Hypertension can be classified into either essential or secondary.
Essential Hypertension: No specific medical cause can be found to explain the patient's condition. However, there appears to be a relationship with high blood pressure and many other factors. Some of these include: Genetic factors: High blood pressure tends to run in families. This may be explained, at least, by shared environmental influences. However, there is still a prominent, unidentifiable genetic component. Fetal factors: Low birth weight is associated with subsequent high blood pressure. Environmental factors: Obesity, high alcohol intake, high sodium intake and stress can raise blood pressure. Insulin Resistance: A positive correlation between diabetes and hypertension has long been recognised. It also known as metabolic syndrome and is a major risk factor for cardiovascular disease.
Secondary Hypertension: Hypertension which results from an underlying, identifiable, usually correctable cause. (5-10% of hypertensive patients)
A mnemonic to help remember some possible secondary causes hypertension is ABCDE A: apnoea, aldosteronism B: bruits, bad kidneys C: coarctation of the aorta, Cushing’s syndrome D: diet, drugs E: erythropoietin, endocrine disturbances
Apnoea: Obstructive Sleep Apnoea (OSA) is a mechanical problem in the upper airway during sleep. Half of patients have hypertension caused by various mechanisms such as sympathetic activation.
Aldosteronism: Over productivity of aldosterone (by the adrenal cortex) which results in over-retention of salt and water. Increases K+ secretion in the urine and detection of elevated aldosterone in relation to plasma renin can diagnose this.
Bruits: (Renal Vascular hypertension) When there is hypertension caused by a compromised artertial supply to the kidneys. Many of these patients will have an abdominal bruit (abnormal sound reflecting turbulent flow) on examination.
Bad kidneys: (Renal parachymal disease)can be a cause of consequence of hypertension. Progressive renal disease interferes with kidneys ability to excrete Na+ and excess fluid. Diagnosed by increased serum creatine levels and decreased urine creatine clearance. Treatment with ACE inhibitors protects kidney function.
Coarctation of the aorta: congenital narrowing of the aortic lumen. Most often occurs just distal to the branch of the left subclavian. Diagnosed by high upper extremity blood pressure and weak lower extremity pulses and the “3 sign” (dilation of the aorta above and below the stenosis)
Cushing’s: hypertensive effects of increased corticosteroirds.
Diet: -high salt (increased water retention) -overweight people have a higher incidence of hypertension
Erythropoietin: Increased EPO levels can be endogenous ( EPO production in chronic hypoxia ie. COPD) or exogenous (to treat anemia). It leads to hypertension by increasing blood viscosity.
Endocrine disorders: HypOthyroidism causes decreased cardiac output with a increase in vascular tone to compensate (INCREASED DIASTOLIC MORE MARKED). HypErthyroidism also causes hypertension by increasing cardiac output. (INCREASED SYSTOLIC MORE MARKED) Preganancy also causes hypertension (causes not fully understood)
References: Kumar and Clark, Wikipedia, http://www.aafp.org/afp/20030101/67.html (American Academy of Family Physicians-article by Edward Onusko)
angela said.... Definition: Persistently high arterial blood pressure Measured after 5 minutes resting (seated) is usually sufficient (standing for testing of orthostatic hypotension however) Measured to the nearest 2mmHg Two consistent measurements should be taken, more if inconsistent When assessing CV risk: average from several visits is more accurate than single visit
From the WHO-International society for hypertension (based on clinical BP): Grade 1 (mild): systolic: 140-149, diastolic: 90-99 i.e.: 140/90+ Grade 2 (moderate): systolic: 160-179, diastolic: 100-109 i.e.: 160/100+ Grade 3 (severe): systolic: ≥180, diastolic: ≥100 If systolic and diastolic fall in different categories, the higher value is taken Threshold for home/self monitoring: higher than 135/85mmHg For ambulatory monitoring: higher than 125/80mmHg Primary hypertension: no known cause Secondary hypertension: associated with other diseases
Incidence: From 1999-2000: Men aged 25+: 30.5% (age-standardised: 32.3%) Men aged 65-74: 69.4% Men aged 75+: 78.8% Women aged 25+: 27.3% (age-standardised: 27.2%) Women aged 65-74: 66.8% Women aged 75+: 74.6% From: AIHW analysis of the 1980, 1983 & 1989 Risk Factor Prevalence Surveys; 1995 National Nutrition Survey; 1999–2000 Australian Diabetes, Obesity and Lifestyle (AusDiab) study.
