Cardiology Flashcards

1
Q

what is the main problem with atherosclerosis

A

plaque rupture - thrombus formation and partial/complete arterial blockage leading to heart attack

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2
Q

what is the best known risk factor for coronary artery disease

A

age

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3
Q

risk factors for atherosclerosis

A

age, tobacco smoking, high serum cholesterol, obesity, diabetes, hypertension, family history

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4
Q

where are atherosclerotic plaques most commonly distributed

A

peripheral and coronary arteries

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5
Q

what factors might govern the distribution of atherosclerotic plaque

A
  • changes in flow/turbulence (bifurcations)
  • wall thickness
  • altered gene expression
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6
Q

what is found within an atherosclerotic plaque

A
  • lipid
  • Necrotic core
  • Connective tissue
  • Fibrous cap
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7
Q

what are the outcomes of an atherosclerotic plaque

A

it will either occlude the vessel lumen or it could rupture

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8
Q

what inflammatory cytokines can be found in plaques

A

IL-1, IL-6, IL-8, IFN-y, TGF-b, MCP-1 and C reactive protein

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9
Q

what are the steps in leukocyte recruitment and movement through the vessel wall

A

Capture
Rolling
Slow Rolling
Firm adhesion
Transmigration

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10
Q

what are the features of a fatty streak

A
  1. the earliest lesion of atherosclerosis
  2. Appear at a very early age (<10 years)
  3. consist of aggregations of foam cells and T lymphocytes within the intimal layer of the vessel
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11
Q

what are intermediate lesions

A

they progress from the fatty streak, containing foam cells, vascular smooth muscle cells, T lymphocytes, and platelet adhesion. They also contain isolates pools of extracellular lipid

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12
Q

what are the features of a fibrous cap (or advanced lesions)

A
  • impedes blood flow
  • prone to rupture
  • covered by a dense fibrous cap made from
    extracellular matrix proteins or collagen and elastin
  • contains a lipid core and necrotic debris
  • may be calcified
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13
Q

what does a fibrous cap contain

A

smooth muscle cells
macrophages
foam cells
T lymphocytes

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14
Q

what causes a plaque rupture

A

if the balance is shifted and there are high inflammatory conditions, and increased enzyme activity, the cap becomes weak and the plaque can rupture

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15
Q

what is plaque erosion

A

this is where lesions tend to be small early lesions. A thickened fibrous cap may lead to collagen triggering thrombosis. A platelet-rich clot may cover the luminal surface and there is a small lipid core

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16
Q

what is a red thrombus

A

where there are red blood cells and fibrin present

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17
Q

what is a white thrombus

A

when there are platelets and fibrinogen present

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18
Q

what are the clinical characteristics that predispose someone to a plaque rupture

A

dyslipidemia
hypertension
diabetes Mellitus
chronic kidney disease
multi vessel disease

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19
Q

what can be done when someone gets a ruptured plaque

A
  • stent implantation
  • distal embolisation
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20
Q

what are clinical characteristics which predispose someone to plaque erosion

A

smoking
being female
being younger than 50
having anterior ischemia

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21
Q

how is coronary artery disease treated

A

PCI - percutaneous coronary intervention
stent

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22
Q

what are coronary stents made of

A

stainless steel

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23
Q

what action does aspirin

A

it irreversibly inhibits platelet cyclo-oxygenase

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24
Q

what is the action of clopidogrel or ticagrelor

A

it inhibits P2Y12 ADP receptors on platelets and therefore has antiplatelet action

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25
Q

what are statins used for

A

to lower cholesterol

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26
Q

what is the action of statins

A

it inhibits HMG CoA reductase and therefore reduces cholesterol synthesis

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27
Q

what is a PCSK9 inhibitor

A

it is a monoclonal antibody that inhibits PCSK9 protein in the liver and leads to improved clearance of cholesterol from the blood

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28
Q

what are the major cell types involved in atherosclerosis

A

epithelium, macrophages, smooth muscle cells and platelets

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29
Q

what are examples of acute coronary syndromes

A

Q wave MI
ST elevation MI
Non Q wave MI
Non ST elevation MI
unstable angina
Non ECG changes

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30
Q

what are the characteristics of an unstable angina

A

pain at rest
crescendo pattern

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31
Q

how would you diagnose an unstable angina

A
  • history
  • ECG
  • troponin test - not normally risen in angina
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32
Q

what is the management for a myocardial infarction

A

300mg of aspirin immediately
- blood test
- ECG
- oxygen therapy
- pain relief
- Aspirin +/- platelet P2Y12 inhibitor
- Consider beta blockers
- Consider antiangial therapy
- Consider urgent angiography

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33
Q

what are other reasons someone may have acute coronary syndrome other than MI

A

stress-induced cardiomyopathy
vasospasm
drug abuse
dissection

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34
Q

what is troponin C a marker of

A

its a biological marker of myocardial damage and is used as a diagnostic tool for cardiac injury

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35
Q

what does aspirin do

A

it prevents platelet clotting

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36
Q

what is the side effect of using aspirin and P2Y12 inhibitors (clopidogrel, prasugrel and ticagrelor) together

A

it increases the risk of bleeding

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37
Q

why are GP2b/3a blockers not used in clinical practice very often anymore

A

as they increase the risk of major bleeding

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38
Q

what medication is the most effective against angina

A

beta blockers

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39
Q

what is a major issue with using clopidogrel

A

it is a prodrug and it is unreliable as it can rapidly inactivate. therefore you can have different responses in different people and it is unpredictable

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40
Q

what factors can alter clopidogrel’s activity

A
  • weight
  • hight
  • drug interactions
  • genetic variations - CYP2C19 loss of function mutation
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41
Q

what is the process of Atherogenesis

A

There is damage to the endothelial cells which causes LDLs to move into the intima.
Due to the damage the endothelium secretes chemoattractants
leukocytes migrate and accumulate in the intima absorbing the LDLs and becoming foam cells
This forms a fatty streak
foam cells will rupture and release lipids
smooth muscle cells migrate from the media to the intima
a dense fibrous cap with a necrotic core is formed
this plaque can partially occlude the lumen and blood flow can be restricted.
this plaque can rupture ad a thrombus formed which can fully occlude the lumen

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42
Q

which cardiac arteries does atherogenesis affect most commonly

A

LAD, circumflex and RCA

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43
Q

what risk factors increase your chance of atheroma formation

A

age
smoking
obesity - high serum cholesterol
diabetes
hypertension
family history
male

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44
Q

put these in ascending order of severity
- stable angina, NSTEMI, STEMI, unstable angina

A

Stable angina> unstable angina > NSTEMI> STEMI

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45
Q

what are the main causes of cardiac myocyte damage

A

atheroma, valvular disease (stenosis) and anaemia

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46
Q

what is angina

A

Angina is the result of myocardial ischaemia, where blood supply < metabolic demand

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47
Q

what is stable angina

A

chest pain after cold/exercise and lasts about 1-5 minutes. it is relieved by rest or GTN spray

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48
Q

what is unstable angina/NSTEMI/STEMI

A

chest pain at rest and prolonged (longer than 20 minutes). there is no release at rest

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49
Q

what is seen on ECG during a STEMI

A

ST elevations

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50
Q

what does STEMI stand for

A

ST-elevation myocardial infarction

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51
Q

what is prinzmetal’s angina

A

it is caused by coronary artery spasms; occur at rest or at night

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52
Q

what are the symptoms of ischemic heart disease

A

chest pain - discomfort, heaviness
radiation - left arm, shoulder, jaw
NSFW - nausea, sweating, fatigue and weak breathing

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53
Q

what are atypical presentations of ischemic heart disease

A

no pain
low grade fever
pale, cool, clammy skin
hyper/hypotension

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54
Q

how do you diagnose ischemic heart disease

A

history taking and physical examination
- resting ECG
- exercise ECG
blood tests - HBA1C, full blood count, cholesterol profile
CT - coronary angiography
biological markers: troponin, myoglobulin, CK

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55
Q

what is heart contraction initiated by

A

depolarisation and changes intracellular calcium concentrations

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56
Q

what needs to occur for heart muscle relaxation to occur

A

removal of calcium - energy dependent

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57
Q

what are the two types of cardiac myocytes

A
  • atrioventricular conduction system - slightly faster
  • general cardiac myocytes
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58
Q

is blood flow through the myocardium from the aortic root diastolic or non-diastolic

A

diastolic

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59
Q

what is the normal systolic ejection fraction

A

about 60-65%

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60
Q

as venous return increases does cardiac/volume increase or decrease

A

it increases

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61
Q

what happens if you exceed the stretch capacity of the sarcomeres in the heart

A

then the cardiac contraction force diminishes

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62
Q

when can myocardial hypertrophy be an adaptive or physiological response

A

in athletes or in pregnancy

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63
Q

what is the myocardial hypertrophic response triggered by

A

angiotensin 2
ET-1
IGF-1
TGF - b
these activate mitogen-activated protein kinase

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64
Q

what happens in left sided cardiac failure

A

there is pulmonary congestion and then overload of the right side

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65
Q

what happens in right sided heart failure

A

there is venous hypertension and congestion

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66
Q

what is diastolic cardiac failure (HFpEF)

A

it is when the left ventricle of the heart becomes stiff and unable to fill properly

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67
Q

what happens in fetal embryogenesis of the heart

A
  • the heart comprises a single chamber until week 5 of gestation
  • it is then divided by intra-ventricular and intra-atrial septa from endocardial cushions
  • the muscular intra-ventricular septum grows upward from the apex producing four chambers and allowing valves to develop
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68
Q

what does congenital heart disease result from

A

results from a faulty embryonic development
- misplaced structures or arrest of the progression of normal structure development

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69
Q

what percentage of live births can congenital heart disease complicate

A

may complicate up to 1% of live births

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70
Q

what are the four most common congenital heart defects

A

Ventricular septal defect -25-30%
Atrial septal defect - 10-15%
Patent ductus arteriosus - 10-20%
Fallots 4-10%

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71
Q

what single gene conditions are associated with an increased risk of congenital heart disease

A
  • Trisomy 21
  • Turners syndrome XO
  • di-George syndrome
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72
Q

what infection in pregnancy is associated with an increased risk of congenital heart disease

A

rubella

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73
Q

What drugs in pregnancy increase the risk of congenital heart disease

A

thalidomide, alcohol, phenytoin, amphetamines, lithium, oestrogenic steroids

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74
Q

what classifications are used for congenital heart disease

A
  • if cyanosis is present or absent
  • whether it occurs from birth or whether it develops later
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75
Q

what types of congenital heart disease show an initial left to right shunt

A

Ventricular septal defect
atrial septal defect
patent ductus arteriosis
anonymous pulmonary venous drainage
hypoplastic left heart syndrome

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76
Q

what types of congenital heart disease show a right to left shunt

A

tetralogy of Fallot
tricuspid atresia

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77
Q

what types congenital heart disease show no shunt

A

complete transposition of great vessels
coarctation
pulmonary stenosis
aortic stenosis
coronary artery origin from pulmonary artery
Ebstein malformation
Endocardial fibroelastosis

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78
Q

what is patent foramen ovale

A

hole in the heart between the right and left atria that doesn’t close correctly after birth.
can be found in the central septum (90%) or in the lower part of the septum primum.

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79
Q

what can a patent foramen ovale lead to

A

cardiac arrhythmias, pulmonary hypertension, right ventricular hypertrophy, and cardiac failure. Also has a risk of infective endocarditis

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80
Q

what is patent ductus arteriosus

A

where the ductus arteriosus persists beyond birth

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81
Q

what can a patent ductus arteriosus lead to

A

the left-to-right shunting eventually means the lung circulation is overloaded with pulmonary hypertension and right-sided cardiac failure subsequently

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82
Q

can a patent ductus arteriosus be closed

A

yes can be closed surgically, by catheters or my prostaglandin inhibitors (idomethacin)

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83
Q

what is tetralogy of Fallot

A

It has four main features
1. Pulmonary stenosis
2. Ventricular septal defect
3. Dextraposition/over-riding ventricular septal defect
4. Right ventricle hypertrophy

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84
Q

what is the characteristic shape of Tetralogy of Fallot on radiology and macroscopically

A

boot shaped

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85
Q

What happens due to a Tetralogy of Fallot

A

As a result of the pulmonary stenosis, right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction usually is performed during the first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases

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86
Q

What is complete transposition of the great arteries (TGA)

A

it involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle.

