Common Cardiovascular Conditions Flashcards

1
Q

What is a congenital heart condition?

A

A range of developmental defects that affect the heart

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2
Q

Define arrhythmias.

A

abnormalities of the electric rhythm of the heart

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3
Q

Define bradycardia

A

abnormally slow rhythm of the heart

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4
Q

Define tachycardia.

A

abnormally fast rhythm of the heart

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5
Q

What are the aetiologies of congenital heart conditions?

A

genetic linkage
environmental factors
maternal illness
exposure to toxins during pregnancy

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6
Q

What are the general categories of congenital heart conditions?

A

Apparent at or before birth
week to months before detection
years after or even in adulthood

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7
Q

What are the key anatomical features before birth?

A

early development = sinus venosus becomes coronary sinus/part of the right atrial wall
before birth = ductus arteriosus, connects pulmonary trunk to aorta and foramen ovale, connects both to atria

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8
Q

What are the 4 main congenital heart defects?

A

Atrial septal defects (ASD)
Ventricular septal defects (VSD)
Patent ductus arteriosus (PDA)
Congenital valve stenosis (CVS)

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9
Q

What happens in atrial septal defects?

A

It is a hole in the heart which increases the amount of blood that flows through the lungs. Oxygenated blood from systemic enters pulmonary circulation, usually acyanotic. It is similar to sinus venosus defect where the pulmonary veins/left atrium shunts into the right ventricle. Also, similar to patent foramen ovale where the foramen ovale remain open post birth, can be unnoticed for years.

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10
Q

What happens in ventricular septal defects?

A

The opening in the interventricular septum. Blood often flows from the left ventricle through the VSD to the right ventricle into the lungs, can cause a volume overload

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11
Q

What happens in patent ductus arteriosus?

A

PDA results when the ductus fails to close, and left to right shunt can occur. The4re is normally a volume overload of pulmonary circulation, which can lead to left ventricular dilation or heart failure.

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12
Q

What happens in congenital valve stenosis?

A

The aortic valve stenosis can cause the left ventricle hypertrophy, fatigue and tachypnoea. The pulmic valve can cause right ventricle hypertrophy, fatigue, dyspnoea with exertion and exercise intolerance.

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13
Q

Explain what dilated cardiomyopathy does.

A

It is an acquired heart condition in childhood, and it can cause viral infection, septal defects, genetic linkage, reduced pumping efficiency, tachycardia, arrhythmia, and can lead to lung congestion or heart failure.

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14
Q

Explain what endocarditis does.

A

It is an acquired heart condition in childhood, and it is relatively rare, it can cause infection of the heart valves and candida, and is more common in congenital heart disease or valve conditions.

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15
Q

Explain what myocarditis does.

A

It is an acquired heart condition in childhood, and it is the necrosis and inflammation of the myocardium, which is usually linked to an infection. It can decreased the myocardial function, enlarge the heart, and cause pulmonary edema and congestive heart failure.

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16
Q

Explain what pericarditis does.

A

It is an acquired heart condition in childhood and it is the infection of pericardium which causes fluid accumulation in pericardial space and cardiac tamponade. It causes a restricted place for the heart to work and haemodynamic compromise as pressure builds up around the heart. It also causes severe limitation to venous return and cardiac output, eventually severe hypotension, cerebral hypoperfusion and cardiac arrest.

17
Q

What is atherosclerosis?

A

An acquired condition in adults, which is the thickening or hardening of the arteries. This is caused by the buildup of plaque in the arteries, which causes a blockage or hypertension in the artery wall.

18
Q

What can happen after the removal of plaque?

A

It could lead to a severe stroke and ischemic necrosis of the brain tissue

19
Q

What are the risk factors of atherosclerosis?

A
Hyperlipidaemia
smoking
age
hypertension 
diabetes 
obesity 
genetic linkage
20
Q

What is an atherogenic lipoprotein?

A

It is a low density protein which is small, crosses endothelium easily, and facilitates carrying of lipids into the arterial wall. LDL above 190mg/dl is high risk, and LDL below 100mg/dl is low risk.

21
Q

What is an antiatherogenic lipoprotein?

A

It is a high density protein which is large, less able to cross endothelium, has poor transport of cholesterol into arterial wall. It captures cholesterol and carries it back to the liver. HDL below 40mg/dl is right risk, and HDL above 50mg/dl is low risk.

22
Q

Explain what happens in atherosclerosis in children.