Sorry! I wasn’t able to find any data on the separate incidences of primary and secondary hypertension!
Research Topic: Investigations required to exclude secondary causes of Hypertension.
It is not necessarily required for the doctor to prescribe numerous investigations. The usual tests include: 1) Measuring sugar and creatine levels. 2) Urine analysis.
•There are many investigations that can be undertaken in order to eliminate the secondary causes of Hypertension. So in order to keep it simple, I will only expand on those tests relevant to this case. •Some drugs, like diuretics, ARBs, and ACE inhibitors, can modify the concentration of potassium in the blood (kaliemia) and the functioning of the kidneys. This warrants a blood test to measure the level of minerals in the blood (blood electrolytes).
For Renal System: •Blood test to monitor sugar and creatine levels in order to diagnose Diabetic Nephropathy or Glomerular disease (defective purification of kidneys). •Urine test- 1) Looking for blood in the urine is carried out with a dipstick. If the dipstick is positive, the result is confirmed by a microscope examination of the urine. 2) Looking for albumin in the urine (proteinuria or albuminuria) is also carried out with a dipstick. If it is positive, it may be necessary to measure the level in the urine over 24 hours. 3) Check urine output as patient could be suffering from Hydronephrosis where certain parts of one or both kidneys become plugged, thus blocking urine flow and raising blood pressure. •Ultrasound Examination – Patients can undergo a renal ultrasound or Doppler Ultrasonography of their arteries in order to eliminate the possibility of Polycystic Kidney disease (which may be inherited, so check family history) or Renovascular Hypertension which may be caused by stenosis of the renal arteries due to build-up of fatty plaque.
For Adrenal Glands: •Blood test – In order to monitor the level of a) Cortisol secretion as an excess may raise blood pressure and is as a result of Cushing’s syndrome (Corticosteroids, pituitary tumour may overstimulate adrenals). b) Aldosterone secretion by the adrenals due to the presence of a tumour or increased growth of normal cells which forces the kidneys to retain salt and water and loose too much potassium. This causes an increase in blood pressure. c) Noradrenaline and adrenaline which again can be a result of tumours (Pheochromocytoma) on the adrenals and also results in raised blood pressure levels.
For Thyroid Glands: •Blood test – In order to monitor the levels of thyroxine secretion. Too little can cause Hypothyroidism and too much can cause Hyperthyroidism (where the activity of epinephrine and norepinephrine is increased), with both cases resulting in an increase in blood pressure.
For Parathyroid Glands: •Blood test – The parathyroid glands regulate levels of calcium and phosphorus in the body. Increased secretion of the parathyroid hormone raises the amount of calcium in the blood, thus raising blood pressure.
The Kidneys As the kidneys are responsible for long-term regulation of blood pressure, it is important to examine their function in hypertension. Renal flow impairment is usually a good indication of hypertensive damage. - Radio-marked flow markers injected into arteries - Gold standard – insulin - EDTA and DTPA can also be used - Measure either rate of elimination from plasma, or excretion into urine.
The Eye The blood vessels in the eye are both highly sensitive, and visible without surgery, and as such are a good place to get an indication of possible systemic hypertensive damage. Opthalmoscopic examination of the eye can reveal signs of possible hypertensive damage: Retinal arterioles: - Generalised and focal narrowing - Irregularity and tortuosity - Increased light reflex - Loss of transparency Veins become indistinct where crossing behind arteries Retinal haemorrhage Retinal white spots Macular oedema Macular stars Blurring of optic disc margins Papilloedema
The Brain Cerebral circulation is not usually affected by hypertension - Adaptation prevents excessive blood flow to brain - Vascular hypertrophy and remodelling This adaptation, however, can decrease the range of the vasodilator reflex due to encroachment on the vascular lumen If the adaptation fails in any way, it can result in: - Hypertensive encephalopathy - Cerebral haemorrhage - Ischaemic stroke
We would obviously want to prevent this, so if hypertensive adaptation is suspected we can perform a cerebral angiography Detects vascular hypertrophy - Risky procedure - Allows us time to treat hypertension and hopefully reverse effects Sudden drops in blood pressure can cause cerebral hypoxia as vasculature has adapted to hypertension – treatment needs to be gradual.
