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5 Human Diseases > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

irreversible risk factors for CVD?

A

age <older
sex <male
family history

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2
Q

reversible risk factors for CVD by patient?

A

smoking - damage blood vessels -> clots
obesity - fatty material damage and clog vessels
diet
exercise

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3
Q

reversible risk factors for CVD by medication?

A

hypertension - damage to heart and blood vessels
hyperlipidemia (high cholesterol) - fatty deposits
diabetes - damage blood vessels and nerves

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4
Q

define primary prevention for cardiovascular disease

A

preventing the disease

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5
Q

define secondary prevention for cardiovascular disease?

A

preventing further disease following diagnosis

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6
Q

define claudication

A

cramping pain in leg following exercise caused by obstruction of arteries

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7
Q

how is cardiovascular disease prevented 4

A

lifestyle changes
control cholesterol
control hypertension
anti-platelet drugs (aspirin)

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8
Q

what lifestyle changes are required to prevent cardiovascular disease?

A

exercise, diet, smoking

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9
Q

what level is controlled cholesterol?

A

<5.00mmol/L or 25%

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10
Q

how is cholesterol controlled

A

statin treatment

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11
Q

what level is controlled hypertension?

A

Reduce blood pressure to <140/85

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12
Q

when are antiplatelet drugs used in cardiovascular disease?

A

if have cvd
if high risk of developing cvd

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13
Q

what is hypertension?

A

high blood pressure

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14
Q

Blood pressure at which harm occurs

A

140/90mmHg

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15
Q

how is blood pressure taken? 2

A

3 measurements at 3 times sitting and rested
Ambulatory measuring -> see how blood pressure changes over 24 or 72hrs

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16
Q

why is age a risk factor for hypertension?

A

stiffer arteries - high blood pressure

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17
Q

why is race a risk factor for hypertension?

A

racism - stress
salt sensitivity
body mass index

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18
Q

why is obesity a risk factor for hypertension?

A

fatty build up in arteries
increased heart work

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19
Q

why is alcohol a risk factor for hypertension?

A

increase in hormone renin which causes vasoconstriction

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20
Q

why is pregnancy a risk factor for hypertension?

A

placenta issues and increase heart work

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21
Q

why is stress a risk factor for hypertension?

A

sympathetic nervous system response causing vasoconstriction and increased heart rate

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22
Q

what are the possible outcomes of hypertension? 2

A

accelerated atherosclerosis -> MI, stroke, peripheral vascular disease

renal damage - renal failure makes hypertension worse

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23
Q

causes of hypertension? 3

A

commonly none

renal artery stenosis -> constriction of arteries to kidney, kidney thinks drop in blood pressure, releases aldosterone so water is retained

endocrine tumours
- Phaeochromocytoma (Adrenergic tumour -> releases adrenaline which causes vasoconstriction and hypertension)
- Conn’s syndrome (Aldosterone = increases the circulating blood volume)
- Cushing’s syndrome (too much cortisol - Salt and water retention increases the circulating blood volume)

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24
Q

signs and symptoms of hypertension 3

A

Usually none

May get a headache

May get Transient Ischaemic attacks -> mini strokes with full neurological return in 24hrs

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25
Q

investigations for hypertension 3

A

Of the blood -> urinalysis, serum biochemistry, serum lipids

ECG

Occasionally renal ultrasounds, renal angiography, hormone estimations

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26
Q

treatment for hypertension 3

A

Aim of treatment to get blood pressure < 120/90mmHg

Modify risk factors -> weight loss, exercise

Single daily dose drug (single to improve compliance but can add more to control)

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27
Q

remember for hypertension

A

Monitoring is important as treatment need changes over time, review at least annually when stable
Monitor blood biochemistry effects of drugs Na/K changes and dehydration

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28
Q

what are the two processes that cause acute coronary syndromes?

A

blood vessel narrowing - ischaemia

blood vessel occlusion - infarction

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29
Q

what is ischaemia?

A

inadequate oxygen delivery for tissue needs

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30
Q

how does blood vessel narrowing cause acute coronary syndromes?

