Cardiac Pathology Practical Flashcards
Have a look at the cardiovascular risk charts and familiarise yourself with the main risk factors for the development of atherosclerosis
Diabetes (due to the hyperglycaemia), increasing age, being male, smoking, systemic hypertension, hyperlipidaemia (increased LDL & reduced HDL).
Note that the aboriginal and Torres Strait Islander populations are at heightened risk so have lower targets & are screened at an earlier age. These populations are also at greater risk of Systemic hypertension, kidney disease, diabetes and hyperlipidaemia.
Why do we focus on the above and not genetics, visceral fat, alcohol etc.? Some people have a strong genetic predisposition but they are in a minority, most of us have inherited many traits that have a slight contribution to both reducing and increasing our risks. Visceral adiposity is a risk factor & often correlates with truncal obesity BUT NOT ALWAYS & in men particularly, you can appear thin but carry a lot of visceral fat.
‘Diet’ alone is not a risk factor as diets vary and it depends upon overall calorie consumption, type of foods consumed, energy expenditure and many genetic traits. Alcohol too is more complex as a risk factor as it depends upon genetics, amount consumed & diet. However, we will learn later in Semester that steatosis or fatty liver increases the risk of hyperlipidaemia & dyslipidaemia and may occur is some individuals who are overweight/obese, eat a high fat diet (NAFLD) or consume too much alcohol.
What is atherosclerosis and what vascular pathology does it cause?
A chronic inflammatory process within the wall of an artery. It predisposes towards the formation of an aneurysm, thrombus and embolus. The former may rupture causing haemorrhage while the latter can cause infarction to the tissue being supplied by that artery.
Atherosclerosis also causes increase resistance to blood flow and gradually reduces blood supply to target tissue which accelerates age-related atrophy.
How does atherosclerosis contribute to systemic hypertension?
Atherosclerosis can cause systemic hypertension by reducing vessel contractility and increasing resistance to blood flow.
Atherosclerosis can directly injure the kidney and increase RAAS activity, which in turn results in greater systemic hypertension from the increase in blood volume and increased vascular resistance. Plus, crosstalk with the SNS leads to an increase in HR and force of ventricular contraction.
How does systemic hypertension lead to atherosclerosis?
Systemic hypertension increases the chance of endothelial injury due to turbulent blood flow, areas where arteries naturally branch are particularly vulnerable.
How can large aneurysms place greater stress on the heart?
The formation of an aneurysm results in a pocket of lost space that increases the workload of the heart as blood is diverted from its more efficient luminal flow into the out-pouch/aneurysm.
Remember from last week that aneurysms are dangerous because they can rupture and they can encourage the formation of a thrombus/embolus although the thrombi and emboli may occur in the absence of an aneurysm too.
What does the kidney do in response to hypotension?
In response to a real or perceived fall in blood pressure/cardiac output the kidneys activate the renin-angiotensin II-aldosterone system (RAAS), which results in:
Angiotensin II leads to vasoconstriction –> increased vascular resistance.
Aldosterone from the adrenal glands increases sodium and water reabsorption by the kidney –> increasing blood volume.
This is also the forward effects of Heart failure.
(info)
The sympathetic nervous system and RAAS potentiate each other, the activation of one leads to increase activity of the other so increased RAAS leads to increased sympathetic tone (vasoconstriction and up regulation of B adrenergic receptors in the heart increased heart rate & force of contraction & arterial/arteriole vasoconstriction). You do not need to remember this point for this subject but will cover it in pharmacology/clinical therapeutics.
In response to hypoxiaemia the kidneys increase the release of erythropoietin (EPO), which in the long-term increases haematocrit/numbers of RBCs
Activation of RAAS also leads to the release of ADH (anti-diuretic hormone) from the posterior pituitary gland, which increases water retention and promotes increased thirst.
b. What does the kidney do in response to systemic hypertension?
