A Simple Guide of Liver Cirrhosis II
--------------------------------------------------
What are the complications of Liver Cirrhosis?
-----------------------------------------------------
Complications may develop with progression of the cirrhosis.
1.Bruising and bleeding due to decreased production of coagulation factors.
2.Jaundice due to decreased processing of bilirubin
3.Itching (pruritis due to bile products deposited in the skin).
4.Hepatic encephalopathy - the liver does not clear ammonia and related nitrogenous substances from the blood, which are carried to the brain, affecting cerebral functioning:
a.neglect of personal appearance,
b.unresponsiveness,
c.forgetfulness,
d.trouble concentrating,
e.changes in sleep habits.
f.Sensitivity to medication due to decreased metabolism of the active compounds.
5.Hepatocellular carcinoma is primary liver cancer one of the common complication of cirrhosis and has a high mortality rate.
6.Portal hypertension - blood normally carried from the intestines and spleen through the hepatic portal vein flows more slowly and the pressure increases causing :
a.Ascites - fluid leaks through the vasculature into the abdominal cavity.
b.Esophageal varices - collateral portal blood flow through vessels in the stomach and esophagus. These blood vessels may become enlarged and are more likely to burst.
7.Immune system dysfunction, leading to
a.nonspecific infection in the body organs
b..Spontaneous bacterial peritonitis -fluid in the abdomen may become infected with bacteria normally present in the intestines
8.Hepatorenal syndrome - insufficient blood supply to the kidneys, causing acute renal failure and a very high mortality (over 50%).
9.Hepatopulmonary syndrome - blood bypassing the normal lung circulation leading to cyanosis and dyspnea (shortness of breath) characteristically worse on sitting up
10.Portopulmonary hypertension - increased blood pressure over the lungs as a consequence of portal hypertension.
What is the treatment of Liver Cirrhosis?
-----------------------------------------------------
In all cases of liver cirrhosis, the liver damage from cirrhosis cannot be repaired so treatment is aimed at reducing progression and complications of the disease.
1. A healthy fat free diet is needed as energy use in cirrhosis is high
2.Close monitoring of the liver function is important.
3.Antibiotics will be prescribed for infections,
4.Antihistamines can help with itching.
5.Laxatives such as lactulose decrease risk of constipation
6.Treating alcoholism
Alcoholic cirrhosis caused by alcoholism is treated by abstaining from alcohol.
7.Treatment for hepatitis-related cirrhosis involves medications to treat the different types of hepatitis, such as
a.interferon for viral hepatitis
b.corticosteroids for autoimmune hepatitis.
8.Cirrhosis caused by Wilson's disease in which copper builds up in organs is treated with chelation therapy (e.g. penicillamine ) to remove the copper.
9.Preventing complications:
---------------------------------
a. Ascites
Salt restriction
Diuretics may be necessary to reduce fluid in abdomen.
b. Esophageal variceal bleeding -
Vasopressin
surgical portacaval shunting
c. portal hypertension
propranolol lower blood pressure over the portal system.
Transjugular intrahepatic portosystemic shunting will relieve pressure on the portal vein as a temporary measure .
c. Spontaneous bacterial peritonitis
antibiotics.
10. Decompensated cirrhosis
-----------------------------------
Decompensation in previously stable patients may occur due to various causes:
a.constipation
b.infection
c.increased alcohol intake,
d.medication
e.bleeding from esophageal varices
f.dehydration.
Patients with decompensated cirrhosis has to be admitted to hospital for
1.close monitoring of the:
fluid balance
mental status,
2.emphasis on adequate nutrition
3.medical treatment -
a.diuretics
b.antibiotics
c.laxatives
d.enemas
e.thiamine
f.steroids
g.acetylcysteine
h.pentoxifylline
Surgical Liver Transplantation
------------------------------------
Liver transplantation is necessary if:
liver stop functioning
severe complications cannot be controlled
Survival rate from liver transplantation has improved to 80% for five year postoperative period.
