SlideShare a Scribd company logo
1 of 45
Download to read offline
HYPERTENSION
Dr. Ndungu J. R.
Systemic and local blood pressure must be tightly
regulated.
Although hypertension is a common health problem, it
typically remains asymptomatic until late in its course.
Hypertension contributes to the pathogenesis of
coronary heart disease and cerebrovascular
accidents, cause cardiac hypertrophy and heart
failure (hypertensive heart disease), aortic
dissection, and renal failure.
The mechanisms of hypertension in the vast
majority of people remain unknown; referred to as
"essential hypertension".
A sustained diastolic pressure greater than 90 mm
Hg, or a sustained systolic pressure in excess of
140 mm Hg, constitutes hypertension; systolic
blood pressure is more important than diastolic
blood pressure in determining cardiovascular risk.
Accurate Blood Pressure Measurement
 The equipment should be regularly inspected and validated.
 The operator should be trained and regularly retrained.
 The patient must be properly prepared and positioned and
seated quietly for at least 5 minutes in a chair.
 The auscultatory method should be used.
 Caffeine, exercise, and smoking should be avoided for at
least 30 minutes before BP measurement.
 An appropriately sized cuff should be used.
25% of individuals in the general population are
hypertensive.
The prevalence and vulnerability to complications
increase with age.
They are also higher in African .
Worldwide prevalence estimates for HTN may be as
much as 1 billion.
7.1 million deaths per year may be attributable to
hypertension.
Regulation of Blood Pressure
Blood pressure is a complex trait involving the
interaction of multiple genetic and environmental
factors that influence two hemodynamic variables:
cardiac output
peripheral vascular resistance
Cardiac output is affected by blood volume which
is strongly dependent on sodium concentrations.
Peripheral resistance is regulated predominantly
at the level of the arterioles and is influenced by
neural and hormonal inputs.
Normal vascular tone reflects an interplay
between circulating factors that induce
vasoconstriction (e.g., angiotensin II and
catecholamines) and vasodilation (e.g., kinins,
prostaglandins, and nitric oxide)
Resistance vessels also exhibit autoregulation.
Other local factors such as pH and hypoxia,
neural interactions (α- and β-adrenergic systems),
are also involved.
The kidneys (primarily) and adrenals (secondarily)
are central players in blood pressure regulation;
they interact with each other to modify vessel tone
and blood volume, as follows;
renin-angiotensin - aldosterone system
prostaglandins and nitric oxide
Atrial natriuretic peptide, secreted by heart atria in
response to volume expansion (e.g., in heart
failure) inhibits sodium reabsorption in distal
tubules and causes global vasodilation.
Pathogenesis of Hypertension
Ninety percent to 95% of hypertension is
idiopathic (essential hypertension), which is
compatible with long life.
Most of the remainder of "benign hypertension" is
secondary hypertension.
Classification
 Essential vs secondary HT
 Benign vs malignant HT
• Essential HT
90 - 95% of cases.
Pathogenetic mechanisms multifactorial and poorly
understood.
• Secondary HT
5 - 10% of cases.
Hypertension due to a recognisable disease.
About 5% of hypertensive persons show a rapidly
rising blood pressure that if untreated leads to
death within 1 or 2 years.
Termed accelerated or malignant hypertension.
The clinical syndrome is characterized by;
 severe hypertension (diastolic pressure over
120mmHg)
 renal failure
 retinal hemorrhages and exudates, with or
without papilledema.
Benign HT
- moderate increase in blood pressure.
- long clinical course.
- little clinical effects in early stages.
Malignant HT
- diastolic pressure > 130 mm Hg
- severe impact on cardiovascular system,
kidneys and central nervous system.
Malignant HT:
- May arise in previously normotensive individuals,
but
more commonly as a complication of benign HT.
- Relatively uncommon (1-5% of hypertensive
patients).
- Aggressive treatment is required.
Hypertensive Urgencies
 Severe elevated BP in the upper range of
stage II hypertension.
 Without progressive end-organ dysfunction.
 Examples: Highly elevated BP without severe
headache, shortness of breath or chest pain.
