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Anat 1082 Multiple Choice Revision > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

Cardiovascular disease incorporates other diseases/ illnesses/ ailments
What are they?

A
  • Hypertension
  • Ischemic heart disease
  • Angina pictorial myocardial infarction
  • Stroke
  • Rheumatic heart disease
  • Congenital cardiac defects
  • Heart failure.

Most Of the disease grouped under the heading CVD are interrelated

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2
Q

Cardiovascular 🫀 disease (CVD) is the primary cause of heart failure.
However there are a variety of other factors that can also cause heart failure.
What are these?

A
  • Heart valve defects caused by, disease such as rheumatic fever or infection
  • Primary disease of the heart muscle AKA cardiomyopathy
  • Congenital heart disease.
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3
Q

What causes Cardiovascular 🫀 Disease(CVD)

A
  • Mostly caused by atheromatous this is a build up of plaque on the intima or the inner layer if the arterial wall
  • Hypertension and strokes are often manifestations of the same process in arteries of the body and the brain.
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4
Q

How can the numbers of people suffering with cardiovascular 🫀 disease decline?

A
  • Can be accomplished through modifications of the major risks know to be associated with atherosclerosis (the build up of fat)
  • EG through diet and exercise.
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5
Q

What are the risk factors for Cardiovascular 🫀 disease?

A
  • Age
  • Sex - Males are at a higher risk.
  • Family history of CVD
  • Ethnic background
  • Smoking
  • Raised BP
  • Raised cholesterol
  • Low income/ social deprivation (north/ south divide)
  • Air pollution.
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6
Q

What is total cholesterol?

A

This is the overall amount of cholesterol in the blood including both good and bad cholesterol

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7
Q

What is Good cholesterol (HDL)?

A

This makes you less likely to have heart problems or a stroke

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8
Q

What is bad cholesterol (LDL or non- HDL)?

A

This contributes to atherosclerosis and makes you more likely to have heart problems or a stroke

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9
Q

What are triglycerides?

A

These are fatty substances similar to bad cholesterol and are considered as the steps before developing cholesterol

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10
Q

What is the genetic link to cardiovascular 🫀 disease (CVD)?

A
  • Genetics can influence the risk for heart disease a family history of CVD modifies the future risk of CVD depending on the number and age of affected 1st degree relatives
  • Many cardiac problems are inherited including arrhythmia’s, congenital heart disease, cardiomyopathy and high cholesterol.
  • CVD leading to heart attack stroke and heart failure can run in families
  • Variants in chromosomes 6, 9, and 12 are associated with heart disease
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11
Q

Cardiovascular 🫀 disease in relation to fetal development ?

A
  • Studies suggest that impaired fetal growth is related to the higher risk of hypertension, diabetes and CVD
  • Neonatal abdominal circumference has also shown to predict plasma cholesterol and fibrinogen levels in men later in life CVD is also linked to this
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12
Q

Size of babies in relation to cardiovascular 🫀 disease?

A
  • Babies born small in relation to size of their placenta have an increased risk of developing hypertension.
  • Babies who are large compared to their placenta are at a higher risk of developing type 2 diabetes sometimes in combination with hypertension
  • Babies born small tent to have higher basal plasma cortisol levels
  • Reduced birthweight has been linked to chronic lung disease.
  • Large birthweight had been linked with increased risk of polycystic ovarian disease and hormone related concerns such as breast, prostate and testicular cancer.
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13
Q

Associations with small birth size?

A
  • Hypertension
  • Coronary heart disease
  • Non insulin dependent diabetes
  • Stroke
  • Dislipidaemia
  • Elevated clotting factors
  • ## Impaired neuro development
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14
Q

Associations with larger birth size?

A
  • Polycystic ovarian cancer
  • Breast cancer
  • Prostate cancer
  • Testicular cancer
  • Childhood leukaemia
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15
Q

What is the Barkers Hypothesis?

A
  • States that adverse influences early in development and particularly during intrauterine life can result in per infant changes in the physiology and metabolism resulting in increased disease in adulthood
  • The fetal origins hypothesis states that fetal under- nutrition in the middle to late gestation leads to disproportionate fetal growth programmes later coronary heart disease
  • Like other living creatures in early life human beings are ‘plastic’ and able to adapt to their environments
  • the development of sweat glands are an example of this.
  • the growth of babies has to constrained by the size of the mother otherwise normal birth could not occur
  • In pregnancies after ovum donation women have smaller babies even if the woman donating them was large.
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16
Q

Please give an example of Plasticity…

A
  • All humans have a similar number of sweat glands at birth but none of them function.
  • In the first 3 years after birth a proportion of the glands become functional depending in the temperature to which the child os exposed.
  • The hotter the conditions the greater the number of sweat glands that are programmed to function.
  • After three years programming is complete and the number of sweat glands are fixed
  • The child who has experienced hot conditions will be better equipped to adapt to similar conditions later in lie because people with more functioning sweat glands cool down faster.
17
Q

Diabetes and hypertension in relation birth size…

A
  • People who where small at birth remain biologically different from people who where born larger at birth.
  • These differences include an increased susceptibility to hypertension and type 2 diabetes
  • In both sexes risk of disease falls with increasing birth weight and sizes white rapid weight gain in early childhood.
  • This rapid weight gain is associated with CVD
18
Q

What role does the placenta play in terms of fetal development?

A
  • If the placenta does not develop properly throughout pregnancy fetal development is impaired as the placenta is the only fetal supply line.
  • Placental size directly affects the capacity for nutrient transfer
19
Q

How does maternal nutrition affect the development of type 2 diabetes, obesity and CVD?

