DOC I AM BLIND
Blindness is the inability to see.
The degree of blindness depends on the extent of loss of vision.
The causes of blindness are:
1.cataract
2.glaucoma
Glaucoma is due to a build-up of pressure within the eye causing damage to the optic nerve transmitting visual information from eye to the brain.
The damage is progressive with loss of peripheral vision followed by reduction in central vision resulting in blindness.
3.Age-related macular degeneration
Age-related Macular degeneration (AMD) is a degenerative disorder affecting the macula at the back the eye.
4.Corneal opacities are often caused by infections or damage to the cornea
5.Retinal detachment
Retinal detachment occurs with ageing and myopia (nearsightedness) may cause the retina to be pulled and detached.
6.Trachoma and other infections of the eye often cause loss of vision
7.Accidents (such as chemical burns,fireworks or sports injuries) affects the cornea of the eye
8.Vitamin A deficiency
Vitamin A deficiency leads to decreased production of a photosensitive pigment in the rods of the eye resulting in night blindness .
Three-quarters of all blindness can be prevented or treated.
Blindness is a lack of vision.
It may also refer to a loss of vision that cannot be corrected with glasses or contact lenses.
1.Partial blindness means that there is very limited visual ability
2.Complete blindness means a total loss of visual or light perception .
3.People with a vision worse than 20/200 are usually legally blind.
Treatment of blindness:
1.Blindness due to some causes such as infection, Vitamin A deficiency or glaucoma can be prevented through early detection and appropriate treatment.
2.Although visual loss cannot be completely restored, medical and surgical treatment can prevent the loss from further progress and complete blindness.
3.Because many serious forms of visual loss are painless, any forms of vision loss will need to be detected early and treated to prevent blindness.
Prevention of blindness
1.Vitamin A deficiency cna be treated with Vitamin A to prevent scarring of the eye and the ensuing blindness
2.Diabetes must be well controlled and regular eye examinations are necessary to prevent retinopathy
3.Majority of eye injuries can be prevented by using safe physical activities and proper eye protection.
4.Ensure good lighting and install handrails along stairs to prevent falling especially among the elderly.
5.Sharp corners and edges of furniture may be padded or cushioned.
6.Protective eye glasses are used to prevent insecticides and corrosive liquids from entering the eyes
7.Children should avoid toys with sharp points, shafts, spikes, rods and sharp edges to prevent eye injuries.
Friday, August 19, 2011
Wednesday, August 17, 2011
A Family Doctor's Tale - GIANT CELL ARTERITIS
DOC I HAVE GIANT CELL ARTERITIS
Giant Cell Arteritis is an inflammatory syndrome of cranial arteries especially the temporal artery.
It may be associated with blindness and may be part of the polymyalgia rheumatica syndrome.
It is rare under the age of 50 years.
Women are more affected than men.
There are some signs that Giant cell cell arteritis may be inherited because the illness have found to run in families.
The causes of Giant Cell Arteritis are:
The cause is unknown although it may be postulated that an immune response may have caused the inflammation.
It has been associated with severe infection and high doses of antibiotics.
There is inflammation of all layers of medium sized arteries within the carotid distribution from the neck, head, arms and even other arteries in the rest of the body.
The symptoms and signs of Giant Cell Arteritis are:
1.pain and tenderness of the scalp arteries with palpable thickening
2.headache and systemic upset such as weight loss
3.visual disturbance with loss of visual fields and blindness in severe cases
4.loss of appetite
5.Fever and sweating
6.weakness and fatigue
7.associated depression
8.claudication pain of jaw muscles while talking or eating
Other symptoms may be:
1.bleeding gums
2.mouth ulcers
3.hearing loss
4.joint pains of jaws, face and body
The Diagnosis of Giant Cell Arteritis is made by:
1.classical symptoms of headache and tenderness of the temporal arteries of the scalp
2.high ESR rate
3.biopsy of temporal artery under local anesthetic is diagnostic with multinucleared giant cells seen with fibrous proliferation of intima and fragmentation of elastic tissue
4.MRI of the brain
5.Ultrasound of the temporal arteries
The Complications of Giant Cell Arteritis are:
1.Development of aneurysm of blood vessels in the brain
2.Sudden transient ischemic attacks or stroke
3.sudden blindness of eyes or weakness of the eyelids
The Treatment of Giant Cell Arteritis is by using:
1.high dose corticosteroids (60mg prednisolone by mouth daily).
