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CRV week 3 > Clinical aspects of Cardiovascular disease > Flashcards

Clinical aspects of Cardiovascular disease Flashcards

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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
what are the indicators of acute coronary syndromes?
unstable angina NSTEMI STEMI (ST elevation MI)
25
what is treatment for an NSTEMI?
- 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)
26
what is a STEMI (ST-elevation MI)?
has more heart damage as 'trans-mural' complete vessel occlusion
27
what are the coronary interventions available for a type 1 STEMI?
systemic thrombolysis primary percutaneous coronary intervention interventional cardiac centre
28
what are the goals of a systemic thrombolysis?
to reestablish the coronary latency salvage the myocardium improve survival
29
what are the complications of acute MI?
extension/ ischemia arrhythmia expansion/ aneurysm acute MI pericarditis RV infarct mechanical heart failure mural thrombosis
30
what are the treatments of coronary artery disease?
-primary prevention -anti-anginal drugs -anti-platelet drugs -thrombolytic drugs -agioplasty and stents -CABG surgery -secondary prevention
31
what is atherosclerosis?
-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
why do we use lipid lowering therapy?
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
what are lipid lowering therapies?
statins are the mainstay of lipid lowering therapy -ezetimibe -PCSK9 inhibitors
34
how do statins work?
-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
what are some examples of statins?
Atorvastatin, Simvastatin, Rosuvastatin, Pravastatin
36
what data do we have that suggest statins work?
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
how does ezetimibe work?
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
what are PCSK9 inhibitors?
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
what is the mechanism of action of aspirin?
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
what is the normal dosage of aspirin?
200mg in acute setting 75mg daily maintenance dose
41
what is the pharmacokinetics of aspirin?
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
what are the uses of aspirin?
Angina Myocardial Infarction Embolic / Thrombotic CVA Transient Ischaemic Attack (TIA) Percutaneous coronary intervention Prevent miscarriage in pro-thrombotic conditions Analgesia
43
what are some contradictions of aspirin?
Under 16’s Breast feeding mothers Peptic ulceration Haemophilia Previous hypersensitivity reaction to NSAID’s Severe renal failure Hepatic Cirrhosis
44
what are some adverse effects of aspirin?
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
what is clopidogrel?
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
what is ticagrelor?
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
what is prasugrel?
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
how do short acting nitrates work for angina relief?
GTN Spray sublingual administration or nitroglycerin tablet SE – Headache, Dizziness
49
how does long acting nitrate for angina prophylaxis work?
Isosorbide mononitrate or isosorbide dinitrate Oral preparation or transdermal patch Losses efficacy with prolonged administration Need nitrate free period SE – hypotension, headache, flushing
50
what are the commonly used beta blockers?
bisoprolol, atenolol and carvedilol
51
how do beta blockers work as anti-ischaemic drugs?
Slow heart rate and decrease myocardial oxygen demand Aim for heart rate 55-60bpm
52
what are the side effects of beta blockers?
Don’t stop abruptly SE - fatigue, depression, bradycardia, heart block, bronchospasm, peripheral vasoconstriction, postural hypotension, impotence, and masking of hypoglycaemia symptoms
53
what are non-dihydropyridine agents?
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
what are some examples of non-dihydropyridine agents?
verapamil and diltiazem
55
what are the side effects of non-dihydropyridine agents?
bradycardia and dizziness
56
what are dihydropyridine agents?
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
what is ivabradine?
Selective If channel inhibitor SE – bradycardia and dizziness
58
what is nicorandil?
Nitrate and potassium channel activator SE - nausea, vomiting, and potentially severe oral, intestinal, and mucosal ulcerations
59
what is ranolazine?
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
what is the criteria for thrombolysis?
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
what are some thrombolysis agents?
Streptokinase (GISSI Trial) Tissue Plasminogen Activator (t-PA) (GUSTO Trial)
62
what are some contradictions of thrombolysis?
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
what are some advantages of thrombolysis?
Can be given quickly Can be given by anyone Relatively cheap Very effective if given quickly after onset of pain (<1 hour)
64
what are some disadvantages of thrombolysis?
Haemorrhage Need to wait 90 minutes to see if it has worked Less effective in late presenters Allergic reactions Contraindications
65
what is the management of an NSTEMI?
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
what is a grace score?
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
what is ezetimibe?
inhibitor of intestinal cholesterol absorption
68
what kind of drugs are Evolocumab and Alirocumab
PCSK9 inhibitors
69
during platelet activation which molecule forms cross links between adjacent platelets?
fibrinogen
70
what drug should not be given to a patient taking warfarin?
aspirin

CRV week 3 (8 decks)

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