Transplantation necessitates the use of immune suppressants for life.
What is the prognosis for Liver Cirrhosis?
---------------------------------------------------
Prognosis is generally not good unless detected at very early stage.
Most liver cirrhosis patient are in the moderate to advanced stage of the disease when detected.
If there are complications, the prognosis is poor.
What is the best prevention for Liver Cirrhosis?
---------------------------------------------------
1. Alcohol- stop the abuse of alcohol
2. Vaccination against hepatitis B
3. Reduce fat in obese -fat cells in liver can lead to cirrhosis
Wednesday, October 29, 2008
Tuesday, October 28, 2008
A Simple Guide to Liver Cirrhosis I
A Simple Guide to Liver Cirrhosis I
-------------------------------------------
What is Liver Cirrhosis?
---------------------------
Liver Cirrhosis is a chronic liver disease where the normal liver tissue is replaced by bands of fibrous scar tissue separating nodules of regenerated liver cells resulting in gradual loss of liver function.
Who is at risk of getting Liver Cirrhosis?
-------------------------------------------
1.Alcohol abuse
2.Genetic causes of Biliary Obstruction such as biliary atresia
3.Hepatitis viral infection
4.Obese -fatty liver can end in liver cirrhosis
5.Exposure to excessive chemicals(factory) or medications(eg statins)
What are the causes of Liver Cirrhosis?
-----------------------------------------------
The main causes of Liver Cirrhosis are:
1.chronic alcoholism:
Alcohol tends to block the normal metabolism of protein, fats, and carbohydrates leaving toxic material behind which can injure the liver and ends in liver cirrhosis.
2.hepatitis C virus infection:
Chronic hepatitis c viral infection causes inflammation of the liver which over the years can damage the liver and lead to cirrhosis.
3.Primary biliary and secondary cirrhosis:
Primary biliary cirrhosis cause is unknown.
Secondary biliary cirrhosis results from chronic obstruction of the biliary tract resulting in chronic inflammation of the liver cells and fibrosis of the liver.
Nodular regeneration of the liver cells occurs subsequently.
Obstruction to the bile ducts can be caused by:
Cholecystitis
Gallstones
Biliary cholangitis
4.Others:
Metabolic diseases:
Hemachromatosis
Wilson Disease
Parasitic Disease:
Schistosomiasis
Cardiac cirrhosis
Liver congestion results from right sided heart failure
Autoimmune Diseases:
Autoimmune hepatitis
Exposure to chemicals and medications
Glycogen storage disease
What are the Symptoms and signs of Liver Cirrhosis?
-----------------------------------------------
Common symptoms of Liver Cirrhosis are:
1.Anorexia
2.fatigue and weakness
3.Gradual onset of jaundice(Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin)
4.weight loss.
5.Fetor hepaticus - odor in breath due to increased dimethyl sulfide
Signs:
1.Spider nevi- central arteriole surrounded by many smaller vessels due to an increase in estradiol .
2.Palmar erythema -redness of the palms due to impaired sex hormone metabolism.
3.Liver size. Can be enlarged, normal, or shrunken.
4.Splenomegaly - Due to congestion of the spleen as a result of portal hypertension.
5.Ascites . Accumulation of fluid in the peritoneal cavity
6.hydrocele and penile flomation (swelling of the penile shaft)
7.Hypogonadism - impotence, infertility, poor sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
8.Gynecomastia - This is due to increased estradiol in male patients.
9.Hypertrophic osteoarthropathy - Chronic proliferative periostitis of the ribs can be very painful.
10.Dupuytren's contracture -palmar fascia tightens to cause flexion deformities of the fingers.
11.Nail changes:
Muehrcke's nails - paired horizontal bands due to hypoalbuminemia
Terry's nails - proximal 2/3 of the nail appears white with distal one-third red due to hypoalbuminemia
Clubbing - angle between the nail plate and proximal nail fold > 180 degrees
12.Caput medusa -In portal hypertension, the umbilical vein may be distended.