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87
Q

does complete transposition of the great arteries have a male or female bias

A

male bias

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88
Q

is survival possible with complete transposition of the great vessels

A

only possible if there is communication between the circuits and virtually all have an atrial septal defect allowing for blood mixing

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89
Q

what is the treatment for complete transposition of the great vessels

A

arterial switch - less than 10% overall mortality

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90
Q

what is coarctation of the aorta

A

this is secondary to an excessive obliterating process that normally closes the ductus arteriosus, extending into the aortic wall. The net result is a narrowing of the aorta after the arch witch excessive blood flow diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body

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91
Q

What are the complications of coarctation of the aorta

A
  • associated with berry aneurysms
  • cardiac failure
  • rupture of dissecting aneurysm
  • infective endarteritis
  • cerebral haemorrhage
  • stenosis of the bicuspid aortic valve
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92
Q

what is the treatment for coarctation of the aorta

A

dilatation (stenting) of the stenosed segment

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93
Q

what is endocardial fibroelastosis

A

secondary -complication of congenital aortic stenosis and coarctation. Profound dense collagen and elastic tissues deposited on endocardial aspect of the left ventricle produces progressive stiffening of the heart and cardiac failure. Similar changes may affect the valves.
primary - may follow a familial pattern

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94
Q

what is Dextrocardia

A

the normal anatomy of the heart is versed with a rightward orientation
- often associated with severe cardiovascular abnormalities

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95
Q

what are the different types of angina

A

standard, prinzmetal/unstable, accelerated/Crescendo

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96
Q

what are risk factors for ischaemic heart disease

A

systemic hypertension
cigarette smoking
diabetes mellitus
elevated cholesterol
Sex
obesity
age
family history
sedentary life

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97
Q

what are some reasons for an imperfect blood supply to the heart

A

atherosclerosis
thrombosis
thromboemboli
artery spasm
collateral blood vessels
blood pressure/cardiac output/heart rate
arteritis

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98
Q

what conditions can limit coronary flow

A

Coronary arteritis
Dissecting aneurysm of aorta
Syphilitic aortitis, congenital abnormality of coronary artery origin
Myocardial bridge

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99
Q

what can occur upon reperfusion of ischaemic myocardium

A

reperfusion of completely infarcted tissue can produce significant haemorrhage. It can allow oxygen delivery and a further degree of injury as a result of generation of superoxide radicals

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100
Q

what are pathological complications of ischaemic damage of the heart

A

Arrhythmias (supraventricular and ventricular)
Left ventricular failure – cardiogenic shock.
Generally reflects >40% muscle damage
Extension of infarction, rupture of the myocardium (into pericardial space, between chambers, across papillary muscle insertion)

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101
Q

what is an aneurysm

A

it is a dilation of part of the myocardia wall, usually associated with fibrosis and atrophy of myocytes

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102
Q

what is pericarditis (dressler syndrome)

A

this is a delayed pericarditic reaction following infarction (2-10 weeks)

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103
Q

what is the WHO classification of hypertension

A

> 140/90mm Hg

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104
Q

what is hypertensive heart disease

A

it reflects cardiac enlargement due to hypertension and in the absence of other causes
there is compensatory hypertrophy of the heart with increased myocyte size. Eventually, the hypertrophy will no longer be able to compensate and oxygen delivery will start to fail

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105
Q

what is the most common reason for angina

A

ischemic heart disease

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106
Q

what are exacerbating factors of angina

A

supply - anaemia, hypoxia, polycythemia, hypothermia, hypovolaemia, hypervolaemia
demand - hypertension, tachyarrhythmia, hypertrophic cardiomyopathy, hyperthyroidism (should be treated)

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107
Q

what environmental factors can bring on angina

A

exercise
cold weather
heavy meals
emotional stress

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108
Q

what is ohms law in biology

A

pressure = flow X resistance
P=QR

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109
Q

what is poiseuilles law in biology

A

P = 8uLQ / pi r^4
essentially coronary flow falls off with the 4th power of the radius

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110
Q

what is microvascular angina

A

small blood vessels are affected, main coronary vessels mostly normal

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111
Q

what is the treatment for angina

A

lifestyle - stop smoking, weight, exercise, diet
advice for emergency
medication - GTN spray, aspirin and beta blocker
revascularisation

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112
Q

what is the gold standard non-invasive test for angina (IHD) diagnosis

A

a perfusion MRI

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113
Q

what is the gold standard (but invasive) test for angina (IHD) diagnosis

A

coronary angiography

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114
Q

what are beta blockers affect on the heart

A

bradycardia
reduce contractility
decrease cardiac output

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115
Q

what are contra-indications of beta blockers

A

in severe asthma will block beta receptors in the lungs and can cause bronchoconstriction

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116
Q

How do nitrates work

A

dilates veins, reducing the venous return and therefore preload. Can also dilate arterioles, reducing blood pressure and afterload

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117
Q

what are side effects of nitrates

A

headache due to venous dilation

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118
Q

what are side effects of beta blockers

A

tiredness
bradycardia
erectile dysfunction
cold hands and feet

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119
Q

what are the effects of calcium channel blockers

A

decreased contraction therefore work the heart has to do and its oxygen demand
decrease heart rate
cause arterial dilation, decreasing BP and afterload

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120
Q

what are side effects of calcium channel blockers

A

flushing
postural hypertension
swollen ankles

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121
Q

what is a major side effect of aspirin therapy

A

gastric ulceration

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122
Q

why would you give an ACE inhibitor to someone with IHD

A

inhibits the production of angiotensin 2 and therefore prevents vasoconstriction and increases sodium and water excretion. This will reduce blood pressure

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123
Q

when is bypass surgery used in cardiac disease

A

when there is multivessel disease

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124
Q

how is bypass surgery performed

A

there is internal mammary graft from the chest, to the right coronary artery past the blockage. Can use veins from your leg (long saphenous vein), if other coronary arteried have blockages as well

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125
Q

what are the pros and cons of Percutaneous Coronary Intervention (stent)

A

pros - less invasive, convenient, repeatable, acceptable
cons - risk stent thrombosis, risk restenosis, cant deal with complex disease, dual antiplatelet therapy

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126
Q

what are the pros and cons of coronary artery bypass graft

A

pros - prognosis is better, deals with complex disease
cons - invasive, risk of stroke/bleeding, can’t do if frail, one time treatment, long length of stay, long recovery time

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127
Q

what is acute pericarditis

A

it is an inflammatory pericardial syndrome

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128
Q

what is Cor pulmonale

A

it is right ventricular hypertrophy and dilation due to pulmonary hypertension

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129
Q

what can cause Cor pulmonale

A
  • embolisation of material into the pulmonary circuit
  • chronic bronchitis and emphysema
  • pulmonary fibrosis
  • cystic fibrosis
  • recurrent emboli
  • primary pulmonary hypertension
  • peripheral pulmonary stenosis
  • IV drug use
  • high altitude
  • abnormal movement of the thoracic cage
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130
Q

what are features of right sided heart failure

A

venous overload, peripheral oedema, and progressive hepatic congestion

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131
Q

what bacteria causes acute rheumatic fever

A

Group A b-haemolytic streptococcus infection

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132
Q

what remains a major factor with regard to heart disease in developing countries

A

acute rheumatic fever

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133
Q

why can acute rheumatic fever cause cardiac dysfunction

A

development of immunity against streptococcal pharyngitis produces antibodies that cross-react with cardiac myocytes and valvular glycoproteins. This produces localised inflammation and subsequent scarring

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134
Q

what are the clinical features of acute Rheumatic fever

A

Carditis (cardiomegaly, murmurs, pericarditis and cardiac failure)
Polyarthritis
chorea - sudden, uncontrolled jerky movement
erythema - redness of skin/mucus membranes
marginatum - rash
subcutaneous nodules

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135
Q

What are minor criteria for acute rheumatic fever diagnosis

A

previous history of rheumatic fever, arthralgia, raised CRP, ESR, and white cell count. Antibodies against group A strep antigens, anti-streptolysin O, anti-DNAsa B and anti-hyaluronidase

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136
Q

how long does it take for symptoms of acute rheumatic fever to diminish

A

3-6 months

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137
Q

what other disorders can affect cardiac valves

A

SLE, Rheumatoid arthritis, ankylosing and other connective tissue disorders

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138
Q

How can progressive cardiac dysfunction occur due to acute rheumatic fever

A

Chronically scarring and deformity produces contracture of the valve and chordae tendinae. These may subsequently calcify and distort blood flow allowing localised thrombosis. They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis.

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139
Q

what is infective endocarditis

A

Infective endocarditis, also called bacterial endocarditis, is an infection caused by bacteria that enter the bloodstream and settle in the heart lining, a heart valve or a blood vessel

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140
Q

what are characteristic microorganisms of infective endocarditis

A

strep. Viridans and Staph. Aures
Fungal and atypical bacteria are also recognised

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141
Q

what occurs in infective endocarditis

A

infection produces a rapidly increasing cardiac valve distortion and disruption, with an acute cardiac dysfunction

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142
Q

what are symptoms of infective endocarditis

A

sudden cardiac failure
septic problems
generation of infected thromboemboli
damage to kidneys
fever
anorexia
fatigue
splenomegaly
clubbing
neurological dysfunction

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143
Q

what is the mortality rate of infective endocarditis

A

30-40% mortality rate

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144
Q

what is the most common cause of infective endocarditis in children

A

congenital heart disease

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145
Q

what are the most common cause of infective endocarditis in adults

A

rheumatic valvular heart
mitral valve prolapse
intravenous drug abuse
prosthetic valves
diabetes
elderly
pregnancy

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146
Q

what is non bacterial thrombotic endocarditis/marantic endocarditis

A
  • sterile thrombotic matter deposits on valves with variable degrees of valve dysfunction
  • degenerative valve disease
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147
Q

what is calcific aortic stenosis

A

it is when there are nodular calcific deposits in the cusps with progressive distortion of valves.

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148
Q

what can nodular calcific stenosis lead to

A

obstruction of left ventricle outflow, leading to pressure overload and cardiac hypertrophy. There can be a risk of sudden cardiac death and MI

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149
Q

what type of valve accelerates development of calcific aortic stenosis

A

bicuspid aortic valves

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150
Q

what is mitral valve disease

A

when there is an issue with the mitral valve and can lead to regurgitation due to a lack of closure

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151
Q

what is one of the main causes of mitral valve stenosis

A

One of the main causes of mitral valve stenosis is rheumatic heart disease. This is where an infection causes the heart to become inflamed

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152
Q

what is mitral valve prolapse

A

it is the degeneration of the mitral valve such that the inner fibrosa becomes loose and fragment, with fragments of mucopolysaccharide material

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153
Q

what can occur in mitral valve prolapse

A

it can cause the valve cusp to bow upwards and may not close which can produce incompetence regurgitation.

