Study Material on Biology and Psychology

This study material on biology and psychology covers topics such as nutrition, saturated fats, high carbohydrate diets, psychosocial factors for CVD, barriers to cardiac rehab, and more. It includes solved assignments, essays, and dissertations. Explore the content to enhance your understanding of these subjects.

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Nutrition
Saturated fats
Saturated fats increase cholesterol levels in the blood, which increases the risk of CVD. The
American Heart Association recommends roughly 13 grams of saturated fats per day to
reduce the risk of CVD (AHA, 2015). To lower the amount of Saturated fat intake, one
should replace them with whole grains, vegetables, and fruits.
High carbohydrate diets and heart disease
Research has shown a link between high carbohydrate diets and Diabetes in some people.
This is because carbohydrates lead to elevated levels of glucose in the blood and if not
managed, diabetes ensues. The American Heart Association states that high glucose levels in
blood lead to arrhythmias, which are linked to heart failure and other cardiovascular
conditions (AHA, 2019).
Dietary manipulations for an individual with hypertension
Reduced sodium Intake by avoiding canned and processed foods, using salt free seasonings
and ensuring the salt consumption does not exceed 2300mg in a day. High sodium levels in
the blood affect the ability of water excretion in the kidneys, leading to strain in the blood
vessels which subsequently causes high blood pressure (Bazzano, et al., 2015,7).

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Consumption of foods rich in Omega 3 fatty acids has been found to decrease the pressure of
blood among other cardiovascular benefits (Bazzano, et al., 2015, 5). Patient should increase
their intake of walnuts, Salmon, Herring and flaxseeds.
Psychology
Psychosocial factors for CVD (concentrating on stress and personality).
Depression is one of the factors linked to development of heart disease. Depressed patients
are more likely to practice risky activities like alcohol intake and smoking which increases
risk for heart disease (Ziegelstein, n.a). In addition, feelings of depression and stress increase
risk for abnormal heart rhythms and hypertension. Depression is also associated with low-
grade inflammation, which caused artery clogging and rupture of plaque, it also leads to
release of stress hormones which reduces the response of the heart to the body’s demand for
increased blood flow. It also leads to activation of platelets, which increases risk for
formation of blood clots in the blood stream (Ziegelstein, n.a)
Barriers to Cardiac Rehab and uptake
Some barriers to uptake of Cardiac rehab include limited self-motivation, individual’s
perception of abilities to adhere to cardiac rehab, and old age and lower physical activity
(Evenson & Fleury, 2000, 245). Patient education on the importance of adherence to cardiac
rehab while emphasizing on self-motivation is an intervention with the ability to overcome
these barriers.
Psychological strategies to enhance cardiac rehab
Stress management in patients with cardiovascular disease is bound to increase self-
motivation and physical activity (Davies, et al., 2010, 8). Self-motivation is vital for

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adherence to cardiac rehab. It also reduces the risk of patient’s getting involves in health risky
activities like smoking, drinking and non-adherence to medication.
Education of emotional coping strategies have the ability to improve the patient’s quality of
life (Davies, et al., 2010, 11). Coping strategies that involve physical exercise not only
increase motivation in patients, but also have the ability to reduce blood pressure and
improve emotional well-being
Relative and Absolute Risk.
Relative risk refers to the probability ratio of risk of occurrence of cardiovascular disease in
People exposed to risk factors, versus in people who have not been exposed. individuals,
versus occurrence in non-exposed individuals (Tenny & Hoffman, 2019, 1).
Absolute risk refers to the probability of occurrence of cardiovascular disease in relation to
number of previous occurrences (Tenny & Hoffman, 2019, 1).
The process of global risk assessment for cardiovascular disease involves risk assessment
processes, development of risk equations, defining implications for risk assessment, evidence
review and implementation of considerations for risk assessment.
The commonly used toll for risk assessment in the UK is the QRISK calculator. Its calculated
risk is calibrated to the contemporary UK population and is therefore expected to be more
convenient (Tidy, 2016)
What is cholesterol and lipoproteins
Cholesterol is a form of a lipid made from alcohol and a steroid. Lipoproteins are complexes
of lipids and proteins. There are two types of lipoproteins, high density and low-density
lipoproteins. Roughly 50% of the weight of LDL particles is made of cholesterol while only a

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quarter is protein. However, HDL have roughly half protein composition and 20%
cholesterol. HDL are denser than LDL (Feingold & Grunfled, 2018).
Potential beneficial functions of HDL protection from CAD
HDLs have the ability to promote cholesterol efflux from artery walls and macrophages
HDLs inhibit vascular inflammation
HDLs have antioxidant and antithrombotic properties
HDLs improve endothelial function enhancing endothelial repair and increasing angiogenesis
Symptom characteristics of angina pectoris
Chest pain described as pressure, fullness, burning or squeezing
Chest pain intensity does not reduce with respiration, cough or change of position
Breathlessness
Fatigue
sweating
Nausea
Chest pain classification
Chest pain is either categorized as atypical angina, typical angina or chest pain from non-
cardiac sources. The three classifications are defined by three characteristics: Substernal chest
discomfort characterized by quality and duration which is provoked by exertion or
psychological distress and is alleviated by rest and nitro-glycerine (Jevon, 2012, 56). Typical
Angina presents with all the three symptoms mentioned while atypical angina presents with