A

causing ischaemia (inadequate oxygen delivery for tissue needs)

Causes cramp in affected muscle/tissue felt as pain

No damage at first but if goes on for many years it can damage the muscle in particular the heart leading to heart failure

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31
Q

how does blood vessel occlusion cause acute coronary syndromes?Myocardial infarction and stroke (CVA)

A

Tissue death due to no oxygen delivery which causes severe pain and loss of function of tissue

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32
Q

name 2 consequences of ischaemia

A

angina
peripheral vascular disease

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33
Q

name 2 consequences of infarction

A

Myocardial infarction and stroke (CVA)

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34
Q

what is coronary artery disease?

A
  • Plaque builds up in the arteries of the heart reducing blood flow to the muscles of the heart
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35
Q

coronary artery disease tends to happen where?

? blood flow causes ? to the interior surface of the ? allowing the accumulation of ? within the surface which forms ? ?. Their size ? gradually narrowing the ? and ? the blood flow. Limiting ? delivery to the ?

A

areas of stress to the artery

turbulent
damage
artery
fat
atherosclerotic plaques
increases
vessel
decreasing
oxygen
tissues

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36
Q

in coronary artery disease

if the oxygen requirements of the tissue increase what happens?

A

the patient will not be able to match it with increased blood flow

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37
Q

why do more cardiac problems happen at faster heart rates?

A

the time for diastole decreases compromising the cardiac blood flow as blood only flows through the arteries when the valve is shut

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38
Q

Acute ischaemic events affecting the heart have 3 main forms what are they?

A

atherosclerosis

atherosclerosis with blood clot

spasm

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39
Q

how long does ischaemia last for it to cause permanent damage?

A

> 20mins

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40
Q

what causes stable angina?

A

Plaque forms reducing blood flow.

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41
Q

when does pain develop in stable angina?

A

Pain develops during exercise.

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42
Q

what is the ECG in stable angina?

A

normal

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43
Q

what are troponins?

A

chemical released when cardiac tissue death occurs

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44
Q

what are the troponin levels in stable angina?

A

normal

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45
Q

what causes unstable angina?

A

Plaque ruptures and thrombus forms around it causing partial occlusion of the vessel.

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46
Q

when does pain develop in unstable angina?

A

Pain can happen at any time .

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47
Q

what is the ECG of unstable angina?

A
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48
Q

what are the troponin levels in unstable angina?

A

normal

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49
Q

what does NSTEMI stand for?

A

non st segment elevation myocardial infarction

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50
Q

what happens in NSTEMI?

A

Plaque ruptures and thrombus forms around it causing partial occlusion to the vessel.

Causing injury and infarct to the subendocardial myocardium

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51
Q

what is the ECG in NSTEMI?

A
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52
Q

what are the troponin levels in NSTEMI?

A

elevated as cardiac tissue death

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53
Q

what does STEMI stand for?

A

ST segment elevation myocardial infarction

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54
Q

what happens in STEMI?

A

Blood clot completely occludes vessel. No blood flow or O2

Transmural injury and infarct to the myocardium

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55
Q

what is the ECG in STEMI?

A
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56
Q

what are the troponin levels in STEMI?

A

elevated

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57
Q

learn the differences

A
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58
Q

define angina pectoris

A

tightness in the chest

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59
Q

what is angina pectoris caused by?

A

reversible ischaemia of heart muscle - narrowing of one or more coronary arteries

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60
Q

what is the difference in pain between unstable and stable angina?

A

Stable angina -> pain only on exercise, gradual deterioration

Unstable angina -> pain at rest and exercise

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61
Q

what are the symptoms of angina pectoris (PCO)?

A

crushing chest pain can have radiation to arm, back, jaw

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62
Q

what are the signs (clinical findings) of angina pectoris? 2

A

often none

hyperdynamic circulation - mismatch between oxygen delivery and requirement

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63
Q

hyperdynamic circulation (mismatch between oxygen delivery and requirement) causes

?: ? carrying capacity of the blood is ? so the ability of the patient to cope with a ? of the coronary artery is also ?. Restoring the patients ? to normal can reduce ? problems.

?: ? the demand for oxygen by the tissues as it increases the ? ?. Treating the hyperthyroidism will solve the ?

?: body loses more ? than it takes in -> decrease in blood ?

A

anaemia
oxygen
reduced
narrowing
reduced
haemoglobin
angina

hyperthyroidism
increases
metabolic rate
angina

hypovolaemia:
fluid
volume

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64
Q

what is angiography?