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154
Q

what diseases are mitral valve prolapse associated with

A

underlying connective tissue disorders, Marfan’s syndrome and myotonic dystrophy

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155
Q

can mitral valve prolapse lead to sudden cardiac death

A

Yes

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156
Q

what is myocarditis

A

inflammation of the myocardium
usually associated with muscle cell necrosis and degeneration

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157
Q

what is the most common type of myocarditis

A

viral myocarditis
- viral toxicity with associated cell mediated cell damage

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158
Q

what is the most common type of myocarditis

A

viral myocarditis
- viral toxicity with associated cell mediated cell damagewhat are the causes of myocarditis

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159
Q

what is the most common type of myocarditis

A

viral myocarditis
- viral toxicity with associated cell mediated cell damagewhat are the causes of myocarditis

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160
Q

what are the causes of myocarditis

A

viruses - coxsacke, adeno, echo, influenza
Rickettsia
bacteria - Diptheria, staphylococcal, streptococci, borrelia, leptospira
fungi and protozoa parasites - toxoplasmosis and cryptococcus
metazoa - echinococcus

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161
Q

what are non infectious causes of myocarditis

A

hypersensitivity/immune-related diseases - rheumatic fever, SLE, scleroderma, drug reaction, RA
radiation
Miscellaneous - sarcoid and uraemia

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162
Q

what is myocarditis often associated with

A

a preceding upper respiratory tract infection

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163
Q

what is giant cell myocarditis

A

A very rare highly aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells. Often fatal.
Early treatment is transplantation but disease can often recur.

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164
Q

what metabolic diseases are associated with myocarditis

A

Hyperthyroidism, hypothyroidism
Thiamin deficiency (vitamin B1/thiamin)
Particularly association with poor diet

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165
Q

what is cardiomyopathy

A

primary cardiac disease with contractile dysfunction and atypical morphology

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166
Q

what are the different forms of cardiomyopathy

A

dilated cardiomyopathy
hypertrophic cardiomyopathy
arrhythmogenic right ventricular cardiomyopathy
secondary
rare forms

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167
Q

what is dilated cardiomyopathy

A

Dilated cardiomyopathy is a type of heart muscle disease that causes the ventricles to thin and stretch, growing larger. It typically starts in the left ventricle.

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168
Q

is there a genetic component to dilated cardiomyopathy

A

yes - 1/3 familial inheritance but could be more. It is mostly autosomal dominant inheritance.

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169
Q

what mutations are linked with dilated cardiomyopathy

A

dystrophin
troponin T
beta myosin heavy chain
actin
lamin A/C
desmin

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170
Q

what is clinical presentation of dilated cardiomyopathy

A

Shortness of breath, thromboemboli, cardiac failure, dysrhythmias and ultimately death

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171
Q

what are causes of secondary dilated cardiomyopathy

A

alcohol
cobalt toxicity
catecholamines
Micro-infarction
Anthracyclines - dose dependent toxicity
cocaine
pregnancy

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172
Q

what is hypertrophic cardiomyopathy

A

the heart muscle cells enlarge and the walls of the heart chambers thicken. The heart chambers are reduced in size so they cannot hold much blood, and the walls cannot relax properly and may stiffen. Also, the flow of blood through the heart may be obstructed.

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173
Q

what mutations are linked to hypertrophic cardiomyopathy

A

beta myosin
myosin binding protein c
troponin C
titin

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174
Q

what mutations found in hypertrophic cardiomyopathy are linked to clinical features

A

beta myosin - cardiac hypertrophic and dysrhythmias
troponin T - risk of sudden death

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175
Q

what changes occur in hypertrophic cardiomyopathy

A

asymmetric hypertrophy with distortion
increased fibrosis
ventricular outflow distortion
myocyte disarray
variation in small artery structure

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176
Q

at investigations are done for hypertrophic cardiomyopathy

A

echocardiology and other imaging modalities together with investigation of genetics and family history

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177
Q

what is arrhythmogenic right ventricular cardiomyopathy

A

a degenerative condition with progressive dilatation of right ventricle, with fibrosis, lymphoid infiltrate and fatty tissue replacement

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178
Q

what is restrictive cardiomyopathy

A

this is a group of diseases in which poor dilation of the heart restricts the ability of the heart to take on blood and pass it to the rest of the body.

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179
Q

what causes restrictive cardiomyopathy

A

amyloid - cardiac or amyloidosis AL/AA
deposits in the heart and stiffens it

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180
Q

what does restrictive cardiomyopathy show on an ECG

A

a low voltage ECG

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181
Q

what is endomyocardial disease

A

Endomyocardial fibrosis (EMF) is a disease of rural poverty that is characterized by fibrosis of the apical endocardium of the right ventricle (RV), left ventricle (LV), or both.

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182
Q

clinical signs of endomyocardial disease

A

high grade eosinophilia
rash
progressive endocarditis
cardiac failure

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183
Q

what is glycogen storage disease

A

Glycogen storage disease (GSD) is a rare condition that changes the way the body uses and stores glycogen, a form of sugar. It is passed down from parents to children (inherited). For most GSDs, each parent must pass on one abnormal copy of the same gene. Most parents do not show any signs of GSD.
type 2, 3 and 4

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184
Q

what is hurler syndrome

A

Mucopolysaccharosis-glycosaminoglycans deposition in cells

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185
Q

what is hemochromotosis

A

multiorgan dysfunction with excess iron deposition in multiple tissues.

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186
Q

what is a sarcoidosis

A

A chronic granulomatous disease with numerous granulomas of non-caseating giant cell type. May involve the heart producing widespread areas of fibrosis and compensatory hypertrophy. It can produce a restrictive disorder. If it involves the conduction system then this may be the prime pathology of the patients with the risk of sudden death.

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187
Q

what is cardiac myxoma

A

cardiac tumour (75%) with bias towards the atria.
proliferation of myxoid cells with endothelial vascular channels and usually produces obstructive symptoms

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188
Q

what is rhabdomyoma

A

paediatric tumour with similarity to fetal cardiac cells
probably a hamartoma

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189
Q

what is a cardiac sarcoma

A

Cardiac sarcoma is a rare type of primary malignant (cancerous) tumor that occurs in the heart
These are rare and can show differentiation towards vascular, fibrous and muscle phenotypes. Almost invariably fatal.

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190
Q

what is the definition of haemopericardium

A

direct bleeding from the vascular wall through the ventricular wall fallowing a MI

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191
Q

what is the definition of haemopericardium

A

direct bleeding from the vascular wall through the ventricular wall fallowing a MI

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192
Q

what is cardiac tamponade

A

it is compression of the heart leading to acute cardiac failure following bleeding into the pericardial space direct bleeding from the vascular wall through the ventricular wall fallowing a MI

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193
Q

what is a cardiac tamponade

A

compression of the heart leading to acute cardiac failure following bleeding into the pericardial space

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194
Q

what is acute pericarditis

A

Acute pericarditis is an inflammatory process involving the pericardium that results in a clinical syndrome characterized by chest pain, pericardial friction rub, changes in the electrocardiogram (ECG) and occasionally, a pericardial effusion.2 Generally, the diagnosis requires 2 of these 3 features.

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195
Q

what are the signs and symptoms of acute pericarditis

A

Acute pericarditis typically presents with acute onset severe, sharp retrosternal chest pain, often radiating to the neck, shoulders, or back. Positional changes are characteristic with worsening of the pain in the supine position and with inspiration; and improvement with sitting upright and leaning forward.
Classically, a scratchy, grating, high-pitched friction rub is heard. This is felt to be caused by fibrinous deposits in the inflamed pericardial space.

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196
Q

where is the pericardial friction rub best heard

A

It is best heard during inspiration at the left lower sternal border, with the patient leaning forward. The rub may disappear with the development of an effusion and impending cardiac tamponade.

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197
Q

what are the features of elastic arteries

A

have two elastic laminae along with
tunica interna
tunica media
tunica adventitia
they also contain vasa vasorum

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198
Q

how does clot lysis occur

A

plasminogen is converted into plasmin. This then acts on fibrin to produce fibrin degradation products, and remove the fibrin cap on the clot.

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199
Q

what are complicated plaques

A

when there is calcification, mural thrombus or a vulnerable plaque

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200
Q

what are complications of plaque rupture

A

acute occlusion due to thrombus
chronic narrowing of vessel lumen with healing of the local thrombus
aneurysm change
embolism of thrombus +/- plaque lipid content

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201
Q

what is essential hypertension

A

Essential (primary) hypertension occurs when you have abnormally high blood pressure that’s not the result of a medical condition. This form of high blood pressure is often due to obesity, family history and an unhealthy diet. The condition is reversible with medications and lifestyle changes

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202
Q

what is the relationship between resistance and lumen size

A

resistance = 1/r^4

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203
Q

what are acquired causes of hypertension

A

chronic vascular disease - diabetes, primary elevation of aldosterone, cushings syndrome, pheochromocytoma, hyperthyroidism, coarctation or the aorta and rennin secreting tumours

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204
Q

what is arteriosclerosis

A

deposition of basement membrane like material and accumulation of plasma proteins within the vessel wall

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205
Q

in what conditions can arteriosclerosis be accelerated

A

diabetes and hypertension

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206
Q

what blood pressure indicates malignant or accelerated hypertension

A

> 160/110 mmHg

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207
Q

what is malignant or accelerated hypertension

A

Malignant/Accelerated hypertension is defined as a recent significant increase over baseline BP that is associated with target organ damage.
often seen in fundoscopic examination and is a medical emergency

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208
Q

what is raynaud’s phenomenon

A

Intermittent bilateral ischaemia of digits/extremities precipitated by motional cold temperature. Accelerated in cases of scleroderma and SLE. May produce distal atrophy and ulceration.

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209
Q

what is fibromuscular dysplasia

A

Abnormal architecture for the arteries producing variable lumen narrowing and distal poverty of circulation.
Particular importance in the renal arteries which produce renal vascular insufficiency and progressive hypertension due to renin-angiotensin stimulation.

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210
Q

what is vasculitis

A

an inflammatory and variably necrotic process centered on the blood vessels that can involve arteries veins and capillaries

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211
Q

how does vasculitis occur

A

it has an immune background of one of the following
- there is deposition of immune complexes
- there is direct attack on vessels by antibodies
- cell mediated immunity
viral infection

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212
Q

what viral antigens have been found in human vasculitis cases

A

HSV, CMV, parvovirus

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213
Q

what is polyarteritis nodosa

A

patchy necrotising arteries, affecting small and medium arteries. It is associated with neutrophils, lymphocytes, plasma cells and macrophages

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214
Q

what can polyarteritis nodosa lead to

A

can thrombose and cause a distal infarction, or heal with subsequent aneurysms. can cause widespread damage to the kidneys, cerebrocirculation and cardiac tissue. Can be rapidly fatal without treatment

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215
Q

what is hypersensitivity angiitis

A

it is a disease that involves deposition of immune complexesis causing inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura.
- can also be a feature of vascular disease

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216
Q

what is a diagnostic marker of hypersensitivity angiitis

A

palpable purpura

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217
Q

what drugs can cause hypersensitivity angiitis

A

aspirin
penicillin
phenytoin (Dilantin, an antiseizure medication)
allopurinol (used for gout)

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218
Q

what infections can cause hypersensitivity angiitis

A

streptococci
staphylococci
viral hepatitis
TB
bacterial endocarditis

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219
Q

what is Churg -Strauss syndrome

A

Churg-Strauss syndrome is a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA).

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220
Q

what organs can Churg -Strauss syndrome affect

A

lungs, spleen, kidney, heart, liver, CAN

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221
Q

what drug can be used to improve Churg-Strauss syndrome

A

steroids

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222
Q

what are features of Churg - Strauss syndrome

A

granulomatous inflammation with intense eosinophilic infiltrates

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223
Q

what is giant cell arteritis

A

an inflammation of the lining of your arteries. Most often, it affects the arteries in your head, especially those in your temples

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224
Q

what is the commonest type of vasculitis

A

giant cell vasculitis

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225
Q

what are risk factors for giant cell arteritis

A

Age. Giant cell arteritis affects adults only, and rarely those under 50
Sex. Women are about two times more likely to develop the condition than men are
Race and geographic region
Polymyalgia rheumatica
Family history.

