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CRV week 3 > Clinical aspects of Cardiovascular disease > Flashcards

Clinical aspects of Cardiovascular disease Flashcards

1
Q

what are the modifiable risk factors for atherosclerosis?

A

smoking
hypertension
hyperlipidaemia
diabetes
obesity

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2
Q

what are the non modifiable risk factors for atherosclerosis?

A

age
male gender
family history

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3
Q

what are the cardiac causes of chest pain?

A

aortic dissection
pulmonary embolism
aortic stenosis
pericarditis
myocarditis
takotsubo cardiomyopathy
cardiac ischaemia

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4
Q

how do you test for cardiac ischaemia?

A

troponin positive
-type I MI -physcial blockage of artery
-type II MI- physical artery okay but there is a blockage/aneurism/spasm
-SCAD
-coronory spasm

Troponin negative
-angina- stable vs unstable
-cor spasm
-microvasular/endothelial

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5
Q

what is an aortic dissection?

A

process where layers of aortic wall split like an onion, very painful

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6
Q

what is a pulmonary embolism?

A

big clots going up to lungs; tends to be one sided

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7
Q

what ia aortic stenosis?

A

heart muscle grows significantly and outgrows its blood supply

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8
Q

what is pericarditis?

A

inflammation of pericardium

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9
Q

what is myocarditis?

A

inflammation of heart muscle ( not normally painful)

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10
Q

what is takotsubo cardiomyopathy?

A

broken heart syndrome - from Amin and jawad

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11
Q

what are the respiratory causes of chest pain?

A

pneumonia
pneumothorax
oesophagitis/ reflux disease
oesophageal rupture/ mediastinitis

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12
Q

what are some other causes for chest pain?

A
  • Cancer
  • Neuralgia
  • Psychogenic
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12
Q

what are the GI causes of chest pain?

A
  • Pancreatitis
  • Gallstones
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13
Q

what are the stages of the sequence of progression of atherosclerosis?

A

endothelial cell injury
lipoprotein deposition
inflammatory reaction
smooth muscle cell cap formation

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14
Q

what happens during endothelial cell injury stage?

A

This is likely the initial factor that begins the process of atherosclerotic plaque formation. Because the endothelium is constantly exposed to the circulation, any toxin present can result in damage, as occurs during tobacco use, diabetes and dyslipidemia. The continuous physical force exerted upon the endothelium also commonly plays a role, as the greatest atherosclerotic plaque occurs at arterial bifurcations ― i.e. the bifurcation of the left main coronary artery and the left anterior descending. Hypertension increases the physical force present.

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15
Q

what happens during the lipoprotein deposition phase?

A

When the endothelium is injured or disrupted, lipoprotein molecules can gain entry where they are then modified by oxidation (via free radicals or oxidizing enzymes) or glycation (in diabetes). This modified lipoprotein, or LDL, is inflammatory and able to be ingested by macrophages, creating “foam cells” and causing a “fatty streak” in the arterial wall.

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16
Q

what is the good cholesterol?

A

HDL

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17
Q

what is the bad cholesterol?

A

LDL

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18
Q

what happens during the inflammatory reaction phase?

A

The modified LDL is antigenic and attracts inflammatory cells into the arterial wall. Also, after endothelial injury, inflammatory mediators are released further, increasing leukocyte recruitment.

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19
Q

what happens during the smooth muscle cell cap formation stage?

A

Smooth muscle cells migrate to the surface of the plaque, creating a “fibrous cap.” When this cap is thick, the plaque is stable; however, thin capped atherosclerotic plaques are thought to be more prone to rupture or erosion, causing thrombosis.

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20
Q

how do wer diagnose chest pain?

A
  • Inpatients
    • Layered history
    • Observations
    • Laboratory tests
    • ECG
    • Serial ECG
    • CXR
  • Outpatients
    • Dual history
    • ECG
    • Chronology
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21
Q

what investigations are required before diagnosis of chest pain?