A
  • During periods of maternal under-nutrition when glucose availability to the fetus reduces insulin secretion and increases peripheral insulin resistance, directing more glucose to the brain and heart and less to the peripheries because glucose availability is low.
  • Nutrient availability becomes abundant after birth this may cause glucose intolerance and eventually diabetes
  • This potentially explains why it is mainly these babies that then become overweight during childhood who are prone to developing type 2 diabetes
  • Poverty has a huge role to play in the development of CVD
20
Q

What is acute coronary syndrome?

A
  • This term encompasses a range of conditions including unstable angina, non-ST-segment-elevation myocardial infarction (NSTEMI) and ST-segment-elevation myocardial infarction (STEMI)
  • All are due to sudden reduction of blood flow to the heart usually caused by rupture of an atherosclerotic plaque within the wall of a coronary artery, and may cause the formation of a blood clot
  • Non-ST-segment-elevation myocardial infarction (NSTEMI) is an unstable coronary syndrome which is differentiated from unstable angina by a subsequent rise in cardiac enzymes
21
Q

What is atherosclerosis?

A
  • It is caused by the build up of fatty deposits in the lumen of the artery
  • As the fatty deposits build up they cause plaques or atheroma to develop
  • These plaques cause a narrowing of the artery lumen
  • This narrowing means that there is reduced blood flow to the myocardium.
22
Q

What does atherosclerosis cause?

A

1- Response to injury theory repetitive injury to the inner lining of the artery

23
Q

How does Atheroma Form?

A
  • Damage to the lunica intima
  • LDL entered (cholesterol)
  • Oxidation of LDL
  • Macrophages engulf
  • Identified as fatty streaks
  • Fat moves into the intima = Buldge
  • Area hardens with white plaque meaning the area looses elasticity
  • Area ulcerates - platelet aggregation- Thrombosis
24
Q

What is stable angina?

A
  • It is not an acute coronary syndrome. The pain usually experienced on exertion is predictable and relieved with rest.
  • Pain is controlled, preventative therapy on movement or after meals, partial occlusion is relieved with GTN.
25
Q

What is Glyceryl trinitrate (GTN)?

A
  • This is a spray used to relieve angina.
  • When sprayed under the tongue it relaxes and widens blood vessels in the heart and in the rest of the body improving O2 delivery
26
Q

What is Angina?

A
  • Chest pain caused when the blood supply to the muscles of the heart is restricted.
27
Q

Chest pain can be angina if….

A
  • The chest feels tight, dull or heavy although some people (especially women) may have sharp stabbing pain.
  • Pain spreads to the arm, neck, jaw, or back
  • Triggered by physical exertion or stress
  • Steps within a few mins of resting
    Angina can also cause:
  • Breathlessness
  • Nausea
  • Pain similar to indigestion
  • Tiredness
    Sable angina occurs when 70-75% of the artery is occluded
28
Q

How to assess pain using the PQRST assessment ?

A 
P= Provoking Factors - what makes it worse?
P= Palliative Factors - what makes it better

Q= Quality - what does the pain feel like

R= Radiation ☢️ - does the pain spread anywhere

S= Severity - how severe is it, how much does it affect your life

T= Temporal factors - is it there all of the time or does it come and go?

29
Q

Causes of unstable angina?

A

It is defined by one or more of the following:
1- Angina of effort occurring over a few days with increased frequency provoked by less exertion
2- Angina that occurs unpredictably and recurrently without specific provaction . Usually short lived may settle spontaneously or be relieved temporarily by GTN but will recur within in a few hours

30
Q

Definition of unstable angina?

A
  • Is an unprovoked and prolonged episode of chest pain raising suspicion of an acute myocardial infarction but without definitive ECG or blood result changes
  • when myocardial is he is is present but without evidence of actual myocardial necrosis (normal serum tropic level) the clinical syndrome is described as unstable angina
31
Q

What is myocardial infarction?

A
  • Occurs when an artery becomes blocked or significantly narrowed
  • Caused by atheroma
  • Indicates defined area of myocardial necrosis caused by local ischemia.
  • Myocardial necrosis begins within approximately 20-30 mins of the time of coronary artery occlusion.
  • Location of Myocardial infarction is determined by site of the occlusion whiten the coronary circulation.
32
Q

How is myocardial infarction identified?

A

Chest pain

  • Feels like it is being pressed or squeezed by a heavy object
  • Pain can radiate across the chest, jaw and back of arms
  • Accompanied by shortness of breath
  • Weak/ Lightheaded
  • overwhelming anxiety
  • Only relieved with opiates

ECG changes
Blood tests changes

33
Q

What is troponin?

A
  • Troponin is a contractile protein
  • Different organisations may use any of the troponin (C, I, or T) as a cardiac marker and the normal parameters can vary in each lab
  • However normal troponin levels are generally accepted as 0.01ng/ ml
  • Measurement of troponin levels are recommended to be taken by nice 2014 10-12 hours from first onset of chest pain then a second test a further 10-12 hours later.
  • Normal troponin levels cannot be detected if there is an increase this is a sign that there has been damage to the heart.
34
Q

3 points of relevance for cardiovascular 🫀 disease

A
  • Diseases of the heart and circulatory system (cardiovascular disease) accounts for almost 155000 deaths in the UK 🇬🇧 and an estimated 17 million worldwide each year.
  • Around 640000 men and nearly 275000 women currently living in the UK have had a heart attack
  • 1in 7 men and 1in 10 women die from coronary heart disease.

Anat 1082 Multiple Choice Revision (20 decks)

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