Pathology of Hypertension

25,131 views 28 slides Apr 13, 2017
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About This Presentation

Pathology of HTN


Slide Content

Hypertension ( HBP/HTN) Pathology 4 th year pharmacy Dr: Nemat Mohammed By: Darya Osman , Eman Salah , Moaz Ahmed, Manal Saeed

F orce exerted by circulating blood on the arterial walls . One of principal vital signs . Maximum (systolic) pressure – pressure in the artery when the left ventricle is contracting to force the blood into aorta and other arteries . Minimum (diastolic) pressure – pressure in the artery when the ventricles are relaxing and the heart is filling up, receiving blood from veins . Sphygmomanometer – device used to measure BP Blood pressure

Heart Rate Stroke volume Cardiac output Peripheral resistance Blood Pressure + +

R egulation of BP Baroreceptor reflex – changes in arterial pressure – medulla (brain stem) Location : left and right carotid sinuses, aortic arch Renin – angiotensin system (RAS) Long – term adjustment of arterial pressure Kidney - compensation Endogenous vasoconstrictor – angiotensin I Aldosterone release (adrenal cortex) Stimulates sodium retention and potassium excretion by the kidney Increases fluid retention and indirectly arterial pressure

Hypertension (HTN) Chronic medical condition in which blood pressure is elevated A systolic blood pressure >139 mmHg and diastolic > 89 mmHg Based on the average of two or more properly measured, seated BP reading on two different doctor’s visits

Types of HTN Primary HTN also known as essential HTN . Accounts for 95% cases of HTN. No universally established cause known. Secondary HTN less common cause of HTN ( 5%). secondary to other potentially rectifiable causes.

Primary HTN No medical cause Risk factors : Sedentary lifestyle Obesity ( body mass index greater than 25 ) Salt ( sodium ) sensitivity Alcohol , smoking Family history

Secondary HTN Common Intrinsic renal disease Renovascular disease Mineralocorticoid excess Sleep Breathing disorder Uncommon Pheochromocytoma Glucocorticoid excess Coarctation of Aorta Hyper/hypothyroidism

P athophysiology of HTN Inability of the kidneys to excrete sodium An overactive renin – angiotensin system, vasoconstriction and retention of sodium and water – hypertension An overactive sympathetic nervous system

The ANS Increased production of catecholamines (epinephrine and norepinephrine) results in SNS overactivity . This results in an increased heart rate, increased peripheral vascular resistance due to systemic vasoconstriction, and hypertension. Additionally , an overactive SNS effects insulin resistance, vascular remodeling, has procoagulant effects, which can lead to neospasm and narrowing of the blood vessels 

Vascular remodelling

The RAAS

Endothelial Dysfunction Oxidative stress upsets balance between endothelin and Nitric oxide leads to changes in the endothelium and sets up a “vicious cycle” that contributes to the maintenance of high blood pressure Alterations in endothelial function are a reliable indicator of target organ damage and atherosclerotic disease, as well as prognosis

Genetics Caused by single gene mutations which leads to several forms of high blood pressure Ten genes have been identified which cause these monogenic forms of  hypertension. HTN has been linked with several chromosomal regions, including regions linked to familial combined hyperlipidemia, was found.

Risk factors Non Modifiable: Age Sex Race Family history Modifiable : Weight Physical fitness Smoking and alcohol Diet Stress diabetes Certain chromic conditios (e.g. kidney disease, sleep apnea)

Complications of Prolonged Uncontrolled HTN Changes in the vessel wall leading to vessel trauma and arteriosclerosis throughout the vasculature Complications arise due to the “target organ” dysfunction and ultimately failure. Damage to the blood vessels can be seen on fundoscopy .

Target Organs CVS (Heart and Blood Vessels ) The kidneys Nervous system The Eyes

Effects On CVS Ventricular hypertrophy, dysfunction and failure Arrhithymias Coronary artery disease, Acute MI Arterial aneurysm, dissection, and rupture

Effects on The Kidneys Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease Ischemic kidney disease especially when renal artery stenosis is the cause of HTN

Nervous System Stroke intracerebral and subaracnoid hemorrhage Cerebral atrophy and dementia

The Eyes Retinopathy , retinal hemorrhages and impaired vision Vitreous hemorrhage, retinal detachment Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction

SIGNS AND SYMPTOMS No symptoms – many people unaware they have hypertensio n until accidentally found Non–specific symptoms – mild symptoms Headache , Morning headache , Tinnitus , Dizziness , Confusion , Fatigue , Shortness of breath , Changes in vision – blindness , Nausea

T reatment of HTN Antihypertensive drugs – act by lowering blood pressure A im of treatment - <140/ 90 Reduction of blood pressure by 5-6 mm/Hg decreases the risk of stroke by 40%, coronary heart disease by 15- 20%, heart failure and mortality from vascular disease

A ntihypertensive drugs

P revention Weight reduction Aerobic exercise (e.g. walking) Reducing sugar intake Reducing sodium ( salt ) and fat/fat free food Fruits , vegetables Stop ping smoking Reducing stress (relaxation therapy – meditation)