 Hi all. Today's topic of discussion is hypertension. Hypertension, as you all know, it's a condition in which arterial BP is chronically elevated. Then this BP cutoff levels are defined according to their effect on patient's risk. According to American Heart Association guidelines, an individual is said to have normal BP when his systolic blood pressure is less than 120 mmHg and the systolic blood pressure is less than 80 mmHg. If the systolic blood pressure is between 120 to 129 and the systolic blood pressure is less than 80, then the individual is said to have elevated BP. If the systolic blood pressure is between 130 to 139 or having the systolic blood pressure between 80 to 89, then it is stage 1 hypertension. If the systolic blood pressure is more than or equal to 150 or the systolic BP is more than or equal to 90 mmHg, it is called stage 2 hypertension. The systolic BP is determined by stroke volume, whereas the diastolic blood pressure is determined by peripheral vascular resistance. This peripheral vascular resistance increases during the constriction of smaller blood vessels. Then when to make a diagnosis? That if a new patient is coming to you, then how to make a diagnosis? To make a diagnosis, there should be a more than or equal to 2 readings on more than or equal to 2 different occasions. What are the causes of hypertension? In more than 95% of the cases, we won't get a specific underlying causes for hypertension. Such patient is said to have essential or primary hypertension and it's the most common causes of hypertension. Its pathology is also not clear. In about 5% of cases, hypertension is found to be a consequence of specific disease or certain underlying disease. Then it is known as secondary hypertension. Let's see what are the causes of secondary hypertension? Alcohol, obesity, pregnancy or some environmental factors for secondary hypertension. What are the renal causes? Renal causes include renal parankymal disease, such as chronic kidney disease, glomerular nephritis. Here there will be decreased GFR, glomerular filtration rate, which leads to a volume overload. This there occurs hypertension. And another mechanism of action is activation of gross system that is renin angiotensin aldosterone system. When there is a decreased blood flow to the kidney, dextraglomerular apparatus of the kidney is stimulated and it releases renin. Renin converts angiotensinogen to angiotensin 1 and angiotensin converting enzyme converts angiotensin 1 to angiotensin 2. Angiotensin 2 releases the aldosterone from the adrenal gland and causes sodium and water retention by reabsorbing them. Another action of angiotensin 2, it has an action of arteriolar vessel constriction. Thus it increases the blood pressure. In renal vascular causes, for example renal artery stenosis, predominant mechanism of action is raw system only. Third renal cause is congenital actuating mutation of sodium chloride channel. Gainer function of sodium chloride channel, which is present in the distal convoluted tubule and the condition is known as gordon syndrome. Mutation of epithelial sodium channel, which is present in the collecting debt is known as lidel syndrome. Here the occurs increase sodium reabsorption by renal tubules and this increases the hypertension. This increases the BP blood pressure coming to the endocrine causes. The causes of endocrine depends upon the type of BP and edema, which type of BP is increased whether systolic blood pressure or diastolic blood pressure and if edema present or not. If the diastolic blood pressure is increased with non-pitting edema, then it will be due to hypothyroidism with mixed edema because mixed edema will compresses the smaller blood vessels, thus increasing the peripheral vascular resistance and in turn increases the diastolic blood pressure. If you found that systolic blood pressure is elevated without edema, then it is due to hypothyroidism. How? Because increased thyroid hormone will increases the function of beta receptor. This beta receptor has two functions that it increases chromatropic that means the heart rate and increases the ionotropic that is contractility, that it increases the contractility. Increased contractility means increased shock volume thereby in turn increases the systolic blood pressure. Another condition is corn syndrome that is aldosterone producing adrenal edenoma. Your diastolic blood pressure is increased without edema. How the diastolic blood pressure is increased? Because aldosterone in long run causes the fibrosis of blood vessels. It is due to the remodeling effect of aldosterone on cardiovascular system which in turn increases the peripheral vascular resistance and increases diastolic blood pressure. Why edema is absent? If aldosterone is present there should be edema but here the edema is absent because aldosterone also causes increased extracellular fluid volume, easier volume and it causes atria to stretch and releases AMP that is atria natriuretic peptide. It will cause natriuresis that is expression of sodium in urine and prevents edema and this is known as escape phenomena. Another condition is piochromocytoma here both systolic blood pressure and diastolic blood pressure is increased without edema. In piochromocytoma we will get sustained hypertension more than an episodic hypertension. Paroxysmal headache, palpitation and sweating are some symptoms of piochromocytoma. Coming to the miscellaneous cossom secondary hypertension, coactation of iota. In coactation of the iota, opaline is more developed than lower limb. Here we will get a radiofumeral delay and we are not able to palpate the dosalis pyrus atria. Dosalis pyrus atria is not palpable. Here also the mechanism of action is ROS that is renin angiotensin and endosclerone system activation due to the decreased renal blood flow. Next coming to obstrate sleep apnea. Due to repeated awakening during night time, the