13.Cruveilhier-Baumgarten murmur. Venous blood flow hum heard in epigastric region due to portal hypertension
14.Asterixis - Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
How is the diagnosis of Liver Cirrhosis made?
-----------------------------------------------------
1. liver biopsy will confirm liver cirrhosis through a percutaneous laparoscopic , or fine-needle approach but may not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis.
there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications due to liver biopsy
2.Lab findings
The following findings are typical in cirrhosis:
a.Aminotransferases - AST and ALT are moderately elevated, with AST > ALT.
b.Alkaline phosphatase - usually slightly elevated.
c.GGT - correlates with AP levels- much higher in chronic liver disease from alcohol.
d.Bilirubin - may elevate as cirrhosis progresses.
e.Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis
f.Prothrombin time - increases since the liver synthesizes clotting factors.
g.Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
h.Serum sodium is low due to inability to excrete free water resulting from high levels of ADH and aldosterone
i.Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. Platelet count is rarely < 50,000/mL.
j.Leukopenia and neutropenia - due to splenomegaly with splenic margination.
k.Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
l.Serology for hepatitis viruses, autoantibodies (ANA or Anti-nuclear antibody, anti-smooth muscle, anti-mitochondria n.antibody, anti-LKM)
n.Ferritin and transferrin saturation (markers of iron overload),
o.copper and ceruloplasmin Ceruloplasmin> (markers of copper overload)
p.Immunoglobulin levels (IgG, IgM, IgA) - high
To determine various causes
p.Cholesterol and glucose
r.Alpha 1-antitrypsin
3.Imaging
Ultrasound is used to assess the degree of cirrhosis:
a.small and nodular liver in advanced cirrhosis
b.increased echogenicity with irregular appearing areas.
Ultrasound may also screen for
a.hepatocellular carcinoma
b.portal hypertension
c.Budd-Chiari syndrome by checking the blood flow in the hepatic vein
FibroScan (transient elastography) uses elastic waves to assess liver stiffness which can grade the severity of cirrhosis.
Abdominal CT and liver and bile duct MRI - may show the the degree of liver cirrhosis
4.Imaging of the bile ducts, such as
ERCP Endoscopic_retrograde_cholangiopancreatography or
MRCP Magnetic_resonance_cholangiopancreatography (MRI of biliary tract and pancreas)
can show abnormalities in the liver
5.Endoscopy
Gastroscopy is performed in patients with liver cirrhosis to exclude the possibility of esophageal varices.
-------------------------------------------
What is Liver Cirrhosis?
---------------------------
Liver Cirrhosis is a chronic liver disease where the normal liver tissue is replaced by bands of fibrous scar tissue separating nodules of regenerated liver cells resulting in gradual loss of liver function.
Who is at risk of getting Liver Cirrhosis?
-------------------------------------------
1.Alcohol abuse
2.Genetic causes of Biliary Obstruction such as biliary atresia
3.Hepatitis viral infection
4.Obese -fatty liver can end in liver cirrhosis
5.Exposure to excessive chemicals(factory) or medications(eg statins)
What are the causes of Liver Cirrhosis?
-----------------------------------------------
The main causes of Liver Cirrhosis are:
1.chronic alcoholism:
Alcohol tends to block the normal metabolism of protein, fats, and carbohydrates leaving toxic material behind which can injure the liver and ends in liver cirrhosis.
2.hepatitis C virus infection:
Chronic hepatitis c viral infection causes inflammation of the liver which over the years can damage the liver and lead to cirrhosis.
3.Primary biliary and secondary cirrhosis:
Primary biliary cirrhosis cause is unknown.
Secondary biliary cirrhosis results from chronic obstruction of the biliary tract resulting in chronic inflammation of the liver cells and fibrosis of the liver.
Nodular regeneration of the liver cells occurs subsequently.
