Summative Assessment: Anatomy & Physiology of Diseasest

Asthma

This work will explain the anatomy of the trachea, bronchi, and bronchioles and explore the abnormalities resulting from asthma, a chronic inflammatory airway disorder. There is inflammatory infiltration of the bronchial submucosa cells like the mast cells, eosinophils, monocytes, lymphocytes, and neutrophils on the pathophysiologic factors. Eosinophils are recruited in the epithelial airways as a result of chemotactic signals inclusive of the chemokines, cytokines, and cell surface adhesion molecules (Sun et al., 2021), which upon activation releases pro-inflammatory mediators that cause epithelial injury, smooth muscle contraction, increased vascular permeability with mucosal edema and bronchial hyper-responsiveness (Clinical Pharmacist, 2014). Consequently, the lymphocytes produce inflammatory cytokine that induces eosinophil recruitment and activation and differentiation of plasma cells into secretory phenotype. In the endobronchial biopsies, the cytokines work with CD4 T cells in the epithelium to amplify inflammation. The inclusion of CD8 lymphocytes would lead to severe asthma with a decline in lung function. The mast cells that are also leukocytes are strongly linked with the smooth muscle cells where they are degranulated to produce higher amounts of proinflammatoy mediators like histamine, tryptase, and lipid bronchoconstrictor mediators (Fiebiger and Bischoff, 2020). The macrophages also take part since their release into airway leads to activation of many pro-inflammatory signals, and activation of T cells, leading to inflammation and perpetuated airway bronchoconstriction favoring asthmatic condition. Further, the dendritic cells are involved mainly by presenting the antigens to intensify inflammatory response in the epithelium. Finally, neutrophils favor airway diseases through their chemotactic activity leading to oxygen burst reaction and release of neutrophil elastase and oxidants for inflammation. References Fiebiger, E. and Bischoff, S.C., 2020. Mucosal basophils, eosinophils, and mast cells. Principles of Mucosal Immunology, p.203. Clinical Pharmacist, 2014. Asthma: pathophysiology, causes and diagnosis. Sun, R., Jang, J.H., Lauzon, A.M. and Martin, J.G., 2021. Interferon‐γ amplifies airway smooth muscle‐mediated CD4+ T cell recruitment by promoting the secretion of C–X–C‐motif chemokine receptor 3 ligands. The FASEB Journal, 35(1), p.e21228.

Arterial Hypertension

This work will outline abnormalities experienced in the blood vessels (arteries), leading to hypertension or high blood pressure. Hypertension is expressed when there is either diastolic pressure, systolic pressure, or both are experienced in the heart, determined through cardiac output balanced against the systematic vascular resistance. The homeostatic process of maintaining blood pressure in the body is inevitably complicated, thus involving physiological mechanisms like arterial baroreceptors, atrial natriuretic peptide, and endothelin renin-angiotensin-aldosterone system, and mineralocorticoid and glucocorticoid steroids. These complex systems control the vasodilation or the vasoconstriction of the systemic circulation, excretion or retention of water and sodium for maintenance of adequate circulating blood volume. During the neurogenic control mechanism, the arterial baroreceptors increase the afferent impulse activity, decreasing efferent sympathetic activity and vagal tones, leading to vasodilation and bradycardia (Bakris, 2021). For the renin-angiotensin system mechanism, the protease renin trigger angiotensin to produce inactive peptide angiotensin 1, which is converted to active octapeptide and angiotensin II. Angiotensin II acts on specific angiotensin receptors that cause smooth muscle contraction and release of prostacyclin, aldosterone, and catecholamine responsible for controlling arterial blood pressure and sodium balance. In the endothelial mechanisms, the nitric oxide mediates produced by bradykinin, acetylcholine, and sodium nitroprusside. Moreover, inhibition of endothelial-derived relaxation is realized since the endothelium synthesizes the endothelin, which is the most potent vasoconstrictor. Another mechanism that can cause cardiac output is the atrial natriuretic peptide (APN) activity. The ANP produces diuresis, natriuresis alongside decreased blood pressure while decreasing aldosterone and plasma renin. ANP is released due to stimulation of atrial stretch receptors and causes alteration of synaptic transmission from osmoreceptors (Spiranec Spes et al., 2020).

References

Bakris, G., 2021. Hypertension - Cardiovascular Disorders - MSD Manual Professional Edition. [Online] MSD Manual Professional Edition. Available at: [Accessed 14 February 2021].

Špiranec Spes, K., Chen, W., Krebes, L., Völker, K., Abeßer, M., Eder Negrin, P., Cellini, A., Nickel, A., Nikolaev, V.O., Hofmann, F. and Schuh, K., 2020. Heart-Microcirculation Connection: Effects of ANP (Atrial Natriuretic Peptide) on Pericytes Participate in the Acute and Chronic Regulation of Arterial Blood Pressure. Hypertension, 76(5), pp.1637-1648.

