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HYPERTENSION
Roll No. : 46, 47, 48, 49, 50Teacher In charge : Dr. G.S. Ranga
Determinants of arterial pressure
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What is HYPERTENSION ?
Transitory or sustained elevation of systemic arterial blood pressure to a level likely to induce cardiovascular damage or other adverse consequences
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Classification of hypertension
Systolic Diastolic
Normal <120 And <80
Prehypertension 120-139 Or 80-89
Stage 1 hypertension 140-159 Or 90-99
Stage 2 hypertension >=160 Or >=100
Isolated systolic hypertension
>=140 <90
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Etiology of Hypertension
There are two types on the basis of etiology:
•Primary hypertension– 90-95% of cases – also termed “essential” of “idiopathic”
•Secondary hypertension– about 5% of cases
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Primary (Essential) hypertension
•Cause unknown•Tends to be familial•Is a polygenic disorder; different patients
carry different subsets of genes associated with obesity, dyslipidemia, insulin resistance, etc,
•Consequence of interaction between environment and genetic factors
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Risk factors for essential hypertension
•Old age•Smoking•Obesity•Excessive intake of salt•Alcohol consumption•Stress•Family history •Low dietary intake of vitamin D, calcium and
potassium
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Secondary hypertension
•A specific underlying disorder is the cause of hypertension
•Accounts for only 5 – 10% cases
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Causes of secondary hypertension
▫ Metabolic syndromes Dyslipidemia Insulin resistance
▫ Renal parenchymal or renovascular disease
▫ Obstructive sleep apnea▫ Preeclampsia and
eclampsia▫ Neurogenic causes
Acute increased intracranial pressure
Acute spinal cord section
Endocrine disease Phaeochomocytoma Cusings syndrome Conn’s syndrome Acromegaly , hypothyroidism and hyperthyroidism
Coarctation of the aorta Mendelian forms of hypertension Iatrogenic
Hormonal / oral contraceptive NSAIDs
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PATHOGENESIS OFHYPERTENSION
Roll no. 47 – Mohit Chhabra
• Local Regulation – Autoregulation, Vasodilator metabolites, Localized vasoconstriction
• Endothelial factors – NO, Endothelins, Prostacyclins and Thromboxane A2
• Systemic regulation by hormones – Kinins, Natriuretic hormones (ABC), circulating vasoconstrictors (vasopressin, norepinephrine, angiotensin II).
• Vasoconstrictive influences: Ion transport/ Endothelial factors
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Vascular Regulatory Mechanisms
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Increased Na+-H+ activity in the vessel wall
Increased intracellular Na+
Increased intracellular pH
Increased smooth muscle contractility and vasoconstriction
Vascular Regulatory Mechanisms
• Baroreceptors monitoring the arterial circulation are present in the carotid sinus and the aortic arch.
• Stimulated by distention/raised BP• Increased baroreceptor discharge inhibits
tonic discharge of the sympathetic nervous system
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Regulatory Mechanisms of the Autonomic Nervous System: Baroreceptors
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Action of Baroreceptors
Regulatory Mechanisms of the Autonomic Nervous System
Inhibition of RVLM/ Vasomotor Center
Inhibited α receptors on blood vessels
Inhibited β receptors in heart
Decreased HR & CO
Decreased PVR
Lowered Blood Pressure
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• Kidney regulates BP by two main mechanisms:1. Regulation of sodium and water homeostasis2. Renin-Angiotensin-Aldosterone-System
• Significant renal impairment is associated with hypertension in large part due to disturbance in sodium handling.
• Reduced renal perfusion leading to raised BP, relates to the activity of the Renin-Angiotensin-Aldosterone System.
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Regulatory Mechanisms of the Kidney
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Sodium Homeostasis
• There are 3 major stimuli for renin secretion:1. Decreased NaCl transport to the macula densa2. Decreased stretch within the renal afferent
arteriole (Baroreceptor mechanism)3. Stimulation of β1 adrenoreceptors in JG cells
• Other stimulatory factors – Prostaglandins• Other inhibitory factors – Angiotensin II,
Vasopressin
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Renin-Angiotensin-Aldosterone System
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Renin-Angiotensin-Aldosterone Axis
Increased activity of the renin-angiotensin-aldosterone axis is not
invariably associated with hypertension
• The main effector molecules of RAAS are Angiotensin II and Aldosterone.