Obstruction to the bile ducts can be caused by:
Cholecystitis
Gallstones
Biliary cholangitis
4.Others:
Metabolic diseases:
Hemachromatosis
Wilson Disease
Parasitic Disease:
Schistosomiasis
Cardiac cirrhosis
Liver congestion results from right sided heart failure
Autoimmune Diseases:
Autoimmune hepatitis
Exposure to chemicals and medications
Glycogen storage disease
What are the Symptoms and signs of Liver Cirrhosis?
-----------------------------------------------
Common symptoms of Liver Cirrhosis are:
1.Anorexia
2.fatigue and weakness
3.Gradual onset of jaundice(Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin)
4.weight loss.
5.Fetor hepaticus - odor in breath due to increased dimethyl sulfide
Signs:
1.Spider nevi- central arteriole surrounded by many smaller vessels due to an increase in estradiol .
2.Palmar erythema -redness of the palms due to impaired sex hormone metabolism.
3.Liver size. Can be enlarged, normal, or shrunken.
4.Splenomegaly - Due to congestion of the spleen as a result of portal hypertension.
5.Ascites . Accumulation of fluid in the peritoneal cavity
6.hydrocele and penile flomation (swelling of the penile shaft)
7.Hypogonadism - impotence, infertility, poor sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
8.Gynecomastia - This is due to increased estradiol in male patients.
9.Hypertrophic osteoarthropathy - Chronic proliferative periostitis of the ribs can be very painful.
10.Dupuytren's contracture -palmar fascia tightens to cause flexion deformities of the fingers.
11.Nail changes:
Muehrcke's nails - paired horizontal bands due to hypoalbuminemia
Terry's nails - proximal 2/3 of the nail appears white with distal one-third red due to hypoalbuminemia
Clubbing - angle between the nail plate and proximal nail fold > 180 degrees
12.Caput medusa -In portal hypertension, the umbilical vein may be distended.
13.Cruveilhier-Baumgarten murmur. Venous blood flow hum heard in epigastric region due to portal hypertension
14.Asterixis - Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
How is the diagnosis of Liver Cirrhosis made?
-----------------------------------------------------
1. liver biopsy will confirm liver cirrhosis through a percutaneous laparoscopic , or fine-needle approach but may not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis.
there is a small but significant risk to liver biopsy, and cirrhosis itself predisposes for complications due to liver biopsy
2.Lab findings
The following findings are typical in cirrhosis:
a.Aminotransferases - AST and ALT are moderately elevated, with AST > ALT.
b.Alkaline phosphatase - usually slightly elevated.
c.GGT - correlates with AP levels- much higher in chronic liver disease from alcohol.
d.Bilirubin - may elevate as cirrhosis progresses.
e.Albumin - levels fall as the synthetic function of the liver declines with worsening cirrhosis
f.Prothrombin time - increases since the liver synthesizes clotting factors.
g.Globulins - increased due to shunting of bacterial antigens away from the liver to lymphoid tissue.
h.Serum sodium is low due to inability to excrete free water resulting from high levels of ADH and aldosterone
i.Thrombocytopenia - due to both congestive splenomegaly as well as decreased thrombopoietin from the liver. Platelet count is rarely < 50,000/mL.
j.Leukopenia and neutropenia - due to splenomegaly with splenic margination.
k.Coagulation defects - the liver produces most of the coagulation factors and thus coagulopathy correlates with worsening liver disease.
l.Serology for hepatitis viruses, autoantibodies (ANA or Anti-nuclear antibody, anti-smooth muscle, anti-mitochondria n.antibody, anti-LKM)
n.Ferritin and transferrin saturation (markers of iron overload),
o.copper and ceruloplasmin Ceruloplasmin> (markers of copper overload)
p.Immunoglobulin levels (IgG, IgM, IgA) - high
To determine various causes
p.Cholesterol and glucose
r.Alpha 1-antitrypsin
3.Imaging
Ultrasound is used to assess the degree of cirrhosis:
a.small and nodular liver in advanced cirrhosis
b.increased echogenicity with irregular appearing areas.
