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L5 & 6 effects of htn on vessels & heart 20 (2)


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L5 & 6 effects of htn on vessels & heart 20 (2)

  1. 1. Effects of Hypertension on Vessels and Heart 2020
  2. 2. LOs • Mention types of hypertension. • Enlist causes of secondary hypertension. • Know the pathogenesis of pathological effects of hypertension on heart and vessels. • Describe the pathological changes in the heart and vessels due to hypertension. • Know the outcome of hypertension.
  3. 3. Hypertension (HTN) Hypertension; an elevation in blood pressure (B.P) beyond normal values of 120/80 mmHg. Sustained diastolic pressures greater than 90 mm Hg or sustained systolic pressures in excess of 140 mm Hg are reliably associated with an increased risk for atherosclerosis and are therefore used as cutoffs in diagnosing hypertension in clinical practice. Three forms of hypertension Systemic Pulmonary Portal
  4. 4. Systemic HTN Types of Systemic Hypertension: Essential (Primary) HTN Secondary HTN Malignant hypertension; Approximately 5% of hypertensive patients (when systolic B.P = 200 mm and diastolic B.P is above 120 mmHg ), if untreated, leads to death in within 1 to 2 years. Malignant hypertension is frequently associated with renal failure and retinal hemorrhages, with or without papilledema. It may develop in previously normotensive persons but more often is superimposed on preexisting benign hypertension, either essential or secondary.
  5. 5. Essential (Primary) HTN Essential (idiopathic) HTN (95% of cases) Gradual age-associated rise in B.P “essential” for normal perfusion of end organs such as the brain. Pathogenesis: Specific triggers unknown However essential HTN results from the interplay of several genetic polymorphisms and environmental factors, which alter renal sodium handling, increase blood volume and /or peripheral resistance.
  6. 6. Essential (Primary) HTN Mechanisms Reduced renal sodium excretion (probably a key pathogenic feature); In the presence of normal arterial pressure; decrease sodium excretion causes an obligatory increase in fluid volume and increased cardiac output, thereby elevating B.P. At the new higher B.P, the kidneys excrete additional sodium. Thus, a new steady state of sodium excretion is achieved, but at the expense of an elevated B.P Increased vascular resistance; may stem from chronic vasoconstriction may result in permanent thickening of the walls of affected vessels. Genetic factors; play an important role in determining B.P, as shown by familial clustering of hypertension. In a small proportion of cases of essential hypertension there is linkage to specific angiotensinogen polymorphisms and angiotensin II receptor variants Environmental factors; Stress, obesity, smoking, physical inactivity, and high levels of salt consumption, modify the impact of genetic determinants.
  7. 7. Essential HTN Risk Associated with Essential HTN: Essential HTN is compatible with long life unless following complication supervenes. 1. Stroke 2. Hypertensive heart disease (coronary heart disease, cardiac hypertrophy and heart failure) 3. Aortic dissection 4. Multi-infarct dementia 5. Renal failure (Without appropriate treatment, some 50% of hypertensive patients die of ischemic heart disease (IHD) or congestive heart failure, and another third succumb to stroke)
  8. 8. Secondary HTN Secondary HTN: with known causes Pathogenesis: Most of the cases are due to; Primary renal disease Renal artery narrowing (renovascular hypertension) Adrenal disorders Single-gene disorders affecting renal sodium resorption, several relatively rare disorders include the following: • Gene defects in enzymes involved in aldosterone metabolism • Mutations in proteins that affect sodium resorption Prognosis: Depends on adequate treatment of the underlying cause.
  9. 9. Causes of Secondary HTN RENAL Acute glomerulonephritis Chronic renal disease Polycystic disease Renal artery stenosis Renal vasculitis Renin-producing tumors CARDIOVASCULAR Coarctation of aorta Polyarteritis nodosa Increased intravascular volume Increased cardiac output Rigidity of the aorta NEUROLOGIC Psychogenicnial pressure Sleep apne Increased intracraa Acute stress, including surgery ENDOCRINE Adrenocortical hyper function (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, licorice ingestion) Exogenous hormones (glucocorticoids, estrogen [including pregnancy-induced and oral contraceptives], sympathomimetics and tyramine-containing foods, monoamine oxidase inhibitors) Pheochromocytoma Acromegaly Hypothyroidism (myxedema) Hyperthyroidism (thyrotoxicosis) Pregnancy-induced (pre-eclampsia)
  10. 10. Vascular Pathology in Hypertension Injury to the vessel wall and in particular to ECs is the fundamental basis. Injurious stimuli may be biochemical, immunologic, or hemodynamic. The integrated function of ECs and the underlying SMCs is critical for the vasculature to respond to various stimuli; such responses can be adaptive or may lead to pathologic lesions. Thus, EC injury or dysfunction contributes to a host of pathologic processes including thrombosis, atherosclerosis, and hypertensive vascular lesions. Ensuing SMC prolifération and matrix synthesis can help to repair a damaged vessel wall, but also can eventually lead to luminal occlusion. In addition to accelerating atherogenesis, hypertension-associated degenerative changes in the walls of large and medium arteries can potentiate both aortic dissection and cerebrovascular hemorrhage.