• Angiotensin II acts on AT1 receptors:– In the adrenal cortex to release Aldosterone which
increases Na+ reabsorption by epithelial sodium channel (ENaC) on the collecting duct with resultant hypokalemia and alkalosis to maintain electric neutrality.
– In the arterioles to cause vasoconstriction
• AT2 receptor antagonizes AT1 by causing vasodilation and sodium excretion.
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Renin-Angiotensin-Aldosterone System
Main factors involved in the pathogenesis of hypertension are:•Genetic factors•Environmental and lifestyle influences•Impact of fetal and infant growth•Prehypertension•Renal mechanisms•Vascular mechanisms•Neurohumoral control systems
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Pathogenesis of Essential Hypertension
Genetic Factors
Gene Role
Angiotensinogen Substrate for Renin
ACE Converts AI to AII
Angiotensin II receptor Type I Vascular receptor for Angiotensin II
Aldosterone synthase Promotes aldosterone synthesis
ENaC in collecting duct (Liddle Syndrome) Site of action of aldosterone
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It is more likely that essential hypertension results from interactions of mutations or polymorphisms at several
loci that influence blood pressure
Lancet, 349, 1353-7
Environmental & Lifestyle Influences
• Dietary salt intake influences not only blood pressure but also cardiovascular disease outcomes. Sodium balance has an impact on blood pressure.
• Visceral adiposity seems important in defining the relationship between blood pressure and obesity.
• Alcohol intake – Intervention trials confirm that blood pressure falls when alcohol is withdrawn from heavy drinkers.
• Clear cut association between obstructive sleep apnea and hypertension.
• Psychosocial stress and blood pressure.
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Impact of fetal and infant growth
• Association between low birth weight and risk of developing hypertension.
• Inverse relationship between birth weight & gestational age with systolic BP.
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Prehypertension
• Annual rate of progression to hypertension is higher amongst pre-hypertensives.
• Prehypertension is also more common in people with diabetes
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• For most forms underlying pathways are well understood:
Pathogenesis of Secondary Hypertension
Secondary Hypertension
Renal diseases – Reno vascular diseases, Renin-producing tumors, AGN*
Endocrine – Cushing’s, Conn’s, Phaeochromocytoma, Hypo/hyperthyroidism
Cardiovascular – Coarctation of aorta
Neurologic – Raised ICP
* http://books.google.co.in/books?id=QfsjuUncJE0C&pg=PA147&lpg=PA147&dq=AGN+and+hypertension&source=bl&ots=MEsoSD5bTf&sig=lN_zKxoD1j5hXR7nKiGSZFlgCPs&hl=en&ei=VzOCTtYHo6mIB9avpf0O&sa=X&oi=book_result&ct=result&resnum=4&ved=0CDcQ6AEwAw#v=onepage&q=AGN%20and%20hypertension&f=false06:18 AM
SOURCES
Harrison’s Principles of Internal Medicine, 18/eRobbins and Cotran Pathologic Basis of Disease,
8/eOxford Textbook of Medicine, 5/eGanong’s Review of Medical Physiology, 23/ePrinciples of Pharmacology by KK Sharma, 2/e
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DIAGNOSIS OF HYPERTENSION
Roll no. 48 – Mohit Garg06:18 AM
• A complete history should be taken which assess the following points:
Duration Previous therapies Family history of hypertension and cardiovascular
diseasesDietary and psychosocial historyOther risk factors : weight change, dyslipidemia,
smoking, diabetes and physical activity Evidence of secondary hypertension: spells of
sweating, palpitations, tremors, erratic sleep and snoring etc.
History
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• Body habitus, including weight and height.
• At the initial examination, blood pressure should be measured in both arms
• Heart rate
• The neck should be palpated for an enlarged thyroid gland, and patients should be assessed for signs of hypo- and hyperthyroidism
• Examination of blood vessels
• Kidneys of patients with polycystic kidney disease may be palpable in the abdomen.