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only two symptoms. Chest pain from non-cardiac sources does not present with any of the
three characteristics mentioned.
Other symptoms may include Chest pain that goes together with either neck pain, arm and
shoulder pain or back pain.
Stable and Unstable Angina
Stable angina is chest pain and breathlessness that follows a certain predictable pattern, while
unstable angina is a medical emergency that occurs suddenly with no predictability. It may
also not go away with rest or medication.
Unstable angina results when perfusion of the myocardium is impeded by Intraluminal
plaque, intraluminal thrombosis, high blood pressure or vasospasms (Roman, 2018).
Myocardial Infarction
Myocardial infarction (MI) refers to necrosis of the myocardium resulting deprivation of
circulating blood and oxygen. Two types of MI include type 1 and type 2. Type 1 Myocardial
Infarction results from an acute atherothrombotic coronary event, whereas Type 2 is more
heterogenous It results from conditions other than coronary artery disease causing imbalance
in oxygen and demand (Gupta, et al., 2017, 349).
In diagnosis, MI type 1 is associated with troponin levels higher than in Mi type 2. Type 2 is
also associated with conditions that cause high oxygen demand like tachycardia and
hypotension. Type 1 is associated with ST segment depression and elevation, while Type 2
has minimal or absent ECG changes (Gupta, et al., 2017, 350).
Steps in the diagnosis of a myocardial infarction.
Diagnosis of Myocardial Infarction is based of patient history and laboratory tests. Fist,
patient history and physical examination is done to check for signs of heart attack such as

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pallor, increased respiration rate, irregular pulse, low-grade fever in some patients, and
history of previous myocardial infarction (Barstow. & Rice, 2017)
Laboratory tests include Electrocardiogram to detect ischemia or acute coronary injury, and
blood test to check for cardiac biomarkers like troponin and a Complete blood count to rule
out anaemia.
Types of Heart Failure
Heart failure refers to a clinical syndrome that causes the heart to fail to pump blood at the
rate required for effective metabolism.
Left sided heart failure occurs when the left ventricle is unable to pump enough blood. This
causes build-up of blood in pulmonary veins leading to shortness of breath or coughing
during physical activity. It is the most common type.
Right sided heart failure happens when the right ventricle is unable to pump enough blood to
the lungs. This leads to build up of blood in the veins caused increased pressure in the veins
and surrounding tissue and subsequent oedema in the legs, abdomen and sometimes genital
area (AHA, 2017).
RAAS system response to heart failure
The RAAS system is a signalling pathway whose function is regulation of blood pressure.
When the blood pressure is low, the kidneys are stimulated to produce Renin, which signals a
transduction pathway. Renin then causes angiotensinogen to produce angiotensin 1 which is
converted by Angiotensin-converting enzyme to angiotensin II. Angiotensin II then causes
vasoconstriction and stimulates secretion of vasopressin from the pituitary. It also causes
production of adrenalin, aldosterone, and noradrenalin from adrenal glands. Aldosterone
enhances infiltration in the kidneys causing sodium and water retention. This process caused

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overall increase in the blood volume which is pumped through constricted arteries, causing
increased blood pressure (Pacurari, et al., 2014).
However, the RAAS system in patients with heart failure may cause sympathetic activation
and cardiac remodelling. For instance, elevated levels of renin have been observed in patients
with dilated cardiomyopathy. Again, angiotensin, aldosterone and vasopressin are involved in
cardiomegaly, which causes scar tissue formation and subsequent heart attack (Pacurari, et
al., 2014).
Echocardiography in the diagnostic assessment of cardiac patients.
Echocardiography utilizes high frequency sound waves to show heart abnormalities. During
an echocardiogram, a hand held wand is placed on the chest to provide a picture of the heart
valves and chamber. It is also used for evaluation of the Left ventricular systolic and diastolic
performance, assessment of cardiac output, diagnosis of valvular disease and assessment of
pulmonary artery and ventricular filling pressure. It is a non-invasive procedure and is
preferred in diagnosis if most cardiovascular diseases
ACE inhibitors and diuretics in heart failure
ACE inhibitors cause vasodilation through inhibition of Angiotensin II and preventing
formation of bradykinin. The effect is reduced arterial pressure which enhances cardiac
functioning. They also decrease sympathetic activity through thwarting the influence of
Angiotensin II on the body’s sympathetic nervous. ACE inhibitors as well enhance excretion
of sodium and water through the renal system, which causes a reduction in the volume of
blood, reduced arterial pressure and decreased venous pressure. They also play a role in
inhibition of cardiac remodelling which happens due to myocardial infarction, hypertension
or heart failure. Diuretics also enhance excretion of water, relieving symptoms of congestive
Heart Failure (Casu and Merella, 2015, 43).

