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3rd BDS IHD > Cardio Vascular System > Flashcards

Cardio Vascular System Flashcards

1
Q

what is stenosis

A

where only a small amount of blood can get through the valve = heart has to work really hard at a higher pressure = doesn’t open properly

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2
Q

what is incompetence

A

is where the valve doesn’t shut properly or has a hole in it = backflow = extra work for the heart

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3
Q

what are the three major causes of heart valve pathology

A

Rheumatic Fever
Calcific Aortic Valve disease
Age related disease

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4
Q

how does rheumatic fever cause heart problems

A

Low prevalence
Yellow swollen tonsils
Strep. Pyogenes
Body fights it off and cross reaction with self antigens
inflammation in myocardium and causes fibrosis in heart valves and ruffled, white, damaged
(90% mitral, 40% aortic)

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5
Q

what is calcific aortic valve disease

A

Calcium in the aortic valve appearing age related
Sometimes amplified where the valve is abnormal
Knobbly yellow lumps, very hard calcifications
Causes problems closing and opening causing stenosis and incompetence

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6
Q

why is aortic valve disease a problem for heart health

A

coronary arteries that supply the heart branch off just after the aortic arch
less blood can get through, heart has to pump harder and gets stronger = left ventricular hypertrophy
same amount of blood gets to coronary arteries so heart muscle gets tired

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7
Q

what is age relate valve disease likely to effect and how

A

Degrading mitral valve
Easily seen on a echo mycogram
Floppy mitral valve, very thin

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8
Q

how would we detect a weak mitral valve

A

mycogram

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9
Q

what types of artificial heat valves can be provided

A

Synthetic = ball and cage, tilting disc, synthetically grown forom pericardium
Biological = porcine, human

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10
Q

what tissue are heart valves made from

A

pericardium

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11
Q

what complications can we get from valve replacements

A

haemolysis
Coagulation - anticoagulation therapy needed with metal or plastic
mechanical failure - cage can break and ball can be released from ball and cage
calcification
infective endocarditis as rough surface is retentive for bacteria
Stitches too tight in sewed
rejection e.g. porcine

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12
Q

how might rheumatic fever lead to risk of endocarditis

A

rheumatic fever is a Strep. Pyogenes infection
Body fights it off and cross reaction with self antigens
causes inflammation and damage/fibrosis of heart valves
This roughens the surface of the valves and forms retention for bacteria that cause infective endocarditis

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13
Q

in what case might a patient be at risk of infective endocarditis with healthy heart valves and which valve might it effect

A

if the patient is an intravenous drug user
staph aureus can cause tricuspid valve infective endocarditis

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14
Q

what valve would be affected if a patient with healthy valves was to get infective endocarditis from IV drug use

A

Tricuspid

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15
Q

what are the local (2) and systemic (3) effects of infective endocarditis

A

Local:
Valve stenosis/incompetence
myocarditis infection of the myocardium heart muscle

Systemic:
general effects of illness
embolisms = organ infarcts, black rashes, splinter haemorrhages
glomerulonephritis (immune complex deposition)

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16
Q

how can infective endocarditis cause major organ infarcts (4)

A

infarct is death of tissue due to loss of blood supply
Valves form ‘vegetations’ - fibrin and bacteria and fragile valves
This can dislodge and form embolisms in major organs
this can cut off blood supply leading to death of parts of organs

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17
Q

give three micro-organism that can cause infective endocarditis and their route

A

risk of EC = Strep. Viridians from oral cavity through transient bacteraemia
healthy = IV drug user, Staph. Aureus
immunocompromised = natural fungus e.g. aspergillus
Strep pyogenes- rheumatic fever?

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18
Q

what percent of deaths does coronary heart disease cause

A

30% in men

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19
Q

what is another name for coronary artery disease

A

ischaemic heart disease

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20
Q

what are the three pre-disposing factors for vessel injury and atherosclerosis

A

Change in blood flow laminar → turbulent (high BP)
Change in vessel wall e.g. injury
Change in blood constituents e.g. too many platelets

Also high blood pressure, smoking, high cholesterol, obesity

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21
Q

what are the three causes of ischaemic heart disease

A

atherosclerosis, myocardial hypertrophy and small vessel disease

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22
Q

what are some risk factors for atherosclerotic plaque formation (4)

A

smoking
uncontrolled diabetes (controlled diabetes = no risk at all)
hyperlipidaemia
Hypertension

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23
Q

why might we get left ventricular hypertrophy? and what can this cause

A

This occurs if there are constricted vessels or faulty valves where the heart has to work harder to pump the same amount of blood. This strengthens the ventricles and leads to left ventricular hypertrophy and however the blood supply to the heart muscle itself does not increase meaning bigger muscle gets the same blood supply, making it more likely to fatigue

causes ischaemic heart disease

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24
Q

what causes small vessel disease and what can cause it

A

non obstructed blood vessels can still cause pain, down to arteriole level
Nitric oxide is a vasodilator so if nitric oxide is either underproduced or over destructed, this causes smooth muscle constriction
this can contribute to ischaemic heart disease