A
  • Exercise Tolerance Test (ETT)
    • Sensitivity and specificity ~70%
    • Low risk (<1:10,000)
    • Low resource
    • Many patients unsuitable/submaximal/indeterminate
  • Invasive Coronary Angiogram
    • Gold standard
    • Low risk (but highest risk) —> MI/CVA/Arrhythmia
    • High resource
    • Patient selection
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22
Q

what is unstable angina?

A

unpredictable pain
-unstable plaque without myocardial necrosis
-critical coronary disease

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23
Q

what is the mechanism of action of anti-anginal drugs?

A

reduce cardiac workload
-slow HR
-reduce force of contraction
-reduce pre-load/ after-load
-improve blood supply
-coronory vasodilation

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24
Q

what are the indicators of acute coronary syndromes?

A

unstable angina
NSTEMI
STEMI (ST elevation MI)

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25
Q

what is treatment for an NSTEMI?

A
  • Dual antiplatelet therapy - Aspirin + Clopidogrel
  • LMWH/fondaparinux - Heparin as anti-coagulant
  • Statin - for correction of cholesterol (HDL)
  • ACE-I - Affects LV modelling
  • β-blocker
  • Risk stratification (ECG, TnT, GRACE, Echo, other investigation)
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26
Q

what is a STEMI (ST-elevation MI)?

A

has more heart damage as ‘trans-mural’
complete vessel occlusion

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27
Q

what are the coronary interventions available for a type 1 STEMI?

A

systemic thrombolysis
primary percutaneous coronary intervention
interventional cardiac centre

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28
Q

what are the goals of a systemic thrombolysis?

A

to reestablish the coronary latency
salvage the myocardium
improve survival

29
Q

what are the complications of acute MI?

A

extension/ ischemia
arrhythmia
expansion/ aneurysm
acute MI
pericarditis
RV infarct
mechanical
heart failure
mural thrombosis

30
Q

what are the treatments of coronary artery disease?

A

-primary prevention
-anti-anginal drugs
-anti-platelet drugs
-thrombolytic drugs
-agioplasty and stents
-CABG surgery
-secondary prevention

31
Q

what is atherosclerosis?

A

-the build up of fatty and fibrous material within the intima of the arteries
-over time the plaque can become fibrous and calcified
-as plaque builds up it can obstruct the lumen of arteries causing ischemia
-even non-obstructive plaque can promote thrombus formation and occlude the arterial lumen

32
Q

why do we use lipid lowering therapy?

A

Multiple clinical trials have shown that reducing LDL-C reduces the risk of cardiovascular events proportionately to the reduction and independent of other risk factors

33
Q

what are lipid lowering therapies?

A

statins are the mainstay of lipid lowering therapy
-ezetimibe
-PCSK9 inhibitors

34
Q

how do statins work?

A

-Inhibit 3-hydroxy-3-methylglutaryl-​ CoA reductase (HMG-​CoAR) which is the rate-​limiting enzyme in the synthesis of cholesterol
-22% reduction in the risk of major CVD events per millimole per litre reduction in LDL-​C
-Huge amounts of safety data for statins
-Main reason for discontinuation is myalgia

35
Q

what are some examples of statins?

A

Atorvastatin, Simvastatin, Rosuvastatin, Pravastatin

36
Q

what data do we have that suggest statins work?

A

Statin treatment for an average of 5 years provided an ongoing reduction in the risk of coronary events for an additional period of up to 10 years

37
Q

how does ezetimibe work?

A

Inhibits cholesterol absorption by enterocytes and augments expression of liver LDL receptors
When added to statins further reduces LDL-​C by 15–20%
IMPROVE-​IT study showed that in patients who survived an acute coronary syndrome, adding ezetimibe to a statin associated with a 6.5% proportional reduction in major CVD events

38
Q

what are PCSK9 inhibitors?

