Topic: Hypertension Faculty: Pathology Course: BSc ATOT - 2nd year Definition, Classification, Pathogenesis, Complications

1. HYPERTENSION
Dr. Salman Ansari
Kanachur Institute of Medical Sciences

2. Hypertension
● Definition
● Classification
● Normal regulation of BP
● Pathogenesis of HTN
● Pathology
● Complications

3. Hypertension
- Definition: defined as persistently elevated systolic blood
pressure (SBP) values of 130 mm Hg or more or diastolic blood
pressure (DBP) of more than 80 mm Hg.
- 15% of the population suffers from hypertension
- Can affect the young as well as elderly

5. Normal blood pressure:
- Systolic BP <120 mmHg
- Diastolic BP <80 mmHg
Pre-hypertension: old term for BP between normal and
hypertension

7. Classification of hypertension
Primary or essential hypertension: 85% of cases
Secondary hypertension: 15% of cases

8. Causes of HTN
Primary HTN(85%): cause is unknown - usually have positive family
history
Secondary HTN(15%): due to an abnormality or disease in the body

9. Causes of secondary HTN:
- Renal causes: diabetic nephropathy, glomerulonephritis,
polycystic kidney disease
- Endocrine causes: Cushing’s syndrome,
pheochromocytoma
- Cardiovascular causes: coarctation of aorta
- Neurological causes: psychogenic
- Medications/toxins: alcohol, drugs like corticosteroids,
NSAIDs
- Stress

10. Risk factors for HTN
- Genetic: runs in families
- Environmental factors like:
- Obesity
- Alcohol intake
- Sodium intake
- stress

11. Regulation of Normal Blood Pressure
- The major factors include age, sex, body mass index
and diet, particularly sodium intake, exertion, emotional
state and others.
- Blood pressure depends on two hemodynamic
variables, namely cardiac output and peripheral
vascular resistance

12. ● Cardiac output: It depends on stroke volume, and
heart rate. Stroke volume in turn is influenced by the
sodium homeostasis. Heart rate and contractility of
myocardium (affects stroke volume) are regulated by
the α- and β-adrenergic systems (also effects on
vascular tone).
● Peripheral vascular resistance: It is determined by
functional and anatomic changes in small arteries and
arterioles. Vascular tone depends on the balance
between vasoconstrictors and vasodilators. Blood
pressure is also influenced by tissue pH and hypoxia.

13. Role of Kidney
Renin-angiotensin system:
● Renin: Whenever there is a fall in blood pressure,
renin is secreted by the juxtaglomerular cells of the
kidney and released into the blood circulation.
● It breaks down plasma angiotensinogen to
angiotensin I, which is then converted to angiotensin
II by angiotensin converting enzyme.

14. ● Angiotensin II:
● It raises blood pressure by increasing both
peripheral resistance (direct action on vascular
smooth muscle cells and causes vasoconstriction)
● It raises blood volume (by stimulating secretion
of aldosterone by the adrenal zona glomerulosa,
and increased reabsorption of sodium in distal
tubules).

15. ● Sodium homeostasis and blood volume:
● When blood volume is reduced, the glomerular
filtration rate falls → leads to increased reabsorption of
sodium by proximal tubules of kidney → thereby
conserves sodium and expands blood volume.
● When blood volume is increased, natriuretic factors
(natriuretic peptides) are secreted by atrial and
ventricular myocardium. They inhibit sodium
reabsorption in distal tubules and cause excretion of
sodium and diuresis.
● Natriuretic peptides also cause vasodilation and may
be considered as endogenous inhibitors of the renin-
angiotensin system

16. Pathogenesis of Hypertension
● Complex and multifactorial disorder
● Decreased renal sodium excretion: It is probably the key
feature.
● Decreased excretion of sodium by kidney → leads to an
increase in fluid volume, cardiac output, and peripheral
vasoconstriction → raises the blood pressure.

17. ● Raised vascular resistance: Factors that
produce vasoconstriction or stimuli that cause
structural changes in the vessel wall → result in
an increase in peripheral vascular resistance →
cause primary hypertension.

18. ● Genetic factors: The genetic defects may be in the
enzymes involved in aldosterone metabolism,
sodium reabsorption and smooth muscle cell
growth.
● Environmental factors: These include stress,
obesity, smoking, lack of physical activity and
heavy intake of sodium salt.

19. Pathogenesis of Secondary Hypertension
Mechanism of renovascular hypertension:
● Renal artery stenosis → decreased glomerular flow and pressure in the
afferent arteriole of the glomerulus → stimulates renin secretion and
production of angiotensin II → vasoconstriction → increased
peripheral resistance.
● Renal artery stenosis also increases sodium reabsorption → increases
blood volume through the aldosterone mechanism.
● Primary hyperaldosteronism: It is one of the most common causes of
secondary hypertension.

21. Pathogenesis
- Decreased sodium excretion
- Impairment of renin-angiotensin-aldosterone system(RAAS)
- Increased sympathetic nervous system activation
- Increased total peripheral resistance
- Increased afterload on heart
- Development of hypertension

22. Pathology
Large and Medium Vessel Disease: Atherosclerosis
● Causes degenerative changes in the walls of large and
medium arteries.
● Predisposes to: (1) Aortic dissection and (2)
Cerebrovascular hemorrhage.

23. Small Vessel Diseases
Two forms can occur in hypertension: (1) Hyaline
arteriolosclerosis, and (2) hyperplastic arteriolosclerosis.
1. Hyaline arteriolosclerosis: It is seen in the arterioles
in patients with benign hypertension.
Microscopy: It shows thickening of the wall due to
homogeneous, pink hyaline material and narrowing of the
lumen

24. 2. Hyperplastic arteriolosclerosis: It occurs in severe
(malignant) hypertension.
Microscopy: The blood vessels show “onion-skin,”
concentric, laminated thickening of the arteriolar walls and
narrowing of the arteriolar lumen

25. Complications of HTN(Target Organ Damage)

26. CNS complications:
- Transient Ischemic Attack(TIA)
- Cerebrovascular accident(CVA) or stroke: due to cerebral
bleeding
- Subarachnoid hemorrhage(SAH)
- Hypertensive encephalopathy

27. Ophthalmic or retinal complications:
- Hypertensive retinopathy: arterioles become narrow
CVS complications:
- Coronary artery disease: angina, myocardial infarction
- Left ventricular failure
- Atrial fibrillation

28. Blood vessels complications:
- Atherosclerosis
- Aortic aneurysm
- Aortic dissection
Renal complications:
- Proteinuria
- Hematuria
- Renal failure

29. Accelerated or malignant hypertension
It is characterized by rapid raise in blood pressure (i.e.,
systolic pressure over 200 mm Hg, diastolic pressure
over 120 mm Hg) → renal failure, and retinal
hemorrhages and exudates, with or without papilledema.
● It may develop in normotensive individuals but more
common in patients with preexisting benign
hypertension (essential or secondary).
● It develops in ~5% of hypertensive persons. If not
treated, death occurs within a year or two.

30. For PPT, scan: For notes, click here or
scan:
References:
Ramadas Nayak - Prep Manual for Undergraduates - Pathology
Questions:
salman.s.ansari92@gmail.com