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PATHOPHYSIOLOGY > Cardiovascular Disorders > Flashcards

Cardiovascular Disorders Flashcards

1
Q

Define atherosclerosis:

A

Build up of fatty plaque in the walls of the arteries leading to damage and restriction of blood flow

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2
Q

Are cardiovascular disorders more likely to occur in men or women?

A

Men (older)

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3
Q

Define hyperlipidaemia:

A

Blood containing too many lipids (fats) (e.g. cholesterol or trigleycerides).

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4
Q

Name the three main consequences of developing atherosclerosis:

A
  1. ischaemic heart disease
  2. stroke
  3. peripheral vascular disease
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5
Q

Name 8 potentially modifiable risk factors for cardiovascular disease:

A
  1. stress
  2. poor diet
  3. lack of exercise
  4. high blood cholesterol
  5. high blood pressure
  6. obesity
  7. diabetes
  8. smoking
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6
Q

Name 4 non-modifiable risk factors for cardiovascular disease:

A
  1. age (more common in older adults)
  2. gender (more common in men)
  3. ethnic origin
  4. family history of cardiovascular disease
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7
Q

When is cardiovascular disease most likely to occur in women and what does this suggest?

A

Following the menopause which suggests that the female sex hormones may act to prevent episodes of cardiovascular disease

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8
Q

Which ethnic origin carries that greatest incidence of cardiovascular disease?

A

South asian

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9
Q

Are lipids soluble or insoluble in water?

A

Insoluble

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10
Q

Why do free cholesterol or triglycerides block up blood vessels?

A

Because they do not dissolve freely in water (they are not soluble) and so they do not dissolve in the plasma. Instead they remain in the vessels causing a blockage.

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11
Q

What are cholesterol and triglycerides carried in the blood as?

A

Lipoprotein particles which allow for the transportation of cholesterol in the blood stream

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12
Q

Which 2 particular types of lipoprotein molecule are associated with increased/decreased risk of cardiovascular disease?

A

Low density lipoprotein molecules (increase the risk of developing cardiovascular disease) and high density lipoprotein molecules (which help to lower the risks associated with low density lipoprotein molecules).

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13
Q

Where are low density lipoprotein molecules produced?

A

In the liver

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14
Q

What is the primary function of low density lipoprotein molecules?

A

They transport cholesterol from the liver to where in the body it is needed.

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15
Q

What is the primary function of high density lipoprotein molecules?

A

They transport cholesterol from tissues back to the liver

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16
Q

What do our plasma cholesterol levels depend on?

A

Our dietry intake of cholesterol and the amount of cholesterol made by the liver.

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17
Q

Which is the most common genetic condition which leads to extremely high cholesterol levels?

A

Familial hypercholesterolaemia

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18
Q

What occurs in familial hypercholesterolaemia?

A

There is a gentic mutation in the coding for low density lipoprotein receptors in the cell membranes of liver cells. Normally, low density lipoproteins will attach themselves to these receptors and are taken up by the liver cells- reducing the levels of low density lipoprotein in the blood plasma.

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19
Q

What is considered the healthy number of total plasma cholesterol levels?

A

5mmol/L

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20
Q

What is generally the number of total plasma cholesterol levels in someone with one faulty low density lipoprotein receptor gene?

A

7.5mmol/L

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21
Q

What is generally the number of total plasma cholesterol levels in someone with two faulty low density lipoprotein receptor genes?

A

13mmol/L

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22
Q

big

A

chungus

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23
Q

Which arteries are predominantly affected by atherosclerosis?

A

Medium and larger sized arteries.

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24
Q

What is atherosclerosis characterised by?

A

A build up of fatty plaques in the walls of the arteries causing a gradual narrowing of the artery lumen reducing the blood flow through the artery.

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25
Q

What does atherosclerosis evolve from?

A

Fatty streaks in the walls of the arteries which are collections of lipid filled foam cells.

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26
Q

What can damage the endothelium of the artery? Name three things.

A

Toxins from tobacco smoking, hyperglycemia in diabetes, stress from blood flow linked to hypertension.

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27
Q

What provides the foetus with oxygen?

A

The maternal placenta.

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28
Q

How does the foetus combat low oxygen saturations?

A

By increasing its cardiac output and having a higher haemoglobin affinity to oxygen.

29
Q

Which two features of the foetal heart close at birth?

A

The foreman ovale and the ductus arteriolus.

30
Q

What is a ventricular septal defect?

A

A hole in the heart wall between the two ventricles causing blood to flow between both sides. Oxygen rich blood gets pumped to the lungs rather than to the body. Symptoms include poor feeding, breathlessness and easy tiring.

31
Q

What is a arterial septal defect?

A

A hole in the wall of the heart dividing the two atrium. Symptoms include shortness of breath, stroke, heart murmur.

32
Q

What is patent ductus arteriosus?

A

The ductus arteriosus which normally closes at birth remains open. This causes blood to flow in the wrong direction causing the heart muscle to weaken. May cause breathlessness, increased heart rate and fatigue.

33
Q

Where is the ductus arteriosus located?

A

Between the aorta and the pulmonary artery.

34
Q

What is coarction of the aorta?

A

A condition where the aorta becomes narrowed which can lead to heart failure because the left ventricle has to work harder.

35
Q

What is pulmonary stenosis?

A

Obstruction of blood flow from the right ventricle to the pulmonary artery normally occurring at the pulmonary valve. Normal oxygen saturation’s cannot be maintained causing cyanosis.

36
Q

What is pulmonary atresia?

A

The pulmonary valve does not form correctly preventing blood from flowing from the heart to the lungs. Symptoms include cyanosis, shortness of breath and fatigue.

37
Q

What is cyanotic heart disease?