sympathetic activity of an individual is increased. So the patient presents with you with a complaint of daytime sleepiness and excessive snoring. It is due to increased sympathetic activity thereby leading to hypertension. Then some drugs are also reason for hypertension such as NSIDs. NSIDs decreases the GFR by inhibiting prostaglandins thereby causing the volume overload and lead to hypertension. Corticosteroids. This cortisol has mineralocorticoid receptor affinity that is the mechanism of action in corticosteroid. Psyroxine overdose I have already mentioned about it. Cocaine use. It also stimulates the sympathetic activity thereby increasing the hypertension. Increases the BP. Coming to the clinical features. Clinical features symptoms include early morning occipital headache. The reason is not known. Disnea. It's due to digestive heart failure. Hypertension will lead to digestive heart failure. Then you will get dysnea. What are the signs of hypertension? Epical heat. It is due to left ventricular hypertrophy. On palpation you will get left ventricular fourth heart sound. Also due to left ventricular hypertrophy, left ventricular becomes stiff. So you will get fourth heart sound. Charged organ damage. It's the adverse effect of BP on organs. First it's blood vessels. In larger arteries the internal elastic lamina is thickened and muscle is hypertrophic. Moog muscle is hypertrophic. Fibrous tissue is deposited thereby making the whistle wall less compliant. In smaller arteries there occurs hyaline arteriosclerosis which lead to aneurysm of the smaller blood vessels. This may lead to carotere and cerebrovascular disease. What are the CNS features? CNS features include stroke. Stroke is a common complication of hypertension. It is due to cerebral hemorrhage or infarction. Carotid atheroma and transient ischemic attacks are more common. Subarachnoid hemorrhage is also associated with hypertension. Hypertension and kephylopathy is a rare condition in which it is characterized by high BP and neurological symptoms including transient disturbance of speech or vision. Parasitia is orientation with some loss of consciousness. In eye we get hypertensive retinopathy. Hypertensive retinopathy cotton wool exhibits are associated with retinal ischemia or infarction and hypertension is also associated with central retinal vein thrombosis. In heart left ventricular hypertrophy because high BP places a pressure load on the heart and lead to left ventricular hypertrophy. Another feature is atrial fibrillation. It is also due to left ventricular hypertrophy because the left ventricular blood filling is impaired causing the diastolic dysfunction thereby leading to left ventricular hypertrophy. Due to left ventricular hypertrophy atrial fibrillation occurs. In kidney proteinuria and alternately leading to renal failure that what is malignant or accelerated hypertension. It is due to accelerated microvascular damage with necrosis in the walls of small arteries and arterioles. Then the diagnosis is based on the evidence of high BP and rapidly processing and organ damage that is rate 3 or rate 4 retinopathy, renal dysfunction and hypertensive encephalopathy. Investigation include urine analysis for blood, protein and glucose, blooduria, electrolytes and creatinine, blood glucose, serum total and HDL cholesterol, then 12-layered ECG. ECG findings of hypertension include left ventricular hypertrophy that is left atrial enlargement will be there, left ventricular hypertrophy voltage criteria is present, left axis deviation. Coming to the treatment. Treatment is according to the BP rating. If it is elevated BP, we advise only lifestyle modification. Lifestyle modification include decreased sodium intake that is sodium intake should restrict to 1.5 gram per day. Then increase potassium intake because this potassium intake will relax the smooth muscles of the blood vessels. Reducing alcohol intake and quitting mocking. Then regular physical exercise. There should be more than or equal to 150 minutes of exercise per week and this exercise will lead to increased basal vagal discharge. An important one is dash diet that is dietary approach to stop hypertension that includes increased intake of fruits and vegetables and low fat dietary product then one have to adopt that diet which is low in saturated fat. In stage 1 hypertension ask for history of coronary artery disease if it is absent then lifestyle modification is advised and if it is present then we have to go for we have to start lifestyle modification along with breath. In stage 2 hypertension also lifestyle modification with breath. Start first line breath. Start with any one first line breath. First line breaths are ac inhibitors or angiotensin receptor blockers, calcium channel blockers and diuretics. Beta blockers are no longer the first line treatment except in the angina patient with hypertension. Ac inhibitors which include enlapril, ramipril, lisinopril and ARBs. ARBs when ac inhibitors are intolerant of side effect of ac inhibitors such as fry cough occurs then we can choose ARBs or better start with ARB like termicertan, valcertan, indisertan. Calcium channel blockers which includes amlotypin, dillchiasm, verapermil, mainly dihydroperidins with dihydroperidins. Diuretics such as purosamide and thiazide like diuretics. If your patient is younger than 55 years then start with either with ac inhibitors or ARBs. If your patient is 55 years or older or black patients of an age that is African or Caribbean descent then start with either with calcium channel blockers or diuretics it's the first step and the BB is not controlled you can combine both. You can combine with angiotensin receptor blockers with calcium channel blockers or angiotensin inhibitors or ARBs with diuretics and BB is not controlled you can combine all these A plus C plus D. If need add further diuretic therapy or alpha blocker or beta blocker.