 Usually due to under-controlled HTN
Hypertensive Emergencies
 Severely elevated BP (>180/120mmHg).
 With progressive target organ dysfunction.
 Require emergent lowering of BP.
 Examples: Severely elevated BP with:
Hypertensive encephalopathy
Acute left ventricular failure with pulmonary edema
Acute MI or unstable angina pectoris
Dissecting aortic aneurysm
Types and Causes of secondary
Hypertension
RENAL
 Acute glomerulonephritis
 Chronic renal disease
 Polycystic disease
Renal artery stenosis
Renal vasculitis
Renin-producing tumors
Endocrine
- Adrenocortical hyperfunction/tumour (Cushing,
Conn)
- Exogenous glucocorticoids
- Pheochromocytoma
- Acromegaly
- Hyperthyroidism
- Pregnancy-induced
CARDIOVASCULAR
Coarctation of aorta
Polyarteritis nodosa
Increased intravascular volume
Increased cardiac output
Rigidity of the aorta
NEUROLOGIC
Psychogenic
Increased intracranial pressure
Sleep apnea
Acute stress, including surgery
Secondary HTN-Clues in Medical
History
 Onset: at age < 30 yrs ( Fibromuscular dysplasia) or
> 55 (athelosclerotic renal artery stenosis), sudden
onset (thrombus or cholesterol embolism).
 Severity: Grade II, unresponsive to treatment.
 Episodic, headache and chest pain/palpitation
(pheochromocytoma, thyroid dysfunction).
 Morbid obesity with history of snoring and daytime
sleepiness (sleep disorders)
Secondary HTN-clues on Exam
 Pallor, edema, other signs of renal disease.
 Abdominal bruit especially with a diastolic
component (renovascular)
 Truncal obesity, purple striae, buffalo hump
(hypercortisolism)
Secondary HTN-Clues on Routine Labs
 Increased creatinine, abnormal urinalysis
( renovascular and renal parenchymal
disease)
 Unexplained hypokalemia
(hyperaldosteronism)
 Impaired blood glucose
( hypercortisolism)
 Impaired TFT (Hypo-/hyper- thyroidism)
Essential Hypertension
Both increased blood volume and increased
peripheral resistance contribute to the increased
pressure.
Essential hypertension results from an interplay
of multiple genetic and environmental factors
affecting cardiac output and/or peripheral
resistance.
Essential hypertension is associated with:
-  peripheral vascular resistance
(pathogenesis poorly understood)
- Sodium and water retention
  blood volume,  cardiac output
Genetic variants in the renin-angiotensin system
may contribute to the known racial differences in
blood pressure regulation.
Environmental factors; stress, obesity, smoking,
physical inactivity, and heavy consumption of salt
Vascular Pathology in Hypertension
Hyaline Arteriolosclerosis. consists of a
homogeneous pink hyaline thickening of the walls
of arterioles with loss of underlying structural
detail and with narrowing of the lumen
Hyperplastic Arteriolosclerosis; associated with
"onion-skin," concentric, laminated thickening of
the walls of arterioles with luminal narrowing.
Characteristic of (but not limited to) malignant
hypertension.
In malignant hypertension, these hyperplastic
changes are accompanied by fibrinoid necrosis.
Complications of systemic HT
 Cardiovascular
 CNS
 Renal
Eyes
Cardiovascular
 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.
Arrhithymias
Coronary artery disease, Acute MI
Arterial aneurysm, dissection, and rupture.
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 (of Bouchard) in brain.
CNS
- 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).
Renal complications
Arteriolosclerosis
 Ischaemic sclerosis of glomeruli and
tubular atrophy.
Proteinuria and microscopic haematuria,
especially in malignant HT .
The Eyes
 Retinopathy, retinal hemorrhages and
impaired vision.
 Vitreous hemorrhage, retinal detachment
 Neuropathy of the nerves leading to
extraoccular muscle paralysis and dysfunction
Patient Evaluation Objectives
 (1) To assess lifestyle and identify other
cardiovascular risk factors or concomitant disorders
that may affect prognosis and guide treatment
 (2) To reveal identifiable causes of high BP
 (3) To assess the presence or absence of target
organ damage and CVD
Cardiovascular Risk factors
 Hypertension
 Cigarette smoking
 Obesity (body mass index ≥30 kg/m2)
 Physical inactivity
 Dyslipidemia
 Diabetes mellitus
 Microalbuminuria or estimated GFR <60 mL/min
 Age (older than 55 for men, 65 for women)
 Family history of premature cardiovascular disease (men
under age 55 or women under age 65)