Essential hypertension: The pathophysiology of essential hypertension is not entirely understood, it appears that it results from a complex mix of lifestyle, physiological and genetic factors.
Cardiac Output and Total Peripheral Resistance: Normal blood pressure relies on the body maintaining a balance between CO and TPR. In hypertensive patients CO tends to be normal but arterial resistance is raised, which suggests contraction of the small arterioles.
Cardiac Output can be increased via a number of factors: - Renin-angiotensin system: Renin is a hormone released by the kidney in response to underperfusion of the glomerulus in the kidney, or reduced salt intake. Renin converts angiotensinogen into angiotensin 1, which in turn is converted in angiotensin II by the angiotensin converting enzyme. Angiotensin II acts on the vascular endothelium causing vasoconstriction and causes the adrenal cortex to release aldosterone which promotes salt re-uptake by the kidney (and water by solvent drag) and the release of the Anti-diuretic Hormone which promotes water re-absorption. This system means that with low salt levels renin is released, producing increased blood volume, and thus increased cardiac output and arterial pressure. So if a patient had a chronic high salt-intake then they may become salt-resistant (or via genetic polymorphisms), thus needing high levels of salt to inhibit renin release. However in hypertension, it is TPR that increases, not CO. This has been explained through autoregulation of the organs, as explained earlier, which decreases CO back to ‘normal’. - Sympathetic Overactivity: Not thought to have much long term effect, so unlikely to produce hypertension. - Endothelial Dysfunction: The endothelial of the vascular system is important in producing vasodilators such as nitric oxide. If the endothelium fails to produce NO, then smooth muscle relaxation may be inhibited, causing thickening. - Genetic factors: Several genes have been identified as contributing to hypertension, most of which cause a dysfunction of the renin-angiotensin-aldosterone system. - Diet: A high salt diet will result in increased water retention, increasing blood volume. Potassium and magnesium reduce blood pressure, so diets low in these minerals promote HT. Obesity puts stress on the body to produce longer and additional peripheral blood vessels to supply the extra body mass, increasing TPR. - Nicotine: Nicotine causes stimulation of the myocardium and causes vasoconstriction, both increasing arterial pressure. - Age: Stiffening of blood vessels by an increase in collagen fibers in the artery walls produces a smaller cross-section in systole.
Secondary hypertension:
Renal Hypertension: Any disease that decreases the perfusion of the glomerulus of the kidney will activate the renin-angiotensin-aldosterone system, producing the effects described earlier.
Adrenal Hypertension: Can occur through a number of adrenal cortex abnormalities. Hyper-aldosteronism will produce increased sodium retention. Pheochromocytoma results in increased secretion of catecholamines (adrenaline and noradrenaline) overstimulating the sympathetic nervous system (peripheral constriction and cardiac stimulation).
End Organ Damage:
The Heart: Heart damage occurs as the increased afterload causes the heart to work harder to expel blood. The ventricles hypertrophy to the point that they stretch and become less efficient. At the same time, more oxygen is required by the myocardium. In the peripheral vascular system the sheering stress on the endothelium may cause it to rip, resulting in lesions that may become atherosclerotic.
The Brain: Hypertension causes the brain to autoregulate, decreasing cerebral blood flow (leading to hypoperfusion), and increasing the chance of cerebral ischaemia.
Eye: A diastolic blood pressure of over 120 mmHg will result in haemorrhaging of the retinal blood vessels.
Kidney: The renal arterioles thicken in response to the stress, decreasing the size of their lumens, decreasing blood flow to the kidney. This activates the renin-angiotensin-aldosterone system, worsening the hypertension. Eventually the kidney will be hypoperfused leading to hypoxia and death.