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25
Q

testing blood for someone with chest pain, what would we be looking for

A

nitric oxide levels (small vessel disease)
lipid levels (hyperlipidaemia)
blood pressure

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26
Q

what are the three results of ischaemic heart disease

A

regional transmural myocardial infarction
subendocardial myocardial infarction
chronic ischaemia

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27
Q

what is the most common heart attack

A

regional transmural myocardial infarction

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28
Q

explain regional transmural myocardial infarction

A

Chunk of of heart tissue has died that is the full thickness of the heart
Due to blockage in coronary artery
acute occluding event in one of the three main coronary arteries
lack of collateral circulation from the other vessels

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29
Q

explain subendocardial myocardial infarction

A

Occurs more in hospitals
Just inner part of ventricle dies (furthest from blood supply)
Severe atherosclerosis in all three coronary arteries
Occurs when sudden reduction in blood flow e.g. hypotension in medical procedure or GA
Pale parts of heart are lack of blood supply

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30
Q

if a patient has a heart attack in a hospital and has severe coronary artery atherosclerosis, what type of heart failure is this likely to be

A

subendocardial myocardial infarction

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31
Q

explain chronic ischaemia

A

‘fixed’ atherosclerotic lesions
angina
myocardial fibrosis
hibernating myocardium
stunned myocardium

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32
Q

which type of ischaemia causes fibrosis

A

chronic ischaemia

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33
Q

what are some complications of infarctions

A

sudden death
Arrhythmias - fibrillation caused by muscle not completely contracting just doing random movements so not pumping blood around the body This is where basic life training comes in, After serious exercise
cardiac failure
If muscle has been degraded = Reduced pump function
mitral incompetence = rupture or necrosis of papillary muscles
pericarditis
cardiac rupture = weakening of wall due to muscle necrosis and acute inflammation, 3-7 days after infarction, rupture into pericardial sac, rupture of interventricular septum
mural thrombosis
ventricular aneurysm - Instead of rupturing it can stretch and form an aneurysm and fill with blood
pulmonary embolism

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34
Q

why can arrhythmias cause myocardial infarction

A

pumping in an irregular manor means no blood is getting efficiently pumped
heart and brain quickly deprived of blood and oxygen

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35
Q

what is ‘cardiac failure’

A

if muscle has been degraded, necrosed or infarcted
reduced pump function
<55% inject compared to normal 75%

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36
Q

what is a cardiac rupture and when is this likely

A

weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac
rupture of interventricular septum

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37
Q

what is an aneurism

A

a bulge that forms in the thinning wall of an artery that can bulge or it can rupture and form a bleed and swelling

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38
Q

what is the cause and sign of mitral valve incompetence

A

necrosis or damage to papillary muscles
causes a pan systolic murmur

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39
Q

a patient has pan systolic murmur, what does this indicate

A

mitral valve incompetence

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40
Q

what would a heart look like if it had had a rupture into the pericardial sac and what may cause this

A

black bulges full of blood
weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac

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41
Q

what would a heart look like if it had had a rupture into the pericardial sac and what may cause this

A

black bulges full of blood
weakening of wall due to muscle necrosis and acute inflammation
3-7 days after infarction
rupture into pericardial sac

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42
Q

what might happen 3-7 days after a heart attack

A

cardiac rupture into the pericardial sac
due to weakened/damaged muscle tissue

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43
Q

what is a mural thrombosis

A

thrombosis on the abnormal endothelial surface following infarction
7-14 days after infarction
embolization to any arterial site

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44
Q

what is a ventricular aneurism

A

stretching of newly-formed collagenous scar tissue
4 weeks or more after infraction
may be associated with cardiac failure
may contain thrombus or stretch

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45
Q

what is the clinical importance of hypertension (3)

A

commonest cause of heart failure in most countries
major risk factor for atherosclerosis
major risk factor for cerebral haemorrhage

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46
Q

what is systole and diastole

A

s = contraction
d = relaxation and filling with blood

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47
Q

in the heart, what does pressure go from and compare this to the aorta

A

In the heart the pressure goes from 0-120. In the aorta, since it stretches, it goes from 120-180 and this varies over the day.

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48
Q

what is seen as normal blood pressure

A

120-130 / 80-85 mmHg

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49
Q

what is seen as severe hypertension

A

> 180/110 mmHg

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50
Q

what are the 2 classifications of hypertension

A

primary and secondary
benign and malignant

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51
Q

what is primary hypertension and what is it affected by (3)

A

no definitely identified cause
affected by:
Balance between sodium and water
Adrenaline levels by adrenal gland
Renin angiotensin aldosterone system

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52
Q

what is secondary hypertension (3)

A

easy to identify and exclude
renal
-renin dependent
-salt and water overload
-Something wrong with kidneys increases BP
endocrine
-Cushing’s, Conn’s, pheochromocytoma
-Too many corticosteroids either from tumours or given

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53
Q

what can cause secondary hypertension (3)

A

renal: renin dependent, salt and water overload, Something wrong with kidneys increases BP
endocrine: Cushing’s, Conn’s, pheochromocytoma, Too many corticosteroids either from tumours or given
drug therapy: corticosteroids, NSAIDs