More Related Content

What's hot

Secondary hypertension
Secondary hypertensionSecondary hypertension
Secondary hypertension
raj kumar
 
INTERNAL MEDICINE - Secondary Hypertension
INTERNAL MEDICINE - Secondary HypertensionINTERNAL MEDICINE - Secondary Hypertension
INTERNAL MEDICINE - Secondary Hypertension
Nian Baring
 

What's hot (20)

Bartter’S And Gittleman’S Syndromes
Bartter’S And Gittleman’S SyndromesBartter’S And Gittleman’S Syndromes
Bartter’S And Gittleman’S Syndromes
 
Right and left ventricular hypertrophy
Right and left ventricular hypertrophyRight and left ventricular hypertrophy
Right and left ventricular hypertrophy
 
Hypertension
HypertensionHypertension
Hypertension
 
Secondary hypertension
Secondary hypertensionSecondary hypertension
Secondary hypertension
 
Hypertension and renal diseases
Hypertension and renal diseasesHypertension and renal diseases
Hypertension and renal diseases
 
secondary hypertension
secondary hypertensionsecondary hypertension
secondary hypertension
 
Diabete coma
Diabete comaDiabete coma
Diabete coma
 
Hypertension, its causes, types and management
Hypertension, its causes, types and managementHypertension, its causes, types and management
Hypertension, its causes, types and management
 
Hypertension lecture
Hypertension lecture Hypertension lecture
Hypertension lecture
 
Hypertension
HypertensionHypertension
Hypertension
 
INTERNAL MEDICINE - Secondary Hypertension
INTERNAL MEDICINE - Secondary HypertensionINTERNAL MEDICINE - Secondary Hypertension
INTERNAL MEDICINE - Secondary Hypertension
 
Heart failure basics
Heart failure basicsHeart failure basics
Heart failure basics
 
Hypertension
HypertensionHypertension
Hypertension
 
Cardiorenal syndromes and management
Cardiorenal syndromes and managementCardiorenal syndromes and management
Cardiorenal syndromes and management
 
Heart Failure Approach class.pptx
Heart Failure Approach class.pptxHeart Failure Approach class.pptx
Heart Failure Approach class.pptx
 
End organ damages of hypertension 2
End organ damages of hypertension 2End organ damages of hypertension 2
End organ damages of hypertension 2
 
ATRIAL FIBRILLATION 2016
ATRIAL FIBRILLATION 2016ATRIAL FIBRILLATION 2016
ATRIAL FIBRILLATION 2016
 
Secondary hypertension by dr Raj kishor
Secondary hypertension by dr Raj kishor Secondary hypertension by dr Raj kishor
Secondary hypertension by dr Raj kishor
 
Hyperaldosteronism
HyperaldosteronismHyperaldosteronism
Hyperaldosteronism
 
2018 ESC/ESH Guidelines for the management of arterial hypertension
2018 ESC/ESH Guidelines for the management of arterial hypertension2018 ESC/ESH Guidelines for the management of arterial hypertension
2018 ESC/ESH Guidelines for the management of arterial hypertension
 

Similar to HYPERTENSION

PATHOLOGY OF HYPERTENSION .ppt
PATHOLOGY OF HYPERTENSION           .pptPATHOLOGY OF HYPERTENSION           .ppt
PATHOLOGY OF HYPERTENSION .ppt
Imtiyaz60
 
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
imrana tanvir
 
HTN CRISIS SEMINER.pptx
HTN CRISIS SEMINER.pptxHTN CRISIS SEMINER.pptx
HTN CRISIS SEMINER.pptx
ImanuIliyas
 

Similar to HYPERTENSION (20)

PATHOLOGY OF HYPERTENSION .ppt
PATHOLOGY OF HYPERTENSION           .pptPATHOLOGY OF HYPERTENSION           .ppt
PATHOLOGY OF HYPERTENSION .ppt
 
10 hypertension
10 hypertension10 hypertension
10 hypertension
 
Hypertension
HypertensionHypertension
Hypertension
 
Internal Medicine Lecture 1 Arterial Hypertension.pptx
Internal Medicine Lecture 1 Arterial Hypertension.pptxInternal Medicine Lecture 1 Arterial Hypertension.pptx
Internal Medicine Lecture 1 Arterial Hypertension.pptx
 
Management of hypertensive crisis
Management of hypertensive crisisManagement of hypertensive crisis
Management of hypertensive crisis
 
Mgt of htn crisis by gelaye
Mgt of htn crisis  by gelayeMgt of htn crisis  by gelaye
Mgt of htn crisis by gelaye
 
Lect_Bloo_vesp.ppt
Lect_Bloo_vesp.pptLect_Bloo_vesp.ppt
Lect_Bloo_vesp.ppt
 
hypertension.docx
hypertension.docxhypertension.docx
hypertension.docx
 
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
L5 &amp; 6 effects of htn on vessels &amp; heart 20 (2)
 