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226
Q

What happens to vessels during giant cell arteritis

A

blood vessel is often thickened
there is granulomatous inflammation involving the full thickness of the wall - macrophages, lymphocytes, plasma cells, neutrophils involved.
variable necrosis
giant cells congregate in internal elastic lamina
thrombosis may occur

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227
Q

what can giant cell arteritis lead to

A

tends to be self-limiting but it can lead to blindness if it affects the ocular artery

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228
Q

what is Wegener’s granulomatosis

A

this is vasculitis of the respiratory tract and the kidney

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229
Q

what can Wegener’s granulomatosis cause in the lungs

A

bilateral pneumonitis with nodular infiltrates that can undergo cavitation mimics TB. Chronic sinusitis and ulcers of the nasal tissues are also common

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230
Q

what can Wegener’s granulomatosis cause in the kidney

A

focal necrotizing glomerulonephritis which progresses to crescentic glomerulonephritis

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231
Q

what are common symptoms of Wegener’s granulomatosis

A

pneumonitis
sinusitis
haematuria
proteinuria
skin rash
joint pains
neurological changes

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232
Q

what gender bias does Wegener’s granulomatosis have

A

male bias

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233
Q

what is Buerger disease

A

this is an inflammatory disease of medium and small arteries affecting the distal limbs

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234
Q

what does Buergers disease have a strong association risk with

A

tobacco smoking

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235
Q

what is the pathophysiology of Beurger disease

A

there is cell-mediated hypersensitivity to collagen type 2 and 3 with impaired endothelium - can have thrombotic and micro-abscess change
this can cause distal ischaemic symptoms and necrosis

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236
Q

stopping what can lead to remission of beurgers disease

A

stopping smoking

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237
Q

what is kawasaki disease

A

it is mucocutaneous lymph node syndrome - generation of antigens that bind to MHCII receptors

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238
Q

what arteries does Kawasaki syndrome principally effect

A

the coronary arteries

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239
Q

what pathogens is Kawasaki disease associated with

A

parvovirus B19
Coronovirus
staphylococci
streptococci
chlamydia infection

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240
Q

what is an aneurysm

A

dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels

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241
Q

what are aneurysms described as

A

fusiform
saccular
dissecting
arterio-venous

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242
Q

what is an abdominal aortic aneurysm

A

it is when there is over 50% dilation of the aortic diameter

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243
Q

are the majority of abdominal aortic aneurysms found

A

below the renal arteries

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244
Q

what is the major problem with abdominal aortic aneurysms

A

aneurysm rupture - those greater than 5-6 cm at increased risk

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245
Q

what are different treatment options for abdominal aortic aneurysms

A

waiting for rupture - higher mortality risk
prophylactic replacement with Dacron graft
endoluminal prosthesis - stent with prosthetic cover

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246
Q

what is a berry aneurysm

A

vascular dilation found in the cerebral circulation

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247
Q

what is a berry aneurism a consequence of

A

longstanding hypertension and/or focal area of weakness within the artery

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248
Q

where in the cerebrum are berry aneurysms commonly found

A

circle of Willis leading to a subarachnoid haemorrhage

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249
Q

what is a dissecting aneurysm

A

a tear occurs in the inner layer of the body’s main artery (aorta). Blood rushes through the tear, causing the inner and middle layers of the aorta to split (dissect)

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250
Q

where do the majority of dissecting aneurysms occur

A

just above the aortic ring

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251
Q

what disorders can predispose someone to getting a dissecting aneurysm

A

Marfans syndrome and other connective tissue disorders

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252
Q

what is syphilitic aortitis

A

an inflammatory disease affecting the vasa vasorum in the late stages of syphilis

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253
Q

what is the pathophysiology of syphilitic aortitis

A

Syphilitic aortitis begins as inflammation of the outermost layer of the blood vessel, including the blood vessels that supply the aorta itself with blood, the vasa vasorum
As it worsens, the vasa vasorum undergo hyperplastic thickening of their walls thereby restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall.
Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm

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254
Q

what are varicose veins

A

an enlarged and torturous vein, principally affecting the superficial leg veins

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255
Q

what are risk factors for varicose veins

A

age
female
hereditary
posture
obesity

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256
Q

wht causes varicose veins

A

progressive incompetence of valves with back pressure on venous circuit. This can cause thinning and dilation of the vascular wall with patchy calcification

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257
Q

what is lymphatic vessel obstruction

A

Lymphatic obstruction is a blockage of the lymph vessels that drain fluid from tissues throughout the body and allow immune cells to travel where they are needed. Lymphatic obstruction may cause lymphedema, which means swelling due to a blockage of the lymph passages.

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258
Q

what can cause lymphatic vessel obstruction

A

Infections with parasites, such as filariasis
Injury
Radiation therapy
Skin infections, such as cellulitis (more common in obese people)
Surgery
Tumors

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259
Q

at is the common surgical cause of lymphatic vessel obstruction

A

A common cause of lymphedema is removal of the breast (mastectomy) and underarm lymph tissue for breast cancer treatment. This causes lymphedema of the arm in some people, because the lymphatic drainage of the arm passes through the armpit (axilla)

260
Q

what is a haemangioma

A

this is a benign proliferation of blood vessel tissue - name varies on the site and age of the patient

261
Q

what are the different classifications of a haemangioma

A

capillary haemangioma
juvenile haemangioma
cavernous haemangioma

262
Q

what is a glomus tumour

A

a benign neoplasm involving the glomus body (component of the dermis layer of the skin, involved in body temperature regulation)

263
Q

what is mainly affected in a glomus tumour

A

the hands - painful

264
Q

what is a haemangioendothelioma

A

a vascular tumour of endothelial cells of low grade malignancy (can metastasise)

265
Q

what is an angiosarcoma

A

it is a highly aggressive malignant neoplasm of endothelial cells

266
Q

where is angiosarcoma commonly found

A

skin, soft tissue, breast, bone, liver and spleen

267
Q

what environmental carcinogens can cause angiosarcoma

A

arsenic and vinyl chloride

268
Q

what infection does karposi’s sarcoma have a link with

A

HIV and AIDS

269
Q

what virus causes karposi’s sarcoma

A

human herpes virus 8

270
Q

is karposi’s sarcoma often seen

A

on the skin

271
Q

what are risk factors for developing a deep vein thrombosis

A

venous flow stasis
injury - trauma, surgery, childbirth
hypercoagulability - pregnancy, cancer, inherited disorders
advanced age
sickle cell disease

272
Q

what are outcomes of DVT

A

lysis
organisation
provocation
embolism

273
Q

what symptoms may reflect a DVT

A

painful or tender calves - Homan sign

274
Q

what is the treatment for DVT

A

anticoagulants mainly

275
Q

what is an embolism

A

it is the passage of material (often thrombus) through the venous or arterial circulations.

276
Q

what is a paradoxical embolism

A

an embolus that travels through the venous circuit and then across from the right to left side of the heart through patent foramen ovale

277
Q

what are sources of embolism

A

atherosclerotic plaques
mural thrombus in heart or vasculature
infective endocarditis

278
Q

what are sites particularly vulnerable of an emboli

A

brain, intestine, distal limb, kidneys and coronary circulation

279
Q

what are other types of emboli (other than thrombus) are there

A

air embolism
acute decompression sickness
amniotic fluid embolism
fat embolism
bone marrow embolism
talc/cotton or other materials from intravascular injection

280
Q

how do you treat ischemic heart disease

A
  • statin: simvastatin
  • nitrate: GTN spray
  • Dual antiplatelet: aspirin and clopidogrel
    In acute NSTEMI - beta blockers, morphine, oxygen, aspirin and nitrate
    Acute STEMI - PCI (stent) if not fibrinolysis (streptokinase)
    surgical interventions - PCI and CABG
281
Q

what is pericarditis

A

inflammation of the pericardium with/without effusion

282
Q

what are causes of acute pericarditis

A

infectious - viral (common), coxsackievirus
Bacterial (mycobacterium tuberculosis
Non infectious - Trauma (common), uraemia, myocardial infarction

283
Q

what are signs of pericarditis

A

Chest pain, relieved by sitting forward/worsened by lying down and inspiration
- fever
- shortness of breath
- pericardial friction rub (high-pitched scratchy sound heard loudest on midline during inspiration)

284
Q

what investigations are done with suspected pericarditis

A
  • ECG (diagnostic) - saddle-shaped ST elevation with PR depression
  • do an echo/chest X-ray if suspect effusion
285
Q

how do you manage pericarditis

A

NSAIDS (ibuprofen) and colchicine
limit exercise

286
Q

what are complications of pericarditis

A

cardiac tamponade

287
Q

what is a cardiac tamponade

A

it is a life threatening condition whereby there is an accumulation of fluid in the pericardial space

288
Q

what is the pathophysiology of a cardiac tamponade

A

fluid in the pericardial space causes compression of the heart chambers and a decrease in venous return. Therefore decreases in filling of the heart and therefore cardiac output

289
Q

what are signs/symptoms of cardiac tamponade

A

Becks triad
- falling BP
- rising JVP
- muffled heart sounds
Pulsus paradoxus

290
Q

what is pulsus paradoxus

A

large decrease in stroke volume - where the systolic blood pressure drops by over 10mmHg on inspiration
- eventually unable to feel distal pulse

291
Q

what is the gold standard investigation for cardiac tamponade

A

Echo

292
Q

what is the management of cardiac tamponade

A

pericardiocentesis - removal of the fluids from the pericardial space

293
Q

what is kaussmaul’s sign

A

an increase in jugular venous pressure rather than a fall that you would expect.

294
Q

what are the major risks when someone has hypertension

A
  • stroke
  • MI
  • renal disease
  • cognitive decline -dementia
  • premature death
295
Q

what part of the cardiovascular system impact hypertension the most

A

peripheral resistance

296
Q

what can impact peripheral resistance

A

the renin-angiotensin-ldosterone system
sympathetic nervous system

297
Q

when is hypertension suspected in clinic

A

when BP is 140/90mmHg or higher

298
Q

what are people with suspected hypertension offered to confirm diagnosis of hypertension

A

ambulatory blood pressure monitoring

299
Q

what is stage 1 hypertension

A

clinic BP = 140/90
ABMP = 135/85

300
Q

what is stage 2 hypertension

A

clinic BP = 160/100
ABMP = 150/95

301
Q

what is severe hypertension

A

SBP = 180
DBP = 110

302
Q

what is the treatment for primary (essential) hypertension

A
  1. lifestyle modification
  2. antihypertensive drug therapy
303
Q

when do you offer antihypertensive drug treatment for someone with stage 1 hypertension

A

someone under 80 who has one of the following
target organ damage
established cardiovascular disease
renal disease
diabetes
10 year cardiovascular disease of 20% or greater

304
Q

when do you offer antihypertensive drug treatment in stage 2 hypertension

A

start them on treatment at any age

305
Q

what are the targets for antihypertensive therapy

A
  1. peripheral resistance (and cardiac output)
  2. RAAS
  3. Sympathetic nervous system
  4. Local vascular vasocontrictor and dilator mediator
306
Q

what is the action of angiotensin II in the body

A

vascular hyperplasia and hypertrophy
aldosterone release
tubular sodium reabsorption
also acts as a vasoconstrictor and increases cardiac output

307
Q

what is the action of noradrenaline in the cardiovascular system

A

peripheral resistance increase
increase cardiac output
(also increases renin release)

308
Q

What are the main uses of ace inhibitors

A

used in hypertension, heart failure, diabetic nephropathy

309
Q

give examples of ACE inhibitors

A

Ramipril
Enalapril
Perindopril
Trandolapril

310
Q

What are the main adverse effects of ACE inhibitors

A
  1. Related to reduced angiotensin II formation: hypotension, Acute renal failure, Hyperkalaemia, teratogenic effects in pregnancy
  2. Related to increased kinin production: cough, Rash, anaphylactoid reactions
311
Q

why does kinin production increase with ACE inhibitors

A

ACE also converts bradykinin to inactive peptides. With ACE inhibitors you increase bradykinin production, getting side effects like cough and rash.