Ultrasound may also screen for
a.hepatocellular carcinoma
b.portal hypertension
c.Budd-Chiari syndrome by checking the blood flow in the hepatic vein
FibroScan (transient elastography) uses elastic waves to assess liver stiffness which can grade the severity of cirrhosis.
Abdominal CT and liver and bile duct MRI - may show the the degree of liver cirrhosis
4.Imaging of the bile ducts, such as
ERCP Endoscopic_retrograde_cholangiopancreatography or
MRCP Magnetic_resonance_cholangiopancreatography (MRI of biliary tract and pancreas)
can show abnormalities in the liver
5.Endoscopy
Gastroscopy is performed in patients with liver cirrhosis to exclude the possibility of esophageal varices.
Saturday, October 25, 2008
A Simple Guide to Cutaneous Larva migrans
A Simple Guide to Cutaneous Larva migrans
----------------------------------------------
What is Cutaneous Larva migrans?
------------------------------------
Cutaneous Larva migrans is a common skin condition which appears as a red snake-like itchy rash caused by penetration and subsequent migration of larvae of various worm parasites.
The condition is benign and self-limited.
It is most commonly found in tropical countries.
Who is at risk from Cutaneous Larva migrans?
---------------------------------------
1.People of all ages are affected but it is more common in children
2.It is more common in hot tropical climates
3.Certain occupations that involve contact with warm, moist, sandy soil:
Farmer
Gardener
4.Certain hobbies that involve contact with warm, moist, sandy soil:
Tropical climate travellers
Barefoot beach goers
Children building sandcastles
What are the causes of Cutaneous Larva migrans?
--------------------------------------------------
The larvae usually hatch from eggs laid in animal faeces and then penetrate through the intact skin of the children or adults.
After shedding their covering, they begin migrating in the epidermis.
Because they are unable to penetrate through the dermis, the disease remains limited to the skin of humans.
THE MOST COMMON PARASITES ARE:
DOG HOOKWORMS:
Ancylostoma braziliense
Ancylostoma caninum
Uncinaria stenocephala
Rarer causes are:
Ancylostoma tubaeforme (cat hookworm)
Necator americanus (human hookworm)
Ancylostoma duodenale
What are Signs and symptoms of Cutaneous Larva migrans?
----------------------------------------------------------
Symptoms:
1.prickling sensation at the site within 30 minutes of larva penetration of the skin
2.Intense itchiness
3.Red linear lesions that moves
4.walking barefoot on the beach in a tropical location
Signs:
1.Itchy, red, raised papules or vesicles
2.snakelike, slightly elevated, red tunnels that are 2-3mm wide and 3-4 cm long from the penetration site
3.Vesicles with clear fluid
4.Tract movement of 1-2 cm/day
5.peripheral eosinophilia (Loeffler syndrome),
6.migratory lung infiltrates,
7.Lesions are typically present on the distal lower extremities,
the dorsa of the feet and the interdigital spaces of the toes,
anogenital region,
the buttocks,
the hands, and
the knees.
How is the diagnosis of Cutaneous Larva migrans made?
--------------------------------------------------------
Diagnosis is mostly based on the
1.classic clinical appearance of the eruption.
2.peripheral eosinophilia on a Complete Blood Count
3.increased IgE levels on total serum immunoglobulin determinations.
4. skin biopsy taken just before leading edge of a tract may show
a larva (periodic acid-Schiff positive) in a
suprabasalar burrow,
basal layer tracts,
spongiosis
intraepidermal vesicles,
necrotic keratinocytes,
an epidermal and upper dermal chronic inflammatory infiltrate with many eosinophils.
What are the complications of Cutaneous Larva migrans?
-----------------------------------------------
1. secondary bacterial infection, usually with Streptococcus pyogenes, may lead to cellulitis.
2. Allergic reactions may occur.
What is the treatment of Cutaneous Larva migrans?
---------------------------------------------------------
The condition is usually self-limiting.
The intense itchiness and risk for infection may require treatment.
Invasive treatment:
---------------------
1.liquid nitrogen cryotherapy for progressive end of larval burrow.