HTN CRISIS SEMINER.pptx
HTN CRISIS SEMINER.pptxHTN CRISIS SEMINER.pptx
HTN CRISIS SEMINER.pptx
 
18.kidney in pregnancy, HTN.pptx
18.kidney in pregnancy, HTN.pptx18.kidney in pregnancy, HTN.pptx
18.kidney in pregnancy, HTN.pptx
 
Hypertension
HypertensionHypertension
Hypertension
 
Htn
HtnHtn
Htn
 
Pathology of Hypertension
Pathology of HypertensionPathology of Hypertension
Pathology of Hypertension
 
Hypertensive Emergencies
Hypertensive EmergenciesHypertensive Emergencies
Hypertensive Emergencies
 
CVS pathology -4 Hypertension (HTN) 2019, sufia husain
CVS pathology -4 Hypertension (HTN) 2019, sufia husainCVS pathology -4 Hypertension (HTN) 2019, sufia husain
CVS pathology -4 Hypertension (HTN) 2019, sufia husain
 
Hypertension - Approach & Management
Hypertension - Approach & ManagementHypertension - Approach & Management
Hypertension - Approach & Management
 
Hypertension
HypertensionHypertension
Hypertension
 
Hypertension
HypertensionHypertension
Hypertension
 
Hypertension
HypertensionHypertension
Hypertension
 

Recently uploaded

💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
Sheetaleventcompany
 
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
Sheetaleventcompany
 
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
Sheetaleventcompany
 
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Sheetaleventcompany
 
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
Sheetaleventcompany
 
Difference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac MusclesDifference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac Muscles
MedicoseAcademics
 
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Sheetaleventcompany
 

Recently uploaded (20)

tongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacytongue disease lecture Dr Assadawy legacy
tongue disease lecture Dr Assadawy legacy
 
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
💰Call Girl In Bangalore☎️7304373326💰 Call Girl service in Bangalore☎️Bangalor...
 
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
💚Chandigarh Call Girls Service 💯Piya 📲🔝8868886958🔝Call Girls In Chandigarh No...
 
❤️Call Girl Service In Chandigarh☎️9814379184☎️ Call Girl in Chandigarh☎️ Cha...
❤️Call Girl Service In Chandigarh☎️9814379184☎️ Call Girl in Chandigarh☎️ Cha...❤️Call Girl Service In Chandigarh☎️9814379184☎️ Call Girl in Chandigarh☎️ Cha...
❤️Call Girl Service In Chandigarh☎️9814379184☎️ Call Girl in Chandigarh☎️ Cha...
 
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
Goa Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Goa No💰Advanc...
 
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
Call Girls in Lucknow Just Call 👉👉8630512678 Top Class Call Girl Service Avai...
 
Chennai ❣️ Call Girl 6378878445 Call Girls in Chennai Escort service book now
Chennai ❣️ Call Girl 6378878445 Call Girls in Chennai Escort service book nowChennai ❣️ Call Girl 6378878445 Call Girls in Chennai Escort service book now
Chennai ❣️ Call Girl 6378878445 Call Girls in Chennai Escort service book now
 
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
Call Girls in Lucknow Just Call 👉👉 8875999948 Top Class Call Girl Service Ava...
 
Race Course Road } Book Call Girls in Bangalore | Whatsapp No 6378878445 VIP ...
Race Course Road } Book Call Girls in Bangalore | Whatsapp No 6378878445 VIP ...Race Course Road } Book Call Girls in Bangalore | Whatsapp No 6378878445 VIP ...
Race Course Road } Book Call Girls in Bangalore | Whatsapp No 6378878445 VIP ...
 
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service AvailableCall Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
Call Girls Rishikesh Just Call 9667172968 Top Class Call Girl Service Available
 
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
💚Reliable Call Girls Chandigarh 💯Niamh 📲🔝8868886958🔝Call Girl In Chandigarh N...
 
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
❤️Amritsar Escorts Service☎️9815674956☎️ Call Girl service in Amritsar☎️ Amri...
 
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
❤️Chandigarh Escorts Service☎️9814379184☎️ Call Girl service in Chandigarh☎️ ...
 
ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptxANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx
ANATOMY AND PHYSIOLOGY OF REPRODUCTIVE SYSTEM.pptx
 
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
Premium Call Girls Dehradun {8854095900} ❤️VVIP ANJU Call Girls in Dehradun U...
 