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54
Q

what is benign hypertension

A

long asymptomatic period
increased frequency of complications later

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55
Q

what is malignant hypertension

A

markedly raised diastolic pressure
symptomatic
rapidly fatal if untreated
haemorrhages in the retina with impairment is common

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56
Q

give 6 effects of hypertesnion

A

accelerated atherosclerosis
sclerosis of smaller vessels
microaneurysms and haemorrhages
heart failure
kidney failure
cerebral haemorrhages = ‘strokes

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57
Q

what are the 4 major components of the heart that can go wrong, with relative consequences

A

myocardium = ventricles = heart failure (ventricles weaker than needed)
valves = infective endocarditis, heart failure
conduction system = tachycardia, bradycardia
coronary artery supply = most problems = atherosclerotic plaque = angina, MI

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58
Q

what is heart failure and what causes it

A

when the heart is pumping in-effectively for the body and heart <55%
an be idiopathic, previous heart failure, high BP, drugs

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59
Q

what is the gold standard assessment for pump function of the heart

A

transthoracic echocardiography (ultra sound)

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60
Q

what are symptoms of heart failure and what causes these problems

A

Reduced cardiac output increases fluid pressure in lungs (left heart failure), reduces venous return to the heart via vena cava (right heart failure) and compensatory responses cause fluid retention and vasoconstriction. This causes;

Breathlessness (increased fluid pressure in lungs)
Swelling (increased fluid pressure in venous system)
Also; dizziness, tiredness, weight loss

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61
Q

what causes the symptoms of heart failure

A

Reduced cardiac output increases fluid pressure in lungs (left heart failure), reduces venous return to the heart via vena cava (right heart failure) and compensatory responses cause fluid retention and vasoconstriction.

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62
Q

what are crepitations and what are they a sign of

A

‘crackles’ in the lungs
heart failure

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63
Q

what are the sign of heart failure

A

low blood pressure
increased heart rate
Crepitations in lungs
haziness in lung radiograph = liquid = increased fluid pressure
Raised jugular venous pressure
Pitting ankle oedema / ascites

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64
Q

what are the causes of valve problems (5)

A

Degeneration (ie it just happens)
Rheumatic fever = increased risk of infective endocarditis
Congenitally abnormal valve
Endocarditis
Papillary muscle rupture after MI

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65
Q

how do we test for arrhythmias

A

Echocardiogram to test the electric signals in the heart

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66
Q

what classes as tachycardia or bradycardia

A

tac = >100bmp
brad = <60 bmp

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67
Q

what is an ectopic beat and are they a risk

A

extra occasional narrow or broad QRS complexes, feels like missed/skipped beat, type of tacchycardia
common in normal, healthy people but more common in heart disease
low risk

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68
Q

what is the most common ‘serious’ arrhythmia and how many people have it over 80

A

Atrial fibrillation
found in 1 in 4 people over 80

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69
Q

hat are risk factors for atrial fibrillation and what can it be a risk for

A

Hypertension, heart failure, valve disease, alcohol, age, obesity, lung disease, hyperthyroidism
Increases risk of stroke

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70
Q

compare atrial fibrillation and atrial flutter

A

similar symptoms, risks and treatment
fibrillation = No P waves, irregular QRS rate
flutter = Rapid abnormal P waves, often 2 per QRS

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71
Q

what are common symptoms and signs of atrial flutter/fibrillation

A

dizziness, tiredness, high heart rate (higher rate, higher risk of symptoms), palpitations, often asymptomatic

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72
Q

what is the second most common arrythmia after atrial fibrilation/flutter

A

Supraventricular tachycardia (SVT)

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73
Q

what is a Supraventricular tachycardia (SVT) and who is at risk of this

A

Narrow QRS complex tachycardia, often absent P waves
Can probably happen to anyone, few predisposing factors, can be born with accessory pathway that increases chances

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74
Q

what are the symptoms of supraventricular tachycardia SVT

A

many palpitations (dizziness and breathless )
rarely dangerous and if lasting a long time (more than minutes) then go to hospital

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75
Q

what is the most dangerous and 3rd most common arrhythmia group

A

ventricular tachycardia or fibrillation

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76
Q

what can cause ventricular tachycardia or fibrillation

A

any problem that affects the ventricles e.g. heart attack, drugs, idiopathic

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77
Q

compare ventricular tachycardia and ventricular fibrillation

A

tachycardia = Broad QRS tachycardia
Fibrillation = Coarse fibrillation waves with no organised QRS

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78
Q

compare 3rd and 2nd degree heart block

A

2nd = Intermittent failure to conduct between P wave and QRS
3rd = No relationship between P waves and QRS, slow QRS rate

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79
Q

how do we test for coronary artery disease

A

coronary angiogram

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80
Q

what is a ‘stable’ atherosclerotic plaque and what does this cause

A

a strong fibrous cap protects the blood from exposure to the lipid core of the lesion, preventing thrombosis
this causes angina

