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Keep
Smiling….!

“It will help you to grow up
in
greater happiness & Love for
each
other.
"
Pathology of
Hypertension
Work by : Elgilani Zaher
Regulation of BP
BP = Cardiac Output x Peripheral Resistance
• Endocrine Factors
– Renin, Angiotensin, ANP, ADH, Aldosterone.
• Neural Factors
– Sympathetic & Parasympathetic
• Blood Volume
– Sodium, Mineralocorticoids(steroids), ANP
• Cardiac Factors
– Heart rate & Contractility.
Hypertension
• Silent Killer – painless – complications
• dizziness, headache, and visual difficulties,
• It is the leading risk factor – MI, Stroke
• Responsible for the majority of emergency visits.
• Number one reason for drug prescription.
• Complications bring to diagnosis but late…
• Chronic, end organ & vascular damage
Characters of HTN
• “Sustained increase in blood
pressure”
•Systolic >140, Diastolic > 90 mmHg
• Normal* < 130 <85 (120/80 +/- 10/5)
• Mild + 20, Moderate +40 Severe +80
• Malignant - > 210/120
Etiologic Classification
• Essential (Primary) Hypertension (95%)
–Unknown etiology, Increased peripheral resistance, Life style, genetic
• Secondary Hypertension (5-10%)
– Renal – GN, RAAS, Renin tumors
– Endocrine – Cushing syndrome , OCP, Thyrotoxicosis
Myxedema, Pheochromocytoma, Acromegaly.
– Vascular – Coarctation of Aorta, PAN, Aortic
insufficiency.
– Neurogenic – Psychogenic, Intracranial
pressure, polyneuritis.
Pathological types of hypertension
The commonest type 95% Rare 5%
Usually above 40 years Younger age (25-53)
Slowly progressive Rabidly progressive
Long term (30 or more) Short fatal
Malignant Hypertension
• Rapidly progressive end organ damage.
• May complicate any type of HTN.
• Artery necrosis with thrombosis.
• Rapidly developing renal failure.
• Hypertensive encephalopathy.
• Left ventricular failure.
• less time  No hypertrophy …!
Pathogenesis of Renovascular HTN
GF
R
Renin
Angiotensin
II
Vasoconstrictio
n P.
Resistance
Sodium
Retention
Blood
Volume
Aldosteron
e
Hypertensio
n
Morphology
• Large Blood Vessels – Macroangiopathy
– Atherosclerosis and its complications.
• Small Blood Vessels – Microangiopathy
– Hyperplastic arteriolosclerosis (thick arterioles)
• Heart
– LVH, Hypertensive cardiomyopathy IHD, MI
• Kidney
– Benign nephrosclerosis.
• Eyes:
– Hypertensive retinopathy
• Brain:
– Haemorrhage, infarction
(splinter hemorrhages & Lacunar infarcts)
Left Ventricular Hypertrophy
Left Ventricular
Hypertrophy
Left Ventricular
Hypertrophy
Hyperplastic Arteriolosclerosis
Onion Skin
Thickening
Onion Skin
Thickening
Of
arterioles.
Of
arterioles.
Narrow
Lumen
Narrow
Lumen
Nephrosclerosis in HTN
Necrotizing arteriole( Malignant HTN)
Fibrinoid
Necrosis
Fibrinoid
Necrosis
Thrombosi
s
Thrombosi
s
Normal Retina (Fundoscopy)
Cause of death
Herat failure (60%) Acute renal failure
Cerebral hemorrhage (30%)
Chronic renal failure (10%)
Cerebral hemorrhage
Heart failure
Conclusions
• Persistent increased blood pressure..
• 95% Essential, 5% secondary - Renovascular
• Benign and Malignant types (>120 Diastolic)
• Vessel damage & Arteriolosclerosis
• Complicates - Atherosclerosis, Diabetes, IHD
• Ischemia or Infarction in end organs.
• Kidney, Brain, Heart & Eyes.
• Complications: Nephrosclerosis, renal damage,
IHD, MI, Stroke & Retinopathy.
Pathology of hypertention.pptx