References: Saladin, Anatomy and Physiology, McGraw Hill, 2006 Beevers, G, ABC of Hypertension: The pathophysiology of hypertension, BMJ 2001; 322:912-916 http://www.4um.com/tutorial/anaesth/highbp.htm
MANAGEMENT OF HYPERTENSION – MEDS AND DRUG THERAPY
• The aim of drug treatment is to reduce the risk of complications of hypertension • This can be achieved by reducing BP to 135/85 or less (120/80 in diabetics) • Commonly used drugs are the ABCDs: ACE inhibitors and Angiotensin antagonists Beta blockers Calcium-channel blockers Diuretics
ACE inhibitors • Inhibits conversion of angiotensin I to angiotensin II (potent vasoconstrictor, causes aldosterone secretion, sodium and water retention). Also inhibits breakdown of bradykinin (vasodilator). Results in a fall in TPR, increase sodium and water excretion. • Eg: Captopril, Enalapril, Perindopril • Adverse effects: Dry cough, headache, marked hypotension, hyperkalemia.
Angiotensin antagonists • Blocks angiotensin(AT) receptors. Results in decrease in TPR and increase sodium and water excretion. • Eg: losartan, irbesartan, candesartan • Adverse effects: similar to ACE inhibitors, however does not cause dry cough (does not inhibit BK breakdown)
Beta Blockers • Block β-receptors of sympathetic NS at the heart. Initially causes decrease in HR and CO and increase TPR (reflex). However inhibition of renin release (required in angiotensin synthesis) causes decrease in TPR and return of CO to normal. • Eg: propanolol, atenolol, metoprolol • Adverse effects: Bronchoconstriction (respiratory), decreased heart contractility, bradycardia, AV block (CVS), depression, sedation, sleep problems (Brain), exacerbate/mask hypoglycemia (diabetes)
High blood pressure usually causes no symptoms. Even if high blood pressure does cause symptoms, the symptoms are usually mild and nonspecific (vague, or suggesting many different disorders). Thus, high blood pressure often is labeled "the silent killer." People who have high blood pressure typically don't know it until their blood pressure is measured. Sometimes people with high blood pressure have symptoms including headache, shortness of breath, dizziness, blurred vision and nausea.
People often do not seek medical care until they have symptoms arising from the organ damage caused by chronic (ongoing, long-term) high blood pressure. The following types of organ damage are commonly seen in chronic high blood pressure: heart attack, heart failure, stroke or "mini stroke" (transient ischemic attack, TIA), kidney failure, eye damage with loss of vision, peripheral arterial disease.
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10 comments:
Aetiology of hypertension:
Hypertension can be classified into either essential or secondary.
Essential Hypertension: No specific medical cause can be found to explain the patient's condition. However, there appears to be a relationship with high blood pressure and many other factors. Some of these include:
Genetic factors: High blood pressure tends to run in families. This may be explained, at least, by shared environmental influences. However, there is still a prominent, unidentifiable genetic component.
Fetal factors: Low birth weight is associated with subsequent high blood pressure.
Environmental factors: Obesity, high alcohol intake, high sodium intake and stress can raise blood pressure.
Insulin Resistance: A positive correlation between diabetes and hypertension has long been recognised. It also known as metabolic syndrome and is a major risk factor for cardiovascular disease.
Secondary Hypertension: Hypertension which results from an underlying, identifiable, usually correctable cause. (5-10% of hypertensive patients)
A mnemonic to help remember some possible secondary causes hypertension is ABCDE
A: apnoea, aldosteronism
B: bruits, bad kidneys
C: coarctation of the aorta, Cushing’s syndrome
D: diet, drugs
E: erythropoietin, endocrine disturbances
Apnoea: Obstructive Sleep Apnoea (OSA) is a mechanical problem in the upper airway during sleep. Half of patients have hypertension caused by various mechanisms such as sympathetic activation.
Aldosteronism: Over productivity of aldosterone (by the adrenal cortex) which results in over-retention of salt and water. Increases K+ secretion in the urine and detection of elevated aldosterone in relation to plasma renin can diagnose this.
Bruits: (Renal Vascular hypertension) When there is hypertension caused by a compromised artertial supply to the kidneys. Many of these patients will have an abdominal bruit (abnormal sound reflecting turbulent flow) on examination.