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
Bhawanipatna Call Girls 📞9332606886 Call Girls in Bhawanipatna Escorts servic...
 
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
Pune Call Girl Service 📞9xx000xx09📞Just Call Divya📲 Call Girl In Pune No💰Adva...
 
Difference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac MusclesDifference Between Skeletal Smooth and Cardiac Muscles
Difference Between Skeletal Smooth and Cardiac Muscles
 
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Kathua Just Call 8250077686 Top Class Call Girl Service Available
 
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
Kolkata Call Girls Service ❤️🍑 9xx000xx09 👄🫦 Independent Escort Service Kolka...
 

HYPERTENSION

  • 2. Systemic and local blood pressure must be tightly regulated. Although hypertension is a common health problem, it typically remains asymptomatic until late in its course.
  • 3. Hypertension contributes to the pathogenesis of coronary heart disease and cerebrovascular accidents, cause cardiac hypertrophy and heart failure (hypertensive heart disease), aortic dissection, and renal failure.
  • 4. The mechanisms of hypertension in the vast majority of people remain unknown; referred to as "essential hypertension".
  • 5. A sustained diastolic pressure greater than 90 mm Hg, or a sustained systolic pressure in excess of 140 mm Hg, constitutes hypertension; systolic blood pressure is more important than diastolic blood pressure in determining cardiovascular risk.
  • 6. Accurate Blood Pressure Measurement  The equipment should be regularly inspected and validated.  The operator should be trained and regularly retrained.  The patient must be properly prepared and positioned and seated quietly for at least 5 minutes in a chair.  The auscultatory method should be used.  Caffeine, exercise, and smoking should be avoided for at least 30 minutes before BP measurement.  An appropriately sized cuff should be used.
  • 7. 25% of individuals in the general population are hypertensive. The prevalence and vulnerability to complications increase with age. They are also higher in African .
  • 8. Worldwide prevalence estimates for HTN may be as much as 1 billion. 7.1 million deaths per year may be attributable to hypertension.
  • 9. Regulation of Blood Pressure Blood pressure is a complex trait involving the interaction of multiple genetic and environmental factors that influence two hemodynamic variables: cardiac output peripheral vascular resistance
  • 10. Cardiac output is affected by blood volume which is strongly dependent on sodium concentrations. Peripheral resistance is regulated predominantly at the level of the arterioles and is influenced by neural and hormonal inputs.
  • 11. Normal vascular tone reflects an interplay between circulating factors that induce vasoconstriction (e.g., angiotensin II and catecholamines) and vasodilation (e.g., kinins, prostaglandins, and nitric oxide)
  • 12. Resistance vessels also exhibit autoregulation. Other local factors such as pH and hypoxia, neural interactions (α- and β-adrenergic systems), are also involved.
  • 13. The kidneys (primarily) and adrenals (secondarily) are central players in blood pressure regulation; they interact with each other to modify vessel tone and blood volume, as follows; renin-angiotensin - aldosterone system prostaglandins and nitric oxide
  • 14. Atrial natriuretic peptide, secreted by heart atria in response to volume expansion (e.g., in heart failure) inhibits sodium reabsorption in distal tubules and causes global vasodilation.
  • 15. Pathogenesis of Hypertension Ninety percent to 95% of hypertension is idiopathic (essential hypertension), which is compatible with long life. Most of the remainder of "benign hypertension" is secondary hypertension.
  • 16. Classification  Essential vs secondary HT  Benign vs malignant HT • Essential HT 90 - 95% of cases. Pathogenetic mechanisms multifactorial and poorly understood. • Secondary HT 5 - 10% of cases. Hypertension due to a recognisable disease.
  • 17. About 5% of hypertensive persons show a rapidly rising blood pressure that if untreated leads to death within 1 or 2 years. Termed accelerated or malignant hypertension.
  • 18. The clinical syndrome is characterized by;  severe hypertension (diastolic pressure over 120mmHg)  renal failure  retinal hemorrhages and exudates, with or without papilledema.
  • 19. Benign HT - moderate increase in blood pressure. - long clinical course. - little clinical effects in early stages. Malignant HT - diastolic pressure > 130 mm Hg - severe impact on cardiovascular system, kidneys and central nervous system.