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Methodology and the key findings of Hambrecht’s study on physical activity and the
regression of atherosclerosis (Hambrecht et al., 1993)
In their Study, Hambrecht et al (1993) included male patients with stable angina. The subjects
asked to not take any beta-adrenergic blockers and antianginal medicine for 48hrs before the
study. They were also asked to fast overnight. The patients were then subjected to the tests
that followed a Balke-ware protocol on a treadmill. They were asked to exercise until they
were exhausted physically or developed dyspnoea, chest pain or when an ST segment
depression of 3mm horizontally was attained. Through out the exercise, respiratory gas
exchange was measured, cardiac catheterization performed and evaluation of coronary
angiogram performed.
The study found that regular physical exercise delayed onset of ventilatory threshold and
improved the maximal oxygen uptake in people ailing from symptomatic coronary artery
disease. However, patients had to use up at least 1400 k/Cal a week in physical activities to
achieve these results. In addition, to achieve regression of coronary atherosclerotic lesions,
patients had to expend more calories, approximately 2200K/Cal per week (Hambrecht , et al.,
1993).

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References
AHA, 2015. Saturated Fat. [Online] Available at: https://www.heart.org/en/healthy-
living/healthy-eating/eat-smart/fats/saturated-fats [Accessed 8 May 2019].
AHA, 2017. Types of Heart Failure. [Online] Available at: https://www.heart.org/en/health-
topics/heart-failure/what-is-heart-failure/types-of-heart-failure [Accessed 8 May
2019].
AHA, 2019. Carbohydrates and Blood Sugar. [Online] Available at:
https://www.hsph.harvard.edu/nutritionsource/carbohydrates/carbohydrates-and-
blood-sugar/ [Accessed 8 May 2019].
Barstow., C. & Rice, M., 2017. Acute Coronary Syndrome: Diagnostic Evaluation. American
Family Physician, 95(3), pp. 170-177.
Bazzano, L. A., Green, T., Harrison, T. N. & Reybolds, K., 2015. Dietary Approaches to
Prevent Hypertension. Current Hypoertension reports, 15(6), pp. 1-16.
Casu, G. & Merella, P., 2015. Diuretic Therapy in Heart Failure – Current Approaches.
European Cardiology Review, 10(1), pp. 42-47.
Davies, P. et al., 2010. Promoting patient uptake and adherence in cardiac rehabilitation.
Cochrane Database of Systematic Reviews, Volume 7, pp. 1-16.
Evenson, K. R. & Fleury, J., 2000. Barriers to Outpatient Cardiac Rehabilitation Participation
and Adherence. Journal of Cardiopulmonary Rehabilitation, 20(4), pp. 241-246.
Feingold, K. & Grunfled, C., 2018. Introduction to Lipids and Lipoproteins. [Online]
Available at: https://www.ncbi.nlm.nih.gov/books/NBK305896/ [Accessed 8 May
2019].

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Gupta, S. et al., 2017. Type 2 versus type 1 myocardial infarction: a comparison of clinical
characteristics and outcomes with a meta-analysis of observational studies.
Cardiovascular Diagnosis and Therapy, 7(4), pp. 348-358.
Hambrecht , R. et al., 1993. Various intensities of leisure time physical activity in patients
with coronary artery disease: effects on cardiorespiratory fitness and progression of
coronary atherosclerotic lesions. Journal of American College of Cardiology, 22(2),
pp. 468-477.
Jevon, P., 2012. Angina and Heart Attack. s.l.:OUP Oxford.
Pacurari, M., Kafoury, R., Tchounwo, P. & Ndebele, K., 2014. Activation of the renin-
angiotensin-aldosterone system in heart failure. nternational Journal of Inflammation,
pp. 1-13.
Roman, P. N. a. Z., 2018. Angina, Unstable. [Online] Available at:
https://www.ncbi.nlm.nih.gov/books/NBK442000/ [Accessed 8 May 2019].
Tenny, S. & Hoffman, M., 2019. Relative Risk. [Online] Available at:
https://www.ncbi.nlm.nih.gov/books/NBK430824/ [Accessed 8 May 2019].
Tidy, C., 2016. Cardiovascular Risk Assessment. [Online] Available at:
https://patient.info/doctor/cardiovascular-risk-assessment [Accessed 8 May 2019].
Ziegelstein, R., n.a. Depression and Heart Disease. [Online] Available at:
https://www.hopkinsmedicine.org/heart_vascular_institute/clinical_services/centers_e
xcellence/womens_cardiovascular_health_center/patient_information/health_topics/d
epression_heart_disease.html [Accessed 8 May 2019].

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