Bad kidneys: (Renal parachymal disease)can be a cause of consequence of hypertension. Progressive renal disease interferes with kidneys ability to excrete Na+ and excess fluid. Diagnosed by increased serum creatine levels and decreased urine creatine clearance. Treatment with ACE inhibitors protects kidney function.
Coarctation of the aorta: congenital narrowing of the aortic lumen. Most often occurs just distal to the branch of the left subclavian. Diagnosed by high upper extremity blood pressure and weak lower extremity pulses and the “3 sign” (dilation of the aorta above and below the stenosis)
Cushing’s: hypertensive effects of increased corticosteroirds.
Diet:
-high salt (increased water retention)
-overweight people have a higher incidence of hypertension
Drugs:
-NSAIDs (by inhibiting prostoglandins)
-the pill,
-cold and flu preparations (containing sympathomimetics)
-caffeine
-alcohol
-cocaine
Erythropoietin: Increased EPO levels can be endogenous ( EPO production in chronic hypoxia ie. COPD) or exogenous (to treat anemia). It leads to hypertension by increasing blood viscosity.
Endocrine disorders: HypOthyroidism causes decreased cardiac output with a increase in vascular tone to compensate (INCREASED DIASTOLIC MORE MARKED). HypErthyroidism also causes hypertension by increasing cardiac output. (INCREASED SYSTOLIC MORE MARKED)
Preganancy also causes hypertension (causes not fully understood)
References: Kumar and Clark, Wikipedia, http://www.aafp.org/afp/20030101/67.html
(American Academy of Family Physicians-article by Edward Onusko)
angela said....
Definition:
Persistently high arterial blood pressure
Measured after 5 minutes resting (seated) is usually sufficient (standing for testing of orthostatic hypotension however)
Measured to the nearest 2mmHg
Two consistent measurements should be taken, more if inconsistent
When assessing CV risk: average from several visits is more accurate than single visit
From the WHO-International society for hypertension (based on clinical BP):
Grade 1 (mild): systolic: 140-149, diastolic: 90-99 i.e.: 140/90+
Grade 2 (moderate): systolic: 160-179, diastolic: 100-109 i.e.: 160/100+
Grade 3 (severe): systolic: ≥180, diastolic: ≥100
If systolic and diastolic fall in different categories, the higher value is taken
Threshold for home/self monitoring: higher than 135/85mmHg
For ambulatory monitoring: higher than 125/80mmHg
Primary hypertension: no known cause
Secondary hypertension: associated with other diseases
Incidence:
From 1999-2000:
Men aged 25+: 30.5% (age-standardised: 32.3%)
Men aged 65-74: 69.4%
Men aged 75+: 78.8%
Women aged 25+: 27.3% (age-standardised: 27.2%)
Women aged 65-74: 66.8%
Women aged 75+: 74.6%
From: AIHW analysis of the 1980, 1983 & 1989 Risk Factor Prevalence Surveys; 1995 National Nutrition Survey; 1999–2000 Australian Diabetes, Obesity and Lifestyle (AusDiab) study.
Sorry! I wasn’t able to find any data on the separate incidences of primary and secondary hypertension!
Sources: Kumar and Clark, 6th ed. : Systemic hypertension, page 857
http://medical-dictionary.thefreedictionary.com/Essential+(Primary)+Hypertension
Research Topic: Investigations required to exclude secondary causes of Hypertension.
It is not necessarily required for the doctor to prescribe numerous investigations.
The usual tests include: 1) Measuring sugar and creatine levels.
2) Urine analysis.
•There are many investigations that can be undertaken in order to eliminate the secondary causes of Hypertension. So in order to keep it simple, I will only expand on those tests relevant to this case.
•Some drugs, like diuretics, ARBs, and ACE inhibitors, can modify the concentration of potassium in the blood (kaliemia) and the functioning of the kidneys. This warrants a blood test to measure the level of minerals in the blood (blood electrolytes).
For Renal System:
•Blood test to monitor sugar and creatine levels in order to diagnose Diabetic Nephropathy or Glomerular disease (defective purification of kidneys).