• The physical examination also should include evaluation for signs of CHF and a neurologic examination.
Physical Examination
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Measured using a sphygmomanometer
Seated quietly for 5 minutes
Centre of the cuff at the level of the heart.
Width of the bladder cuff should equal at least 40% of the arm circumference
the length of the cuff bladder should be enough to encircle at least 80% of the arm circumference
Inflate 20-30 mmHg above loss of radial pulse
Deflate at 2mmHg per second
Physical Examination
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Systolic Diastolic
Normal <120 And <80
Prehypertension 120-139 Or 80-89
Stage 1 hypertension 140-159 Or 90-99
Stage 2 hypertension >=160 Or >=100
Isolated systolic hypertension
>=140 <90
Classification of hypertension
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Laboratory Tests
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COMPLICATIONS OF HYPERTENSION
Roll no. 49 – Mohit Sharma
Complications of Hypertension
• Damage Heart - CHF, MI, Sudden death, angina
Kidneys - renal failure, proteinuria
Peripheral Vascular disease
CNS - Stroke, retina damage
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Cardiovascular complications
Heart
- Increased workload on left ventricle
Left ventricular hypertrophy
left ventricular failure.
- Greater thickness of left ventricle
decreased perfusion and ischaemia of
subendocardial region of myocardium.
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Consequences of Hypertension
• Cardiac - LVH
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Arteries
- Accelerated atherogenesis.
- risk of developing aortic dissecting aneurism.
Arterioles: Arteriolosclerosis
- Benign HT:
Deposition of eosinophilic (‘hyaline’) material in vessel
walls due to influx of plasma proteins.
- Malignant HT:
Thickening of intima.
Necrosis of vessel walls ('fibrinoid' necrosis) and
formation of micro-aneurisms in brain.06:18 AM
CNS Complications:- Rupture of micro-aneurisms of small penetrating
arteries Intracerebral haemorrhage.
- Risk of cerebral infarction due to atherosclerosis
of circle of Willis.
- Acute malignant HT: ‘Hypertensive encephalopathy’
due to cerebral oedema (headache, nausea and vomiting,
visual disturbances, seizures and disturbances of
consciousness).
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Consequences of Hypertension - CNS
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Peripheral vascular disease
Classical presentation : Intermittent claudication (aching pain in calves or
buttocks while walking that is relived by rest)
Ankle-brachial index:-Ratio of SBP ankle to arm- <0.90 : diagnostic
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Peripheral Vascular Disease
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Renal complications
Arteriolosclerosis
Ischaemic sclerosis of glomeruli and
tubular atrophy.
Proteinuria and microscopic haematuria,
especially in malignant HT .
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Consequences of Hypertension -Kidney
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Factors responsible:
-Vasoconstriction
-Vascular leakage: lead to flame shaped retinal hmg & retinal edema
-Arterioloscelerotic changes
Consequences of Hypertension - Retina
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Grading- Hypertensive retinopathy
Grade 1: subtle broadening of the arteriolar light reflex, mild generalized arteriolar
attenuation, particularly of small branches, and vein concealment Grade 2: obvious broadening of the arteriolar light reflex and deflection of veins at
arteriovenous crossings (Salus sign) Grade 3:-‘Copper-wiring’ of arterioles -Banking of veins distal to arteriovenous crossings (Bonnet sign)-Tapering of veins on both sides of the crossings (Gunn sign) and right-angled
deflection of veins.Grade 4: ‘Silver-wiring’ of arterioles & papilloedema associated with grade 3 changes
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Consequences of Hypertension - Retina
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MANAGEMENT OF HYPERTENSION
Roll no. 50 – Naman Bansal
Learning Objectives
• Who to treat?• When to treat?• How to treat?
Treatment options• Till when to treat?