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81
Q

what is angina and what makes this worse

A

Angina is a recurrent feeling of chest pressure/heaviness/pain/indigestion, sometimes radiating to the arm, neck, or back
Angina is almost always precipitated by exertion or stress (circumstances where the heart needs a greater blood supply)

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82
Q

compare unstable angina and stable angina

A

Angina rarely lasts more than 10minutes, and rarely is at rest = stable = no increase in symptoms
Angina itself isn’t dangerous. However “Unstable angina” (increasing frequency, duration, or onset at rest) is a sign of risk and warrants immediate assessment

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83
Q

what is myocardial infarction

A

MI occurs when an atherosclerotic plaque in a coronary artery ruptures, opening up the lipid core triggering thrombus formation.
This causes permanent death of some myocardium (unlike angina)

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84
Q

compare angina and MI

A

both caused by constricted coronary arteries and atherosclerotic plaque
MI causes complete thrombosis and death of myocardium, angina does not

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85
Q

what is the time difference in angina and MI pain

A

angina = upt to 10 minutes
MI is more than 10 minutes usually but can activate instantly

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86
Q

what causes atherosclerotic plaque rupture

A

not know, can happen under stress, exercise, rest, sleep

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87
Q

why is an exercise ECG not a good way of measuring coronary heart disease

A

50% of women show the ‘positive’ change in ECG even without the disease

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88
Q

explain the myocardial perfusion test

A

test for coronary heart disease
injected with a radio-showing fluid that is picked up by herat tissue
under relaxation, all of heart is seen
under stress, a portion of heart may not be seen = this part of the heart is affected by coronary heart disease

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89
Q

what is the gold standard for diagnosing coronary heart disease

A

CT angiography and invasive angiography if CT positive

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90
Q

when do we use invasive over CT angiography

A

risk of MI or if we need to stent

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91
Q

give three ways to diagnose coronary heart disease

A

exercise ECG
myocardial perfusion test
invase/CT angiography

92
Q

how do we treat coronary heart disease

A

better diet: low processed foods, fats and salts. more fruit and veg, oily fish, olive oil, nuts
exerise more
cholesterol lowering drugs e.g statins
lifestyle : control stress, anxiety, obesity, smoking, diabetes

93
Q

how do we treat angina due to CAD

A

treat CAD which improves prognosis, not symptoms
no treat if no bother
medications: beta blockers, calcium channel blockers,
If medication not working/side effects; stenting or coronary artery bypass grafting
(these improve symptoms but not prognosis)

94
Q

if someone has had a stent, why might this be and what effects does this have (prognosis/symptoms)

A

treat angina: improve symptoms but not prognosis
previous MI: improve prognosis- but not for long

95
Q

what 2 investigations do we do if someone thinks they are having a heart attack

A

ECG imediately to see if the ST is raised = ST elevated MI
could be a non-elevated ST MI so also test:
Serum Troponin in blood - immediate and 6 hours after pain

96
Q

if heart muscle is damaged, what substance would be found in the blood

A

serum Troponin

97
Q

what is the immediate treatment for MI (3)

A

immediate dual action medications of antiplatelet e.g. Aspirin, clopidogrel, and pain releif e.g. morphine
Anticoagulation for 24-72hrs; Heparin, Fondapariux or similar
Both STEMI and NSTEMI should have angiography and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications

98
Q

compare the treatment of STEMI and NSTEMI

A

Both STEMI and NSTEMI should have angiography (invasive) and if possible stenting; STEMI immediately, NSTEMI within 72hrs or sooner if complications

99
Q

when should oxygen be given and what can it do if given at the wrong time

A

only if the patient is hypoxic
may constrict coronary arteries and cause MI

100
Q

what should be given to a patient if they suddenly get chest pain and you are waiting for an ambulance

A

aspirin under the tongue

101
Q

what is the secondary treatment for MI

A

DAPT (dual antiplatelet therapy) for a year then Aspirin alone, Statin, Betablocker for a year, ACE inhibitor, and treatment of any complication (heart failure, arrhythmia, etc).
Cardiac rehabilitation; exercise, education, diet, smoking cessation

102
Q

how do we diagnose and test for heart failure

A

referring to the ventricles, so look at the ventricles
test blood for B-type Natriuretic Peptide (BNP)
if positive (as can be other things) do a transthoracic echocardiogram
best way is MRI

103
Q

what is the gold standard to investigate ventricular function and heart failure

A

MRI
more accurate and higher resolution than ultrasound Transthoracic echocardiogram

104
Q

if a patient describes a CT scan or a MRI scan for a heart diagnosis, what was the problem likely to be

A

CT = injected with fluid = angiography testing coronary arteries
MRI = dark tube = ventricular heart failure

105
Q

what are ACE inhibitors

A

angiotensin-converting enzyme inhibitors
lowers blood pressure and used for treating heart failure

106
Q

what is the function of steroid medication for heart failure

A

aldosterone antagonists
aldosterone seen as disadvantageous for the heart

107
Q

what medications are given if a pt has heat failure

A

ACE inhibitors e.g. Ramipril - REMEBER
Beta blockers e.g. bisoprolol - REMEBER
Aldosterone antagoniosts
treatment of complications like anaemia and thyroid