•Urine test- 1) Looking for blood in the urine is carried out with a dipstick. If the dipstick is positive, the result is confirmed by a microscope examination of the urine.
2) Looking for albumin in the urine (proteinuria or albuminuria) is also carried out with a dipstick. If it is positive, it may be necessary to measure the level in the urine over 24 hours.
3) Check urine output as patient could be suffering from Hydronephrosis where certain parts of one or both kidneys become plugged, thus blocking urine flow and raising blood pressure.
•Ultrasound Examination – Patients can undergo a renal ultrasound or Doppler Ultrasonography of their arteries in order to eliminate the possibility of Polycystic Kidney disease (which may be inherited, so check family history) or Renovascular Hypertension which may be caused by stenosis of the renal arteries due to build-up of fatty plaque.
For Adrenal Glands:
•Blood test – In order to monitor the level of a) Cortisol secretion as an excess may raise blood pressure and is as a result of Cushing’s syndrome (Corticosteroids, pituitary tumour may overstimulate adrenals). b) Aldosterone secretion by the adrenals due to the presence of a tumour or increased growth of normal cells which forces the kidneys to retain salt and water and loose too much potassium. This causes an increase in blood pressure. c) Noradrenaline and adrenaline which again can be a result of tumours (Pheochromocytoma) on the adrenals and also results in raised blood pressure levels.
For Thyroid Glands:
•Blood test – In order to monitor the levels of thyroxine secretion. Too little can cause Hypothyroidism and too much can cause Hyperthyroidism (where the activity of epinephrine and norepinephrine is increased), with both cases resulting in an increase in blood pressure.
For Parathyroid Glands:
•Blood test – The parathyroid glands regulate levels of calcium and phosphorus in the body. Increased secretion of the parathyroid hormone raises the amount of calcium in the blood, thus raising blood pressure.
References:
•http://www.servier.com/patient/cardiologie/hypertension/8.asp
•http://www.mayoclinic.com/health/high-blood-pressure/HQ01345/MOTT=DS00100
Investigations – Detecting End-Organ Damage
The Kidneys
As the kidneys are responsible for long-term regulation of blood pressure, it is important to examine their function in hypertension.
Renal flow impairment is usually a good indication of hypertensive damage.
- Radio-marked flow markers injected into arteries
- Gold standard – insulin
- EDTA and DTPA can also be used
- Measure either rate of elimination from plasma, or excretion into urine.
The Eye
The blood vessels in the eye are both highly sensitive, and visible without surgery, and as such are a good place to get an indication of possible systemic hypertensive damage.
Opthalmoscopic examination of the eye can reveal signs of possible hypertensive damage:
Retinal arterioles:
- Generalised and focal narrowing
- Irregularity and tortuosity
- Increased light reflex
- Loss of transparency
Veins become indistinct where crossing behind arteries
Retinal haemorrhage
Retinal white spots
Macular oedema
Macular stars
Blurring of optic disc margins
Papilloedema
The Brain
Cerebral circulation is not usually affected by hypertension
- Adaptation prevents excessive blood flow to brain
- Vascular hypertrophy and remodelling
This adaptation, however, can decrease the range of the vasodilator reflex due to encroachment on the vascular lumen
If the adaptation fails in any way, it can result in:
- Hypertensive encephalopathy
- Cerebral haemorrhage
- Ischaemic stroke
We would obviously want to prevent this, so if hypertensive adaptation is suspected we can perform a cerebral angiography
Detects vascular hypertrophy
- Risky procedure
- Allows us time to treat hypertension and hopefully reverse effects
Sudden drops in blood pressure can cause cerebral hypoxia as vasculature has adapted to hypertension – treatment needs to be gradual.
Well, the comment above would be mine, and you'd probably like a reference...
Handbook of Hypertension, Vol 18: "Assessment of Hypertensive Organ Damage"
L. Hansson, W.H. Birkenhager
Cheers,
Shane
Robb said…..
Hypertension: Pathophysiology.
Essential hypertension:
The pathophysiology of essential hypertension is not entirely understood, it appears that it results from a complex mix of lifestyle, physiological and genetic factors.