312
Q

what diseases do you use angiotensin II receptor blockers in

A

hypertension
diabetic nephropathy
Heart failure (when you cant use ACE inhibitors)

313
Q

what examples of angiotensin II receptor blockers

A

Candesartan
Losartan
Valsartan
Irbesartan
Telmisartan

314
Q

what are the main adverse effects of angiotensin II receptor blockers

A

systemic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angioedema

315
Q

are angiotensin II receptor blockers contraindicated in pregnancy

A

YES

316
Q

what conditions are calcium channel blockers used in

A

hypertension
arrhythmia (tachycardia)
ischemic heart disease

317
Q

What are examples of calcium channel blockers

A

Amlodipine
Nifedipine
Felodipine
Lacidipine
Diltiazem
Verapamil

318
Q

what are the three subtypes of calcium channel blockers

A
  1. Dihydropyridines
  2. Phenylalkylamines
  3. Benzothiazepines
319
Q

what is the action of dihydropyridines (CCB)

A

Preferentially affects vascular smooth muscle - peripheral arterial vasodilators

320
Q

what are examples of dihydropyridines (CCB)

A

Amlodipine
Nifedipine
Felodipine

321
Q

what is the action of phenylalkylamines

A

the main effect is on the heart
- Negatively chronotropic (reduced heartbeat)
- Negatively inotropic (reduced contractility)

322
Q

what is an example of phenylalkylamines

A

Verapamil

323
Q

what is the action of benzothiazepines

A

intermediate heart/peripheral vascular effects

324
Q

what is an example of benzothiazepine

A

diltiazem

325
Q

what are the adverse effects of calcium channel blockers

A
  1. due to peripheral vasodilation: flushing, headache, oedema, palpitations
  2. Due to negative chronotropic effects: bradycardia, AV block
  3. Negative ionotropic effects: worsening of cardiac failure
  4. verapamil causes constipation
326
Q

what calcium channel blockers cause adverse effects due to negative chronotropic effects

A

verapamil
diltiazem

327
Q

what calcium channel clocker causes adverse effects due to peripheral vasodilation

A

mainly dihydropyridines

328
Q

what calcium channel blocker causes adverse effects due to inotropic effects

A

verapamil

329
Q

what are the uses of beta - adrenoceptor blockers

A

ischaemic heart disease
heart failure
arrhythmia
hypertension

330
Q

what are examples of beta blockers

A

bisoprolol
propranolol
carvedilol
metoprolol
atenolol
nadolol

331
Q

what does the word cardioselective mean

A

often used to imply B-1 selectivity
- this is a misnomer since up to 40% of cardiac beta adrenoceptors are B2

332
Q

what beta blockers are beta 1 selective

A

metoprolol
Bisoprolol

333
Q

what beta blockers are non selective

A

propranolol
Nadolol
Carvedilol
(atenolol is slightly B 1 selective but not very)

334
Q

what are the main adverse effects of beta blockers

A

fatigue
headache
sleep disturbance/nightmares
bradycardia
hypotension
cold peripheries
erectile dysfunction

335
Q

what can beta blockers cause worsening of

A

asthma, or COPD
PERIPHERAL VASCULAR DISEASE - claudication or Raynaud’s
heart failure - given standard dose or acutely (need to start dose small and slowly up the dose)

336
Q

what are diuretics used for (CVD)

A

hypertension
heart failure

337
Q

what are the different classes of diuretics

A
  1. thiazides and related drugs (distal tubule)
  2. Loop diuretics
  3. Potassium-sparing diuretics
  4. aldosterone antagonists
338
Q

what are examples of thiazides

A

bendroflumethiazide
hydrochlorothiazide
chlorthalidone

339
Q

what are examples of loop diuretics

A

furosemide
bumetanide

340
Q

what are examples of potassium sparing diuretics

A

amiloride
triamterine
spironolactone - also aldosterone agonist
eplerenone - also aldosterone agonist

341
Q

what are the main adverse effects of diuretics

A

hypovolaemia
hypotension
low serum potassium, sodium, magnesium and calcium
raised uric acid (gout)
erectile dysfunction - thiazides
impaired glucose tolerance

342
Q

what are other examples of antihypertensives

A

alpha 1 adrenoceptor blockers
centrally acting antihypertensives
direct renin inhibitor

343
Q

what is an example of an alpha 1 adrenoceptor blocker

A

doxazosin

344
Q

at is an example of a centrally-acting antihypertensive

A

moxonidinl
methyldopa

345
Q

what is an example of a direct renin inhibitor

A

aliskiren

346
Q

according to NICE what is the hypertensive treatment for those over 55 or Afro-Caribbean of any age

A

Calcium channel blocker

347
Q

according to NICE what antihypertenside treatment do you give an under 55 patient

A

ACE - inhibitor or Angiotensin II receptor blocker

348
Q

what happens when someone doesnt respond to first like hypertension drugs

A

you combine ACE-inhibitor or angiotensin II receptor blocker PLUS calcium channel blocker

349
Q

what happens when someone doesnt respond to second-line hypertension drugs

A

you combine ACE-I/ARB + CCB
+ thiazide - like - diuretic

350
Q

How do you treat acute UA/NSTEMI

A

BMOAN
- Beta blocker
- morphine
- oxygen
- aspirin
- nitrate

351
Q

how do you treat acute STEMI

A
  • if available within 120 minutes of medical contact then PCI
  • if not then fibrinolysis (streptokinase/alteplase)
352
Q

what surgical interventions do you use to treat IHD

A
  • PCI (stent)
  • CABG (preferred in patients with diabetes and over 65)
353
Q

what is the definition of heart failure

A

the inability of the heart to deliver blood and thus oxygen at a rate that is commensurate with the requirements of the body

354
Q

what can heart failure result from

A

can result from structural or functional cardiac disorder that impairs the hearts ability to function

355
Q

what compensatory mechanisms occur when the heart starts to fail

A

BP falls which is detected by baroreceptors causing an increase in sympathetic activation. This leads to positive inotropic and chronotropic effects thus increasing the cardiac output
Activation of the RAAS system

356
Q

what are causes of heart failure

A
  • ischemic heart disease
  • cardiomyopathy
  • valvular heart disease (AS/MR)
  • hypertension
  • alcohol excess
  • Cor pulmonale
  • anemia, arrhythmia, hyperthyroidism
  • congestive heart failure (both sided)
357
Q

what is cor pulmonale

A

it is a disease of the lungs/pulmonary vessels causing pulmonary hypertension and therefore right ventricular hypertrophy. This can cause right sided heart failure with venous overload, peripheral oedema and hepatic congestion

358
Q

what are the different types of heart failure

A

systolic heart failure
diastolic heart failure
acute/chronic
heart failure reserved ejection fraction
heart failure preserved ejection fraction

359
Q

what is systolic heart failure

A

the inability of the ventricle to contract properly

360
Q

what is diastolic heart failure

A

the inability of the ventricle to relax and fill properly

361
Q

what is HF reserved ejection fraction

A

systolic where the ejection fraction is lower than 40%

362
Q

what is HF preserved ejection fraction

A

diastolic where the ejection fraction is larger than 40%

363
Q

what are risk factors of heart failure

A

over 65
male
obese
previous MI
African descent

364
Q

what are the symptoms/signs of heart failure

A

SOFA PC
- shortness of breath
- orthopnea
- fatigue
- ankle swelling
- pulmonary oedema
- cold peripheries
Raised JVP
End respiratory crackles

365
Q

what blood test can you do to diagnose heart failure

A

Brain (B type) natriuretic peptide (BNP)

366
Q

What will heart failure look like on an ECG

A

The ECG may reveal abnormalities such as atrial fibrillation, abnormal Q waves, LV hypertrophy (LVH), and a widened QRS complex

367
Q

what would a transthoracic ECG show in heart failure

A
  • wall motion abnormalities
  • valvular disease
  • cardiomyopathies
368
Q

what could a chest X ray show when someone is heart failure

A
  • Alveolar oedema
  • B-lines
  • Cardiomegaly
  • Dilated upper lobe vessels
  • Effusion (pleural)
369
Q

how can you diagnose heart failure

A

Blood test
ECG
Transthoracic ECG
Chest X-ray

370
Q

how do you treat acute heart failure

A
  • oxygen
  • morphine
  • furosemide
  • GTN spray
371
Q

What lifestyle changed can you make to treat chronic heart failure

A
  • stop smoking!
  • eat less salt, optimise weight and nutrition
  • avoid NSAIDs/verapamil
372
Q

How can you medically treat chronic heart failure

A

AABCDD
1st line: ACE-I and beta blockers
2nd line: ARB and nitrate
3rd line: Cardiac resynchronisation or digoxin
Diuretics: furosemide as a symptom relief

373
Q

What are primary causes of hypertension

A

often primary cause is unknown

374
Q

what are secondary causes of hypertension

A

renal disease
pregnancy
endocrine disease
coarctation
drugs
toxins

375
Q

what signs/symptoms of hypertension

A

Usually asymptomatic
When malignant hypertension look for damage to brain, eye, heart and kidney

376
Q

what head (brain) symptoms can you get in hypertension

A

central oedema, hemorrhage, headache

377
Q

what eye symptoms can you get in hypertension

A

papilledema, cotton wool spots

378
Q

what pecs/heart symptoms do you get in hypertension

A

AF, aortic dissection, chest pain, dysponoea (acute HF)

379
Q

what renal symptoms do you get in hypertension

A

haematuria, proteinuria (acute kidney infarction)

380
Q

how do you diagnose hypertension

A

Recheck patients BP on 2-3 occasions over few weeks/months
if high offer ABPM

381
Q

what happens if stage 1 hypertension is diagnosed

A

Do a QRISK to decide on treatment pathway

382
Q

what happens if stage 2 hypertension is diagnosed

A

start antihypertensive treatment

383
Q

what happens if a patient has malignant hypertension and signs of a papilloedema/and signs of renal haemorrhage

A

they will get same day admission
start antihypertensive drug treatment immediately

384
Q

for diabetics with hypertension what is always the first line treatment

A

ACE-I

385
Q

what antihypertensive treatment is contraindicated in pregnancy (or if patient is on general anesthesia)

A

ACE-I

386
Q

what organisms can cause infective endocarditis

A

staphylococcus aureus (most common for IV drug use)
Streptococcus viridians (mouth/oral surgery and most common for non IV drug users)
Staphylococcus epidermis (prosthetic valves)

387
Q

what are symptoms of infective endocarditis

A

signs of infection - fever, fatigue, loss of appetite)

388
Q

what are the clinical manifestations of infective endocarditis

A

splinter haemorrhages
osler nodes
janeway lesions
roth spots

389
Q

what are Osler nodes

A

tender nodules in fingers

390
Q

what are Janeway lesions

A

nodules on the palms of the hands

391
Q

What are Roth spots

A

haemorrhage with a clear centre on fundoscopy (eye)

392
Q

how do you diagnose infective endocarditis

A

modified dukes criteria
Echo - GOLD STANDARD
ECG - prolonged PR interval

393
Q

what is the Modified dukes criteria - the major criteria

A
  1. blood cultures positive for endocarditis - needs to be from two separate blood cultures or bloods coming in are persistently positive (i.e taken 3 - 12 hours apart)
  2. Evidence of endocardial movement - echocardiogram positive such as abscess, or a new valvular regurgitation
394
Q

what is the minor criteria for the modified duke’s criteria

A
  • predisposing heart condition or IV drug use
  • fever
  • vascular/immunological signs
  • positive blood culture (doesnt meet major criteria)
  • positive echocardiogram (doesnt meet major criteria)
395
Q