A

Deoxygenated blood bypasses the lungs and mixes with oxygenated blood entering the systemic circulation. Encompasses the 4 T’s: truncus arteriosus, transportation of great arteries, tetralogy of fallot and total anomalous pulmonary venous connections.

38
Q

What is truncus arteriosus?

A

A form of congenital heart disease. A condition where a singular large arterial trunk overlies a ventricular septal defect causing a mixture of oxygenated and deoxygenated blood to enter the systemic circulation.

39
Q

What is tetralogy of fallot?

A

A combination of 4 congential abnormalities occuring at once. Includes pulmonary valve stenosis (narrowing of pulmonary valve), ventricular septal defect (hole between the ventricles), overriding aorta (aorta lies above the ventricular septal defect) and right ventricular hypertrophy (thickening of the wall of the right ventricle).

40
Q

What is adult congenital heart disease?

A

Adults living with a heart defect present from birth.

41
Q

What is transposition on the great arteries?

A

The two main arteries leaving the heart (pulmonary artery and the aorta) are switched. Oxygen poor blood circulates the body whilst oxygen rich blood circulates the lungs. Symptoms include cyanosis, fatigue, breathlessness.

42
Q

Give 3 risk factors for transposition of the great arteries:

A
  1. viral infection during pregnancy
  2. increased maternal age
  3. genetic factors
43
Q

What is total anomalous pulmonary venous return?

A

Pulmonary veins are connected to the right side of the heart rather than the left side. Oxygen rich blood does not return to the left atrium, instead it returns to the right side of the heart where oxygen rich and oxygen poor blood mix.

44
Q

Define cardiovascular disease

A

A disease of the heart and blood vessels caused by atherosclerosis

45
Q

Give 4 modifiable risk factors for cardiovascular disease:

A

high BP, smoking, diabetes, inactivity, obesity, high blood cholesterol.

46
Q

Give 4 non modifiable risk factors for cardiovascular disease:

A

age, gender, genetics, race and ethnicity.

47
Q

What are 4 risk factors for hypertension?

A

Age, family history, ethnicity, increased stress, socioeconomic status.

48
Q

What are 4 complications of hypertension?

A

Atherosclerosis, heart failure, kidney failure, stroke.

49
Q

What is essential hypertension?

A

Hypertension with no known cause

50
Q

What is secondary hypertension?

A

Hypertension with a definable cause for example endocrin disease, kidney disease or tumour presence, or as a side effect of medication use.

51
Q

What are short term regulatory factors for hypertension?

A

Increased heartrate and vasoconstriction due to sympathetic control.

52
Q

What are long term regulatory factors for hypertension?

A

Changes in blood volume through the renin angiotensin aldosterone system.

53
Q

Give the path of the cardiac conjunction system

A

Sino atrial node, atrio ventricular node, av bundle (bundle of his) pukinje fibres.

54
Q

What is atrial fibrilation?

A

The atrioventricular node sends chaotic, unregulated signals which cause uneffective contractions. This leads to a reduced cardiac output and reduced blood pressure.

55
Q

What does atrial fibrillation increase the risk of?

A

Stroke (by five times)

56
Q

What is ischaemic heart disease otherwise known as?

A

Coronary heart disease.

57
Q

What can cause damage to coronary arteries?

A

Raised cholesterol, smoking and increased blood pressure.

58
Q

Why does ischaemia occur in coronary heart disease?

A

A build up of plaque in the coronary arteries leads to a reduced blood supply. The heart does not receive enough oxygen during physical activity.

59
Q

Why does pain occur during angina?

A

Adenosine is released which stimulate the pain fibres in the heart

60
Q

Angina is a early sign of:

A

Atherosclerosis

61
Q

Give three preventative treatments of angina:

A

Statins, anti-hypertensive medications and diet and exercise changes.

62
Q

What is angina?

A

Where on exertion, the needs of the heart (oxygen and nutrient demand) cannot be met due to reduced blood supply.

63
Q

Give 3 acute coronary syndromes and state why these occur:

A

-unstable angina
-non ST elevation MI
-ST elevation MI
They occur when atherosclerosis has advanced enough to prevent blood flow to the heart all together.

64
Q

How can we tell the difference between unstable angina, ST elevated MI and non ST elevated MI?

A

Using an ECG and establishing whether or not troponin proteins have been released.

65
Q

What is unstable angina?

A

Narrowing of the coronary arteries due to a thrombus. The heart does not receive a normal supply of blood even at rest. Patient develops chest pain. However, no ECG changes or troponin release.

66
Q

Describe how narrow the coronary arteries are within a. coronary heart disease b. angina c. MI

A

In coronary heart disease, a plaque begins to build up within the coronary arteries but blood can still pass thorugh.
In angina, more plaque is present but makes it difficult for blood to pass through. The hearts needs are not met during exercise.
MI- significant blockage of the coronary arteries causing the hearts needs to not be met even at rest.

67
Q

What happens during a non ST elevation MI (NSTEMI)

A

Extreme narrowing of coronary arteries by thrombus resulting in poor blood flow to the myocardium. Chest pain experienced. Oxygen demand of the heart is not met. ECG changes include ST depression and T wave inversion as well as troponin release as a part of cell ischaemia.

68
Q

What happens during a ST elevation MI (STEMI)

A

Complete blockage of the artery by a thrombus. ECG changes occur including ST elevation which indicates extensive cellular necrosis due to no blood supply reaching the heart. Blood tests show raised troponin levels but a diagnosis must be made using a clinical history, symptoms and ECG recording.

69
Q

Give 3 other reasons why ECG changes may occur:

A
  1. use of drugs e.g. cocaine
  2. tachycardia
  3. trauma

PATHOPHYSIOLOGY (14 decks)

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