changes in hypertension

1. HYPERTENSION
Dr Samiyah Syeed
Prof of Pathology
SABVMCRI

2. Introduction
• High blood pressure is a common
condition, afflicting 29% of the adult
population of the United States
• It is a major risk factor for myocardial
infarction, heart failure, stroke, dementia,
kidney disease, and progressive
atherosclerosis

3. Definition
JNC 7 (Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood
Pressure) Classification
BP
classification
Systolic BP
(mmHg)
Diastolic BP
(mmHg)
Normal <120 and <80
Pre-hypertension 120 - 139 or 80 - 89
Stage 1
hypertension
140 – 159 or 90 – 99
Stage 2
hypertension
> 160 or > 100

4. Causes of hypertension

5. Types and Causes of Hypertension
(Systolic and Diastolic)
1. Essential hypertension (90% to 95% of
cases)
2. Secondary hypertension
A) Renal
• Acute glomerulonephritis
• Chronic renal disease
• Polycystic disease
• Renal artery stenosis
• Renal vasculitis
• Renin-producing tumors

6. B) Endocrine
• Adrenocortical hyperfunction: Cushing syndrome,
primary aldosteronism, congenital adrenal
hyperplasia)
• Exogenous hormones: Glucocorticoids, oral
contraceptives
• Pheochromocytoma
• Acromegaly
• Hypothyroidism (myxedema)
• Hyperthyroidism (thyrotoxicosis)
• Pregnancy-induced

7. C) Cardiovascular
• Coarctation of aorta
• Polyarteritis nodosa
• Increased intravascular
volume
• Increased cardiac output
• Rigidity of the aorta
D) Neurologic
• Psychogenic
• Increased intracranial
pressure
• Sleep apnea
• Acute stress,
including surgery

8. Regulation of Normal Blood pressure

9. Role of Kidney

10. Pathogenesis of hypertension
Essential hypertension is a complex and multifactorial disorder.
1. 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.
2. Raised vascular resistance: Factors that produce vasoconstriction 
structural changes in the vessel wall → result in an increase in peripheral
vascular resistance → cause primary hypertension
3. Genetic factors: They play an important role in the development of
hypertension
4. Environmental factors: These include stress, obesity, smoking, lack of
physical activity and heavy intake of sodium salt.

11. Consequences of hypertension
1. Risk factor: Hypertension is one of the major modifiable risk factors for
atherosclerosis.
2. Lesions/diseases produced: Cardiac hypertrophy, congestive heart
failure and ischemic heart disease , multi-infarct dementia, aortic dissection,
stroke, subarachnoid hemorrhage, hypertensive encephalopathy, retinal
ischemia/ infarction and renal failure.
3. 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.
• develops in ~5%, of hypertensive persons. If not treated, death occurs
within a year or two

12. Comparison of benign and malignant
hypertension
Benign Malignant
Aetiology Usually essential if secondary,
commonly of endocrine type
A few cases arise out of benign essential.
Majority are secondary to renal disease
Age Benign younger than 45 years but is
prolonged into 6 and 7 decades
Young adults 25-35 years
Sex Female > Male Female = Male
Prevalence Very common – at least 15% of
population in western societies
Rare
Course Very slow – may years RAPID – months to 1-2 years
Blood
pressures
Diastolic 90-120 mm Hg very slow
rise
120+
Rapid rise
Arteries Accelerates
Arteriosclerosis;
Potentiates atheroma
Accelerates arteriosclerosis;
Causes intimal fibrous thickening
Hyaline thickening Fibroid necrosis of vessel wall and thrombosis,
especially affecting kidney and abdominal
viscera

13. • EFFECTS AND MAIN COMPLICATIONS IN VARIOUS ORGANS
• Effects and complication are proportional to the height of the blood pressure.
• Therefore drug treatment which lowers the BP lowers the incidence of complications, but
the diseased vessels do not return to normal and organ perfusion may be inadequate at
levels of BP which would usually be considered physiological.
• Modern drug therapy has greatly reduced the morbidity and mortality from malignant
hypertension.
Heart Hypertrophy of left ventricle Hypertrophy of left ventricle
± focal myocardial necrosis
Heart failure Common Acute heart failure
Cerebral
haemorrhage
Due to rupture of damaged artery –
30% of cases
Encephalopathy (fits and loss of
consciousness) due to cerebral oedema and
haemorrhage
Kidney Varying degree of nephrosclerosis but
usually not serious
Severe renal damage – death in uranemia
Eyes Arterial narrowing – retinal exudation Papilloedema; arterial narrowing; haemorrhage
and exudates.

14. Vascular pathology in hypertension
• Hypertension accelerates atherogenesis and
causes degenerative changes in the walls of large
and medium arteries that can lead to aortic
dissection and cerebrovascular hemorrhage.
Morphology
• Hypertension is associated with two forms of
small blood vessel disease:
1. Hyaline Arteriolosclerosis:
• Arterioles show homogeneous, pink hyaline
thickening with associated luminal narrowing.

15. 2. Hyperplastic Arteriosclerosis:
• Occurs in severe (malignant) hypertension;
• vessels exhibit "onion-skin lesions," characterized
by concentric, laminated thickening of the walls
and luminal narrowing .
• The laminations consist of smooth muscle cells
with thickened, reduplicated basement
membranes;
• In malignant hypertension they are accompanied
by fibrinoid deposits and vessel wall
necrosis (necrotizing arteriolitis), particularly in
the kidney.

16. Hyaline arteriosclerosis

17. Hyperplastic arteriosclerosis

18. Atherosclerosis

19. Left ventricular hypertrophy

20. Myocardial infarction

21. Aortic dissection

22. Intra cerebral hemorrhage

23. Cerebral infarct