How do you use the modified dukes criteria to diagnose infective endocarditis

A

Definite IE = 2 major/1 major with 3 minor/all 5 minor

396
Q

what is the treatment for infective endocarditis

A

antibiotics for 4-6 weeks

397
Q

What antibiotic would you use for staphylococcus induced infective endocarditis

A

Flucloxacilin and rifampicin and gentamicin
IF MRSA use vancomycin, rifampicin and gentamicin

398
Q

what antibiotic would you use for a non staphylococcus infective endocarditis

A

benzylpenicillin plus gentamicin

399
Q

what antibiotics would you use for an unknown organism infective endocarditis

A

Flucloxacillin, plus ampilicin and gentamicin

400
Q

what murmur is heard with mitral valve stenosis

A

rumbling mid-diastolic murmur with an opening snap (best heart on expiration and patient on their left side)
- diastolic decrescendo, presystolic crescendo

401
Q

what murmur is heard for mitral regurgitation

A

pansystolic murmur radiating to the left axilla
- systolic holo or pan

402
Q

what murmur is heard for aortic stenosis

A

an ejection systolic murmur which radiates to the carotids and apex
- systolic crescendo/-decrescendo

403
Q

what murmur is heard for aortic regurgitation

A

an early diastolic murmur (best heard on expiration with patient sat forward)
- diastolic decrescendo

404
Q

what are the symptoms of a mitral valve stenosis

A
  • exertional dyspnoea
  • haemoptysis (coughing of blood due to pulmonary oedema)
  • palpitations (AF)
  • chest pain
405
Q

what are the symptoms of mitral valve regurgitation

A
  • palpitations
  • exertional dyspnoea
  • fatigue
  • weakness
406
Q

what are the symptoms of an aortic valve stenosis

A

Triad of
- syncope
- angina
- dyspnoea

407
Q

what are the symptoms of aortic valve regurgitation

A

palpitations
angina
dyspnoea

408
Q

what are the signs of mitral valve stenosis

A

malar flush - plum red discolourisation of high cheeks
atrial fibrillation
tapping apex beat
low volume pulse
loud S1

409
Q

what are the signs of mitral valve regurgitation

A

atrial fibrillation
displaced thrusting apex
soft or absent S1

410
Q

what are the signs of aortic valve stenosis

A

sustained heaving apex
slow rising pulse
narrow pulse pressure
soft S2 if severe

411
Q

what are the signs of aortic valve regurgitation

A

water hammer pulse
wide pulse pressure
displaced apex
carotid pulsation (Corrigan’s sign)
Head nodding with heartbeat (De Musset’s)
Capillary pulsation in nail bed (Quincke’s)

412
Q

what are causes of mitral valve stenosis

A

Rheumatic heart disease - most common
annular calcification
congenital
mucopolysaccharidosis

413
Q

what are causes of mitral valve regurgitation

A

papillary muscle rupture/dysfunction (post MI)
mitral valve prolapse
rheumatic heart disease
infective endocarditis
connective tissue disorders
Myxomatosis mitral valve

414
Q

what are causes of aortic valve stenosis

A

senile calcification of valve
congenital bicuspid valve
rheumatic heart disease

415
Q

what are causes of aortic valve regurgitation

A

acute - aortic dissection and infective endocarditis
chronic - connective tissue disorders, rheumatic heart disease, RA, AS and takayasu’s
Congenital bicuspid valve

416
Q

what is the key complication in the first 24h of an MI

A

Arrhythmia

417
Q

what hypertension medication can cause a dry cough

A

lisinopril

418
Q

how do you work out pulse pressure

A

systolic - diastolic pressure

419
Q

how do you work out the mean arterial pressure

A

diastolic pressure + 1/3 pulse pressure

420
Q

what is the afterload

A

Force against which the ventricles must contract to expel the blood out of the ventricles

421
Q

what vascular changes are seen in hypertension

A
  • accelerated hypertension
  • causes thickening of media of muscular arteries
422
Q

what can happen to the heart in hypertension

A

major risk factor for developing ischemic heart disease

423
Q

what nervous system pathology is seen in hypertension

A

intracerebral haemorrhage

424
Q

what kidney pathology is seen in hypertension

A

can cause or develop from renal disease
kidney size is reduced and small vessels show intimal thickening and hypertrophy

425
Q

what tests do you do to check for end organ damage in hypertension

A

urinalysis - check albumin: creatinine ratio and haematuria
ECG/echo
Fundoscopy
Bloods - look for serum creatinine, eGFR and glucose

426
Q

what is the treatment for malignant hypertension

A

sodium nitroprusside

427
Q

what does lead I on an ECG measure

A

the lateral side of the heart
- supplied by circumflex artery

428
Q

what does lead II on an ECG measure

A

The inferior side of the heart
- supplied by the right coronary artery

429
Q

what does lead III on an ECG measure

A

The inferior side of the heart
- supplied by the right coronary artery

430
Q

what does lead aVL on an ECG measure

A

the lateral side of the heart
- supplied by the circumflex artery

431
Q

what does lead aVF on an ECG measure

A

the inferior boarder of the heart
- supplied by the right coronary artery

432
Q

what does lead V1 on an ECG measure

A

the septal portion of heart
- supplied by the left anterior descending artery

433
Q

what does lead V2 on an ECG measure

A

the septal portion of the heart
- supplied by the left anterior descending artery

434
Q

what does lead V3 measure on an ECG

A

the anterior boarder of the heart

435
Q

what does lead V3 measure on an ECG

A

the anterior boarder of the heart
- supplied by the right coronary artery

436
Q

what does lead V4 measure on an ECG

A

the anterior boarder of the heart
- supplied by the right coronary artery

437
Q

what does lead V5 measure on an ECG

A

the lateral boarder of the heart
- supplied by the circumflex artery

438
Q

what does lead V6 measure on an ECG

A

the lateral boarder of the heart
- supplied by the circumflex artery

439
Q

in what ECG lead are all waves negative

A

in lead avR !!!

440
Q

what are the ten rules of ECG

A
  1. PR = 120-200 ms (3-5 small squares)
  2. QRS not wider than 110ms (3 little squares)
  3. QRS upright in leads I and II
  4. QRS and T waves have same direction in leads I, II and III
  5. ALL waves negative in aVR lead
  6. R wave increases in size from V1-V4, S wave grows from V1 to 3 and is absent in V6
  7. ST segment is isoelectric in all leads except V1 and V2 where it may be slightly raised (very raised is bad)
  8. P waves upright in I and II and V2-V6
  9. There should be no Q waves larger than 0,04s in I, II, V2-V6
  10. T wave upright in I, II, V2-V6
441
Q

what does right atrial enlargement look like on ECG

A

Tal (>2.5mm) and pointed P waves in limb leads

442
Q

what does left atrial enlargement look like on an ECG

A

Notched/bifid M shaped P waves in the limb leads

443
Q

what disorders causes short PR intervals

A

Wolff-Parkinson-white syndrome
Accessory pathway (Bundle of Kent) allows early activation of the ventricle (delta wave and short PR interval)

444
Q

what disorders cause a long PR interval

A

first degree heart block

445
Q

what is a pathological Q wave

A

when its more than 2mm deep and over 1mm wide, OR, over 25% amplitude of the subsequent R wave

446
Q

what is the J point

A

it is the junction point between QRs and ST segment

447
Q

what are U waves on an ECG

A

U wave related to after depolarisations which follow repolarisations
U waves are small, round, symmetrical and positive in lead II, with amplitude < 2 mm
U wave direction is the same as T wave
More prominent at slow heart rates

448
Q

what percent of births have a congenital heart defect

A

1%

449
Q

how percentage of congenital heart defects are tetralogy of fallot

A

10%

450
Q

how can you resolve a tetralogy of fallot

A

surgical intervention

451
Q

what are the common structural heart defects

A

ventricular septal defect
atrial septal defect
atrioventricular septal defect
patent ductus arteriosus
coarctaction of the aorta
bicuspid aortic valve and aortopathy
pulmonary stenosis
tetralogy of fallot
eisenmenger syndrome

452
Q

what is ventricular septal defect

A

an abnormal connection between the two ventricles

453
Q

what is the outcomes of having a ventricular septal defect

A

high pressure in the left ventricle
low pressure in the right ventricle
blood flows from the high pressure to low, flowing back into the right ventricle and increasing blood flow through the lungs

454
Q

what does a large ventricular septal defect lead to

A

a very high pulmonary blood flow in infancy
breathlessness
poor feeding
failure to thrive

455
Q

what can a large ventricular septal defect lead to

A

Eisenmenger’s syndrome and right ventricle hypertrophy

456
Q

How do you fix a large ventricular septal defect

A

PA band, complete repair

457
Q

what happens when you have a small ventricular septal defect

A

there is a small increase in pulmonary blood flow only
- often asymptomatic

458
Q

what do you have an increased risk of if you have a small ventricular septal defect

A

endocarditis

459
Q

How do you fix a small ventricular septal defect

A

no intervention is needed

460
Q

what are the clinical signs of a large ventricular septal defect

A

small breathless skinny baby
increased respiratory rate
tachycardia
big heart on chest X ray
murmur varies in intensity

461
Q

what are the clinical signs of a small ventricular septal defect

A

loud systolic murmur
thrill (buzzing sensation)
will have a normal heart rate and size

462
Q

What is Eisenmengers syndrome

A

In Eisenmenger syndrome, there is irregular blood flow in the heart and lungs. This causes the blood vessels in the lungs to become stiff and narrow causing pulmonary arterial hypertension. Eisenmenger syndrome permanently damages the blood vessels in the lungs.

463
Q

what is the pathophysiology behind Eisenmengers syndrome

A

There is a high pressure pulmonary blood flow (due to irregular connection in heart), which damages the pulmonary vasculature. This leads to an increased resistance through the lungs, increasing the right ventricular pressure.
This causes the shunt to reverse and the patient becomes BLUE

464
Q

what is an atrial septal defect

A

an abnormal connection between the two atria (premium, secundum and sinus venosus)

465
Q

at what age does atrial septal defects normally present

A

often present in adulthood

466
Q

what is the physiology of an arterial septal defect

A

there is a sightly higher pressure in the left atria than the right and therefore the shunt is from the left to the right. This causes an increased flow into the right hear and therefore the lungs

467
Q

what occurs in a large atrial septal defect

A

there is a significant increase in flow through the right heart and lungs during childhood which leads to a right heart dilation.
shortness of breath on exertion
increased chest infections
if there is any stretch on the right side of the heart, the shunt should be closed

468
Q

what occurs in a small arterial septal defect

A

there is a small increase in flow
no right heart dilation
no symptoms
leave this alone

469
Q

what are the the clinical signs of an arterial septal defect

A

pulmonary flow murmur
fixed split second heart sound - delayed closure of PV because more blood)
big pulmonary arteries on chest X ray
big heart on chest X ray

470
Q

how do you close an arterial septal defect

A
  • surgical intervention
  • key hole technique
471
Q

what is an atrio-ventricular septal defect

A

hole in the middle of the heart - involves the ventricular and atrial septum, the mitral and tricuspid valves (can be complete or partial)

472
Q

what genetic condition do you often see atrio-ventricular septal defects

A

Downs syndrome

473
Q

What is the pathophysiology of atrio-ventricular septal defect

A

instead of two separate AV valves there is one large malformed one

474
Q

what happens when there is a complete AVSD defect

A

breathlessness as neonate
poor weight gain
poor feeding
torrential pulmonary blood flow

475
Q

how do you repair complete AVSD

A

PA band in infancy (surgery)

476
Q

what happens in a partial AVSD defect

A

can present like a small ventricular or arterial septal defect - can be left along if there is no right heart dilation

477
Q

what are clinical signs of a patent ductus arteriosus

A

a continuous ‘machinery’ murmur
if its large you can have heart hypertrophy and breathlessness
can lead to Eisenmengers syndrome

478
Q

how do you close a patent ductus arteriosus

A

surgical or percutaneous

479
Q

what are the clinical signs of coarctation of the aorta

A

right arm hypertension
bruits of the scapulae and back from collateral vessels
murmur

480
Q

what is a bicuspid AV

A

when you only have two cusps rather than three in the aortic valve

481
Q

what is pulmonary stenosis

A

narrowing of the outflow of the right ventricle

482
Q

what can severe pulmonary stenosis lead to

A

right ventricular failure as neonate
collapse
poor pulmonary blood flow
right ventricular hypertension
tricuspid valve regurgitation

483
Q

what is the treatment for pulmonary stenosis

A

balloon valvuloplasty
open valvotomy
open trans-annular patch
shunt

484
Q

What do you give someone who has resistant hypertension

A

ACE-I/ARB + CCB + thiazide - like diuretic
with the addition of spironolactone, high dose thiazide, alpha blocker, beta blocker

485
Q

What is a NSTEMI (subendocardial infarct )

A

an unstable plaque with a thrombus occluding over 90% of the vessel. Blood flow is restricted enough that cells start to die. This patient often has pain at rest.