108
Q

what are the 4 valves of the heart

A

Aortic - aorta
Tricuspid = right atrium –> ventricle
Bicuspid/Pulmonary = to the lungs from right ventricle
Mitral = left atrium –> ventricle

109
Q

which valves are more likely to be a cause of disruption in the heart (2)

A

mitral and Aortic

110
Q

why do we rarely see mitral stenosis these days

A

this is primarily caused by rheumatic fever which we are vaccinated against

111
Q

what investigation is good for valve movements in the heart (2)

A

transthoracic echocardiogram
transoesophageal is more accurate but unpleasant for patient
BE CAREFUL - this does not help diagnose coronary heart disease

112
Q

why artery could be used for a less invase valve replacement for aortic stenosis

A

femoral artery - same as angiogram

113
Q

what MUST a patient with metallic valve replacement be on and for how long

A

warfarin lifelong
nothing else, no DOACs or NOACs

114
Q

if a patient with a metallic heart valve needed a high bleeding risk surgery, what would we have to do

A

pt would be on warfarin so would stop warfarin and bridge with heparin and this must be done in a specialist clinic
never stop warfarin without consulting and maybe never stop if metal

115
Q

how can we diagnose and study arrhythmias

A

ECG but obviously cannot predict when arrhythmia occurs
can give smartphone app with watch to detect ECG at time
or small implanted loop ECG constantly recording

116
Q

other than ECG, what can we investigate with Arrhythmic patients

A

Ventricular fibrillation and tachycardia usually due to the left ventricle so
echocardiogram for heart failure
angiogram for coronary artery disease
family screening for patients with possible genetic problems

117
Q

what is the P wave on an ECG

A

small atrial depolarisation

118
Q

what is the P wave on an ECG

A

small atrial depolarisation

119
Q

what is QRS complex on an ECG

A

ventricular depolarisation

120
Q

what is the T spike on an ECG

A

ventricular repolarisation

121
Q

give the order of the ECG spikes

A

P wave = atrial depolarisation
QRS complex = ventricular depolarisation
T wave = Ventricular repolarisation

122
Q

if we accidently injected intravenous lignocaine, what would we see on an ECG and how do we treat

A

wide QRS and very close complexes = ventricular tacchycardia
immediate defibrillation

123
Q

if the P wave is irregular what is the patient likely to have and how do we treat

A

ventricular bradycardia
pacemaker
usually caused by old age

124
Q

what does the CHADS-2Vasc score tell us and what score is significant

A

risk of stroke with Atrial fibrillation and flutter
weather or not to give warfarin or NOAC anticoagulant
score of 1 or over = give anticoagulant

125
Q

how do we treat atrial fibrillation/flutter

A

reduce risk of stroke with anticoagulants
if tachycardia slow the rate with beta blockers or calcium ion channel blockers

126
Q

how can we correct SVT

A

supraventricular tachycardia
can do a defibrillation or treat with adenosine or vasovagal maneouvors
to prevent happening again = ablation (surgical correction of electric current)

127
Q

how do we treat ventricular fibrillation or arrhythmia

A

immediate defibrillation
prevent with beta blockers or implanted cardiovascular defibrillator under the skin

128
Q

how and when do we provide a pacemaker

A

above skin of heart we place the pacemaker in with wires in the veins of right atrium and ventricle
when bradycardic

129
Q

give three types of heart devices we can implant

A

dual chamber pacemaker box = only for bradycardia
Cardioverter/Defibrillator = Treats ventricular tachycardia or VF. Can also pace bradycardias
Cardiac Resynchronisation Therapy (CRT) = Treats heart failure + bradycardia (CRT-P) + CRT-D also has ICD

130
Q

when should angina prevent dental treatment

A

stable angina is fine and well controlled
if the pain comes when they are at rest or pain worsening, they should get this seen an d prevent treatment

131
Q

when a patient has heart failure, when should we defer dental treatment

A

well controlled heart failure is safe, if on beta blockers or calcium blockers, breathless on exertion or can lie flat at night
if cannot lie flat at night, getting more breathless or swollen ankles, refer to GP immediately

132
Q

after a heart attack, how do we manage dental treatment

A

at high risk of another heart attack
Recent MI (within 6 weeks); defer until 3-6 months post MI, longer if possible.

133
Q

what type of arrhythmia should defer a dental treatment

A

when there are frequent attacks of disabling tachycardia (few times a week)

134
Q

if a patient is awaiting valve surgery, how does this affect treatment

A

if stable, continue with treatment
try do treatment before as when valve replaced = more likely infective endocarditis

135
Q

what are 95% of hypertensions?