Cardiac Output and Total Peripheral Resistance: Normal blood pressure relies on the body maintaining a balance between CO and TPR. In hypertensive patients CO tends to be normal but arterial resistance is raised, which suggests contraction of the small arterioles.
Cardiac Output can be increased via a number of factors:
- Renin-angiotensin system: Renin is a hormone released by the kidney in response to underperfusion of the glomerulus in the kidney, or reduced salt intake. Renin converts angiotensinogen into angiotensin 1, which in turn is converted in angiotensin II by the angiotensin converting enzyme. Angiotensin II acts on the vascular endothelium causing vasoconstriction and causes the adrenal cortex to release aldosterone which promotes salt re-uptake by the kidney (and water by solvent drag) and the release of the Anti-diuretic Hormone which promotes water re-absorption. This system means that with low salt levels renin is released, producing increased blood volume, and thus increased cardiac output and arterial pressure. So if a patient had a chronic high salt-intake then they may become salt-resistant (or via genetic polymorphisms), thus needing high levels of salt to inhibit renin release. However in hypertension, it is TPR that increases, not CO. This has been explained through autoregulation of the organs, as explained earlier, which decreases CO back to ‘normal’.
- Sympathetic Overactivity: Not thought to have much long term effect, so unlikely to produce hypertension.
- Endothelial Dysfunction: The endothelial of the vascular system is important in producing vasodilators such as nitric oxide. If the endothelium fails to produce NO, then smooth muscle relaxation may be inhibited, causing thickening.
- Genetic factors: Several genes have been identified as contributing to hypertension, most of which cause a dysfunction of the renin-angiotensin-aldosterone system.
- Diet: A high salt diet will result in increased water retention, increasing blood volume. Potassium and magnesium reduce blood pressure, so diets low in these minerals promote HT. Obesity puts stress on the body to produce longer and additional peripheral blood vessels to supply the extra body mass, increasing TPR.
- Nicotine: Nicotine causes stimulation of the myocardium and causes vasoconstriction, both increasing arterial pressure.
- Age: Stiffening of blood vessels by an increase in collagen fibers in the artery walls produces a smaller cross-section in systole.
Secondary hypertension:
Renal Hypertension: Any disease that decreases the perfusion of the glomerulus of the kidney will activate the renin-angiotensin-aldosterone system, producing the effects described earlier.
Adrenal Hypertension: Can occur through a number of adrenal cortex abnormalities. Hyper-aldosteronism will produce increased sodium retention. Pheochromocytoma results in increased secretion of catecholamines (adrenaline and noradrenaline) overstimulating the sympathetic nervous system (peripheral constriction and cardiac stimulation).
End Organ Damage:
The Heart: Heart damage occurs as the increased afterload causes the heart to work harder to expel blood. The ventricles hypertrophy to the point that they stretch and become less efficient. At the same time, more oxygen is required by the myocardium. In the peripheral vascular system the sheering stress on the endothelium may cause it to rip, resulting in lesions that may become atherosclerotic.
The Brain: Hypertension causes the brain to autoregulate, decreasing cerebral blood flow (leading to hypoperfusion), and increasing the chance of cerebral ischaemia.
Eye: A diastolic blood pressure of over 120 mmHg will result in haemorrhaging of the retinal blood vessels.
Kidney: The renal arterioles thicken in response to the stress, decreasing the size of their lumens, decreasing blood flow to the kidney. This activates the renin-angiotensin-aldosterone system, worsening the hypertension. Eventually the kidney will be hypoperfused leading to hypoxia and death.
References: Saladin, Anatomy and Physiology, McGraw Hill, 2006
Beevers, G, ABC of Hypertension: The pathophysiology of hypertension, BMJ 2001; 322:912-916
http://www.4um.com/tutorial/anaesth/highbp.htm
MANAGEMENT OF HYPERTENSION – MEDS AND DRUG THERAPY
• The aim of drug treatment is to reduce the risk of complications of hypertension
• This can be achieved by reducing BP to 135/85 or less (120/80 in diabetics)
• Commonly used drugs are the ABCDs:
ACE inhibitors and Angiotensin antagonists
Beta blockers
Calcium-channel blockers
Diuretics
ACE inhibitors
• Inhibits conversion of angiotensin I to angiotensin II (potent vasoconstrictor, causes aldosterone secretion, sodium and water retention). Also inhibits breakdown of bradykinin (vasodilator). Results in a fall in TPR, increase sodium and water excretion.