A

Using a dye to look at the patency of the arteries

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65
Q

what is ecocardiography?

A

Ultrasound to look at the function of the heart valves and ventricles

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66
Q

what do isotope studies do?

A

Looks at the proportion of blood ejected from the left ventricle shows how much residual function is present

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67
Q

what 2 things do you have to do to treat angina pectoris?

A

Reduce oxygen demands of the heart

Increase oxygen delivery to the tissues

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68
Q

when treating angina pectoris what do you have to do to reduce the oxygen demands of the heart? 3

A

reduce afterload (blood pressure)

reduce preload (venous filling pressure)

correct mechanical issues (valves/septal defects)

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69
Q

when treating angina pectoris how can you increase oxygen delivery to tissues? 2

A

Angioplasty -> dilate blocked, narrowed vessels

CABG coronary artery bypass grafting -> creates a new route for blood to flow around blocked/narrowed arteries

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70
Q

what non-drug therapies are used to treat angina pecoris?

A

Explanation of illness to understand what triggers it so they can manage it by living within limitations

Modify risk factors : smoking cessation, exercise, diet

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71
Q

drug therapies for angina pectoris

Reduce MI risk Aspirin -> reduce chance of platelets adhering to atherosclerotic plaque

Reduce hypertension (afterload) -> diuretics, Ca channel antagonists, ACE inhibitors, B blockers

Reduce ? -> dilate coronary vessels through ?

Emergency treatment -> ? ? to reduce preload, short shelf life

A

aspirin
platelets

hypertension (afterload)

preload (venous filling pressure)
nitrates

GTN spray

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72
Q

what is CABG?

A

(bypas) -> can only be carried out once, lasts 10yrs, major surgery (mortality)

Veins grafted from the leg and attached to the aorta as a new blood supply to bypass the obstruction

It is only possible if the blockage is close to the origin of the artery

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73
Q

what is angioplasty?

A

dilate blocked, narrowed vessels

lower risk (percutaneous intervention) and benefit, risk of vessel rupture during procedure, need antiplatelet therapy

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74
Q

what is peripheral vascular disease?

A

angina of the tissues - usually lower limbs (like angina but doesn’t affect cardiac tissue ).

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75
Q

what are the symptoms of peripheral vascular disease?

A

claudication pain in limb on exercise

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76
Q

peripheral vascular disease has an MI risk as ? is a ? disease so if they have it in there peripheral vessels they also have it in the ? vessels

A

atherosclerosis
systemic
cardiac

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77
Q

what are the outcomes of peripheral vascular disease? 3

A

Limitation of function

poor wound healing

May lead to tissue necrosis and gangrene

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78
Q

how does ischaemia lead to infarction?

A

Embolization: piece of atherosclerotic plaque breaks off and blocks a smaller vessel downstream. Lack of blood flow to that area will cause tissue death if it persists for more than 20 minutes

79
Q

Infarction is an issue with the heart but also affects the ? and ?

A

limbs
brain

80
Q

Stroke: Happens through carotid artery atherosclerosis which allows platelet clots and other clots to embolise up the carotid artery and into the brain causing ischaemia in the short term and eventually infarction of the brain tissue in the obstructed area

A

carotid
atherosclerosis
platelet
embolise
brain
ischaemia
infarction

81
Q

define myocardial infarction

A

Blockage of a coronary artery without collateral blood supply. Therefore all the tissue distal to the blockage will suffer necrosis

82
Q

how is tissue loss from necrosis reduced when treating mi? 2

A

by opening blood flow to ischaemic tissue
- Thrombolysis: using drugs to absorb the blood clot which is causing the blockage
- Angioplasty

By bypassing the obstruction
- CABG, fem/pop bypass

83
Q

how are further episodes of MI prevented?

A

risk factor management and aspirin

84
Q

if a patient is having an MI what do u give?

A

analgesics, aspirin, reassurance,

85
Q

what basic life support may be required if a patient has a mi?

A

cardiac arrest due to an arrythmia from altered electrical conduction in the heart tissues

86
Q

bls for cardiac arrrest?

A

approach with caution
verbal and pain stimulus
call for help
head tilt chin lift
assess breathing 10s
no breathing = cardiac arrest
call 999
30 chest compressions
2 rescue breaths

87
Q

hospital treatment for MI is dependant on time from onset of symptoms

<3hrs angioplasty and stenting

<6hrs thrombolysis if suitable

Drug treatment to reduce tissue damage

A
88
Q

signs and symptoms of mi

A

Pain, nausea, pale, sweaty, feel like going to die

89
Q

what are the outcomes of mi?