2.Dosage of corticosteroids can be reduced 2-3 weeks after symptoms disappear
3.maintenance dose of corticosteroids should be continues for six to eight months
Because of the prolonged use of corticosteroids, the bones may become porous and fragile:
1.additional calcium and collagen producing drugs are needed to strengthen the bones
2.walking and weight bearing exercises are needed
3.avoid smoking and alcohol
The Prognosis of Giant Cell Arteritis is:
Prognosis is good with prompt onset of corticosteroids treatment before loss of vision however treatment may be needed to continue for 1-2 years. Even then recurrence may occur.
Any loss of vision is irreversible once it occurred
Giant Cell Arteritis is an inflammatory syndrome of cranial arteries especially the temporal artery.
It may be associated with blindness and may be part of the polymyalgia rheumatica syndrome.
It is rare under the age of 50 years.
Women are more affected than men.
There are some signs that Giant cell cell arteritis may be inherited because the illness have found to run in families.
The causes of Giant Cell Arteritis are:
The cause is unknown although it may be postulated that an immune response may have caused the inflammation.
It has been associated with severe infection and high doses of antibiotics.
There is inflammation of all layers of medium sized arteries within the carotid distribution from the neck, head, arms and even other arteries in the rest of the body.
The symptoms and signs of Giant Cell Arteritis are:
1.pain and tenderness of the scalp arteries with palpable thickening
2.headache and systemic upset such as weight loss
3.visual disturbance with loss of visual fields and blindness in severe cases
4.loss of appetite
5.Fever and sweating
6.weakness and fatigue
7.associated depression
8.claudication pain of jaw muscles while talking or eating
Other symptoms may be:
1.bleeding gums
2.mouth ulcers
3.hearing loss
4.joint pains of jaws, face and body
The Diagnosis of Giant Cell Arteritis is made by:
1.classical symptoms of headache and tenderness of the temporal arteries of the scalp
2.high ESR rate
3.biopsy of temporal artery under local anesthetic is diagnostic with multinucleared giant cells seen with fibrous proliferation of intima and fragmentation of elastic tissue
4.MRI of the brain
5.Ultrasound of the temporal arteries
The Complications of Giant Cell Arteritis are:
1.Development of aneurysm of blood vessels in the brain
2.Sudden transient ischemic attacks or stroke
3.sudden blindness of eyes or weakness of the eyelids
The Treatment of Giant Cell Arteritis is by using:
1.high dose corticosteroids (60mg prednisolone by mouth daily).
2.Dosage of corticosteroids can be reduced 2-3 weeks after symptoms disappear
3.maintenance dose of corticosteroids should be continues for six to eight months
Because of the prolonged use of corticosteroids, the bones may become porous and fragile:
1.additional calcium and collagen producing drugs are needed to strengthen the bones
2.walking and weight bearing exercises are needed
3.avoid smoking and alcohol
The Prognosis of Giant Cell Arteritis is:
Prognosis is good with prompt onset of corticosteroids treatment before loss of vision however treatment may be needed to continue for 1-2 years. Even then recurrence may occur.
Any loss of vision is irreversible once it occurred
Monday, August 15, 2011
A Family Doctor's Tale - DIABETES INSIPUS
DOC I HAVE DIABETES INSIPUS
Diabetes Insipidus is an endocrine disease resulting from the loss of antidiuretic hormone (ADH) also known as vasopressin stored in the pituitary gland in the brain.
It is characterized by the copious flow of dilute urine (hence the term diabetes) and excessive thirst .
The Causes of Diabetes Insipidus are:
The cause of diabetes insipidus is unknown in 45 per cent of cases.
A.When it is caused by the lack of ADH, it is called Central Diabetes Insipus.
This usually results from any condition damaging the the neuro-hypophyseal (pituitary gland) system of the brain
It can occur at any age and affects either sex.
It is unusual in infants but can commence in early childhood.
Possible causes of central diabetes insipus are:
1.head injuries or birth injuries
2.neoplasm of the pititary gland
3.eosinophilic granuloma
4.primary or secondary cancer (particlarly breast cancer)
5.sarcoidosis
6.familial diabetes insipus
B.When it is caused by a failure of the kidneys to respond to the ADH hormone, the condition is known as Nephrogenic Diabetes Insipus
There is a defect in the parts of the kidneys that help to reabsorb water back into the bloodstream.
It may occur as a sex-linked inherited disorder where male children receive the abnormal gene from their mothers.
