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HYPERTENSION

HYPERTENSION. Sufia Husain Pathology Department KSU, Riyadh March 2014. LECTURE OUTLINE. R. L. Introduction Definition Classification Primary vs secondary HTN Benign vs malignant HTN Causes of secondary HTN Pathogenesis Regulation of blood pressure Vascular morphology in HTN

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HYPERTENSION

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  1. HYPERTENSION Sufia Husain Pathology Department KSU, Riyadh March 2014

  2. LECTURE OUTLINE R L • Introduction • Definition • Classification • Primary vs secondary HTN • Benign vs malignant HTN • Causes of secondary HTN • Pathogenesis • Regulation of blood pressure • Vascular morphology in HTN • Heart in HTN • Complications of HTN

  3. Hypertension - Introduction • Common problem (25% of population) • Asymptomatic until late- Silent Killer – painless – • Leading risk factor – MI & Stroke • Complications alert to diagnosis but late…

  4. Hypertension and Hypertensive Vascular Disease • Hypertension:Definition: a sustained diastolic pressure more than 90 mm Hg or a sustained systolic pressure in excess of 140 mm Hg (>140/90) • In the early stages of HTN there are few or no symptoms. • Hypertension is an important factor which contributes in development of: • Coronary heart disease. • Cerebrovascular accidents (stroke) • cardiac hypertrophy • Congestive heart failure. • Aortic dissection. • Renal failure. • retinopathy

  5. Risk factors for Hypertension • Hereditary,Genetics- family history • Race. African-Americans • Gender. Men & postmenopausal women • Age • Obesity • Diet, particularly sodium intake • Lifestyle-stressful • Heavy alcohol consumption • Diabetes • Use of oral contraceptives • Sedentary or inactive lifestyle

  6. Classification: based on etiology/cause • Primary/Essential Hypertension (95%) : Mechanisms largely unknown. It is idiopathic. • Secondary Hypertension (5-10%): it can be due to pathology in the renal, endocrine, vascular or neurogenic systems

  7. Causes of Secondary Hypertension

  8. Polycystic kidney Renal Artery stenosis - Atrophy

  9. Hypertension classification based on clinical • Benign hypertension: it can be essential/idiopathic HTN or secondary HTN • Malignant hypertension: it can be essential/idiopathic HTN or secondary HTN

  10. Classification based on clinical features. • Benign: • Modest level. • Fairly stable over years to decades. • Compatible with long life. • Malignant(5%): • there is rapidly rising BP which often leads to end organ damage • It can complicate any type of HTN (i.e. essential or secondary) • It is seen in 5% of HTNive patients. • The diastolic pressure is usually over 120mmHg • It is associated with: • Widespread arterial necrosis and thrombosis • Rapid development of renal failure • Retinal hemorrhage and exudate, with/without papilledema • Hypertensive encephalopathy • Left ventricular failure • Leads to death in 1 or 2 years if untreated.

  11. Postulated mechanisms/PATHOGENESIS of Essential Hypertension 1.Defect in sodium excretion 2.Defect in cell membrane function: -Na/Ca transport 3.Increased sympathetic/ vasoconstrictive response

  12. Regulation of Blood Pressure (BP) BP = Cardiac Output x Peripheral Resistance • Endocrine Factors • Renin, Angiotensin, ADH, Aldosterone • Neural Factors • Sympathetic & Parasympathetic • Humoral factors • vasoconstrictors and vasodilators • Blood Volume • Sodium, Mineralocorticoids • Cardiac Factors • Heart rate & Contractility NOTE: • Peripheral resistance is regulated predominantly at the level of the arterioles. • Reduced renal sodium excretion in the presence of normal arterial pressure is probably a key initiating event; it is a final common pathway for the pathogenesis of most forms of hypertension

  13. Regulation of Blood Pressure (BP)

  14. GFR Combination of endocrine and other factors Renin by JGA Aldosterone Angiotensin II Sodium Retention Blood Volume Vasoconstriction  P. Resistance Hypertension

  15. Blood pressure regulation • Blood pressure is a function of cardiac output and peripheral vascular resistance  two hemodynamic variables that are influenced by multiple genetic, environmental, and demographic factors

  16. Atrialnatriuretic peptide/factor/Hormone (Cardionatrine/Cardiodilatine/atriopeptin) • It is a powerful vasodilator, and a protein (polypeptide) hormone secreted the heart muscle cells in the atria (atrial myocytes).It is involved in the homeostatic control of body water, sodium, potassium and fat. • It is released in response to high blood volume. It acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure. • It has exactly the opposite function of the aldosterone secreted by the zona glomerulos.

  17. Renin-angiotensin-aldosterone and atrialnatriuretic peptide rule

  18. Morphology: • Large Blood Vessels (Macroangiopathy) • Atherosclerosis. HT is a major risk factor in AS. • Small Blood Vessels (Microangiopathy) • Arteriolosclerosis • Hyaline arteriolosclerosis • Hyperplastic arteriolosclerosis:

  19. Small Blood Vessels (Microangiopathy) Arteriolosclerosis • Hyaline arteriolosclerosis: • Characteristic of benign hypertension • Can also be seen in elderly without hypertension and in diabetic patients. • Leads to benign nephrosclerosis due to diffuse renal ischemia. • Hyperplastic arteriolosclerosis: • Characteristic of malignant hypertension. • May be associated with necrotizing arteriolitis (fibrinoid necrosis)

  20. Vascular pathology in hypertension. A. Hyaline arteriolosclerosis: hyalinosis of arteriolar wall with narrowing of lumen. B. Hyperplastic arteriolosclerosis (onionskinning) causing luminal obliteration of vascular lumen (periodic acid–Schiff [PAS] stain).

  21. Vascular Pathology in Hypertension • Hyaline/ Benign hypertension • Hyperplastic/ Malignant hypertension Hyperplastic/ Malignant hypertension

  22. Left ventricular cardiac hypertrophy (left sided hypertensive cardiomyopathy/ hypertensive heart disease) • Longstanding poorly treated HTN leads to left sided hypertensive heart disease. • Hypertrophy of the heart is an adaptive response to pressure overload due to HTN. • HTN induces left ventricular pressure overload which leads to hypertrophy of the left ventricle with increase in the weight of the heart. The free LV wall is > 2cm and the weight of the heart is > 500 grams • In time, the increased thickness of the left ventricular wall impairs diastolic filling. This often induces left atrial enlargement.

  23. Left Ventricular Hypertrophy

  24. complications/Organ damage in HTN: A • Cardiovascular • Left ventricular cardiac hypertrophy(left sided hypertensive cardiomyopathy/ hypertensive heart disease) • Coronary heart disease • Aortic dissection • Kidney • Benign nephrosclerosis (photo A) • Renal failure in untreated or in malignant hypertension • Eyes • Hypertensive retinopathy (photo B) is especially seen in malignant hypertension. • Brain • Haemorrhage, infarction leading to Cerebrovascular accidents B

  25. Subarachnoid Haemorrhage Cerebral Hemorrhage

  26. Lacunar Infarct Cerebral Infarction

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