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HHD 2 > IHD and ACS > Flashcards

IHD and ACS Flashcards

1
Q

What is ischaemic heart disease?

A

heart problems caused by narrowing of the arteries
narrowing of the arteries leads to less blood and oxygen reaching the heart (therefore affects coronary arteries)

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2
Q

Ischaemic heart disease is also referred to as …

A

coronary artery disease
coronary heart disease

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3
Q

Ischaemic heart disease is a spectrum of diseases which include:

A

stable angina
unstable angina
myocardial infarction

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4
Q

Acute coronary syndrome refers to a group of conditions that include…

A

ST elevations myocardial infarction
Non-ST elevation myocardial infarction
Unstable angina

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5
Q

Angina presents as a “pain in the heart”. Describe the pathophysiology of angina

A

cells do not have enough oxygen and so switch to anaerobic respiration; leading to the production of lactic acid (from pyruvate)

Build up of acid in the heart tissue causes pain

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6
Q

What are some risk factors for ischaemic heart diseases (IHD)?

A

diabetes
obesity
hypertension
smoking

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7
Q

What is a risk factor for atherosclerotic changes to the blood vessels?

A

high blood pressure

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8
Q

Outline the aetiology of IHD

A

Endothelial injury (lining of vessels can be damaged by high blood pressure)

the endothelium becomes exposed to LDL, hormones and pro-inflammatory molecules (smoking)

Expression of adhesion molecules (expression of adhesion molecules is up-regulated in damaged endothelium

leukocytes then adhere to the artery wall (via adhesion molecules) as part of the inflammatory response to the damaged endothelium

Monocytes scavenge lipids and then become foam cells (characteristic of atheroma)

Foam cells release cytokine to stimulate smooth muscle migration in to the media - formation of the fatty streak [smooth muscle cell hyperplasia- further narrowing the blood vessels]

Deposition of lipoprotein in the intima leads to plaque

Obstruction due to plaque, clot or vasospasm

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9
Q

What is the consequence of an atheroma encouraging the splitting of the endothelium ?

A

subendothelium is exposed
platelet plug formation
thrombus is formed

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10
Q

What is an arterial stenosis?

A

narrowing of the artery

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11
Q

What causes angina?

A

this is when the myocardial oxygen demand exceeds the myocardial supply

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12
Q

Give instances where myocardial oxygen demand increases

A

emotional stress
increased physical activity
sexual activity

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13
Q

How is myocardial oxygen supply assessed?

A

coronary blood flow
arterial O2 content

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14
Q

Angina is a ___________ cellular hypoxia

A

reversible

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15
Q

Infarct is an _____________ condition with dead muscle present. What leads to an infarct ?

A

irreversible
complete blockage of the coronary artery

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16
Q

List IHD presentation

A

typical angina
atypical angina
asymptomatic
epigastric pain
jaw/arm pain (left arm, left side of jaw)
fatigue
dyspnoea on exertion
tachycardia
xanthelasma
retinopathy

Delayed healing in pulp/periodontum due to poor circulation

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17
Q

What is xanthelasma?

A

local accumulation of lipid deposits on eyelids

18
Q

Give the characteristics of typical angina

A

chest pressure/squeezing lasting several minutes

provoked by exercise or stress

relieved by rest or GTN

19
Q

What are the clinical presentations of a myocardial infarct?

A

sweating
tachypnea
anxiety (fight or flight)- impending feeling of doom
Pale skin

no GTN relief

20
Q

What are the clinical investigations for IHD?

A

Resting ECG
Haemoglobin (make sure that they are not anaemic)
Fasting lipid profile
Fasting blood glucose
coronary angiography

21
Q

What is the presentation of angina on an ECG

A

ST depression

[there should be a straight line between the S and T segments of the ECG]

22
Q

How is IHD managed for all patients?

A

lifestyle education
antiplatelet therapy (prevent thrombus which narrows arteries)
anti-anginal therapy
statin (lipidaemia, atheroma)
anti-HTN therapy- prevent damage to the endothelial layer of the blood vessels
CABG (coronary artery bypass graft, to bypass obstruction and supply cells in region)/PCI

BM control ? bone marrow??

23
Q

What is the management of acute anginal symptoms ?

A

sublingual GTN

24
Q

ST elevation in ECG is usually an indication of…

A

infarct

25
Q

ST depression in ECG is usually an indication of …

A

angina

26
Q

What is unstable angina?

A

absence of biochemical evidence of an MI
angina lasts >20 minutes
angina at rest (pain at rest)
crescendo angina

27
Q

What is a myocardial infarction (non-ST elevation)?

A

an acute ischaemic event causing myocyte necrosis
no ST elevation on the ECG

28
Q

What is a myocardial infarction (ST- elevation)

A

acute ischaemic event causing myocyte necrosis
evidence of ST elevation on the ECG

29
Q

What is the biochemical evidence of a myocardial infarct?

A

when a muscle dies, various enzymes are releases

However in angina, muscle cells do not die which means enzymes are not releases hence no biochemical evidence being present

30
Q

What is the clinical presentation acute coronary syndrome?

A

angina
radiation to jaw/arm
pallow
dyspnoea
cardiogencic shock- cannot meet the demands of the body- body not getting enough blood flow
nausea and vomiting
sweating
feeling of impending doom
tachycardia
hypotension

epigastric shock may also occur- pain goes through to the back

31
Q

Outline the pathophysiology of ACS

A

rupture of fibrous plaque
exposure of lipid substances
platelet aggregation
thrombus formation
occlusion of vessel
ischaemia (reduction of oxygen) and myocardial necrosis

32
Q

What are the clinical investigations to determine ACS?

A

ECG
cardiac biomarkers (dead muscles leak enzymes)
coronary angiogram
serum, lipids, glucose, U&Es (urea and electrolytes)

33
Q

Give examples of cardiac biomarkers of infarcts

A

Troponin
Creatine kinase (CK)
CK-MB (isoenzyme of creatine kinase)

34
Q

What is the presumptive management of ACS?

A

[MONA]
Morphine- switches off sympathetic nervous system, also for pain
Oxygen
Nitrates (for pain - [acid relief?])
Aspirin (300mg)

employ DR ABC

35
Q

What is the definitive management of ACS?

A

percutaneous coronary intervention (PCI)- stent
anticoagulation (warfarin)
antiplatelet (forever)
statin
thrombolysis

36
Q

When should thrombolysis be performed?

A

if PCI is not available in 90 minutes
if a stent is not placed in 90 minutes

37
Q

PCI (stent) delays …

A

(pushes back) the need for CABG

38
Q

What is the disadvantage of a stent placed in vein ?

A

veins are not meant to undergo arterial pressure
they will eventually narrow

39
Q

What are the dental considerations for stable angina

A

[angina can be provoked by pain and anxiety- emotional stress]

no issues with minor treatment under LA
consider oral sedation, [BZD?]
anything larger than minor treatment, deal with cardiology team

40
Q

What are the dental considerations for unstable angina?

A

higher risk of MI
always discuss with cardiology team prior to treatment, prophylactic GTN

41
Q

What are the dental considerations post myocardial infarction?

A

most complications occur within 6 months (high re-infarction rate)
defer treatment where possible

HHD 2 (37 decks)

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