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Goals of Treatment
1. Reduce cardiovascular and renal morbidity and mortality.
2. Obtain target BP goals of <140/90 mmHg or <130/80 mmHg with diabetes or renal disease.
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Classification of hypertension
Systolic Diastolic
Normal <120 And <80
Prehypertension 120-139 Or 80-89
Stage 1 hypertension 140-159 Or 90-99
Stage 2 hypertension >=160 Or >=100
Isolated systolic hypertension
>=140 <90
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High Risk for Adverse Prognosis
• Black Race• Male Sex• Persistent diastolic pressure >115 mmHg• Smoking• Diabetes Mellitus• Hypercholestrolemia• Obesity• Excess alcohol intake• Evidence of end organ damage
1.Cardiac2.Eyes3.Renal4.Nervous System
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JNC 7 Management Algorithm
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Pharmacologic Therapy
• Only agents shown to decrease morbidity and mortality related to CHD in major trials
• Decrease plasma volume and CO• Reduce peripheral vascular resistance• Most of anti-hypertensive effect at low
doses; biochemical effects are dose related
• Thiazides; loop; potassium sparing
Diuretics
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Diuretics
Adverse effects:• Electrolyte imbalance:
potassium, magnesium, sodium, calcium, uric acid, glucose
• Hypercholesterolemia
Diuretics
Useful in:• All populations• Isolated systolic hypertension• CHF• Renal insufficiency (loop diuretics if
CrCl < 30-50)• Combination with second drug
Beta Adrenergic Blockers
• Decrease HR, CO, renal blood flow• Inhibit vasoconstriction/decrease
peripheral resistance
Beta Adrenergic Blockers
Useful in:• Patients with LVH, angina,
tachycardia, anxiety, migraine, glaucoma
• Patients with CHD; provide significant protection against MI recurrence
Beta Adrenergic Blockers
Adverse effects:• CHF exacerbation acutely; AV block• Bronchospasm (in reversible disease)• CNS (lipid solubility)
o Propranolol, metoprolol >> atenolol
• ? Carbohydrate metabolism• ? Lipid metabolism
Angiotensin Converting Enzyme Inhibitors
• Block formation of angiotensin II• Promote vasodilation &
decrease aldosterone• Increase bradykinin &
vasodilatory PG’s
Angiotensin Converting Enzyme Inhibitors
Preferred in:• Congestive heart failure• Diabetes type I and II• Known coronary heart disease• At high risk for CHD• Nephropathy
Angiotensin Converting Enzyme InhibitorsAdverse effects:• Cough (5-15% of patients)• Skin rash, taste alterations (esp. Captopril)• Hyperkalemia• Hypotension, dizziness• Renal dysfunction (up to 35% inc in SCr)• Rare: angioedema (most frequent in African
Americans), neutropenia, proteinuria• Teratogenic
Angiotensin Receptor Blockers
• Losartan, valsartan, candesartan, et.al.
• No cough, rare angioedema• Less potent antihypertensive
effect--improves if combined with diuretic
• Teratogenic
Calcium Channel Blockers
• Peripheral vasodilators• Non-dihydropiridines: diltiazem,
verapamil• Dihydropiridines: amlodipine,
felodipine, isradipine, nicardipine, nifedipine, nisoldipine
• Short-acting dihydropiridines
Calcium Channel Blockers
Adverse effects:• Dizziness, headache, peripheral
edema• DHP’s: worse edema, flushing,
tachycardia, rash• Non-DHP’s: CHF exacerbation, AV
block, bradycardia, constipation
Calcium Channel Blockers
• Useful in: angina• Most effective in African Americans
as single drug therapy• In patients with DM, its use assoc.
with greater risk of MI compared with ACEI
Alpha Adrenergic Blockers
• Prazosin, terazosin, doxazosin• Can cause postural hypotension and
syncope• Use with caution in elderly• Useful in men with BPH
Central Sympatholytics
• Adverse effects: sedation, drowsiness, dry mouth, bradycardia, heart block
• Clonidine withdrawal: hypertension, headache, palpitations, perspiration
• Methyldopa: hepatitis, lupus-like syndrome, thrombocytopenia, hemolytic anemia
Direct Vasodilators
• Tachycardia can aggravate angina• Headache, dizziness, fluid retention• Hydralazine: lupus-like syndrome,
hepatitis• Minoxidil: hirsutism, pericardial
effusion
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