth it

253
Q

What should do as F1 for infective endocarditis?

A

Query IE for sepsis request ECHO especially if risk factors, Can cause INR to go up

254
Q

Which drugs can increase blood pressure?

A

SNRIs anxiety medications, NSAIDS, corticosteroids oestrogen contraception, Anti-TNF

255
Q

How often should BP be checked one treatment?

A

6months to 12 months to check kidney,

256
Q

When should antihypertensive be stopped?

A

Before general anaesthesia due to risk of hypotension

Phase 2 mine (13 decks)

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