486
Q

What is a STEMI (transmural infarct)

A

an unstable plaque and a thrombus occluding 100% of the lumen - Infarction

487
Q

How would you diagnose prinzmetals angina

A

ST elevation on ECG
Troponin C is negative
The spasm can be reproduced by Ach

488
Q

What patients may have a silent MI (no pain)

A

Diabetics
Elderly
Post heart transplant patients

489
Q

What are signs of a right ventricular MI

A

Jugular venous distension
lower leg oedema
hypotension
bradycardia

490
Q

what are signs of left ventricular MI

A

pulmonary oedema
hypotension
S4 heart sound
Tachycardia (reflex)

491
Q

what do you need to watch out for in the first 24 hours after an MI

A

patient can go into premature ventricular contraction which can lead to ventricular fibrillation if it was a significant infarct.
- have cold extremities
- can cause flash pulmonary oedema

492
Q

what can happen 24hrs to 3 days after a MI

A
  • can get rupture syndromes due to ventricular septal defect, leading to a free wall rupture and blood can leak into the pericardial cavity. This can lead to cardiac tamponade
  • can get mitral regurgitation due to papillary rupture (murmur)
493
Q

what can happen 3-14 days after an MI

A

pericarditis due to inflammation
patient has an increased risk of left ventricular aneurysm causing clots and an increased chance of embolism

494
Q

How would you diagnose an NSTEMI

A

ST depression
T wave inversion
Troponin positive

495
Q

how would you diagnose an unstable angina

A

ST depression
T wave inversion
Troponin negative

496
Q

What is the stress test for IHD

A

make someone exercise and you look for any flow limiting stenosis
- Perform an ECG looking for a reduction in ST or T wave inversion
- Echo looking at wall motion anomalies
- MPI looking for cod spots
you can also do a drug induced stress test using dobutamine

497
Q

what leads to you see an inferior STEMI in

A

leads II III and avF

498
Q

what do you think when you see a hyperacute T wave

A

ischemia that is progressing to infarction

499
Q

why would you give someone nitroglycerine after a MI

A

it causes dilation of the cardiovascular system which causes a reduction in the preload. This reduces stroke volume and therefore the oxygen demand of the heart

500
Q

what type of patient would you not give nitroglycerin to

A

those who are preload dependent - Right ventricular MI

501
Q

what is the definition of a tachyarrhythmia

A

an abnormal rate of above 100bpm

502
Q

what is the definition of a bradyarrhythmia

A

an abnormal rate of below 60bpm

503
Q

what arrythmias are defined as supraventricular tachyarrhythmias

A

sinus tachycardia
atrial tachycardia (focal and multifocal)
atrial fibrillation
atrial flutter
AVN re-entral tachycardia
AVRT

504
Q

what arrythmias are defined as ventricular tachyarrhythmias

A

ventricular tachycardia (monomorphic and polymorphic)
Polymorphic V.T with prolonged QT
Torsades de pointes
Ventricular fibrillation

505
Q

what is sick sinus syndrome

A

The SAN is dysfunctional and produces a sinus bradycardia, From this you can develop SVT

506
Q

what are the different types of bradyarrhythmias

A

sinus bradycardia
first degree heart block
second decree heart block (Mobitz 1 and 2)
third degree heart block

507
Q

What is cushings triad

A

decreased heart rate
increased blood pressure
irregular respiratory rate

508
Q

what metabolic reasons could cause an increase in vagal tone (bradycardia)

A

Hypothyroidism
hyperkalaemia
increase in intercranial pressure (cushings triad)

509
Q

what can cause early after depolerisation

A

Electrolyte imbalance (low potassium, calcium and magnesium)
Drugs such as antibiotics, anti arrhythmia or antipsychotic drugs

510
Q

what is an early after depolerisation

A

Early afterdepolarizations (EADs) are secondary voltage depolarizations during the repolarizing phase of the action potential

511
Q

what can cause a delayed after depolerisation

A

ischemia causing irritation, hypoxia, inflammation, increased sympathetic tone or digoxin toxicity

512
Q

what is delayed after depolerisation

A

The delayed afterdepolarization (DAD) arises from the resting potential after full repolarization of an action potential and it may reach threshold for activation.

513
Q

what would you see on an ECG for early after depolerisation

A

polymorphic V.T with a long QT (torsardes)

514
Q

What would you see on an ECG for delayed after depolerisation

A

Multifocal atrial tachycardia
Focal atrial tachycardia
VT with a normal QT

515
Q

What arrythmias have re-entrance circuits

A

AVN re-entrance tachycardia
Atrioventricular re-entrance tachycardia
Atrial fibrillation
Atrial flutter
Ventricular fibrillation
Ventricular tachycardia

516
Q

what is an AVRT

A

(wolf-Parkinson-White syndrome)
an accessory pathway (bundle of Kent) means electrical impulses can travel between the atria and ventricle without needing to go through the AVN

517
Q

What is AVNRT

A

abnormal pathway within the AV node
- alpha = slow conduction and a short refractory period
- beta = fast conduction and long refractory period
most common is the slow fast pathway

518
Q

what are the two types of AVRT

A

Orthodromic - ventricle back to atria (narrow QRS)
Antidromic - atria to ventricle (depol bottom up) ( wide QRS)

519
Q

why might you get a conduction block

A

inferior wall MI
Fibrosis
Hyperkalaemia
Beta blockers
calcium channel blockers
digoxin
amyloidosis and sarcoidosis

520
Q

What is seen on a sinus tachycardia ECG

A

P waves are present, narrow QRS complex and T wave is present - rapid rate

521
Q

What is seen in a focal atrial tachycardia ECG

A

Inverted P wave (in lead II and upright in avR), narrow QRS

522
Q

What is seen in atrial flutter ECG

A

Saw tooth P waves (II, III, avF)

523
Q

What is seen in an AVRT/AVNRT ECG

A

No P waves seen (can have retrograde P waves) and you will have an narrow QRS

524
Q

what is seen on an atrial fibrillation ECG

A

No P waves
Fibrillation waves in P1
irregular PR intervals
IRREGULARLY IRREGULAR

525
Q

what is seen in multifocal atrial tachycardia ECG

A

morphologically different P waves

526
Q

what is seen in ventricular tachycardia ECG

A

QRS is wider than 0.14 seconds (with atrioventricular dissociation)/ Extreme right axis deviation

527
Q

what is seen in supraventricular tachycardia with a bundle branch block ECG

A

QRS is less than 0.4 seconds and there is no AV dissociation

528
Q

what is seen in atrial fibrillation with bundle branch bock

A

QRS is the same morphology but it is irregular

529
Q

what is seen in a sinus bradycardia ECG

A

normal morphology but it is slower than your normal rate

530
Q

what does a first degree heart block look like on ECG

A

P wave with a prolonged PR interval (over 200ms)

531
Q

what does a second degree heart block look like on ECG

A

There is not a QRS complex for every P wave with a prolonged PR interval

532
Q

what does a mobitz type 2 heart block look like on ECG

A

Not every P wave has a QRS following it but there is a normal PR interval

533
Q

What does a type 3 heart block look like on an ECG

A

Complete AV dissociation, beating independently to eachother

534
Q

What does hypocalcaemia present on an ECG

A

Prolonged QT interval (secondary to a prolonged ST segment)

535
Q

what does hypercalcaemia present on an ECG

A

short QT interval, ST segment shortening with an increased amplitude in the QRS complex. T wave is prolonged and you may have a prominent U wave

536
Q

how does hypokalaemia present on ECG

A

small or inverted T waves, prominent U waves, a long PR interval and depressed ST elevations

537
Q

how does hyperkalaemia present on an ECG

A

tall tented T waves, small P waves, wide QRS, ventricular fibrillations, sine wave

538
Q

what is the most likely cause of sudden cardiac death

A

hypertrophic obstructive cardiomyopathy

539
Q

how long is the bleeding time

A

3-5 minutes (how long it takes to clot)

540
Q

what is the S3 heart sound

A

it shows rapid ventricular filling in early diastole

541
Q

What is the S4 heart sound

A

Pathological gallop - due to blood forced into a stiff hypertrophic ventricle

542
Q

what is the definition of angina pain

A
  1. central crushing chest pain radiating to the neck or jaw
  2. brought on with exertion
  3. relieved by rest or GTN spray
543
Q

what is decubitus angina

A

it is induced when lying flat

544
Q

what is the GRACE score

A

it is a predictor of mortality from MI in the next 6 months to 3 years in patients

545
Q

What is the QRISK score

A

it predicts the risk of CVD in 10 upcoming years. Includes age, blood pressure, socioeconomic status, ethnicity etc.
a score of over 10 (10% increased risk in the next 10 years) starts the patient on lipid lowering therapy

546
Q

when do symptoms start to occur in angina

A

then 70-80% of the lumen is occluded

547
Q

what is acute coronary syndromes

A

It is the umbrella term for unstable angina, NSTEMI and STEMI

548
Q

what ECG changes occur after an MI

A

Hyperacute T wave
pathologially deep Q waves
Left bundle branch block

549
Q

what is seen in ECG for unstable angina

A

Normal - may show some ST depression or T wave inversion

550
Q

What is seen in ECG for NSTEMI

A

ST depression and T wave inversion
- no Q waves

551
Q

What is seen in ECG for STEMI

A

ST segment elevation in local leads (2+)
Q waves - pathological

552
Q

what is a type 1 and type 2 MI

A

type 1 = ischemic heart disease
type 2 = increased demand or cavospasm

553
Q

why might diabetics have silent MIs

A

diabetic neuropathy dont feel the pain and therefore you can miss the diagnosis

554
Q

how do you acutely treat acute coronary syndrome

A

MONAC
- morphine
- O2
- Nitrates
- Aspirin
- Clopidogrel

555
Q

what is the initial loading dose of aspirin

A

300mg

556
Q

What is the long term dose of aspirin

A

75mg

557
Q

what are the acute complications of acute coronary syndromes

A

Heart failure due to ventricular fibrillation, mitral incompetence, left ventricular free wall rupture, cardiogenic shock

558
Q

what are complications that can occur 2 weeks post acute coronary syndromes

A

Dressler syndrome - autoimmune pericarditis
Heart failure
Left ventricular aneurysm

559
Q

what is heart failure with a preserved ejection fraction

A

when ejection fraction is over 50%
- diastolic failure with a preserved pump function so there is filling issues

560
Q

what is heart failure with reduced ejection fraction

A

When ejection fraction is lower than 40%
there is systolic failure and the pump fails, decreasing CO

561
Q

what are three cardinal non specific signs of heart failure

A
  1. shortness of breath
  2. ankle swelling
  3. fatigue
562
Q

what is the new york heart association classes of heart failure severity

A
  1. No limit on physical activity
  2. slight limit on moderate activity
  3. marked limit on moderate and gentle activity
  4. symptoms present at rest
563
Q

what is inactive BNP

A

this is NT proBNP and has levels 5X higher than BNP
- can also be measured in MI diagnosis according to NICE

