Medical Officer/RHEMA MEDICAL GROUP HYPERTENSION Dr Anzo William Adiga WatsApp or Call +256777363201 Medical Officer/RHEMA MEDICAL GROUP

Plan What is hypertension? Causes Pathophysiology Diagnosis Investigation Treatment

Why is it important? Common Morbidity and mortality Effective treatment

What is blood pressure? Blood pressure is the force exerted by blood on the walls of the arteries when the heart beats. When measured, two figures are recorded. The first is called the systolic pressure. This is the pressure in the arteries when the heart contracts. The second, called the diastolic, is the pressure while the heart is filling with blood again as it relaxes.

What is hypertension?

Why does hypertension matter? When the force of blood against the vessel wall increases, it causes changes in the vessels. This occurs in all organs – most importantly the brain, heart, and kidneys

Causes PRIMARY “Essential hypertension” >95% OF CASES SECONDARY Renal disease Renal artery stenosis Glomerulonephritis Chronic kidney disease Polycystic disease Obstructive uropathy Adrenal disease Primary aldosteronism Cushing's syndrome Phaeochromocytoma Drug induced Oral contraceptives Corticosteroids Sympathomimetics Other causes Coarctation of the aorta Pre-eclampsia Raised intracranial pressure

Other ‘hypertensions’ Pulmonary hypertension White coat hypertension Malignant hypertension Pregnancy induced hypertension

Risk factors Age Smoking Cholesterol Genetics Inactivity Obesity Diet Stress

Mechanisms Cardiac output Peripheral resistance Renin-angiotensin-aldosterone system Autonomic nervous system Endothelial dysfunction Other Bradykinin Endothelin Nitric oxide Atrial natriuretic peptide

Pathophysiology of hypertension TOTAL PERIPHERAL RESISTANCE CARDIACOUTPUT = BP X Maintaining a normal blood pressure depends on the balance between cardiac output and total peripheral resistance Most patients with hypertension have a normal cardiac output and a raised peripheral resistance

Pathophysiology : Peripheral resistance Peripheral resistance is dependent on the contraction of the smooth muscle cells in the walls of the small arterioles This is due to an increase in intracellular calcium Prolonged smooth muscle contraction causes structural changes with thickening of the arteriolar vessel walls and an irreversible rise in resistance

Pathophysiology : Renin-angiotension-aldosterone system (RAAS) Released in response to: Glomerular hypoperfusion Decreased sodium in tubules Sympathetic nervous system Aldosterone released: Increased salt and water retention Causes vasoconstriction

Pathophysiology - kidneys By impairing renal perfusion, there is activation of the RAAS stystem This causes worsening hypertension and salt and water retention The increased cardiac load causes further left ventricular hypertrophy

Pathophysiology: Sympathetic nervous system The autonomic nervous system is important in maintaining a normal blood pressure. It mediates short term changes in blood pressure in response to stress and physical exercise.   “Fight or flight”

Pathophysiology : Endothelial dysfunction Vascular endothelial cells produce local vasoactive agents, including the vasodilator molecule nitric oxide and the vasoconstrictor peptide endothelin. Abnormalities of these cells may be important in hypertension

Pathophysiology : Summary Interactions between all the systems discussed are probably responsible for essential hypertension In any case where there are multiple factors suggested, and multiple treatments on offer, the cause has generally not been fully discovered

Pathology - consequences Heart Arteries Kidney Brain Eyes

Coronary artery atheroma Left ventricular hypertrophy Pathology - Cardiac Coronary artery atheroma Left ventricular hypertrophy Heart failure Ischaemia – ‘angina’ Myocardial infarction Sudden cardiac death

Pathology – Left ventricular hypertrophy

Pathology – Coronary artery disease

Pathology – Coronary artery disease

Pathology – Myocardial infarction

Pathology – Heart failure

Pathology - Arteries Medium/large arteries Small arteries Arterioles Accelerates atherosclerosis Small arteries Media and Intimal thickening Arterioles Onion skin thickening Fibrinoid necrosis

Pathology – Large arteries

Pathology - Peripheral vascular disease Large and medium sized vessels – atheroma and degenerative changes

Pathology – Peripheral vascular disease

Pathology – Peripheral vascular disease

Pathology - arterioles Onion skin thickening Fibrinoid necrosis

Pathology - kidney

Pathology - kidney Nephrosclerosis Artery and arteriolar narrowing due to intimal thickening and hyaline deposition Glomerulosclerosis (loss of glomeruli) Tubular atrophy Interstitial fibrosis

Arterial medial hypertrophy Pathology - kidney Arterial medial hypertrophy Glomerular sclerosis Tubular atrophy

Pathology - Cerebral Cerebral infarcts “Stroke” Can cause vascular dementia

Pathology - Cerebral Cerebral haemorrhage

Pathology - Cerebral

Pathology - Eyes Retinal haemorrhages Exudates Papilloedema Retinal artery and venous thrombosis

Symptoms Usually none Headache Visual disturbance Dizziness Symptoms of organ damage

Investigation Cause of hypertension Associated cardiovascular risk factors Evidence of target organ damage

Treatment – Lifestyle Maintain normal weight Low salt intake Limit alcohol intake Stop smoking Aerobic exercise – 30minutes a day 5 portions fruit/veg daily Limit saturated fat intake

Treatment - Pharmacological <50% - BP controlled by one drug alone Common to need 2 or more different drugs This increases the possibility of side effects – compliance important as these patients are generally asymptomatic before they start! Most need treatment for life

DRUG OF CHOICE Bendrofluithiazid (Aprinox) 5mg Od....For life Esinolpril/Lisinopril/Captopril(5mg/5mg of/25mg tds) Propanalolo/Atenolol 40/10mg bB, Carvidolol 3 Arotvastatin Nifedipine, Amylodipine

You start to examine him and start with his hands You start to examine him and start with his hands. They feel very cold and you notice he is sweating quite a lot. You can’t find a radial pulse even though the patient is still talking and decide to call for the Registrar straight away to try and prevent another disaster. You ask the nurse to put some oxygen on the patient and take his observations (pulse, blood pressure, respiratory rate and oxygen levels) while you pop to the phone.

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