  • 20. Malignant HT: - May arise in previously normotensive individuals, but more commonly as a complication of benign HT. - Relatively uncommon (1-5% of hypertensive patients). - Aggressive treatment is required.
  • 21. Hypertensive Urgencies  Severe elevated BP in the upper range of stage II hypertension.  Without progressive end-organ dysfunction.  Examples: Highly elevated BP without severe headache, shortness of breath or chest pain.  Usually due to under-controlled HTN
  • 22. Hypertensive Emergencies  Severely elevated BP (>180/120mmHg).  With progressive target organ dysfunction.  Require emergent lowering of BP.  Examples: Severely elevated BP with: Hypertensive encephalopathy Acute left ventricular failure with pulmonary edema Acute MI or unstable angina pectoris Dissecting aortic aneurysm
  • 23. Types and Causes of secondary Hypertension RENAL  Acute glomerulonephritis  Chronic renal disease  Polycystic disease Renal artery stenosis Renal vasculitis Renin-producing tumors
  • 24.
  • 25. Endocrine - Adrenocortical hyperfunction/tumour (Cushing, Conn) - Exogenous glucocorticoids - Pheochromocytoma - Acromegaly - Hyperthyroidism - Pregnancy-induced
  • 26. CARDIOVASCULAR Coarctation of aorta Polyarteritis nodosa Increased intravascular volume Increased cardiac output Rigidity of the aorta
  • 28. Secondary HTN-Clues in Medical History  Onset: at age < 30 yrs ( Fibromuscular dysplasia) or > 55 (athelosclerotic renal artery stenosis), sudden onset (thrombus or cholesterol embolism).  Severity: Grade II, unresponsive to treatment.  Episodic, headache and chest pain/palpitation (pheochromocytoma, thyroid dysfunction).  Morbid obesity with history of snoring and daytime sleepiness (sleep disorders)
  • 29. Secondary HTN-clues on Exam  Pallor, edema, other signs of renal disease.  Abdominal bruit especially with a diastolic component (renovascular)  Truncal obesity, purple striae, buffalo hump (hypercortisolism)
  • 30. Secondary HTN-Clues on Routine Labs  Increased creatinine, abnormal urinalysis ( renovascular and renal parenchymal disease)  Unexplained hypokalemia (hyperaldosteronism)  Impaired blood glucose ( hypercortisolism)  Impaired TFT (Hypo-/hyper- thyroidism)
  • 31. Essential Hypertension Both increased blood volume and increased peripheral resistance contribute to the increased pressure. Essential hypertension results from an interplay of multiple genetic and environmental factors affecting cardiac output and/or peripheral resistance.
  • 32. Essential hypertension is associated with: -  peripheral vascular resistance (pathogenesis poorly understood) - Sodium and water retention   blood volume,  cardiac output
  • 33. Genetic variants in the renin-angiotensin system may contribute to the known racial differences in blood pressure regulation. Environmental factors; stress, obesity, smoking, physical inactivity, and heavy consumption of salt
  • 34. Vascular Pathology in Hypertension Hyaline Arteriolosclerosis. consists of a homogeneous pink hyaline thickening of the walls of arterioles with loss of underlying structural detail and with narrowing of the lumen
  • 35. Hyperplastic Arteriolosclerosis; associated with "onion-skin," concentric, laminated thickening of the walls of arterioles with luminal narrowing. Characteristic of (but not limited to) malignant hypertension. In malignant hypertension, these hyperplastic changes are accompanied by fibrinoid necrosis.
  • 36.
  • 37. Complications of systemic HT  Cardiovascular  CNS  Renal Eyes
  • 38. Cardiovascular  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.
  • 39. Arrhithymias Coronary artery disease, Acute MI Arterial aneurysm, dissection, and rupture.
  • 40. 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 (of Bouchard) in brain.
  • 41. CNS - 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).
  • 42. Renal complications Arteriolosclerosis  Ischaemic sclerosis of glomeruli and tubular atrophy. Proteinuria and microscopic haematuria, especially in malignant HT .
  • 43. The Eyes  Retinopathy, retinal hemorrhages and impaired vision.  Vitreous hemorrhage, retinal detachment  Neuropathy of the nerves leading to extraoccular muscle paralysis and dysfunction
  • 44. Patient Evaluation Objectives  (1) To assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment  (2) To reveal identifiable causes of high BP  (3) To assess the presence or absence of target organ damage and CVD
  • 45. Cardiovascular Risk factors  Hypertension  Cigarette smoking  Obesity (body mass index ≥30 kg/m2)  Physical inactivity  Dyslipidemia  Diabetes mellitus  Microalbuminuria or estimated GFR <60 mL/min  Age (older than 55 for men, 65 for women)  Family history of premature cardiovascular disease (men under age 55 or women under age 65)