A

PCSK9 binds to LDL receptors and promotes their intracellular degradation
Inhibiting PCSK9 can decrease LDL-​C substantially
PCSK9 inhibitors in addition to statins achieves much lower LDL-​C levels than was previously possible, and this further reduction conferred greater CVD benefit
Expensive so only used in high-risk patients with atherosclerotic disease failing to reach target LDL-C or in patients with severe familial hypercholesterolaemia with substantially elevated LDL-​C levels despite maximal statin−ezetimibe therapy
Evolocumab, Alirocumab

39
Q

what is the mechanism of action of aspirin?

A

Irreversibly binds to the enzyme cyclo-oxygenase
Inhibits platelet synthesis of thromboxane A2
Inhibits platelet adhesion and aggregation
Platelets thereafter unable to synthesise new cyclo-oxgenase however endothelial cells can
At higher doses can inhibit prostacyclin production
(Prostacyclin inhibits platelet aggregation)

40
Q

what is the normal dosage of aspirin?

A

200mg in acute setting
75mg daily maintenance dose

41
Q

what is the pharmacokinetics of aspirin?

A

Oral preparation
Rapid absorption – peak plasma level at 30 – 40 mins
Platelet inhibition is evident at 1 hour
Variable 1st pass metabolism
Metabolic product is salicyluric acid
Oral bioavailability is 40 – 50%
Renal excretion dependent on urinary pH
Rapid clearance (t½ - 20 mins)

42
Q

what are the uses of aspirin?

A

Angina
Myocardial Infarction
Embolic / Thrombotic CVA
Transient Ischaemic Attack (TIA)
Percutaneous coronary intervention
Prevent miscarriage in pro-thrombotic conditions
Analgesia

43
Q

what are some contradictions of aspirin?

A

Under 16’s
Breast feeding mothers
Peptic ulceration
Haemophilia
Previous hypersensitivity reaction to NSAID’s
Severe renal failure
Hepatic Cirrhosis

44
Q

what are some adverse effects of aspirin?

A

Gastrointestinal Irritation – 50%
Gastric erosions / bleeding
Prolongation of bleeding time
Bronchospasm (in hypersensitive patients)
Skin rash (in hypersensitive patients)
Reye’s Syndrome (avoid in under 16’s)

45
Q

what is clopidogrel?

A

Belong to family of thienopyridines

Selectively inhibits adenosine diphosphate (ADP) induced platelet aggregation

Rapid absorption and extensive metabolism

Undergoes hepatic transformation into an active metabolite – SR26334

Selective reduction in ADP binding sites

Plasma elimination t½ - 8 hours

Dose dependent inhibition of ADP-induced platelet aggregation

Inhibition of platelet aggregation detectable at 2 hours (if given 400mg)

46
Q

what is ticagrelor?

A

Reversible and non-competitive ADP receptor antagonist
Directly inhibits P2Y12 receptor - doesn’t need hepatic metabolism for activity
Blocks platelet reactivity more consistently/completely than clopidogrel with less inter-individual response variability
Inhibition of platelet aggregation 30 minutes after 180mg loading dose is similar clopidogrel 600mg at 8 hours
If patient needs CABG after angio – less time to wait for recovery of platelet function (3 days compared to 5 days after clopidogrel)
180mg loading dose then 90mg bd

47
Q

what is prasugrel?

A

Thienopyridine pro-drug like clopidogrel
Irreversible inhibitor of P2Y12 receptor
Needs hepatic biotransformation but only one oxidative step
Therefore faster produced higher concentration of active drug
10 times more potent antiplatelet effect and more consistent
60mg loading dose then 10mg daily thereafter

48
Q

how do short acting nitrates work for angina relief?

A

GTN Spray sublingual administration or nitroglycerin tablet
SE – Headache, Dizziness

49
Q

how does long acting nitrate for angina prophylaxis work?

A

Isosorbide mononitrate or isosorbide dinitrate
Oral preparation or transdermal patch
Losses efficacy with prolonged administration
Need nitrate free period
SE – hypotension, headache, flushing

50
Q

what are the commonly used beta blockers?