A

The development of atherosclerosis begins in early life. Arterial fatty streaks invade LDL carrying lipids, which causes immune cells to have symptomatic changes. The fatty streaks are deposited in the intima of large muscular arteries. In children the risk factors are increased BMI, hypertension, cholesterol levels and LDL levels. The full development of atherosclerosis is rare but possible.

23
Q

What is the first stage of the developmental stages in atheroma’s?

A

Stage one is injury to the endothelium of the blood vessel. There are haemodynamic stresses, such as turbulent blood flow, there is a buildup of cholesterol, pathogenic chemicals enter, such as smoking, hypertension occurs, ineffective agents enter, such as bacteria or viruses, and damaged endothelial tissues release pro-inflammatory signals.

24
Q

What is the second stage of the developmental stages in atheroma’s?

A

Stage two is the accumulation of oxidised lipids. Endothelial damage triggers an inflammatory response, low density lipoprotein carries the lipids into the tunica intima, this lipid then oxidises, the damage surrounding the tissue attracts macrophages, and the macrophages take up the LDL to become foam cells.

25
Q

What is the third stage of developmental stages of atheroma’s?

A

Stage three is the proliferation of smooth muscle and fibrous cap formation. Smooth muscle cells proliferate, lymphocytes get attracted to that area, elastic and collagen fibres accumulate there, some foam cells die and released their lipid content, core of the dead and dying foam cells develops, fibrous cap develops, and the surface of the plaque can become pro-thrombic.

26
Q

What is the complicated plaque?

A

Fragile blood vessels invade the plaque, which can bleed into the mass. Smooth muscle cells differentiate and produce calcified regions. Hydrodynamic forced can lead to erosion or rupture of the unstable plaque, and circulating blood may even undermine and life the plaque. Haemorrhage and thrombosis combine to obstruct the vessel.

27
Q

What are the complications of atherosclerosis?

A

Arterial suffering and hypertension
Vessel constriction leading to chronic ischemia
thrombus - blood clot
acute occlusion with risk of ischemic necrosis
aneurysm formation

28
Q

What are the key sites atherosclerosis can have complications?

A
abdominal aorta iliac arteries 
proximal coronary arteries
thoracic aorta 
main arteries in leg 
main vessels supplying brain
29
Q

What does stable angina endothelial cell look like?

A

The lumen is narrowed by plaque, with vasoconstriction and a reduced blood flow. This can be a trigger for emotional distress or exertion, increased heart rate which increases oxygen consumption, and ischemic condition in myocardium.

30
Q

What does unstable angina endothelial cell look like?

A

The plaque is ruptured, there is platelet aggregation, thrombus formation, unopposed vasoconstriction, unstable atherosclerotic plaque rupture, platelet thrombosis, and a reduced blood flow.

31
Q

What does variant angina endothelial cell look like?

A

There is no overt plaques, intense vasospasm, reduced blood flow due to vasospasm only, no clear evidence of atherosclerosis. Increased heart rate, which increases oxygen consumption, hence ischemic symptoms.

32
Q

What is coronary heart disease?

A

When the coronary arteries cannot deliver enough oxygen rich blood to the heart. It is a very common cause of heart attack. Acute coronary syndromes are usually linked to atherosclerosis.

33
Q

What is the CHD pathway?

A

Disruption of atherosclerotic plaque, platelet aggregation and thrombus formation, risk of embolus formation, thrombus/embolus blocking blood flow to myocardium.

34
Q

What are the aetiologies of myocardial infarction?

A

Atherosclerotic plaque rupture or erosion with super impose thrombus
vasculitis syndromes
coronary embolism
congenital abnormalities of coronary arteries
severe coronary artery spasm
states of reduced oxygen supply

35
Q

Explain how myocardial infarction is associated with pain

A

The location of the blockage determines the site of ischemic damage. Stressed and ischemic cardiomyocytes release inflammatory mediators. The activation of nociceptors results in pain.

36
Q

What is arrhythmias?

A

Abnormalities of the electric rhythm. It is associated with a wide range of common clinical problems, such as common benign palpitation. It can cause problems with impulse formation, abnormally slow heart rhythm and abnormally fast rhythms.

37
Q

Define Angina pectoris

A

Persistent chest pain that is caused by limited blood flow to the heart

38
Q

Define aneurism

A

Blood filled bulge of a blood vessel and swelling in the artery wall