Nephrogenic diabetes insipus can also be caused by:
1.drugs such as lithium or amphotericin B
2.hypercalcemia or high blood calcium
3. Kidney problems such as polycystic kidney disease
The symptoms of Diabetes Insipidus are:
Symptoms:
1.polyuria or frequent passing of urine
a.urine output of 5-10 liters per 24 hours
b.specific gravity of urine 1.001 to 1.005
2.polydipsia or excessive thirst (with craving for cold water)
3.no other evidence of ill health
Diagnosis of Diabetes Insipidus is often based on
1. medical symptoms of polyuria and polydipsia
2.Urinary volume and specific gravity
3.Infusion of vasopressin
4.MRI of brain
The complications of Diabetes Insipidus are:
1. dehydration - fever, tachycardia or fast heart beats, sunken eyes, dry skin or mucosa, low blood pressure
2.electrolyte imbalance - which can affect the heart rhythm, fatigue, muscle aches and irritability of the nervous system
3.death from primary or secondary lesion in the brain
The treatment of Diabetes Insipidus is:
The underlying cause must first be treated.
In the case of Central Diabetes Insipus:
1.vasopressin can be given intravenously or intranasally or as oral medication with very good effect
In the case of Nephrogenic Diabetes Insipus (hereditary or lithium induced)
1. stopping the use of lithium may restore kidney function
2.thiazide diuretics may lower urine output
3.anti-inflammatory medications such as indomethocin given orally may help
The prognosis of Diabetes Insipidus is:
generally good with replacement therapy and if the underlying cause can be treated
Diabetes Insipidus is an endocrine disease resulting from the loss of antidiuretic hormone (ADH) also known as vasopressin stored in the pituitary gland in the brain.
It is characterized by the copious flow of dilute urine (hence the term diabetes) and excessive thirst .
The Causes of Diabetes Insipidus are:
The cause of diabetes insipidus is unknown in 45 per cent of cases.
A.When it is caused by the lack of ADH, it is called Central Diabetes Insipus.
This usually results from any condition damaging the the neuro-hypophyseal (pituitary gland) system of the brain
It can occur at any age and affects either sex.
It is unusual in infants but can commence in early childhood.
Possible causes of central diabetes insipus are:
1.head injuries or birth injuries
2.neoplasm of the pititary gland
3.eosinophilic granuloma
4.primary or secondary cancer (particlarly breast cancer)
5.sarcoidosis
6.familial diabetes insipus
B.When it is caused by a failure of the kidneys to respond to the ADH hormone, the condition is known as Nephrogenic Diabetes Insipus
There is a defect in the parts of the kidneys that help to reabsorb water back into the bloodstream.
It may occur as a sex-linked inherited disorder where male children receive the abnormal gene from their mothers.
Nephrogenic diabetes insipus can also be caused by:
1.drugs such as lithium or amphotericin B
2.hypercalcemia or high blood calcium
3. Kidney problems such as polycystic kidney disease
The symptoms of Diabetes Insipidus are:
Symptoms:
1.polyuria or frequent passing of urine
a.urine output of 5-10 liters per 24 hours
b.specific gravity of urine 1.001 to 1.005
2.polydipsia or excessive thirst (with craving for cold water)
3.no other evidence of ill health
Diagnosis of Diabetes Insipidus is often based on
1. medical symptoms of polyuria and polydipsia
2.Urinary volume and specific gravity
3.Infusion of vasopressin
4.MRI of brain
The complications of Diabetes Insipidus are:
1. dehydration - fever, tachycardia or fast heart beats, sunken eyes, dry skin or mucosa, low blood pressure
2.electrolyte imbalance - which can affect the heart rhythm, fatigue, muscle aches and irritability of the nervous system
3.death from primary or secondary lesion in the brain
The treatment of Diabetes Insipidus is:
The underlying cause must first be treated.
In the case of Central Diabetes Insipus:
1.vasopressin can be given intravenously or intranasally or as oral medication with very good effect
In the case of Nephrogenic Diabetes Insipus (hereditary or lithium induced)
1. stopping the use of lithium may restore kidney function
2.thiazide diuretics may lower urine output
3.anti-inflammatory medications such as indomethocin given orally may help
The prognosis of Diabetes Insipidus is:
generally good with replacement therapy and if the underlying cause can be treated
Saturday, August 13, 2011
A Family Doctor's Tale - MARFAN'S SYNDROME
DOC MY CHILD HAVE MARFAN'S SYNDROME
Marfan's Syndrome is an inherited disorder of the connective tissue as a result of a defective gene called fibrillin-1.
This gene causes defects involving the the collagen and glyccosaminoglycans tissue.
It is characterized by generally weak connective tissue which includes
1.muscles, ligaments and bones.
2.lung tissue
3.the heart and aorta
4.the eyes
5. the skin
6.the meninges
The Causes of Marfan's Syndrome are:
It is an inherited disease caused by an autosomal dominant gene.
Inheritance is passed to 50 per cent of offspring if one parent is affected and 100 per cent of offspring if both parents are affected.