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Pathology of hypertention.pptx

  • 1. Keep Smiling….!  “It will help you to grow up in greater happiness & Love for each other. "
  • 3.
  • 4. Regulation of BP BP = Cardiac Output x Peripheral Resistance • Endocrine Factors – Renin, Angiotensin, ANP, ADH, Aldosterone. • Neural Factors – Sympathetic & Parasympathetic • Blood Volume – Sodium, Mineralocorticoids(steroids), ANP • Cardiac Factors – Heart rate & Contractility.
  • 5. Hypertension • Silent Killer – painless – complications • dizziness, headache, and visual difficulties, • It is the leading risk factor – MI, Stroke • Responsible for the majority of emergency visits. • Number one reason for drug prescription. • Complications bring to diagnosis but late… • Chronic, end organ & vascular damage
  • 6. Characters of HTN • “Sustained increase in blood pressure” •Systolic >140, Diastolic > 90 mmHg • Normal* < 130 <85 (120/80 +/- 10/5) • Mild + 20, Moderate +40 Severe +80 • Malignant - > 210/120
  • 7. Etiologic Classification • Essential (Primary) Hypertension (95%) –Unknown etiology, Increased peripheral resistance, Life style, genetic • Secondary Hypertension (5-10%) – Renal – GN, RAAS, Renin tumors – Endocrine – Cushing syndrome , OCP, Thyrotoxicosis Myxedema, Pheochromocytoma, Acromegaly. – Vascular – Coarctation of Aorta, PAN, Aortic insufficiency. – Neurogenic – Psychogenic, Intracranial pressure, polyneuritis.
  • 8.
  • 9. Pathological types of hypertension The commonest type 95% Rare 5% Usually above 40 years Younger age (25-53) Slowly progressive Rabidly progressive Long term (30 or more) Short fatal
  • 10. Malignant Hypertension • Rapidly progressive end organ damage. • May complicate any type of HTN. • Artery necrosis with thrombosis. • Rapidly developing renal failure. • Hypertensive encephalopathy. • Left ventricular failure. • less time  No hypertrophy …!
  • 11. Pathogenesis of Renovascular HTN GF R Renin Angiotensin II Vasoconstrictio n P. Resistance Sodium Retention Blood Volume Aldosteron e Hypertensio n
  • 12. Morphology • Large Blood Vessels – Macroangiopathy – Atherosclerosis and its complications. • Small Blood Vessels – Microangiopathy – Hyperplastic arteriolosclerosis (thick arterioles) • Heart – LVH, Hypertensive cardiomyopathy IHD, MI • Kidney – Benign nephrosclerosis. • Eyes: – Hypertensive retinopathy • Brain: – Haemorrhage, infarction (splinter hemorrhages & Lacunar infarcts)
  • 13. Left Ventricular Hypertrophy Left Ventricular Hypertrophy Left Ventricular Hypertrophy
  • 14. Hyperplastic Arteriolosclerosis Onion Skin Thickening Onion Skin Thickening Of arterioles. Of arterioles. Narrow Lumen Narrow Lumen
  • 16. Necrotizing arteriole( Malignant HTN) Fibrinoid Necrosis Fibrinoid Necrosis Thrombosi s Thrombosi s
  • 18. Cause of death Herat failure (60%) Acute renal failure Cerebral hemorrhage (30%) Chronic renal failure (10%) Cerebral hemorrhage Heart failure
  • 19. Conclusions • Persistent increased blood pressure.. • 95% Essential, 5% secondary - Renovascular • Benign and Malignant types (>120 Diastolic) • Vessel damage & Arteriolosclerosis • Complicates - Atherosclerosis, Diabetes, IHD • Ischemia or Infarction in end organs. • Kidney, Brain, Heart & Eyes. • Complications: Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy.