Hypertension (HBP/HTN)

Pathology4th year pharmacy

Dr: Nemat Mohammed

By: Darya Osman, Eman Salah, Moaz Ahmed, Manal Saeed

o Force exerted by circulating blood on the arterial walls.

o One of principal vital signs.

o Maximum (systolic) pressure – pressure in the artery when the left ventricle is contracting to force the blood into aorta and other arteries.

o Minimum (diastolic) pressure – pressure in the artery when the ventricles are relaxing and the heart is filling up, receiving blood from veins.

o Sphygmomanometer – device used to measure BP

Blood pressure

Heart Rate Stroke volume

Cardiac output Peripheral resistance

Blood Pressure

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Regulation of BPo Baroreceptor reflex – changes in arterial pressure –

medulla (brain stem)◦ Location : left and right carotid sinuses, aortic arch

o Renin – angiotensin system (RAS)◦ Long – term adjustment of arterial pressure◦ Kidney - compensation◦ Endogenous vasoconstrictor – angiotensin I

o Aldosterone release (adrenal cortex)◦ Stimulates sodium retention and potassium excretion by the

kidney◦ Increases fluid retention and indirectly arterial pressure

Hypertension (HTN)o Chronic medical condition in which blood pressure is

elevated

o A systolic blood pressure >139 mmHg and diastolic > 89 mmHg

o Based on the average of two or more properly measured, seated BP reading on two different doctor’s visits

Types of HTNPRIMARY HTN

o also known as essential HTN.

o Accounts for 95% cases of HTN.

o No universally established cause known.

SECONDARY HTN

o less common cause of HTN ( 5%).

o secondary to other potentially rectifiable causes.

Primary HTN

oNo medical cause

o Risk factors :o Sedentary lifestyleo Obesity ( body mass index

greater than 25)o Salt ( sodium) sensitivityo Alcohol, smokingo Family history

Secondary HTN Common

◦ Intrinsic renal disease

◦ Renovascular disease

◦ Mineralocorticoid excess

◦ Sleep Breathing disorder

Uncommon◦ Pheochromocytoma

◦ Glucocorticoid excess

◦ Coarctation of Aorta

◦ Hyper/hypothyroidism

Pathophysiology of HTNo Inability of the kidneys to excrete sodium

o An overactive renin – angiotensin system, vasoconstriction and retention of sodium and water – hypertension

o An overactive sympathetic nervous system

The ANSo Increased production of catecholamines (epinephrine

and norepinephrine) results in SNS overactivity.

o This results in an increased heart rate, increased peripheral vascular resistance due to systemic vasoconstriction, and hypertension.

o 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

Geneticso Caused by single gene mutations which leads to several forms of high blood

pressure

o Ten genes have been identified which cause these monogenic forms of hypertension.

o HTN has been linked with several chromosomal regions, including regions linked to familial combined hyperlipidemia, was found.

Risk factorso Non Modifiable:

o Age

o Sex

o Race

o Family history

o Modifiable:

o Weight

o Physical fitness

o Smoking and alcohol

o Diet

o Stress

o diabetes

o Certain chromic conditios (e.g. kidney disease, sleep apnea)

Complications of Prolonged Uncontrolled HTN

o Changes in the vessel wall leading to vessel trauma and arteriosclerosis throughout the vasculature

o Complications arise due to the “target organ” dysfunction and ultimately failure.

o Damage to the blood vessels can be seen on fundoscopy.

Target Organs o CVS (Heart and Blood Vessels)

o The kidneys

o Nervous system

o The Eyes

Effects On CVS o Ventricular hypertrophy, dysfunction and failure

o Arrhithymias

o Coronary artery disease, Acute MI

o Arterial aneurysm, dissection, and rupture

Effects on The Kidneyso Glomerular sclerosis leading to impaired kidney function and finally end stage kidney disease

o Ischemic kidney disease especially when renal artery stenosis is the cause of HTN

Nervous Systemo Stroke

o intracerebral and subaracnoid hemorrhage

o Cerebral atrophy and dementia

The Eyeso Retinopathy, retinal hemorrhages and impaired vision

o Vitreous hemorrhage, retinal detachment

o Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction

SIGNS AND SYMPTOMS

o No symptoms – many people unaware they have hypertension until accidentally found

o Non–specific symptoms – mild symptoms

Headache, Morning headache, Tinnitus, Dizziness, Confusion, Fatigue, Shortness of breath, Changes in vision – blindness, Nausea

Treatment of HTNo Antihypertensive drugs – act by lowering blood pressure

o Aim of treatment - <140/ 90

o 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

Antihypertensive drugs

ACE – IARBs

Beta blockersThiazide diuretics

VasodilatorsLong acting CCBAlp

ha blockersCentral agents

Preventiono Weight reduction

o Aerobic exercise (e.g. walking)

o Reducing sugar intake

o Reducing sodium (salt) and fat/fat free food

o Fruits, vegetables

o Stopping smoking

o Reducing stress (relaxation therapy – meditation)