A

Death or functional limitation from reduced cardiac muscle action

90
Q

how is MI diagnosed?

A

STEMI st segment elevation MI, NSTEMI non-st segment elevation MI
§ Note: even after a few weeks the ECG isn’t normal as has a q wave

troponin level elevation

91
Q

long term management of mi?

A

Risk modification
Aspirin, b blocker, ACE inhibitor

92
Q

define valve stenosis

A

narrowed valves

93
Q

define valve incompetence

A

valve not closing properly

94
Q

which valves are most likely to have problems? why?

A

mitral valve and aortic valve due to higher pressure (left heart)

95
Q

heart valve disease is common in the elderly and those with down syndrome

A
96
Q

causes of heart valve disease 4

A

Congenital abnormality
○ Valve doesn’t work effectively, patient often has symptoms of heart failure and need a replacement of the valve

Myocardial infarction -> papillary muscle rupture

Rheumatic fever -> immunological reaction to streptococci which can cause damage to the heart valve -> rheumatic heart disease can also lead to infective endocarditis

Dilation of the aortic root which pulls the cusps apart so they can’t close fully -> caused by syphilis or aneurysm formation

97
Q

how is valve disease investigated?

A
  • Ultrasound scan
    Doppler ultrasound colours the blood based on if it is flowing in or out of the heart
98
Q

why are valve replacements done before heart failure?

A

as it will not fully reverse any heart failure previous to treatment

99
Q

what risk is there with valve replacements?

A

endocarditis risk so may consider antibiotic prophylaxis

100
Q
A
101
Q

list 3 dental implications of valve replacements

A

Anticoagulants

Endocarditis prevention
○ OHI, prevent oral diseases and remove causes of oral sepsis

Consult with patients medical team

102
Q

Infective endocarditis is ? and ? of the ? (inside heart). Bacteria enter (mouth), go into the circulation and settle onto previously ? areas of heart tissue. The bacteria colonise a ? and multiply to cause ? and ? of the infection, leading to ? formation -> thickenings and areas of damage to the valves

A

infection
inflammation
myocardium
damaged
thrombus
damage
spread
vegetation

103
Q

what is the main bacteria for infective endocarditis?

A

oral streptococci so it impacts dental care (bacteraemia).

104
Q

where is infective endocarditis usually found?

A

on the valves

105
Q

patients at risk of infective endocarditis 4

A

Other cardiac disease

Intracardiac device
○ Not angioplasty, stent, CABG, implanted pacemaker or defibrillator

Prosthetic valve

Past endocarditis

106
Q

is diagnosis of infective endocarditis difficult?

A

yes
there is no single test that is reliable

Have to take blood cultures over several days to see if bacteria are present in the blood stream coming from the infection in the heart

107
Q

effects of infective endocarditis 3

A

Prolonged antibiotic treatment

Cardiac valve damage that may require replacement which is risky

Risk of death from disease or its complications

108
Q

which dental procedures increase risk of infective endocarditis?

A

any that involve manipulation of the dento-gingival junction

109
Q

what should a dentist do for patients at risk of infective endocarditis?

A

Identify them -> medical history covering risk conditions

Prevention of oral disease and excellent oral hygiene -> keep bacteria low

110
Q

remember

Nice Guidelines: antibiotic prophylaxis should not be routinely be given to a patient with infective endocarditis

Special consideration: prosthetic valve, previous infective endocarditis, congenital heart disease

A
111
Q

congenital heart defects/disease is often undetected and asymptomatic but suspect they have them if have other congenital body defects

Can detect them through what?

A

doppler ultrasound -> shows blood flow and its direction. easy and non-invasive.

112
Q

what is finger clubbing?

A

swelling of the terminal digits of the hands and changes of the nail bed angle to the finger.

113
Q

what medical issues is finger clubbing seen in? 4

A

Cardiac disease

Lung disease

Inflammatory bowel disease

Liver cirrhosis

114
Q

what is cyanosis?

A

Lack of oxygenated haemoglobin / increase in deoxygenated haemoglobin in the blood

115
Q

how much deoxygenated haemoglobin in the blood is considered cyanosis?

