Hypertension – B. Pharma 2nd Semester Pathophysiology notes pdf


Hypertension - B. Pharma 2nd Semester Pathophysiology notes pdf


At the end of this PDF, student will be able to

         Define hypertension

         Classify various types of hypertension

         Explain the pathogenesis involved in the development of hypertension

        Describe the complications associated with the development of hypertension


Hypertension, often referred to as high blood pressure, is a chronic medical condition where the force of blood against the artery walls is consistently too high. This condition can lead to severe health problems if left unmanaged.

Persistently elevated arterial blood pressure [BP]

Associated with both functional and morphologic alteration of blood vessels

     Arterial BP – generated by the interplay between blood flow and the resistance to blood flow

     Measured in mmHg

2 types of arterial blood pressure

       Systolic BP (SBP)- achieved during cardiac contraction

       Diastolic BP (DBP)- achieved after contraction when the cardiac chambers are filling

SBP – DBP = pulse pressure (measure of arterial wall tension)

     Cardiac output – major determinant of SBP

     Total peripheral resistance determines DBP

       Mean arterial pressure [MAP] – Average pressure throughout the cardiac cycle of contraction

       During cardiac cycle 2/3rd time spent in diastole and 1/3rd time in systole

MAP= [SBP (1/3)] +[DBP (2/3)]

BP= Cardiac output × Total peripheral

Clinical classification of hypertension

Category Systolic (mm Hg) Diastolic (mm Hg)
Normal < 130 <85
High normal 130-139 85-89

     Mild (Stage 1)

140-159 90-99

     Moderate (Stage 2)

160-179 100-109

     Severe (Stage 3)

180-209 110-119

     Very severe (Stage 4)

≥ 210 ≥ 120
Malignant hypertension > 200 ≥ 140

Etiological classification of hypertension

A. Primary essential hypertension

      Genetic factors

     Racial and environmental factors

     Risk factors modifying the course  of HT

B. Secondary hypertension

     Renal – Renovascular

                              Renal parenchymal disease

       Endocrine –  Adrenocortical hyperfunction


Oral contraceptives

       Coarctation of aorta


Clinical classification of primary and secondary hypertension

Benign hypertension

       Observed in 95% of patients

       Slow rise in BP taking years to develop

Malignant/ accelerated hypertension

       Observed in 5-10% of patients

       Rapid rise in BP to 200/140 mm Hg or more

       If left untreated, patient’s life expectancy decreases

Symptoms of Hypertension

When BP is severe, following symptoms are observed

       Nose bleeding

       Irregular heart beat

       Head ache



      Flushed face

      Breathing difficulties

      Strong tendency to uinate

      Vertigo, tinnitus, etc.,

Malignant hypertension is characterized by

       Pulsating headache beneath the eye

       Visual disturbance

       Nausea and vomiting

       Disturbed sleep

Pathogenesis of Hypertension

BP is the product of

       Cardiac output

       Total peripheral vascular resistance

  • Cardiac output

 – Volume of blood that circulates through systemic blood vessels each minute

        Dependent on stroke volume (SV)

        SV – Volume of blood ejected by the left ventricle during each contraction

  • Peripheral resistance depends on

̶           Viscosity of blood

̶           Diameter of the blood vessel

̶           Compliance

       High viscosity – high pressure to pass through vascular bed

       High pressure to pass through constricted and non-complaint blood vessels

BP is controlled by

  • Neural component
  • Peripheral auto regulatory mechanism
  • Humoral mechanism
  • Vascular endothelial mechanism

Neural component

       Both CNS & ANS controls BP

Centers in CNS are

̶         Vasomotor center in Medulla

̶         Vagal nucleus

̶           Area postrema

̶          Nuclues tractus solitarii

̶            Maintenance of BP by sympathetic nervous system through α and β adrenergic receptors

++ post synaptic α1 receptors ―vasoconstriction ― ↑ BP

++ pre synaptic α2  receptors ― negative feedback on NA release

++ β1 in heart ― ↑ HR and contractility

++ β2 in arterioles and venules ― vasodilation

Change in BP senses by barro receptors in carotid artery and aortic arch

       Respond to change in arterial pressure

       Transmitted to brain through IX cranial nerve and vagus nerve

       ↑ discharge from barroreceptors − depression of vasomotor center − excitation of nucleus ambiguus − reverts change in BP

Peripheral auto regulatory mechanism

       Normal case – volume and pressure adaptive mechanism of kidney maintains BP

↓ BP – adaptation of kidney  ̶  more Na+ and H2O retention

↑BP  – adaptation of kidney  ̶  Na+ and H2O excretion –  ↓ blood volume & cardiac output

Humoral mechanism

  • Renin Angiotensin Aldosterone system
  • Natriuretic hormone
  • Insulin resistance and hyperinsulinemia

Renin-Angiotensin-aldosterone system

Renin-Angiotensin-aldosterone system

Natriuretic hormone

       Inhibits Na+ /K+ ATP ase

       Interferes with Na+ transport across cell membrane

       ↑ Na+ in body fluids – ↑ Natriuretic hormone  – ↑ urinary excretion of Na+ and H2O

       Blocks active transport of Na+ out of the walls of arterioles –  ↑ vascular tone and BP

Insulin resistance and hyper insulinemia

       Causes Na+ retention

       Increases sympathetic activity

       Increases vascular resistance

       Increases BP

Vascular endothelial mechanism

       Regulates blood vessel tone

       Vasodilating substances – Nitric oxide, Prostacyclin (PI2) and bradykinin – Hypotension

       Vasoconstrictors – Angiotensin II and Endothelin I – ↑BP

Effect of dietary Na+ Ca2+ K+ on BP

       ↑ intra cellular Ca2+ – alters smooth muscle function on blood vessels – ↑ Peripheral vascular resistance

       K+ depletion – ↑ Peripheral vascular resistance

       ↑ Na+ in body fluids & in arterial wall – ↑ BP

Complications of Hypertension

       Blood vessels
–  Large arterioles dialatess

                        – Smaller arterioles get damaged

       Eye – Arterial narrowing, haemmorhage

       Heart –  Hypertropy of left ventricles, heart failure

       Kidney – Nephrosclerosis, renal damage, death in uremia

       Brain – Rupture of damaged blood vessels, encephalopathy, cerebral edema


       Persistently elevated arterial blood pressure is called hypertension

       Hypertension can be classified as benign or malignant or accelerated hypertension

       HT can also be classifies as primary and secondary HT based on etiology

       BP is controlled by neuronal component, humoral mechanism, peripheral autoregultory mechanism and vascular endothelial mechanism

       Any defects in the functioning of these mechanisms leads to the development of HT

       HT is affects kidneys, blood vessels, brain and predisposed to many cardiovascular diseases

Frequently Asked Questions

  1. What is the leading cause of hypertension?
    • The exact cause of primary hypertension is often unknown, but it’s commonly linked to lifestyle factors, genetics, and age.
  2. Can hypertension be hereditary?
    • Yes, hypertension can run in families, making genetics a significant risk factor.
  3. What are the long-term complications of uncontrolled hypertension?
    • Uncontrolled hypertension can lead to heart disease, stroke, kidney damage, and vision problems.
  4. How is hypertension diagnosed?
    • Hypertension is diagnosed through repeated blood pressure measurements. High readings over time indicate the condition.
  5. Are there natural ways to manage hypertension without medication?
    • Yes, lifestyle modifications such as a heart-healthy diet and regular exercise can help manage hypertension without medication.

Hypertension – B. Pharma 2nd Semester Pathophysiology PDF Notes

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