  11. 11. Stereotypical response to vascular injury Intimal thickening, emphasizing intimal smooth muscle cell migration and proliferation associated with extracellular matrix synthesis. Intimal smooth muscle cells may derive from the underlying media or may be recruited from circulating precursors 3. Elaboration of extracellular matrix 2. SMCs mitosis 1. Recruitment of SMCs or smooth muscle precursor cells to the intima
  12. 12. Arteriolosclerosis A form of cardiovascular disease involving hardening and loss of elasticity of arterioles or small arteries, most often associated with HTN & D. mellitus. Arteriolosclerosis is the term used to describe 3 morphologic forms of vascular disease affecting arterioles and small muscular arteries. These are: 1. Hyaline arteriolosclerosis, 2. Hyperplastic arteriolosclerosis 3. Necrotizing arteriolitis All the three types are common in hypertension but may occur due to other causes as well. Arteriosclerosis: thickening, hardening and loss of elasticity of the walls of arteries
  13. 13. Hyaline arteriolosclerosis Chronic hemodynamic stress in benign HTN induces; leakage of plasma components across injured ECs into vessel walls & increased ECM production by SMCs leads to homogeneous, pink hyaline thickening of arteriolar walls & luminal narrowing. Vessels of older adult patients (normotensive or hypertensive) show same changes but in hypertensive patient hyaline arteriolosclerosis is more generalized and severe Similar lesions also common in diabetic microangiopathy; etiology is hyperglycemia-associated EC dysfunction. In the kidneys of hypertensive, arteriolar narrowing caused by hyaline arteriosclerosis leads to diffuse vascular compromise, ischemic atrophy and nephrosclerosis (glomerular scarring)
  14. 14. Hyperplastic arteriolosclerosis Hyperplastic arteriolosclerosis is more typical of severe hypertension. Vessels exhibit “onion skin,” concentric, laminated thickening of arteriolar walls and luminal narrowing. The laminations consist of SMCs and thickened, reduplicated basement membrane. In malignant hypertension, these changes accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), particularly prominent in the kidney.
  15. 15. Hypertensive Heart Disease (HHD) • Systemic (left sided) HHD • Pulmonary (right sided) HHD
  16. 16. Systemic (left sided) HHD Basics for Diagnosis: History of hypertension Left ventricular hypertrophy in the absence of other causes accounting for hypertrophy The stimulus for hypertrophy is pressure overload
  17. 17. Systemic (left sided) HHD Stages of HHD Compensated HHD: With hypertrophy an adequate cardiac output is maintained. Decompensated HHD: Thickness of muscle wall increase demand for oxygen, decrease compliance, and role of hypertension on atheroma, all contribute to decompensated HHD and eventual dilatation.
  18. 18. Systemic (left sided) HHD Gross: Compensated stage - Concentric ventricular hypertrophy Decompensated stage - Ventricular dilatation (In both stages, heart weight increased) Note: Left atrial dilation due to stiffening of the left ventricle and impaired diastolic relaxation, leading to atrial volume overload Microscopy: Large cardiac muscle fibers with large nuclei, later interstitial fibrosis.
  19. 19. Systemic (left sided) HHD Outcome of HHD: • CHF • Increased risk of sudden cardiac death • Renal disease • Stroke Note: Drug control leads to regression of hypertrophy.
  20. 20. Pulmonary (right sided) HHD - Cor pulmonale Pulmonary hypertension caused by primary disorders of the lung parenchyma or pulmonary vasculature ends up in Cor pulmonale which consists of; Right ventricular hypertrophy Right ventricular dilation Generally, right ventricular dilation and hypertrophy caused by congenital heart disease or by left ventricular failure are excluded by this definition.
  21. 21. Pulmonary (right sided) HHD - Cor pulmonale Types of Cor pulmonale: Acute cor pulmonale: Most commonly follows massive pulmonary embolism with obstruction of >50% of the pulmonary vascular bed. Chronic cor pulmonale: Occurs secondary to prolonged pressure overload caused by obstruction of the pulmonary vasculature, or compression or obliteration of septal capillaries (resulting from emphysema, interstitial pulmonary fibrosis, or primary pulmonary hypertension).
  22. 22. Pulmonary (right sided) HHD - Cor pulmonale Acute cor pulmonale Right ventricle usually dilated but does not show hypertrophy; if an embolism causes sudden death the heart may even be of normal size. Chronic cor pulmonale Right ventricular (and often right atrial) hypertrophy. In extreme cases the thickness of the right ventricular wall may be comparable to or even exceed that of the left ventricle. When ventricular failure develops the right ventricle and atrium may also be dilated. Such dilation may mask right ventricular hypertrophy.
  23. 23. References • Robbins Basic Pathology 10th edition Chapter 10 &11 pages 361 to 440