1. Medical Officer/RHEMA MEDICAL GROUP
HYPERTENSION
Dr Anzo William Adiga
WatsApp or Call
Medical Officer/RHEMA MEDICAL GROUP

2. Plan What is hypertension? Causes Pathophysiology Diagnosis
Investigation
Treatment

3. Why is it important? Common Morbidity and mortality
Effective treatment

4. 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.

5. What is hypertension?

6. 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

7. 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

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

9. Risk factors Age Smoking Cholesterol Genetics Inactivity Obesity Diet
Stress

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

11. 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

12. 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

13. 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

14. 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

15. 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”

16. 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

17. 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

18. Pathology - consequences
Heart
Arteries
Kidney
Brain
Eyes

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

20. Pathology – Left ventricular hypertrophy

21. Pathology – Coronary artery disease

22. Pathology – Coronary artery disease

23. Pathology – Myocardial infarction

24. Pathology – Heart failure

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

26. Pathology – Large arteries

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

28. Pathology – Peripheral vascular disease

29. Pathology – Peripheral vascular disease

30. Pathology - arterioles
Onion skin thickening
Fibrinoid necrosis

31. Pathology - kidney

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

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

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

35. Pathology - Cerebral
Cerebral
haemorrhage

36. Pathology - Cerebral

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

38. Symptoms Usually none Headache Visual disturbance Dizziness
Symptoms of organ damage

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

40. 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

41. 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

42. 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

43. 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.

44. ANY QUESTIONS?