Coronary Artery Disease/ Ischemic heart disease

This work will present the coronary arteries and smooth muscle cells' anatomy and physiology and explain the abnormalities that occur leading to ischemic heart disease. Coronary artery disease is caused by plaque (cholesterol) build-up in the walls of coronary arteries, narrowing them to partially or fully block blood flow into the heart; a condition called atherosclerosis. Atherosclerosis is understood as the complex interaction of the cells of the arterial walls and the blood and the molecular messages they exchange. When arterial endothelium interacts with bacterial products or dyslipidemia and hypertension hormone vasoconstrictors, they produce glycoxidation products associated with hyperglycemia or the pro-inflammatory cytokines that are derived from excessive adipose tissues (Ali et al., 2018). These cells then augment adhesive molecules' expression that causes sticking of the blood leukocytes in the arterial walls' inner surface. Transmigration of these adherent leukocytes is dependent on the expression of chemoattractant cytokines regulated by the risk factors of atherosclerosis. Once they form in the arterial intima, the blood leukocytes communicate with endothelial and smooth muscle cells and the endogenous cells of the arterial walls where the exchanged message depends on the inflammatory mediators. As a consequence of inflammatory ferment, the small muscle cells migrate from tunica media into the intima. They proliferate and elaborate a complex, rich extracellular matrix, which propagates inflammatory response and apoptosis in the created atherosclerotic lesion in the long run (Elosua, Sayols-Baixeras, Lluís-Ganella and Lucas, 2014). The dead lipid-laden macrophages also cause extracellular deposition of the tissue factor that accumulate in the intima to form a lipid-rich core of atherosclerotic plaque.

References

Ali, M., Girgis, S., Hassan, A., Rudick, S. and Becker, R., 2018. Inflammation and coronary artery disease. Coronary Artery Disease, 29(5), pp.429-437.

Elosua, R., Sayols-Baixeras, S., Lluís-Ganella, C. and Lucas, G., 2014. Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants. The Application of Clinical Genetics, p.15.

Cardiac Arrhythmia

This work describes the anatomy and physiology of the arteries and ventricles of the heart and the abnormalities that potentially lead to arrhythmia. Arrhythmia refers to cardiac conditions that cause an irregular heartbeat or where the heart can beat too slow (bradycardia) or too quickly (tachycardia) (Savalia et al., 2017). It can be in varied types like atrial fibrillation attributing to the irregular beating of atrial chambers, atrial flutter or abnormal heart conduction, supraventricular tachycardia (rapid but rhythmic regular heartbeat), ventricular fibrillation, which is an irregular rhythm of rapid, uncoordinated, and fluttering ventricular contractions and the ventricular tachycardia which refers to abnormal electric impulse in the ventricles that causes abnormal heartbeat. In the cardiac conduction system, the junction of the superior vena cava and high lateral atrium is usually filled with a cluster of cells that produces electrical impulses for a normal heartbeat, referred to as the sinus node. The transmission of electric impulses is through the atria to the atrioventricular (AV) node. However, the AV node has a low conduction velocity, thus delay impulse transmission, resulting in lowered cardiac output. Consequently, the atria in the anteroseptal region are not electrically insulated where there is a continuation of AV node that causes a termination of Purkinje fibers. Thus, the arrhythmias result from decreased pacemaker function or blocked conduction in the AV node or Kis-Purkinje system or the re-entry process, which is regarded as circular propagation of impulse around the two interconnected pathways with varied refractory periods and conduction characteristics (Mitchell, 2021).

References

Mitchell, B., 2021. Overview of Arrhythmias - Cardiovascular Disorders - MSD Manual Professional Edition. [online] MSD Manual Professional Edition. Available at: [Accessed 14 February 2021].

Savalia, S., Acosta, E. and Emamian, V., 2017. Classification of cardiovascular disease using feature extraction and artificial neural networks. Journal of Biosciences and Medicines, 5(11), pp.64-79.

Mitral Valve Prolapse (MVP)

This work will describe the mitral valve's anatomy and physiology, whose functions are coordinated by six components: the mitral annulus, left atrium, left ventricle, leaflets, pillar muscle, and chordae tendinous and left ventricular wall in the heart functioning. MVP is typically a myxomatous valve disease where the mitral valve leaflet tissues and chordae become abnormally stretchy so that the mitral valve flops back into the left atrium. Mitral Valve Prolapse is featured with a progressive increase of area and length of the mitral valve tissues (Delling and Vasan, 2014), which causes the leaflets to thicken anatomically and superiorly prolapse towards the left atrium through the mitral annulus during systole to cause the valve dysfunction. The Mitral valve is one of the main four valves in the heart that lies between the left atrium and left ventricle, with the primary function of preventing the backward flow of blood as it moves through the heart. The action is controlled by its anterior and posterior leaflets that open and close to facilitate blood flow. The leaflets meet at the commissures and are connected to the papillary heart muscles by the fan-shaped connective tissues called the chordae tendinae. The capillary muscles then connect to the left ventricular wall, and together with the mitral annulus (ring-like structure connecting left atrium and left ventricle), work in synchrony to cause an effective mechanism of closing and to open the cardiac cycle. Hence, altered physiological functioning of these structures causes Mitral Valve Prolapse (Oliveira et al., 2020).

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References

Delling, F. and Vasan, R., 2014. Epidemiology and Pathophysiology of Mitral Valve Prolapse. Circulation, 129(21), pp.2158-2170.

Oliveira, D., Srinivasan, J., Espino, D., Buchan, K., Dawson, D. and Shepherd, D., 2020. Geometric description for the anatomy of the mitral valve: A review. Journal of Anatomy, 237(2), pp.209-224.