A

5g/dl or more of deoxygenated haemoglobin in the blood

116
Q

central cyanosis is mostly caused by what?

A

congenital heart disease causing Poor oxygenation of the blood or oxygenated and deoxygenated blood mixing

117
Q

what are the signs of central cyanosis?

A

warm tissues being blue e.g. tongue

118
Q

peripheral cyanosis is caused by

A

cold extremeties or vascular spasm
causing slow circulation taking more oxygen out of the haemoglobin in cold tissues

119
Q

what are the signs of peripheral cyanosis?

A

Cold peripheral tissues look blue e.g. hands

120
Q

which septal defects are the most common?

A

atrial

121
Q

what happens in atrial septal defects?

A

oxygenated blood from left atrium leaks into right atrium

122
Q

are atrial septal defects usually cyanotic?

A

no as no deoxygenated blood is going to the left side and to rest of body

123
Q

how do atrial septal defects lead to heart failure?

A

due to increase strain on the heart

On an x-ray shows a bulge in the left side of the heart due to increased workload

124
Q
A
125
Q

what happens in ventricular septal defects?

A

Blood flows from left to right ventricle and pulmonary artery due to higher pressure in left side.

126
Q

how is ventricular septal defects an increased endocarditis risk?

A

more turbulent flow as the volume of blood in the right ventricle and circulating into the lungs is higher

127
Q

are ventricular septal defects usually cyanotic?

A

non-cyanotic as no deoxygenated blood is going to the left side and to res of body

128
Q

treatment for septal defects 2

A

Some shrink naturally (atrial defects often require no intervention)

‘Patch’ repair -> open heart surgery where mesh is place on either side of the defect by arterial access

129
Q

what is coarctation of the aorta?

A

Narrowing of the aorta just after the left carotid artery has exited, restricts blood flow to the left arm and lower limbs.

Blood pressure would differ taken on the right vs left arm, the left arm would have considerably lower blood pressure

130
Q

what is patent ductus arteriosus?

A

The ductus fails to close so the pulmonary artery and aorta are connected.

131
Q

is there cyanosis in patent ductus arteriosus?

A

No cyanosis as oxygenated blood flows into the pulmonary artery due to higher pressure in aorta

132
Q

how can patent ductus arteriosus lead to heart failure and endocarditis risk?

A

due to turbulent blood flow

133
Q

define heart failure

A

output of the heart is incapable of meeting the oxygen demands of the tissues

134
Q

what are the 2 situations where heart failure can occur?

A

Low output failure - most common

High output failure

135
Q

in heart failure what is low output failure?

A

Pump is failing and not strong enough to force liquid around the body

136
Q

what causes low output heart failure?

A

Most commonly due to heart muscle disease, pressure overload, volume overload

Also due to
- Arrhythmias -> Atrial contractile signal not transferred to the ventricle so they continue at a rate independent to the atria
- Drugs e.g. corticosteroids and anticancer drugs can affect heart muscle

137
Q

in heart failure what is high output failure?

A

Demands of the body have exceeded the capacity of the pump

138
Q

what is high output heart failure due to?

A

Due to anaemia, thyrotoxicosis etc.

139
Q

is left or right heart failure more common? why?

A

Left heart failure is more common than right because the left side does the most work.

140
Q

what is congestive heart failure

A

Left heart failure often leads to right as increased blood volume into the lungs causes the right side to have to work harder which then starts to fail -> congestive heart failure

141
Q

what are the 2 mechanisms of heart failure?

A

systolic dysfunction (pumping)

diastolic dysfunction (filling)

142
Q

mechanisms of heart failure

in systolic dysfunction what happens during diastole and systole?

A

diastole: enlarged ventricles fill with blood

systole: ventricles pump out less blood than normal

143
Q

mechanisms of heart failure

systolic dysfunction is due to what?

A

Due to loss of muscle or stiffness of the ventricle wall

144
Q

mechanisms of heart failure

in diastolic dysfunction what happens during diastole and systole?

A

diastole: stiff ventricles fill with less blood than normal

systole: ventricles pump out blood (may be less than normal)

145
Q

heart failure compensation mechanism

how does the body compensate for heart failure? how is this managed?