564
Q

what is seen on a chest X-ray in people with heart failure

A

ABCDE
Alveolar bat wing oedema
Keley B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural Effusion

565
Q

what is the definition of an abdominal aortic aneurysm

A

Permanent aortic dilation exceeding 50%, where the diameter is over 3cm
- typically infrarenal

566
Q

what is the pathophysiology of an abdominal aortic aneurysm

A

smooth muscle, elastic and structural degeneration in all three layers of the vascular tunica with leukocyte infiltrate

567
Q

when can abdominal aortic aneurysms occur in the thoracic aorta

A

during marfans or chlers danlos as well as atherogenesis
- monitor these closely

568
Q

where are the most common locations for an aortic dissection

A
  1. Sinotubular junction - where aortic root becomes tubular near the aortic valve
  2. Just distal to the left subclavian artery
569
Q

What is the stanford classification of aortic dissection location

A

A = proximal to left subclavian 2/3
B = distal to left subclavian 1/3

570
Q

what is the pathophysiology of aortic dissection

A

Blood dissects the media and intima and pools in the false lumen which can propagate forwards or backwards = leads to reduced perfusion of end organs, organ failure and shock

571
Q

what are the symptoms of aortic dissection

A

sudden onset of ripping or tearing chest pain
- shock/hypotension
- new aortic insufficiency murmur
- neurological symptoms
- dicreased peripheral left arm pulse
- cardiac tamponade

572
Q

how do you diagnose aortic dissection

A

widened mediastinum on chest X ray - over 8cm
CT angiogram
TOE - sensitive

573
Q

how do you treat aortic dissection

A

surgical - open repair or EVAR
Medication - Beta blocker Esmolol or labetolol, pluss a partial alpha blocker to prevent reflex tachycardia
Vasodilator sodium nitroprusside

574
Q

what are complications of aortic dissection

A

Cardiac tamponade
Aortic insufficiency - regurgitation
Pre-renal AKI
Stroke

575
Q

what are secondary causes of hypertension

A
  1. phaeochromocytoma
  2. cushings
576
Q

What is a DVT

A

it is a thrombus in the deep leg vein
- if below calf it is less concerning
- if above calf it is life threatening

577
Q

what can pulmonary embolism cause

A

Cor pulmonale

578
Q

what are patient symptoms of pulmonary embolism

A

Sudden onset of pleuric chest pain
Dyspnoea
Evidence of DVT - swollen leg
Tachycardia, hypertensive, increased JVP

579
Q

What are symptoms of a deep vein thrombosis

A

unilateral swollen calf with engorged leg veins, typically warm

580
Q

how do you diagnose a pulmonary embolism

A

ECG - sinus tachycardia S1Q3T3
T wave inversion of anterior and inferior leads
New right bundle branch block

581
Q

how do you diagnose a deep vein thrombosis

A

Use the wells DVT score
if its less than 1 check D dimer, if its not raised there is no pulmonary embolism
if DVT score is over 1 or D dimer is raised then do a duplex ultrasound which is diagnostic

582
Q

what does the D dimer measure

A

it is a measure of clot burden
- if its sensitive it rules in a PE

583
Q

what is a differential diagnosis for DVT

A

CELLULITIS - skin infection typically caused by staph aureus and strep pyogenes
- can cause tender, inflamed and swollen calf

584
Q

what is the pathophysiology of peripheral vascular disease

A

Acute to acute on chronic
Intermittent claudication due to atherosclerotic partial lumen occlusion. This can progress to total limb ischemia

585
Q

what are the 6Ps to remember in acute limb ischemia

A

Pulselessness
Pallar
Pain
Perishingly cold
Paralysis
Parasthesia

586
Q

what happens when the blood vessel to a region becomes occluded

A

irreversible nerve damage - within 6hrs
Irreversible muscle damage - 6-10rhs
Skin symptoms last to appear

587
Q

what are the symptoms of peripheral vascular disease

A
  1. Ankle-brachial pressure index is less than 0.9
  2. lack of lower leg pulse
  3. skin on leg is cooler, colour change
  4. Bruits - pulsitile regions
  5. Buerger test positive
588
Q

what is the Fontaine classification

A
  1. asymptomatic
  2. intermittent claudication
  3. chronic limb ischemia
  4. ischemic ulcers - gangrene
589
Q

How do you diagnose peripheral vascular disease

A

ABPI
- 0.5-0.9 intermittent claudication
- less than 0.5 = ischemia
color duplex or ultrasound

590
Q

what is the treatment for peripheral vascular disease - intermittent claudication

A

risk factor management
- smoking cessation
- change dies
- loose weight

591
Q

What is the treatment for peripheral vascular disease - chronic limb ischemia

A

revascularisation surgery - PCI
amputation if severe

592
Q

what is the treatment for peripheral vascular disease - acute limb threatening ischemia

A

SURGICAL EMERGENCY
Revascularisation within 4-6hrs

593
Q

what are complications of peripheral vascular disease

A

Amputation
Permanent limb weakness
rhabdomyolysis
increased risk of cerebrovascular accidents and CVD

594
Q

what are causes of pericarditis

A

Idiopathic
Viral - coxsackie
Bacterial - TB
Fungal
Autoimmune - SLE
Dressler’s syndrome
Neoplastic

595
Q

WHat is the pathophysiology of pericarditis

A

Inflamed pericardial layers rub against each other exacerbating the inflammation. THis can remain dry or become effusive (extra fluid)

596
Q

what are the symptoms of cardiac tamponade

A

Becks triad - Hypotension, increased JVP, muffled S1+2 sounds
Pulsus paradoxicus

597
Q

what are risk factors of infective endocarditis

A

Male
Elderly
Prosthetic valves
IV drug user
Congenital heart defects
Rheumatic heart disease

598
Q

what is the consequence of regurgitation

A

insufficiency and proximal chamber dilation
- Loss of structural chamber integrity and strength

599
Q

what is the consequence of valve stenosis

A

increase in upstream pressure and proximal chamber hypertrophy
- heart becomes huge and rigid; poorly compliant

600
Q

When are right sided valve defects heard

A

Inspiration

601
Q

What are right sided valve defects

A

defects with pulmonary or tricuspid valves

602
Q

When are left sided defects heard best

A

expiration

603
Q

what are the two types of left sided valve defects

A

aortic valve or mitral valve defects

604
Q

what is tachycardia

A

Any beat higher than 100 bpm

605
Q

what is atrial fibrillation

A

an irregularly irregular heart rhythm

606
Q

What are causes of atrial fibrillation

A

Heart failure
Hypertension
Secondary to mistral stenosis
sometimes idiopathic

607
Q

what are risk factors for developing atrial fibrillation

A

60+
DM (T2)
Hypertension
valve defects
history of MI

608
Q

What is the pathophysiology behind atrial fibrillation

A

Rapid reentrant ectopic foci cause atrial spasm which causes atrial blood to pool instead of pump efficiently to ventricles

609
Q

what are the different types of atrial fibrillation

A

Paroxysmal - episodic
Persistent - longer than 7 days
Permanent

610
Q

how do you diagnose atrial fibrillation

A

ECG diagnostic - narrow QRS (<120ms) and irregularly irregular. No P wave

611
Q

how do you treat atrial fibrillation

A

Beta blockers or CCBs and oral anticoagulants
Cardioversion and warfarin

612
Q

what is important to do when assessing anticoagulation for atrial fibrillation

A

the CHA2DS2 VASc score - stroke risk to determine if someone should start anticoagulation therapy

613
Q

What is the HASBLED score

A

it assesses the risk of major bleeds in AF patients on anticoagulation

614
Q

what is atrial flutter

A

irregular organised atrial firing
- there is atrial spasm but is still coordinated

615
Q

how do you treat atrial flutter

A

If unstable cardiovert
If stable then rhythm or rate control via BBs and oral anticoagulation

616
Q

how do you diagnose Wolff-Parkinson White syndrome

A

ECG
1. Slurred delta waves
2. Short PR interval
3. Wide QRS

617
Q

how do you treat Wolff-Parkinson White

A
  1. Vasalva carotid massage
  2. IV adenosine, 6mg then 12mg then another 12mg
  3. Consider surgical radiofrequency ablation of bundle of kent
618
Q

what is long QT syndrome

A

Ventricular tachyarrhythmia normally caused by a congenital channel disorder affecting cardiac calcium channels

619
Q

what are causes of long QT

A

Romano Ward syndrome
Jerrel lange neilsen syndrome
Hypokalaemia
Hypocalcaemia

620
Q

What is Torsades de pointes

A

Polymorphic ventricular tachycardia in patients with prolonged QT. There are rapid irregular QRS complexes which are round baseline and can cease or develop into ventricular fibrillation

621
Q

what happens during ventricular fibrillation

A

Shapeless rapid oscillations on the ECG
- patient becomes pulseless and goes into cardiac arrest
- need defibrillation

622
Q

what can cause a right bundle branch block

A

Pulmonary emboli, ischemic heart disease, VSD

623
Q

What is seen on EGC in right bundle branch block

A

MaRRoW
M seen in V1 (RSR wave)
W seen in V6 (deep S wave)

624
Q

What are causes of left bundle branch block

A

IHD, valvular disease

625
Q

What is seen on ECG on left bundle branch block

A

WiLLiaM
W seen in V1
M seen in V6

626
Q

what are symptoms of hypertrophic cardiomyopathy

A

May present with sudden death
Others: chest pain, palpitations, shortness of breath, syncope

627
Q

what are symptoms of rheumatic fever

A

New murmur
Uncoordinated jerky movement
arthritis
erythema nodosum
pyrexia

628
Q

how do you diagnose rheumatic fever

A

chest X ray - cardiomegaly
ECHO - look for valvular damage

629
Q

How do you treat rheumatic fever

A

IV benzypenicillin
then phenoxypenecillin for 10 days
Haloperidol for jerky movements

630
Q

what can arial septal defect lead to

A

overloading of the right heart circulation which can lead to hypertrophy and in worse case Eisenmenger syndrome

631
Q

what is atrioventricular septal defect associated with

A

Downs syndrome

632
Q

what is shock

A

Medical emergency - hypoperfusion, life threatening due to acute circulation failure

633
Q

how does shock present

A
  1. Confusion
  2. Skin - pale cold sweaty
  3. Prolonged hypotension
  4. Decreased urine output
  5. Reduced GCS
  6. Weak pulse
634
Q

what is hypovolemic shock

A

due to blood loss/ fluid loss
treat with ABCDE plus IV fluid

635
Q

What is septic shock

A

Uncontrolled bacteria infection
- warm, tachycardic
Treat with ABCDE and broad spectrum antibiotics

636
Q

What is cardiogenic shock

A

Due to heart pump failure
Treat with ABCDE and treat underlying cause

637
Q

what is anaphylactic shock

A

Due to IgE mediated type 1 reaction
Treat with ABCDE and IM adrenaline

638
Q

What is neutrogenic shock

A

Due to spinal cord trauma
Treat with ABCDE with IV atropine (blocks vagal tone)

639
Q

what organs are most at risk of failure during shock

A

Kidney
Lung
Heart
Brain

640
Q

what medication is given in infants who have patents ductus arteriosus

A

Indomethacin - prostaglandin synthase inhibitor

641
Q

What is seen on a chest X Ray in heart failure

A

ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural effusion

642
Q

what are risk factors for mitral stenosis

A

female
older
decreased BMI
post MI
Connective tissue disorder

643
Q

what can cause mitral regurgitation

A

Myxomatoses mitral valve - progressive disarray of the valve where mass of cells in valve connective tissue makes the leaflets heaver and prolapse
papillary muscle rupture

644
Q

what are symptoms of mitral regurgitation

A

excisional dyspnoea
pan systolic murmur radiating to the axilla
S1 soft

645
Q

how do you threat a type three heart block

A

IV atropine and a permanent pacemaker