A

‘essential’ - no secondary cause

136
Q

what effects can untreated hypertension cause around the body

A

• Brain: thrombotic, thromboembolic and haemorrhagic stroke, multiinfarct dementia, hypertensive encephalopathy

• Heart: LVH, LV failure, coronary artery disease

• Kidney: renal, failure

• Eyes: hypertensive, retinopathy

137
Q

what is the main factor contributing to atherosclerotic plaque and then give 3 other factors

A

hypertension 5-10x
smoking 2x
diabetes 2x
hyperlipidaemia 1.5x
obesity 1.5x

138
Q

what does prognosis of hypertension depend on (4)

A

level of systolic and diastolic blood pressure
age, sex other risk factors
evidence of end-organ damage
improved with antihypertensive therapy

139
Q

what are some non-pharma logical treatment of hypertension

A

stop smoking
reduce salt fat and alcohol intake
exercise more
reduce weight
control diabetes

140
Q

give some common anti=hypertensive drugs

A

Thiazide diuretics
ACE inhibitors
Beta blockers]calcium ion channel blockers

141
Q

what do diuretics do

A

reduce the amount of water in the body
inhibit reabsorption of ions into the blood
in turn reducing osmosis of water back into the blood

142
Q

what is the function of thiazide diuretics and hen do we use them

A

inhibit NaCL reabsorption in proximal and early distal tubules of nephron

First line treatment of hypertension

143
Q

what are some common side effects of anti-hypertensive drugs

A

rash
electrolyte disturbance (kidney acting)
postural hypotension

144
Q

how does angiotensin II act

A

direct vasoconstrictor
stimulates adrenal glands to produce aldosterone

145
Q

what frequent (and why) and infrequent side effects do ACE inhibitors usually have

A

cough - alters bradykinin degradation

infrequent:
-hypotension
-rash
hyperkalaemia
renal failure especially in presence of renal artery stenosis
loss of tate/alteration

146
Q

what do ace inhibitors do

A

inhibit conversion of angiotensin I to angiotensin II

147
Q

what a

A
148
Q

if a patient has loss of taste and has high BP, what are they likely taking

A

ACE inhibitors

149
Q

what are losartan, valsartan, candesartan (suffix sartan)

A

Angiotensin II receptor antagonists ARBs

150
Q

compare sympathetic and parasympathetic pathways in term of neurostramsitter and function

A

S:
-norepinephrine
-increased contractility of heart
-increase heart rate
-increase vasoconstriction

P:
-Acetyl Choline
-opposite

151
Q

how do beta blockers act

A

act as antagonists for beta-adrenoreceptors
variable selectivity for cardiac beta 1 receptors

152
Q

what is the most and least selective beta blocker

A

propranolol = least
bisoprolol = most

153
Q

what function do beta blockers have

A

reduce heart rate, blood pressure, cardiac output

154
Q

what are some contraindications for beta blockers

A

asthma, uncontrolled heart failure, bradycardia

155
Q

what common side effects do we get with beta blockers

A

fatigue
hypotension
cold peripheries
bronchospasm
impotence

156
Q

what is the effect of calcium channel blockers

A

vasodilators = reduce systematic vascular tone

157
Q

give 2 types of calcium channel blockers with examples

A

e.. Verapamil = cause bradycardia, inhibit AV node conduction (atrial fibrillation)

e.g. Amlodipine = may cause reflex tachycardia

158
Q

what are common side effects for calcium channel blockers

A

flushing
headache
dizziness
hypotension
oedema

159
Q

give 4 drugs used for anti-anginal purposes

A

beta blocker (hypertension)
calcium channel (hypertension)
nitrates
potassium channel activators

160
Q

how do beta blockers help angina

A

beta adrenal receptor blockers
reduce heart rate, blood pressure and myocardial contractility
lower oxygen demand
put less stress on coronary arteries

161
Q

why must beta blockers be introduced slowly if cardiac failure

A

may exacerbate cardiac failure symptoms:

peripheral vascular disease (leg pain) - claudication
cause bronchospasm

162
Q

if a patient is on beta blockers, why can we not suddenly take them off

A

cause arrhythmia
worsening angina
MI

163
Q

how do nitrates help angina (3)

A

Produce nitric oxide at the endothelial surface leading to vascular smooth
muscle relaxation and arteriolar and venous dilatation

Reduce myocardial oxygen demand (lower preload and afterload) and

increase myocardial oxygen supply (coronary vasodilatation)

164
Q

what type of medication is GTN spray

A

nitrate anti-angina

165
Q

what are the side effects of nitrates

A

headache, flushing, postural hypotension

166
Q

why is postural hypotension important to dentistry

A

if a patient e.g. takes GTN spray in dental chair
then stands up, they will get postural hypotension
may faint, be aware of cause

167
Q

how do calcium antagonists work

A

Lower myocardial oxygen demand by reducing blood pressure and myocardial contractility and increase myocardial oxygen supply by
dilating coronary arteries

168
Q

what type of drugs are Verapamil and diltiazem and when should they NOT be used

A

calcium antagonists - use for arrythmia and angina
never use with heart failure as reduce contractility of the myocardium and heart rate

169
Q

what is the only potassium channel activator that we use and what is its function

A

Nicordandil
arterial and venous dilators
angina relief

170
Q

what side effects are there with potassium channel activators

A

can cause mucocutaneous ulceration - relegated to second line therapy

171
Q

a patient has angina treatment but cant remember their medication but also has white ulceration in the mouth. what is their likely medication

