Pathology 1

Week 3 Assignment Pathology

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Week 3 Assignment Pathology

Question 1 - The Pathophysiological Factors Resulting in Heart Failure

Americans show concerns due to the red alert indicated by heart failure (HF) conditions.

Researchers confirms that HF's disease impacts the lives of around six million individuals within

the periphery of the United States of America. Therefore, the cost of heart failure is evident

among various households, ranging from financial burdens and reduced healthy living standards.

It is possible to reveal the statistical extent of heart failure in the country. Reports confirm that 6-

10% of persons above sixty-five years are highly exposed to the same. Therefore, it further

ensures that heart failure as a condition shares a positive relationship with age; as one grows

older (above 65 years), the likelihood of developing HF also increases It is also vital to

understand that the basis of heart failure is the insufficient supply of oxygen to meet the

metabolic demands of various cells and tissues involved in blood circulation. Mixed

abnormalities are emerging from different environments and varying degrees to disrupt heart

functions. As a result of the breakdown in blood circulation, there is insufficiency in the heart,

thus causing oxygen deficiencies in the heart and the rest of the body; heart failure results.

(Inamdar et al,2016)

The occurrence of a harmful event to the heart, forcing a reduction in the volume of

pumped blood, is the genesis of HF's pathophysiological process. As indicated above, HF

etiology follows extrinsic and intrinsic factors; it holds to mention that it is a multidimensional

process. Some examples resulting from several factors include chronic lung condition,

myocardial infarction, coronary artery failure, and hypertension, among others. Conversely,

other etiological cases emerge from pathological concerns; fibrosis, infiltration disorders,

rheumatic fever, and hemochromatosis. Scientific evidence confirms that are instances of
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genetically or congenital cases influencing heart failure in various groups. An appearance of any

of the above conditions indicates a negative impact on the heart's pumping abilities, thus

introducing the condition's pathogenesis. Before gaining an in-depth insight into the discussion,

it is vital to note two types of heart failures; systolic and diastolic HF. While these two factors

are distinct in their occurrences, they reduce the heart's functionality and output regarding blood

and oxygen supply in various parts of the body

Biologically, the body responds automatically to correct any deficient occurrence it

experiences through a series of processes. The same holds when cardiac functionality is

inefficient. In a bid to meet the output deficits, the cardiac activates the adrenergic nervous,

cytokine, and the renin-angiotensin-aldosterone systems. Through a series of natural biological

processes, the above systems work to aid in correcting the identified failure and restoring

normality in cardiac balance. However, striking this balance comes with some costs since the

process is involving and tiring. When heart failure persists, the involved body systems undergo

tear and wear, causing damage to the left ventricle that is highly responsible for blood pumping.

The harm alters the compensation process since the reliable systems are no longer operational.

The baroreceptors respond by unloading the aortic arch and carotid sinus in the heart's

left ventricle, which causes an imbalance in the central nervous system. The central nervous

system loses parasympathetic tone, hence triggering the pituitary gland to release arginine

vasopressin (AVP) .AVP acts as a permeability catalyst in the renal ducts since it increases the

kidney's water absorption rate. The AVP move calls for a counter-response from the central

nervous system due to the osmolality signal to stimulate the release of renin by the sympathetic

nervous system (SNS). Due to more renin in the system, the kidney responds by releasing

angiotensin II and aldosterone to activate the renin-angiotensin-aldosterone system's

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functionality. The above biological factors force the body to enhance vasoconstriction levels and

going directly to the heart; the development exposes the heart's myocytes to more damages. The

production kills cardiac cells and also causes hypertrophy. As noted above, cells die due to

reduced contractility, which forces the heart to rebuild the matrix responsible for holding

myocardial cells. However, this restructuring is not significant since it results in an unorganized

interstitial collagen matrix, ineffective in supporting the cardiac cells. It explains how the

compensation process fails in the long-run. (Malik et al,2020)

Question 2 - The Distinction between Systolic and Diastolic HF

It is now precise that there exist two types of heart failures in diastolic and systolic.

While the previous section agreed that both types of heart dysfunction have adverse health

effects, there are significant differences. However, the primary peculiarity is on the heart's

destruction area. In DHF, hypertrophy causes a circular thickening of the ventricular walls due to

prolonged system overuse. There is minimal room for blood circulation and filling due to the

thickening effect, thus less blood flow into the heart. In such a scenario, the flexibility of various

heart muscles reduces, and it fails to fill. Conversely, while the problem is with ventricle walls,

systolic heart failure (SHF) causes reduced automatic contraction abilities’ embroils increased

outward muscles, which hinder the heart's contraction abilities making it challenging for the

ventricles to push out the blood (Jeong et al,2015)

Question 3 - The causes of the patient's shortness of breath

The circulation system's perfusion and reduced pulmonary vascular congestion are the

primary input factors in shortness of breath for HF patients. In explaining the same etiology, it is

the development of pulmonary edema due to the heart failure condition. Pulmonary edema's
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causative factors involve the heart's inability to pump and circulate blood effectively. Cardiac

output levels depend on the heart rate, afterload, preload, and myocardial contractility. The

preload is known as the blood volume in the ventricle post diastole. Its determination relies on

the blood levels headed to the ventricle during the diastole and the remaining quantity after the

heart's contraction. Understanding the heart's preload concept is vital since it aids in explaining

the reason behind HF patients' increased blood volume, contraction failures, and incomplete

filling. One of the resulting consequences from increased preload is high pulmonary vein and

capillary pressure. (Hashmi et al,2020)

Conversely, an imbalance in pressure (oncotic < hydrostatic) escalates plasma discharge

pulmonary vessels' walls through interstitial space. In case of any reverse functionality in the

lymphatic system to discharge significant fluid levels from tissues, there body is at risk of

alveolar flooding leading to pulmonary edema. Such issues explain HF patients' breathlessness

and orthopnea. When stomach contents reduce respiratory effectiveness, then orthopnea occurs.

The condition worsens when pulmonary edema occurs since the lungs might be forced into

abnormality due to fluids and the inability to appropriately oxygen transfer. Hence, it explains

why the patient would prop pillow to sleep. Paroxysmal nocturnal dyspnea is the condition

where patients sit upright at night to grasp air. The situation occurs due to pulmonary edema that

causes bronchial pressure. (Berliner et al,2015)

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References

Berliner, D., Schneider, N., Welte, T., & Bauersachs, J. (2016). The Differential Diagnosis of

Dyspnea. Deutsches Arzteblatt international, 113(49), 834–845.

https://doi.org/10.3238/arztebl.2016.0834

Hashmi MF, Modi P, Sharma S. (2020) Dyspnea. . In: StatPearls [Internet]. Treasure Island (FL):

StatPearls Publishing; 2020 Jan-. Available from:

https://www.ncbi.nlm.nih.gov/books/NBK499965/

Inamdar, A. A., & Inamdar, A. C. (2016). Heart Failure: Diagnosis, Management and Utilization.

Journal of clinical medicine, 5(7), 62. https://doi.org/10.3390/jcm5070062

Jeong, E. M., & Dudley, S. C., Jr (2015). Diastolic dysfunction. Circulation journal : official

journal of the Japanese Circulation Society, 79(3), 470–477.

https://doi.org/10.1253/circj.CJ-15-0064

Malik A, Brito D, Chhabra L.(2020) Congestive Heart Failure. In: StatPearls [Internet]. Treasure

Island (FL): StatPearls Publishing; 2020 Jan-. Available from:

https://www.ncbi.nlm.nih.gov/books/NBK430873/