As above which just exacerbates the problem by increasing blood pressure further. Many drugs used to treat systemic hypertension work on the kidney to block the effects of aldosterone, the activation of angiotensin II or the action of angiotensin II. The kidneys are among the first organs to be damaged by systemic hypertension & when damaged, they activate RAAS.
c. Can you think of a reason why evolution favoured such a sensitive response to hypotension rather than hypertension?
Natural selection favours qualities/traits that enhance reproduction not ageing. Without medical assistance the birthing process is a very dangerous endeavour due to the risk of infectious disease and haemorrhage. The high oestrogen levels of pregnancy favour blood clotting and the response of our bodies to hypotension is lifesaving if we suffer a significant haemorrhage. However, now we are fortunate enough to have good medical interventions and so the things that would have killed us off at a young age are being treated and we are now living on past our reproductive lives into old age when these systems unfortunately contribute to pathology.
a. In a person with ischaemic heart disease, which vessels are affected by atherosclerosis?
Coronary arteries, they may have minimal damage to other major arteries yet have considerable atherosclerosis of the coronaries (coronary artery disease CAD), which predisposes them to the ischaemic heart diseases listed above
b. What is the difference between angina and a myocardial infarction?
Angina is the pain associated with ischaemia but blood is restored before there is any necrosis of the myocardium. Angina is caused by transient ischaemia.
c. Explain the inflammatory and reparative changes that occur in the heart following a myocardial infarction:
The infarcted tissue would stimulate the acute inflammatory response so there would be hyperaemia, oedema and the infiltration of the tissue by neutrophils. Hyperaemia increases hydrostatic pressure causing fluid to leak from the vessels into the damaged tissue. In addition, increased vascular permeability allows plasma proteins to also enter the damaged tissue hence the oedema is an exudate.
Because the heart is a permanent tissue, the formation of granulation tissue would follow; macrophages will move into the necrotic tissue and continue to remove it along with the increasingly apoptotic population of neutrophils. Fibroblasts would migrate into the area and secrete collagen fibres to fill in the space once occupied by dead myocytes and new capillaries (angiogenesis) would sprout into the area to provide growth factors, oxygen and nutrients for the granulation tissue.
Once the dead cells are removed and the tissue deficit filled with collagen, the macrophages and fibroblasts migrate away and the new capillaries regress (die of by apoptosis). As this is a case of organization as part of acute inflammation, the granulation tissue would mature into a collagen scar which contracts over time pulling the edges of parenchymal tissue together.
d. Why does the heart heal through organisation, what are the positive and negative consequences?
The adult human myocardial cells are permanent and so incapable of proliferation thus healing is through organisation. It is good that this can occur so that it is possible to survive following a heart attack. However, the scar tissue is weaker than the original myocardium and this area of weakness may form an aneurysm and rupture.
In addition, the scar tissue can encourage a thrombus or blood clot to form over it which can shed emboli into the circulation. The scar tissue will also not relay electrical impulses in the same way as the original tissue and overall the remaining myocytes will have to take on a greater workload.
Why does endocarditis frequently become chronic in nature?
Ironically the heart valves themselves have a poor blood supply so the acute response is frequently ineffectual so inflammation becomes chronic. Being largely acellular, the valves of the heart do not have a rich blood supply of their own and so it is hard to get a sufficient concentration of neutrophils or drug to the site of infection. In addition, platelets and blood proteins like fibrin can coat the vegetations making them harder to penetrate.
What local (within the heart) effects can endocarditis have?
Damage and scarring to the valves, remember that chronic inflammation inevitably results in more tissue damage and scarring/organisation.
Valve Stenosis – valves not opening correctly
Valve insufficiency/incompetence – valves not closing correctly so allowing regurgitation
Depending upon which valve is affected, these problems can lead to left, right or global heart failure.
What other pathology may infective endocarditis cause?
Apart from the systemic effects of heart failure, infective endocarditis can result in infectious emboli being shed into the circulation leading to infarction and infection in organs like the lungs, liver, kidneys, bones and brain.