A

ulceration is mucocutaneous
Nicorandil = potassium channel activator

172
Q

how do antiplatelets work

A

Inhibit platelet aggregation and arterial thrombus formation, thus
preventing heart attack, stroke and CV death

173
Q

how does Aspirin work

A

irreversibly blocks platelet cyclo-oxygenase (COX1) and the
production of thromboxane A2, a platelet activating substance

174
Q

how do Clopidogrel, prasugrel and ticagrelor work

A

platelet ADP (P2Y12) receptor inhibitors (Clopidogrel irreversible, ticagrelor reversible)
used alone or, more often, in combination with aspirin
reduces platelet activation

175
Q

compare Clopidogrel and ticagrelor

A

Both anti-platelet inhibit platelet ADP (P2Y12) receptor
Clopidogrel - irreversible
Ticagrelor - reversible

176
Q

how does aspirin work

A

Aspirin – blocks platelet cyclo-oxygenase (COX1) and the
production of thromboxane A2, a platelet activating substance

177
Q

how to statins work

A

Hydroxymethyl-glutaryl (HMG) CoA reductase inhibitors
Lower LDL cholesterol and may increase HDL cholesterol
Reduce risks of myocardial infarction, stroke and CV death

178
Q

what is heart failure

A

an imprecise term describing the state that develops when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure
Associated with activation of RAS axis and sympathetic nervous system

179
Q

what 2 factors is heart failure associated with

A

Associated with activation of renin-angiotensin system RAS axis
sympathetic nervous system

180
Q

give 7 symptoms of heart failure

A

swollen/tender abdomen and loss of appetite
swollen ankles
breathlessness
struggle to sleep due to breathlessness
chronic tiredness
cough with frothy sputum
increased urination at night

181
Q

what are the 3 types of diuretics

A

K sparing
Thiazides
Loop Diuretics

182
Q

where do loop diuretics work

A

ascending portion of the loop of Henle

183
Q

how and where do K sparing diuretics act

A

Inhibit reabsorption of Na in the distal convoluted and collecting tubule
(aldosterone antagonists)

184
Q

how does aldosterone effect heart function

A

Retention Na+ and Retention H2O = oedema
Excretion K+ and Excretion Mg2+ = arrythmia

185
Q

what is digoxin used for

A

slows conduction in atrial fibrillation
increases vagal tone

186
Q

what Acronym helps remeber the treatment of hypertension

A

ABC
Ace inhibitors (most important)
Beta blockers
Calcium ion channel antagonists

187
Q

what is thrombosis

A

Inappropriate blood coagulation within a vessel

188
Q

compare venous and arterial thrombosis

A

arterial:
high pressure system
Thrombosis is platelet rich bound in fibrin

venous:
low pressure
low pressure system
fibrin rich, very few platelets
Non return valves

189
Q

what happens if a non-return venous valve is damaged

A

discoloration of skin
swelling
pain

190
Q

what are the 2 results of arterial thrombosis

A

Myocardial infarction
Thrombotic stroke

191
Q

what are th reuslts of a venous thrombosis

A

Leg deep vein thrombosis (MI)
Pulmonary embolism (PE)
Cerebral venous thrombosis in the venous sinuses = severe headache, pain, nausea, double vision

192
Q

what are the signs and symptoms of a cerebral venous thrombosis vs a stroke

A

Cerebral venous thrombosis in the venous sinuses = severe headache, pain, nausea, double vision

stroke usually caused by thrombosis in the carotid artery
unilateral drop of face, loss of speech, cannot touch nose

193
Q

how many people with a DVt also have a PE

A

75% of people with DVT will also have a pulmonary embolism so both must be treated

194
Q

in general terms how do we treat arterial thrombosis

A

antiplateletes

195
Q

how do we treat venpous thrombosis

A

anticoagulants

196
Q

explain formation of arterial thrombosis

A

Initial fatty streak under the endothelium
Plaque enlargement
Turbulence due to protrusion into lumen
Loss of endothelium and collagen exposure and pro-coagulants (collagen = prothrombotic)
Platelet activation and adherence = cascade triggered
PLatelet = fibrinogen –> fibrin
Fibrin meshwork deposition and red cell entrapment
More turbulence, more platelet and fibrin deposition
Thrombus of layers of platelets, firbin and red cells

197
Q

what are the main risk factors for arterial thrombosis

A

Family history = hypercholesterolaemia
Diabetes mellitus
Hypertension
Hyperlipidaemia
Smoking - irritates endothelium accelerating arterial disease + peripheral vascular disease
Atrial fibrillation for stroke
congenital high levels of clotting factors e.g. FVIII
male sex

198
Q

how many people above 80 have AF

A

10%

199
Q

explain atrial fibrillation

A

Left atrium becomes enlarged starting to fibrillate uncontrollably = turbulent due to no co-ordination = pro-thrombotic
Irregularly irregular heart rhythm
4% in >60years, 8% in >80years
Left atrial thrombus
Embolization leads to stroke or limb emboli
Impaired cardiac output

Antiplatelet drugs are ineffective for AF

we recommend anticoagulants for this as there is high fibrin in this blood

200
Q

how do we treat AF (3)