A

by increasing blood volume which makes heart failure worse

management needs to fix the cause and prevent the compensatory mechanisms from making things worse

146
Q

what are the signs of left heart failure?

A

Affect systolic blood pressure and systemic tissues

Lungs accumulate more blood than normal and have higher blood pressure than expected

147
Q

what are the signs of right heart failure?

A

Venous pressure increases as systemic veins fill as blood is not taken away and pumped around the body.

This leads to fluid transudate from the blood in the tissues

148
Q

symptoms of heart failure 4

A

Shortness of breath -> fluid in lung tissues prevent alveoli from transmitting oxygen into the blood, worse if patient lies flat as venous pressure in the lungs rises

Swelling of feet and legs -> fluid moving into tissues from RHF due to gravity
○ Pitting oedema: Severity of heart failure is assessed based on how far up the leg it goes

Swollen or tender abdomen -> liver engorgement and fluid

Cough with frothy sputum from air mixing with liquid in the lungs causing irritation

149
Q

what is the treatment for acute heart failure (emergency)

A

oxygen, morphine, frusemide

Patient is short of breath and gasping
due to fluid in lungs

High dose diuretic to remove fluid -> frusemide

150
Q

treatment for chronic heart failure

Improve myocardial function
- Hypertension, valve disease, arrhythmias, anaemia, thyroid disease

Reduce ‘compensation’ effects

Treat the cause where possible

Drugs

Stop negative inotropes - B blocker -> make heart failure worse

A

myocardial function

compensation effects

cause

inotropes

151
Q

drugs used to treat heart failure

? -> increase salt and water loss

? -> reduce water and salt retention

? -> reduce venous filling pressure

? -> treat problems with electrical impulses of the heart by improving heart efficiency and control electrical activity

A

diuretics

ACE inhibitors

nitrates

inotropes

152
Q

name a negative inotrope that can make heart failure worse (medicine)

A

B-blocker

153
Q

cardiac arrhythmias are issues of what?

A

heart rate

154
Q

define tachycardia (tachy arrhythmias)

A

heart rate too fast

155
Q

tachycardia results in impaired ?? by ? the ???. reduced cardiac output leads to ??

A

cardiac function
reducing
diastolic filling time
heart failure

156
Q

what are the 2 groups of tachyarrhythmias?

A

atrial tacchyarrhythmias
ventricular tachyarrhythmias

157
Q

describe the qrs complex on an ECG for atrial tachyarrhthymias

A

narrow

158
Q

describe the qrs complex on an ECG for ventricular tachyarrhythmias

A

broad as the signal passes through multiple tissues

159
Q

what is atrial fibrillation?

A

rapid atrial impulses conducted to ventricles -> irregular and high pulse

160
Q

what is ventricular fibrillation?

A

no organised rhythm or qrs pattern

161
Q

how are tachy arrhythmias treated

A

beta blockers - can result in postural hypotension

162
Q

define brady arrhythmias

A

heart rate too slow

163
Q

what are brady arrhythmias caused by?

A

drug induced or heart block

164
Q

what is heart block?

A

reduction in conduction through the atrioventricular node which prevents another impulse to travel preventing tachy arrhythmia or atrial fibrillation

165
Q

how is a heart block shown on an ECG?

A

prolonged pq interval

166
Q

the level of a heart block is classified based on what?

A

the length of the signal delay. 1 2 or 3, 3 means there is no signal passed to the ventricles so they pulse at their own intrinsic rate

167
Q

what is the treatment for brady arrythmias?

A

cardiac pacemaker -> takes over if pulse drops below a certain rate

168
Q

in normal sinus rhythm what do parts of an ECG represent:

P wave

qrs complex

t wave

A

p wave = atrial repolarisation

qrs complex = ventricular depolarisation

t wave = ventricular repolarisation

169
Q

define asystole

A

no electrical activity

170
Q

this is what asystole looks like on an ECG

A
171
Q

is asystole treated with a defibrillator? why?

A

no as defibrillators dont give electrical activity they just coordinate existing electrical activity

172
Q

how is a pt with asystole treated?

A

adrenaline to try produce electrical activity so a defibrillator can be used

173
Q

is there cardiac output with ventricular fibrillation? why?

A

no as no emptying of the ventricles due to muscle spasm

174
Q

how is ventricular fibrillation treated?

A

with a defibrillator

175
Q

antiplatelet drugs e.g. aspirin reduce the chance of what?

