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Cardiovascular > Coronary heart disease > Flashcards

Coronary heart disease Flashcards

1
Q

What are the mortality rates for CHD?

A

1 in 5 men

1 in 7 women

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2
Q

What is cardiogenic shock?

A

An inadequate perfusion as a result of cardiac dysfuntion

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3
Q

When can cardiogenic shock occur?

A

Acute MI - multivessel disease, particularly occluded LAD
Delayed presentation
Mechanical complications - VSD, MR, rupture

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4
Q

What chemicals are released in response to MI?

A

Systemic inflammatory response - IL-6, TNF alpha, NO

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5
Q

What does the systemic inflammatory response do?

A

Decreases CO and SV. This induces hypotension, reduced coronary perfusion pressure and this leads to ischemia

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6
Q

How is angina clinically diagnosed?

A

Visceral pain from myocardial hypoxia - hard to describe, gestures
Characteristic patterns of provocation, relief and timing
Characteristic background of risk factors

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7
Q

How is anginal pain described?

A

Pressing, squeezing, heaviness, a weigth

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8
Q

Where can anginal pain radiate to?

A

Arms, back, neck, jaw, teeth

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9
Q

What can provoke angina?

A

Exertion, stress, cold wind, after meals

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10
Q

How can anginal pain be relieved?

A

Few minutes, relieved by rest and/or GTN spray

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11
Q

What are differential diagnoses of chest pain?

A

GI tract: reflux (burning, provoked by food)
Peptic ulcer (epigastric, relief by antacids), oesophageal spasm, biliary colic
MSK: Injury (location, tender, prolonged) nerve root pain (character, prolonged)
Pericarditis (central, posture related)
Pleuritic pain (focal, exacerbated by breathing, sharp, catching)

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12
Q

What diagnoses of chest pain are emergencies?

A

MI (severe, autonomic upset, ongoing despite morphine)
PE (breathless, dull pain (poss pleuritic)
Dissection of aorta (Tearing, excruciating pain)

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13
Q

How can angina be diagnosed?

A

History, exercise testing, perfusion scanning, CT angiography, angiography

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14
Q

What are the pros and cons of exercise testing?

A

Cheap, reproducible, risk stratification

Poor diagnostic accuracy in some sub-groups
Sub-maximal tests

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15
Q

What are the pros and cons of perfusion imaging?

A

Non-invasive, more precision than ETT, risk stratification

Radiation, can produce false positives and negative

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16
Q

What are the pros and cons of CT angiography?

A

Non-invasive, anatomical data and risk stratification

Radiation, less precise than angiography, expensive

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17
Q

What are the pros and cons of angiography?

A

“Gold standard”, anatomical and risk straficiation, follow-on angioplasty

Risk 1:1000 death, stroke
Radiation
Contrast: renal dysfunction, rash, nausea

18
Q

How is risk reduced in angina?

A

Drugs
Lifestyle
Revascularisation: CABG, PCI

19
Q

What drugs can be used in the treatment of angina?

A

Aspirin: anti-platelet
Beta-blocker: slows HR, reduce O2 demand
Statin: reduced cholesterol
ACEI: reduces BP

20
Q

What are the complications of CABG?

A 
Death 1-2%
Stroke 2-3% 
MI 3% 
AF
Infection
Cognitive impairement
Sternal malunion 
Renal failure 
Failure to recover
21
Q

What is involved in a PCI techinque?

A

Vascular access, catheter to ostium of coronary, guidwire down vessel, ballons threaded over wire, stent(s) implanted, balloon, catheter and wires removed

22
Q

What is the indication for angiography?

A

Severe symptoms

High risk

23
Q

What is atheroclerosis?

A

A progressive disease that is characteterized by a build-up of plaque within the arteries

24
Q

What makes up plaque?

A

Fatty substances, cholesterol, cellular waste, calcium and fibrin

25
Q

What can happen to a plaque?

A

There can be bleeding into the plaque, or the formation of a clot on the surface of the plaue

26
Q

What is the pathogenesis of atherosclerotic plaques?

A

Endothelial damage
Protective response in production of cellular adhesion molecules
Monocytes and T lymphocytes attach to “sticky” surface of endothelial cells
Migrate through arterial wall to subendothelial space
Macrophages take up oxidised LDL-C
Lipid-rich foam cells
Fatty streak and plaque

27
Q

What can cause endothelial damage?

A 
Haemodynamic forces (shear stress caused by hypertension) 
Vasoactive substances 
Mediators (cytokines) from blood cells 
Cigarette smoke 
Atherogenic diet 
Elevated glucose levels
Oxidised LDL-C
28
Q

What are the cellular adhesion molecules that the cell expresses?

A 
Cytokines (IL-1, TNF-alpha), chemokines (MCP-1, IL8) 
Growth factors (PDGF, bFGF)
29
Q

What does oxidised LDL promote?

A

Death of endothelial cells and an inflammatory response resulting in the impairment of normal function of the endothelium
Also modifies the response to angiotensin 2, resulting in vasdilatory impairment and induces a prothrombotic state by affecting platelets and coagulation factors

30
Q

What does atherothrombosis mean?

A

Describes the formation of an acute thrombus in a vessel affected by atherosclerosis, a process common to a number of CV disorders

31
Q

What wil be exposed when an atherosclerotic plaque ruptures?

A

It will expose components such as collagen and von willebrand factor that allows platelets to adhere to the damaged area and initiate thrombus formation

32
Q

What are the different classes of lipoproteins?

A 
Chylomicrons 
VLDL
IDL
LDL
HDL
33
Q

What is the role of chylomicrons?

A

To transport triglycerides from the gut to the liver

34
Q

What does VLDL do?

A

Transports triglycerides from the liver to the rest of the body. Triglycerides along with cholesterol, cholesterol ester and other lipoprotein molecules are transported in VLDL within the bloodstream where VLDL undergoes delipidation by lipoprotein lipase

35
Q

What occurs once VLDL undergoes delipidation?

A

Trigelyerides are removed from the core and replaced by cholesterol esters principally from HDL.

36
Q

What lipoprotein in VLDL transformed into?

A

LDL, although the larger VLDL particles are lipolysed to IDL which is then removed from the plasma directly

37
Q

What is dietary fat broken down into in the GI tract?

A

Cholesterol, fatty acids and mono and diglycerides
These molecules along with bile acid form water-soluble micelles that carry lipid to the absorptive sites of the duodenum

38
Q

What happens once the chylomicrons enter the bloodstream from the duodenum?

A

It is hydrolysed by LP lipase releasing the triglyceride core, free fatty acids and mono and diglycerides for energy production or storage

39
Q

What happens to the residual chylomicron?

A

It undergoes further delipidation resulting in the formation of chylomicron remnants. These are taken up by the liver, undergo lysosomal degredation and are either used for cell membrane synthesis or excreted as bile salts

40
Q

What is the function of statins?

A 
Recueced total cholesterol and LDL
Improves endothelial dysfunction 
Increases nitric oxide bioavaliability 
Antioxidant properties 
Inhibition of inflammatory responses 
Stabilisation of atherosclerotic plaques
41
Q

How do statins work?

A

They inhibit HMG-CoA synthase preventing the formation of cholesterol

Cardiovascular (27 decks)

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