Marfan Syndrome can also occur from mutation of the genes in 30 per cent of cases.
The symptoms of Marfan's Syndrome are:
Symptoms:
1.Long slender extremities with arm span exceeding height and long tapered fingers (also called spider fingers)
2.Skeletal deformities include:
a.kyphoscoliosis
b.pectus excavatum
c.pigeon chest
d.long narrow face
e.high arched palate
f.pronathism
3.Lax ligaments resulting in:
a.hyperflexiblity of joints
b.easily strained ligaments and joints
c.flat feet
4.Eye problems:
a.dislocation of lens due to lax ligaments
b.myopia
5.Heart problems:
a.dilatation of aorta and aortic aneurysm
b.dilatation of pulmonary artery
6.Learning disabilities
Diagnosis of Marfan's Syndrome is often based on
1. medical examination and appearance
2. measurement of metacarpal index from X-rays
Ratio of length to midpoint width is greater than 8.5
3.Urinary hydroxyproline is excessive indicating increased collagen turnover
4. Genetic analysis
5.ECG and echocardiogram
6.Eye examination and tests
The complications of Marfan's Syndrome are:
1. dissecting aortic aneurym may cause death
2.collapsed lungs
3.retinal detachment
4.heart valve problems
Marfan Syndrome patients generally have a shorter life span because of skeletal deformities and heart problems
The treatment of Marfan's Syndrome:
1.Genetic counseling
2.Prevention of joint strains especially spinal joints
3.Beta blockers can reduce aortic blood flow and prevent dilatation of aorta
4.Avoid competitive sports or strenuous physical activities
5.Antibiotic should be given to prevent endocarditis before any dental treatment
6.Pregnancy should be monitored carefully especially in the third trimester because of the strain on the heart
The prognosis of Marfan's Syndrome:
1.Shorter life span because of heart and skeletal problems
2. Good care and surgery treatment of the heart and eyes may extend the lifespan further.
Prevention of Marfan's Syndrome:
Genetic counseling and testing for Marfan's Syndrome
Marfan's Syndrome is an inherited disorder of the connective tissue as a result of a defective gene called fibrillin-1.
This gene causes defects involving the the collagen and glyccosaminoglycans tissue.
It is characterized by generally weak connective tissue which includes
1.muscles, ligaments and bones.
2.lung tissue
3.the heart and aorta
4.the eyes
5. the skin
6.the meninges
The Causes of Marfan's Syndrome are:
It is an inherited disease caused by an autosomal dominant gene.
Inheritance is passed to 50 per cent of offspring if one parent is affected and 100 per cent of offspring if both parents are affected.
Marfan Syndrome can also occur from mutation of the genes in 30 per cent of cases.
The symptoms of Marfan's Syndrome are:
Symptoms:
1.Long slender extremities with arm span exceeding height and long tapered fingers (also called spider fingers)
2.Skeletal deformities include:
a.kyphoscoliosis
b.pectus excavatum
c.pigeon chest
d.long narrow face
e.high arched palate
f.pronathism
3.Lax ligaments resulting in:
a.hyperflexiblity of joints
b.easily strained ligaments and joints
c.flat feet
4.Eye problems:
a.dislocation of lens due to lax ligaments
b.myopia
5.Heart problems:
a.dilatation of aorta and aortic aneurysm
b.dilatation of pulmonary artery
6.Learning disabilities
Diagnosis of Marfan's Syndrome is often based on
1. medical examination and appearance
2. measurement of metacarpal index from X-rays
Ratio of length to midpoint width is greater than 8.5
3.Urinary hydroxyproline is excessive indicating increased collagen turnover
4. Genetic analysis
5.ECG and echocardiogram
6.Eye examination and tests
The complications of Marfan's Syndrome are:
1. dissecting aortic aneurym may cause death
2.collapsed lungs
3.retinal detachment
4.heart valve problems
Marfan Syndrome patients generally have a shorter life span because of skeletal deformities and heart problems
The treatment of Marfan's Syndrome:
1.Genetic counseling
2.Prevention of joint strains especially spinal joints
3.Beta blockers can reduce aortic blood flow and prevent dilatation of aorta
4.Avoid competitive sports or strenuous physical activities
5.Antibiotic should be given to prevent endocarditis before any dental treatment
6.Pregnancy should be monitored carefully especially in the third trimester because of the strain on the heart
The prognosis of Marfan's Syndrome:
1.Shorter life span because of heart and skeletal problems
2. Good care and surgery treatment of the heart and eyes may extend the lifespan further.
Prevention of Marfan's Syndrome:
Genetic counseling and testing for Marfan's Syndrome
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