• Eg: Captopril, Enalapril, Perindopril
• Adverse effects: Dry cough, headache, marked hypotension, hyperkalemia.
Angiotensin antagonists
• Blocks angiotensin(AT) receptors. Results in decrease in TPR and increase sodium and water excretion.
• Eg: losartan, irbesartan, candesartan
• Adverse effects: similar to ACE inhibitors, however does not cause dry cough (does not inhibit BK breakdown)
Beta Blockers
• Block β-receptors of sympathetic NS at the heart. Initially causes decrease in HR and CO and increase TPR (reflex). However inhibition of renin release (required in angiotensin synthesis) causes decrease in TPR and return of CO to normal.
• Eg: propanolol, atenolol, metoprolol
• Adverse effects: Bronchoconstriction (respiratory), decreased heart contractility, bradycardia, AV block (CVS), depression, sedation, sleep problems (Brain), exacerbate/mask hypoglycemia (diabetes)
Calcium-channel blockers
• Reduces intracellular calcium in smooth muscle and cardiac cells, causing vasodilation, reduced cardiac contractility and reduced AV conduction.
• Eg: Verapamil, Diltiazem, Nifedipine
• Adverse effects: cardiac depression, bradycardia, flushing, oedema, headaches, constipation, nausea, increased digoxin levels (verapamil)
Diuretics
• Increases sodium and water excretion in kidneys and reduces circulating blood volume.
• Eg: Thiazide diuretics – act on distal tubule
Loop diuretics – act on Loop of Henle
Potassium-sparring diuretics – act on collecting duct
• Adverse effects: hyperuricaemia(gout), hypercholesteraemia, hyperglycaemia(diabetes), hyperkalaemia and increased digoxin toxicity (drug interaction)
Other Drugs
• Sympathetic inhibitors
o α-blockers. Eg: prazosin
o mixed α and β blockers. Eg: labetolol
o CNS-acting drugs. Eg: Methyldopa, Clonidine
• Vasodilators. Eg: Hydralazine, Minoxidil, Sodium nitropusside.
References:
• Lecture 19 – Treatment of Hypertension (week 2)
• Medical Pharmacology at a Glance, 5th ed.
• Kumar and Clark
Signs and symptoms of hypertension:
High blood pressure usually causes no symptoms. Even if high blood pressure does cause symptoms, the symptoms are usually mild and nonspecific (vague, or suggesting many different disorders). Thus, high blood pressure often is labeled "the silent killer." People who have high blood pressure typically don't know it until their blood pressure is measured. Sometimes people with high blood pressure have symptoms including headache, shortness of breath, dizziness, blurred vision and nausea.
People often do not seek medical care until they have symptoms arising from the organ damage caused by chronic (ongoing, long-term) high blood pressure. The following types of organ damage are commonly seen in chronic high blood pressure: heart attack, heart failure, stroke or "mini stroke" (transient ischemic attack, TIA), kidney failure, eye damage with loss of vision, peripheral arterial disease.
reference:
http://mens-health.health-cares.net/high-blood-pressure-symptoms.php
--shida--
Lifestyle modifications for hypertension prevention and management:
1. Lose weight if overweight.
2. Limit alcohol intake.
3. Increase aerobic physical activity.
4. Reduce sodium intake.
5. Maintain adequate dietary potassium.
6. Maintain adequate intake of dietary calcium and magnesium for general health.
7. Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.
CURRENT Medical Diagnosis & Treatment 43rd edition. Tierney, L.M, McPhee, S.J & Papadakis, M.A. Lange Medical Books/McGraw-Hill (2004)
Nice blog! Is your theme custom made or did you download
it from somewhere? A design like yours with a few simple adjustements would really make my
blog jump out. Please let me know where you
got your design. Thanks ageless male - ageless male
- ageless male
Look into my weblog ... ageless male
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