HYPERTENSION
Dr Samiyah Syeed
Prof of Pathology
SABVMCRI
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
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
Causes of hypertension
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
B) Endocrine
• Adrenocortical hyperfunction: Cushing syndrome,
primary aldosteronism, congenital adrenal
hyperplasia)
• Exogenous hormones: Glucocorticoids, oral
contraceptives
• Pheochromocytoma
• Acromegaly
• Hypothyroidism (myxedema)
• Hyperthyroidism (thyrotoxicosis)
• Pregnancy-induced
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
Regulation of Normal Blood pressure
Role of Kidney
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.
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
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
• 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.
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.
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.
Hyaline arteriosclerosis
Hyperplastic arteriosclerosis
Atherosclerosis
Left ventricular hypertrophy
Myocardial infarction
Aortic dissection
Intra cerebral hemorrhage
Cerebral infarct

18.kidney in pregnancy, HTN.pptx

  • 1.
  • 2.
    Introduction • High bloodpressure 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 (JointNational 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.
  • 5.
    Types and Causesof 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 • Adrenocorticalhyperfunction: Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia) • Exogenous hormones: Glucocorticoids, oral contraceptives • Pheochromocytoma • Acromegaly • Hypothyroidism (myxedema) • Hyperthyroidism (thyrotoxicosis) • Pregnancy-induced
  • 7.
    C) Cardiovascular • Coarctationof 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 NormalBlood pressure
  • 9.
  • 10.
    Pathogenesis of hypertension Essentialhypertension 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 benignand 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 ANDMAIN 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 inhypertension • 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.
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