A

bisoprolol, atenolol and carvedilol

51
Q

how do beta blockers work as anti-ischaemic drugs?

A

Slow heart rate and decrease myocardial oxygen demand

Aim for heart rate 55-60bpm

52
Q

what are the side effects of beta blockers?

A

Don’t stop abruptly

SE - fatigue, depression, bradycardia, heart block, bronchospasm, peripheral vasoconstriction, postural hypotension, impotence, and masking of hypoglycaemia symptoms

53
Q

what are non-dihydropyridine agents?

A

heart rate lowering calcium channel blockers Both act by peripheral vasodilation, relief of exercise-induced coronary constriction, a modest negative inotropic effect, and sinus node inhibition

54
Q

what are some examples of non-dihydropyridine agents?

A

verapamil and diltiazem

55
Q

what are the side effects of non-dihydropyridine agents?

A

bradycardia and dizziness

56
Q

what are dihydropyridine agents?

A

Long acting Nifedipine or amlodipine
The very long half-life of amlodipine and its good tolerability make it an effective once-a-day antianginal and antihypertensive agent
SE – few, ankle oedema

57
Q

what is ivabradine?

A

Selective If channel inhibitor
SE – bradycardia and dizziness

58
Q

what is nicorandil?

A

Nitrate and potassium channel activator
SE - nausea, vomiting, and potentially severe oral, intestinal, and mucosal ulcerations

59
Q

what is ranolazine?

A

Selective inhibitor of the late inward sodium current
SE - dizziness, nausea, and constipation
Ranolazine increases QTc, and should therefore be used carefully in patients with QT prolongation or on QTprolonging drugs

60
Q

what is the criteria for thrombolysis?

A

Within 12 hours of onset of pain
ST segment elevation ≥2mm in 2 adjacent chest leads
ST segment elevation ≥1mm in 2 adjacent limb leads
True posterior MI
New bundle branch block
Within 12 to 24hrs of onset of pain with ongoing symtomsand ECG evidence of evolving infarction and only if no available cardiac catheterisation laboratory

61
Q

what are some thrombolysis agents?

A

Streptokinase (GISSI Trial)
Tissue Plasminogen Activator (t-PA) (GUSTO Trial)

62
Q

what are some contradictions of thrombolysis?

A

Coagulation disorder
Active GI bleeding ie peptic ulceration
Severe hypertension (IV beta-blockade)
Previous haemorrhagic stroke
Surgery in the last month
Pregnancy
Traumatic CPR
Recent major trauma / head injury
TIA / Ischaemic stroke

63
Q

what are some advantages of thrombolysis?

A

Can be given quickly
Can be given by anyone
Relatively cheap
Very effective if given quickly after onset of pain (<1 hour)

64
Q

what are some disadvantages of thrombolysis?

A

Haemorrhage
Need to wait 90 minutes to see if it has worked
Less effective in late presenters
Allergic reactions
Contraindications

65
Q

what is the management of an NSTEMI?

A

IV access
Oxygen if hypoxic
Aspirin 300mg
Ticagrelor 180mg
Analgesia (opiate + antiemetic)
Fondaparinux 2.5mg S/C
Beta-blocker
ACEI
Risk Stratification
Heart Score
Grace Score
Coronary angiography

66
Q

what is a grace score?

A

Developed from 11,389 patients with ACS
Validated by the GRACE and GUSTO-2B trials
Uses 8 variables (0-258 points)
Age
Heart Rate
SBP
Creatinine
Killip Class (I-IV)
Cardiac Arrest
Elevated Troponin
ECG changes
All cause mortality from hospital discharge up to 6 months

67
Q

what is ezetimibe?

A

inhibitor of intestinal cholesterol absorption

68
Q

what kind of drugs are Evolocumab and Alirocumab

A

PCSK9 inhibitors

69
Q

during platelet activation which molecule forms cross links between adjacent platelets?

A

fibrinogen

70
Q

what drug should not be given to a patient taking warfarin?

A

aspirin

CRV week 3 (8 decks)

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