A

atrial fibrillation
Anticoagulation first so that when put into correct rhythm we don’t get embolism and as embolism is the biggest danger

Heart rate control: Beta blockers, Ca channel blocker, Digoxin, AV junction ablation

DC cardioversion in sedation

201
Q

compare aspirin and clopidogrel

A

both irreversible COX I inhibitors
aspirin has GI affects, clopidogrel doesn’t
clopidogrel is more expensive
clopidogrel is a stronger antiplatelete

202
Q

how does aspirin work

A

COX1 inhibitor
prevents formation of thromboxane which is a pro-platelet factor
Inhibition lasts for the lifespan of platelet: ≈ 1 week.
Risk reduction of non fatal vascular event by 30%.
Risk reduction of fatal vascular event by 15%.

203
Q

must we stop antiplatelet drugs during dental procedures

A

aspirin unlikely to be needed to stop
clopidogrel is stronger so consider removal for a week prior

204
Q

how do we treat an arterial thrombosis

A

fibrinolytics e.g. streptokinase

205
Q

how do we prevent aterial thrombosis

A

lifestyle - reduce factors, stop smoking, lose weight, dietary changes
drugs = antiplateletes e.g. aspirin

206
Q

how do fibrinolytics work e.g. streptokinase

A

activates plasminogen –> plasmin
this factor breaks down fibrin coagulations
high risk of bleeding

207
Q

what are some indications for use of fibrinolytics

A

MI,
stroke within 3 hours,
Life-threatening PE

208
Q

how do we treat MI

A

Percutaneous coronary intervention (with possible cardiac stenting)
Combined with 3 – 12 months aspirin + clopidogrel
Coronary artery bypass grafting
Carotid endarterectomy - stent carotid artery and require anticoagulant therapy therafter

209
Q

what is conoarary artery bypass grafting and when is it done

A

open heart surgery swapping a vein from the leg into the heart to make a new coronary connection
done where it is not possible to stent

210
Q

what is a percutaneous coronary intervention, when is it done and what must it be done with

A

where we use a cannula in the arm to gain access to the coronary arteries to remove a clot
we may then place a stent
it is done when a pt experiences a MI
must be followed by 3-12 months of aspirin and clopidogrel dual therapy

211
Q

how does diabetes increase risk of arterial thrombosis

A

High blood sugar is toxic to endothelium and damages endothelium, increases fatty streak deposit

212
Q

a patient is on clopidogrel and aspirin, what is their likely status

A

recently had a stent placed following an MI

213
Q

what is a newly licensed way of reducing recurrent vascular events

A

Rivaroxaban (anticoagulant) has recently be licensed to prevent recurrent vascular disease in addition to aspirin (anti-platelet) (in low doses)

214
Q

how does AF lead to strokes

A
  1. Blood pools in atria
  2. Blood clot forms
  3. Blood clot breaks off
  4. Blood clot travels to brain and blocks a cerebral artery
    causing a stroke
215
Q

how might high fibrin in blood lead to leg ulcers

A

high fibrin = increased risk of venous thrombosis
= deep vein insufficency
post thrombotic syndrome
leg ulcer

216
Q

what can result of DVT

A

pulmanory emboli –> death or pulmanory hypertension
deep vein insufficency –> post thrombotic syndrome

217
Q

what three factors affect venous thrombosis

A

hypercoagulability (acquired and inherited)
stasis (acquired)
vascular damage (aquire)

218
Q

what increases risk of stasis –> venous thrombosis

A

aeroplane travel
hospitalisation
disability

218
Q

what increases risk of stasis –> venous thrombosis

A

aeroplane travel
hospitalisation
disability

219
Q

what are some inherited risks for venous thrombosis

A

antithrombin deficiency (10-40 fold increase, biggest risk)
Protein C deficiency
protein S deficiency
Factor V Leiden

220
Q

what is the function of protein C and S

A

prevent factor VIII formation
deficiency in this = increased risk of venous thrombosis

221
Q

what is the risk increase of venous thrombosis under hospitalisation

A

150 fold

222
Q

what is the risk increase of venous thrombosis when pregnant

A

15 fold

223
Q

how do we prevent DVT

A

Adequate hydration - reduce pressure
Early mobilisation - reduce stasis
Graduated elastic compression hosiery stockings, tighter in calves
screening for Protein C, Protein S, Factor V andantithrombin deficency
thromboprophylaxis
assess any patients in hospital for thrombophilias

224
Q

what chemical prophylaxis can we give to prevent venous thrombosis

A

Low molecular weight heparin
Direct oral anticoagulants
prevents 50 – 70% of VTE

225
Q

how do we prevent recurrent DVTs (3)

A

anticoagulants for 3 months after a first event.

Provoked events (OCP) do not need anticoagulation >3 months
Distal DVT do not need anticoagulation >3 months

Consider long term anticoagulation after 1st unprovoked thrombosis or a risk factor that is permanent

226
Q

how can we prevent DVTs going to PE

A

vena cava filters
anticoagulants

3rd BDS IHD (14 decks)

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