A

heart attack and stroke in at risk population

176
Q

what are the dental implications of antiplatelet drugs?

A

prolonging the bleeding time after extraction

177
Q

Oral anticoagulants (e.g. warfarin)
inhibit the ?? and reduce the amount of ? formed and therefore ??

A

clotting cascade
fibrin
clotting stability

178
Q

what is the dental imact of oral anticoagulants?

A

increase in post-treatment bleeding a few hours later as no fibrin so unstable clot formation which breaks down after a few hours.

179
Q

warfarin
Inhibits synthesis of ????? (2,7,9,10 and protein ? and protein ?)

Initial ?? as protein C and S ??.

Anticoagulation takes 2-3 days as clotting factors 2,7,9,10 are ? without replacement

so ? is often used initially also given as has instantaneous affect preventing hypercoagulation

A

vitamin k dependant clotting factors
C
S

hypercoagulation
inhibit clotting

consumed

Heparin

180
Q

pt on warfarin have to be monitored using what test?

A

IRN ratio of a healthy volunteers prothrombin time (time to convert prothrombin to thrombin) measured against the patient

Aim for INR between 2 and 4

181
Q

remember
Warfarin and dentistry

Local haemostatic measures e.g. fibrinogen activator, suture, or local anaesthetic with vasoconstrictor

Assume all drugs interact with warfarin -> INR test day after prescribing antibiotics, avoid NSAIDs

A
182
Q

remember
New oral anticoagulants

No significant drug interactions with dentistry

Short half life -> can do extraction just before dose is due when effects of the drug are lowest

A
183
Q

what do statins do?

A

inhibit cholesterol synthesis in the liver

184
Q

what are the side effects of statins?

A

can cause inflammation in the muscles (myositis) with some drug interactions

185
Q

what do B blockers do?

A

reduce the excitability of the cardiac conduction system reducing the risk of cardiac arrest, ventricular fibrillation and death

186
Q

beta blockers can make heart failure and asthma worse. what dental impact do they have?

A

more susceptible to lichenoid reactions

187
Q

Diuretics -> antihypertensive (BP) and for heart failure
Increase ? and ? loss reducing ? volume and ??
can lead to ?? so has to be monitored by looking at ? in the blood periodically

A

salt
water
plasma
cardiac workload

Na/K imbalance
electrolytes

188
Q

what is the dental impact of diuretics?

A

dry mouth if excessive water loss

189
Q

Nitrates -> Used for emergency treatment or long term prevention of ?

dilates the veins -> reducing the preload to the heart

dilates the coronary arteries -> reducing ?? and cardiac ? requirement

This reduces pain from ischaemia as the oxygen needs can be better balanced.

dilates ??? supply -> if narrowed coronary arteries, other blood vessels to the tissue will be enhanced

A

angina

dilates
preload

cardiac workload (afterload)
oxygen

pain
oxygen

collateral coronary artery

190
Q

Calcium channel blockers -> treats ? and ?

They can act on different places for example some act on peripheral blood vessels whilst others act on the heart muscle

Block calcium channels in smooth muscles -> vasodilation and relaxation

Slow conduction of pacing impulses in the heart

A

hypertension
migraines

vasodilation
relaxation

conduction
impulses

191
Q

Angiotensin converting enzyme (ACE) inhibitors do what to things ?

A

reduce blood pressure and reduce water/salt retention

192
Q

Angiotensin converting enzyme (ACE) inhibitors

Inhibit conversion of angiotensin I to angiotensin II

Angiotensin II is a vasoconstrictor and triggers aldosterone dependant resorption of water and salt

direct ? affect on the arteries and also a reduction in ?? by preventing salt and water reabsorption

A

angiotensin I
angiotensin II

vasoconstrictor
aldosterone
water
salt

vasodilatory
plasma volume

193
Q

side effects of ACE inhibitors?

A

hypotension and cough as they cause tissue changes which can irritate
Angiotensin II inhibitors work the same but don’t cause these side effects

194
Q

what is the dental impact of ACE inhibitors? 2

A

More susceptible to lichenoid reaction

Angio-oedema -> sudden increase in tissue fluid due to inhibition of the complement cascade by the ace enzyme -> rapid swelling of the tongue/lips

5 Human Diseases (16 decks)

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