Autopsy Findings in Hypertensive Heart Disease.pptx

Chiibeneme 102 views 18 slides Jun 20, 2024
Slide 1
Slide 1 of 18
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18

About This Presentation

Cardiovascular autopsy findings
renal
pulmonary
liver and spleen complications


Slide Content

Autopsy Findings in Hypertensive Heart Disease Onyema Chidimma Oguchi 19051145007 Medicine and Surgery

Outline Introduction Cardiovascular system Pulmonary complications Renal complications Liver and Spleen complications Neurological complications Conclusion References

Introduction Definition of HHD: Hypertensive heart disease refers to the structural and functional changes in the heart that occur due to chronic high blood pressure. These changes include left ventricular hypertrophy, heart failure, and ischemic heart disease. Clinical Importance: Understanding HHD is crucial for managing and preventing complications that can lead to significant morbidity and mortality. Role of Autopsies: Autopsies help in understanding the extent and nature of the damage caused by hypertension, providing insights that are essential for developing better treatment and prevention strategies.

Autopsy Findings - Cardiovascular System Heart Gross Findings Heart weight often exceeds 400g LV wall thickening (>15 mm) Chamber dilatation Histological Findings Myocyte hypertrophy and disarray Interstitial fibrosis Vessels Patent coronary arteries Evidence of atherosclerosis may or may not be present Pan- Valvular Dilatation This is a common finding in hypertensive cardiovascular disease, indicating that the heart valves are enlarged due to high blood pressure

Hypertension Effects: Chronic high blood pressure increases cardiac workload : Chronic high blood pressure forces the heart to work harder to pump blood against the increased systemic vascular resistance, leading to hypertrophy . Left ventricular hypertrophy (LVH) due to pressure overload: The left ventricle thickens to manage the increased workload, which can initially help maintain cardiac output but eventually leads to stiffness and decreased compliance . Myocardial fibrosis resulting from chronic ischemia and pressure overload Mechanisms Leading to LVH (Left Ventricular Hypertrophy) Pressure Overload : Sustained high blood pressure increases the afterload (resistance the heart must pump against), causing the heart muscle, particularly the left ventricle, to thicken. Neurohormonal Activation : Chronic hypertension activates the renin-angiotensin-aldosterone system (RAAS), promoting vasoconstriction and sodium retention, which contribute to increased blood pressure and myocardial hypertrophy. Cellular Mechanisms : Cardiac myocytes (heart muscle cells) enlarge and produce more extracellular matrix proteins, leading to thickening and stiffening of the ventricular wall.

Pulmonary Complications Pulmonary Edema Mechanism: In left heart failure, the left ventricle cannot effectively pump blood, leading to a backlog of pressure in the pulmonary veins. This increased pressure pushes fluid into the alveolar spaces in the lungs. Autopsy Findings: The lungs appear heavy, and when cut, frothy fluid exudes, indicating the presence of pulmonary edema. Histology : Microscopic examination shows alveolar spaces filled with protein-rich fluid stained pink, typical of edema fluid.

Renal Complications Hypertensive Nephropathy Pathophysiology: Pathophysiology : Chronic hypertension damages the small blood vessels in the kidneys, leading to ischemia of the glomeruli (functional units of the kidney) and activation of the RAAS, which worsens hypertension and kidney damage . The narrowing of the arterial openings due to hyaline deposition, a process known as arteriolosclerosis. The resulting inadequate blood flow produces tubular atrophy, interstitial fibrosis Autopsy Findings : The kidneys often have a granular appearance and are reduced in size due to scarring and loss of nephrons. Histologically, there is thickening of the arterioles (hyperplastic arteriolosclerosis) and scarring of the glomeruli ( glomerulosclerosis ).

Liver and Spleen Complications Chronic Passive Congestion Liver (Nutmeg Liver): Right heart failure causes blood to back up into the hepatic veins, leading to congestion and ischemia in the liver. The liver appears mottled due to centrilobular necrosis. Spleen : Systemic venous congestion from heart failure also affects the spleen, leading to splenomegaly (enlarged spleen) with congestion.

Neurological Complications Intracranial Hemorrhage (Intracerebral and Intraventricular Hemorrhage and Pontine Hemorrhage) Pathophysiology : Hypertension causes microaneurysms (Charcot-Bouchard aneurysms ) in the brain's blood vessels to rupture, leading to hemorrhage within the brain tissue ( intraparenchymal hemorrhage) Autopsy Findings : The brain may show signs of edema, such as flattened gyri and narrowed sulci. Microscopically, there are areas of hemorrhage and gliosis (reactive changes in glial cells).

Conclusion HHD results from chronic hypertension causing multi-organ damage Autopsy findings provide crucial insights into disease progression Effective management of hypertension can prevent severe complications

References Offiah , A. U., Amadi , A. N., Azuamah , Y. C., Igwe , F. E., & Onyesom , E. (2022). Autopsy pathology of hypertensive cardiovascular disease: Case reports. International Journal of Science and Healthcare Research, 7(4), 134-136. DOI: https://doi.org/10.52403/ijshr.20221018 Basso, C., Michaud, K., d'Amati , G., Banner, J., Lucena , J., Cunningham, K., ... & van der Wal , A. C. (2021). Cardiac hypertrophy at autopsy. Virchows Archiv , 478(3), 347-355. DOI: https://doi.org/10.1007/s00428-021-03038-0 Coelho, J. C., Ferretti-Rebustini , R. E. L., Suemoto , C. K., Leite , R. E. P., Jacob- Filho , W., & Pierin , A. M. G. (2019). Hipertensão arterial: estudo post mortem na região metropolitana de São Paulo. Revista da Escola de Enfermagem da USP, 53, e03457. DOI: https://www.ee.usp.br/reeusp/Revista/2019/53/e03457.pdf