Hypertension: Causes, Pathogenesis - Pathology - ATOT

Topic: Hypertension
Faculty: Pathology
Course: BSc ATOT - 2nd year

Definition, Classification, Pathogenesis, Complications

1. HYPERTENSION Dr. Salman Ansari Kanachur Institute of Medical Sciences

2. Hypertension Definition Classification Normal regulation of BP Pathogenesis of HTN Pathology Complications

3. Hypertension Definition : defined as persistently elevated systolic blood pressure (SBP) values of 130 mm Hg or more or diastolic blood pressure (DBP) of more than 80 mm Hg. 15% of the population suffers from hypertension Can affect the young as well as elderly

4. Normal blood pressure : Systolic BP <120 mmHg Diastolic BP <80 mmHg Pre-hypertension: old term for BP between normal and hypertension

5. Classification of hypertension Primary or essential hypertension : 85% of cases Secondary hypertension : 15% of cases

6. Causes of HTN Primary HTN( 85%): cause is unknown - usually have positive family history Secondary HTN (15%): due to an abnormality or disease in the body

7. Causes of secondary HTN: Renal causes : diabetic nephropathy, glomerulonephritis, polycystic kidney disease Endocrine causes : Cushing’s syndrome, pheochromocytoma Cardiovascular causes : coarctation of aorta Neurological causes : psychogenic Medications/toxins : alcohol, drugs like corticosteroids, NSAIDs Stress

8. Risk factors for HTN Genetic : runs in families Environmental factors like: Obesity Alcohol intake Sodium intake stress

9. Regulation of Normal Blood Pressure The major factors include age, sex, body mass index and diet, particularly sodium intake, exertion, emotional state and others. Blood pressure depends on two hemodynamic variables, namely cardiac output and peripheral vascular resistance

10. Cardiac output : It depends on stroke volume, and heart rate. Stroke volume in turn is influenced by the sodium homeostasis. Heart rate and contractility of myocardium (affects stroke volume) are regulated by the α- and β-adrenergic systems (also effects on vascular tone). Peripheral vascular resistance : It is determined by functional and anatomic changes in small arteries and arterioles. Vascular tone depends on the balance between vasoconstrictors and vasodilators. Blood pressure is also influenced by tissue pH and hypoxia.

11. Role of Kidney Renin-angiotensin system : Renin : Whenever there is a fall in blood pressure, renin is secreted by the juxtaglomerular cells of the kidney and released into the blood circulation. It breaks down plasma angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin converting enzyme.

12. Angiotensin II : It raises blood pressure by increasing both peripheral resistance (direct action on vascular smooth muscle cells and causes vasoconstriction) It raises blood volume (by stimulating secretion of aldosterone by the adrenal zona glomerulosa, and increased reabsorption of sodium in distal tubules).

13. Sodium homeostasis and blood volume : When blood volume is reduced , the glomerular filtration rate falls → leads to increased reabsorption of sodium by proximal tubules of kidney → thereby conserves sodium and expands blood volume. When blood volume is increased , natriuretic factors (natriuretic peptides) are secreted by atrial and ventricular myocardium. They inhibit sodium reabsorption in distal tubules and cause excretion of sodium and diuresis. Natriuretic peptides also cause vasodilation and may be considered as endogenous inhibitors of the renin-angiotensin system

14. Pathogenesis of Hypertension Complex and multifactorial disorder Decreased renal sodium excretion : It is probably the key feature. Decreased excretion of sodium by kidney → leads to an increase in fluid volume, cardiac output, and peripheral vasoconstriction → raises the blood pressure.

15. Raised vascular resistance : Factors that produce vasoconstriction or stimuli that cause structural changes in the vessel wall → result in an increase in peripheral vascular resistance → cause primary hypertension.

16. Genetic factors : The genetic defects may be in the enzymes involved in aldosterone metabolism, sodium reabsorption and smooth muscle cell growth. Environmental factors : These include stress, obesity, smoking, lack of physical activity and heavy intake of sodium salt.

17. Pathogenesis of Secondary Hypertension Mechanism of renovascular hypertension : Renal artery stenosis → decreased glomerular flow and pressure in the afferent arteriole of the glomerulus → stimulates renin secretion and production of angiotensin II → vasoconstriction → increased peripheral resistance. Renal artery stenosis also increases sodium reabsorption → increases blood volume through the aldosterone mechanism. Primary hyperaldosteronism: It is one of the most common causes of secondary hypertension.

18. Pathogenesis Decreased sodium excretion Impairment of renin-angiotensin-aldosterone system(RAAS) Increased sympathetic nervous system activation Increased total peripheral resistance Increased afterload on heart Development of hypertension

19. Pathology Large and Medium Vessel Disease : Atherosclerosis Causes degenerative changes in the walls of large and medium arteries. Predisposes to: (1) Aortic dissection and (2) Cerebrovascular hemorrhage.

20. Small Vessel Diseases Two forms can occur in hypertension: (1) Hyaline arteriolosclerosis, and (2) hyperplastic arteriolosclerosis. 1. Hyaline arteriolosclerosis : It is seen in the arterioles in patients with benign hypertension. Microscopy : It shows thickening of the wall due to homogeneous, pink hyaline material and narrowing of the lumen

21. 2. Hyperplastic arteriolosclerosis: It occurs in severe (malignant) hypertension. Microscopy : The blood vessels show “onion-skin,” concentric, laminated thickening of the arteriolar walls and narrowing of the arteriolar lumen

22. Complications of HTN(Target Organ Damage)

23. CNS complications : Transient Ischemic Attack(TIA) Cerebrovascular accident(CVA) or stroke: due to cerebral bleeding Subarachnoid hemorrhage(SAH) Hypertensive encephalopathy

24. Ophthalmic or retinal complications : Hypertensive retinopathy: arterioles become narrow CVS complications : Coronary artery disease: angina, myocardial infarction Left ventricular failure Atrial fibrillation

25. Blood vessels complications : Atherosclerosis Aortic aneurysm Aortic dissection Renal complications : Proteinuria Hematuria Renal failure

26. Accelerated or malignant hypertension It is characterized by rapid raise in blood pressure (i.e., systolic pressure over 200 mm Hg, diastolic pressure over 120 mm Hg) → renal failure, and retinal hemorrhages and exudates, with or without papilledema. It may develop in normotensive individuals but more common in patients with preexisting benign hypertension (essential or secondary). It develops in ~5% of hypertensive persons. If not treated, death occurs within a year or two.

27. For PPT, scan: For notes, click here or scan: References: Ramadas Nayak - Prep Manual for Undergraduates - Pathology Questions: [email protected]