wk 5- cardiac pathology Flashcards
right side of the heart does what
weaker ventricle, pumping poorly oxygenated blood into pulmonary artery (circuit)
left side of the heart does what
stronger ventricle, enters aorta our major artery. pumps oxygenated blood into systemic circuit to the body downstream
what is the difference between angina and myocardial infarction
angina caused by transient ischaemia, no necrosis occurs, loss of blood supply but blood is restored
myocardial infarction caused by acute ischaemia, necrosis occurs in the myocardium
describe the inflammation and repair that occurs following a myocardial infarction
acute inflammation
healing through organisation because it is a permanent organ. granulation tissue and the 3 components.
what 5 complications can occur following an MI
- thrombus
- embolus
- aneurysm
- arrhythmia
- further heart failure and disease
list the causes of left sided heart failure
- ischaemic heart disease
- systemic hypertension
- aortic/mitral valve disease
list the causes of right sided heart failure
- left side failing first
describe backward effects of left sided heart failure and what symptoms they cause
pulmonary congestion
pulmonary oedema
reduced venous return from pulmonary circuit
symptoms: dyspnea
describe backward effects of right sided heart failure and what symptoms they cause
congestion and oedema in the systemic venous circuit leading to peripheral oedema
describe forward effects of heart failure, what compensatory mechanisms are triggered from a reduction in cardiac output
cardiac ouput goes down, kidney activates RAAS.
renin angiotensin aldosterone system
angio- vasoconstrictor increasing vascular resistance
aldo- increase sodium uptake increasing blood volume
list some common causes and possible consequences of endocarditis
inflammation of the inner lining of the heart
causes: necrosis, bacterial infection, trauma all these can lead to inflammation
consequences: stenosis or incompetence
list some common causes and possible consequences of pericarditis
inflammation of the outer sack of the heart
causes: intrinsic heart disease, disease in lungs, pleura, medistinum, generalised disorders, aging
consequences: heart failure (acute or chronic)
stenosis
valve does not open properly
incompetence
valve does not close properly
hypertension
increased blood pressure
systemic hypertension is caused by
cardiac output and systemic vascular resistance
congestive heart failure
heart increases in size to meet demands of maintaining blood pressure and cardiac output
what is a major risk factor for atherosclerosis
aging
what are the impacts of age on cardiovascular system
increase in ischaemic heart disease and heart failure with age. heart valves can become calcified with age also.
main risk factors for atherosclerosis 6
diabetes
increasing age
being male
smoking
systemic hypertension
hyperlipidaemia (increased LDL, decreased HDL)
what is atherosclerosis and what vascular pathology does it cause
a chronic inflammatory process within the wall of an artery.
1.predisposes you towards formation of an aneurysm, thrombus and embolus.
aneurysm can rupture
thrombus/embolus can cause infarctions
2. increases resistance of blood flow and reduces the supply to tissues
how does atherosclerosis contribute to systemic hypertension? 3
- reducing vessel contractility
- increasing resistance of blood flow
3.injure kidneys and increase RAAS which increases systemic hypertension (increased blood volume and vascular resistance)
how does systemic hypertension lead to atherosclerosis
increases the chance of endothelial injury due to the turbulent blood flow.
how can large aneurysms place greater stress on the heart?
the pocket increases the workload of the heart as blood is diverted from its luminal flow
what does the kidney do in response to hypotension
the kidneys activate RAAS - renin- angiotensin II- aldosterone system
which:
angiotensin II leads to vasoconstriction which increases vascular resistance
aldosterone from the adrenal glands increases sodium and water reabsorption by the kidneys which increases blood volume
these are also the forward effects of heart failure
what do the kidneys do in response to systemic hypertension
activate RAAS as well and cause further hypertension
explain the inflammatory and repair that occurs 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.
what local effects can endocarditis have?
damage/scarring to the valves
valve stenosis
valave insufficiency/incompetence
right side heart failure or global heart failure
what are two types of valves diseases
stenosis
insufficiency
what is pericarditis
inflammation of the pericardium, the sack surrounding the heart
what are the most common causes of pericarditis
infection, autoimmune disease, secondary cancer, spread of inflammatory response caused by myocardial infarction
what is congestive heart failure
a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill with or eject blood, thus resulting in congestion of blood trying to enter the failing ventricle and reducing the amount ejected with each contraction
what are the forward effects of left and ride sided heart failure?
Aldosterone increases sodium and water reabsorption by the kidney increasing blood volume
Angiotensin II leads to vasoconstriction increased vascular resistance.
When the heart muscle is failing, the result is the maintenance of cardiac out and blood pressure
within a normal range.
what are the main causes of left sided heart failure
systemic hypertension, ischaemic heart disease, pericarditis and valve disease
pathology that increases in incidence with age
atherosclerosis which increases the risk of heart failure, ischaemic heart disease and valve disease
list causes of left and right sided heart failure separately
left-
ischemic heart disease, valve disease, systemic hypertension
right-
left sided heart failure, pulomary hypertension, valve disease
what are the forward effects of heart failure
decreased cardiac output leads to renal compensation through activation of RAAS
this results in CO and BP often appearing normal
what are the backwards effects of right vs left sided heart failure?
left- congestion, oedema in the lungs, dyspnea
right- congestion and oedema in the venous system ???
what symptoms would someone with right sided heart failure exhibit?
severe swelling of limbs, ascotes and distended jugular vein
what symptoms would someone with left sided exhibit?
dyspnea, especiall when lying down, coughing up blood tinged fluid
which organs are at risk of damage with right heart failure
organs with a large outflow into the inerior vena cava (liver and kidneys)
what organs are at risk with left heart failure?
lungs