2.electrocautery
Medication:
----------------
1.Thiabendazole
Thiabendazole is the best medication
Topical application is used for early, localized lesions.
The oral route is preferred for widespread lesions or unsuccessful topical treatment.
2.Mebendazole (Vermox)
Broad-spectrum anthelmintic that inhibits microtubule assembly and irreversibly blocks glucose uptake, thereby depleting the parasites' glycogen stores.
Other effective treatments include
3.albendazole,
4.ivermectin.
In most cases there is decreased itchiness within 24-48 hours and lesions resolve in 1 week.
5.Antibiotics are given if there are secondary bacterial superinfections.
6.Antihistamines are given for severe itchiness
What is the prognosis of Cutaneous Larva migrans ?
----------------------------------------------------
The prognosis is excellent.
This is a self-limiting disease.
Humans are accidental hosts and the larva usually dies within 4-8 weeks.
The lesions usually will disappear within 8 weeks to 1 year depending on complications.
What are the Preventive measures taken for Cutaneous Larva migrans ?
-----------------------------------------------------------------------------
Travellers to tropical regions and pet owners should be made aware of this condition.
Prevention is by avoiding direct skin contact with possible faecally contaminated soil.
----------------------------------------------
What is Cutaneous Larva migrans?
------------------------------------
Cutaneous Larva migrans is a common skin condition which appears as a red snake-like itchy rash caused by penetration and subsequent migration of larvae of various worm parasites.
The condition is benign and self-limited.
It is most commonly found in tropical countries.
Who is at risk from Cutaneous Larva migrans?
---------------------------------------
1.People of all ages are affected but it is more common in children
2.It is more common in hot tropical climates
3.Certain occupations that involve contact with warm, moist, sandy soil:
Farmer
Gardener
4.Certain hobbies that involve contact with warm, moist, sandy soil:
Tropical climate travellers
Barefoot beach goers
Children building sandcastles
What are the causes of Cutaneous Larva migrans?
--------------------------------------------------
The larvae usually hatch from eggs laid in animal faeces and then penetrate through the intact skin of the children or adults.
After shedding their covering, they begin migrating in the epidermis.
Because they are unable to penetrate through the dermis, the disease remains limited to the skin of humans.
THE MOST COMMON PARASITES ARE:
DOG HOOKWORMS:
Ancylostoma braziliense
Ancylostoma caninum
Uncinaria stenocephala
Rarer causes are:
Ancylostoma tubaeforme (cat hookworm)
Necator americanus (human hookworm)
Ancylostoma duodenale
What are Signs and symptoms of Cutaneous Larva migrans?
----------------------------------------------------------
Symptoms:
1.prickling sensation at the site within 30 minutes of larva penetration of the skin
2.Intense itchiness
3.Red linear lesions that moves
4.walking barefoot on the beach in a tropical location
Signs:
1.Itchy, red, raised papules or vesicles
2.snakelike, slightly elevated, red tunnels that are 2-3mm wide and 3-4 cm long from the penetration site
3.Vesicles with clear fluid
4.Tract movement of 1-2 cm/day
5.peripheral eosinophilia (Loeffler syndrome),
6.migratory lung infiltrates,
7.Lesions are typically present on the distal lower extremities,
the dorsa of the feet and the interdigital spaces of the toes,
anogenital region,
the buttocks,
the hands, and
the knees.
How is the diagnosis of Cutaneous Larva migrans made?
--------------------------------------------------------
Diagnosis is mostly based on the
1.classic clinical appearance of the eruption.
2.peripheral eosinophilia on a Complete Blood Count
3.increased IgE levels on total serum immunoglobulin determinations.
4. skin biopsy taken just before leading edge of a tract may show
a larva (periodic acid-Schiff positive) in a
suprabasalar burrow,
basal layer tracts,
spongiosis
intraepidermal vesicles,
necrotic keratinocytes,
an epidermal and upper dermal chronic inflammatory infiltrate with many eosinophils.
What are the complications of Cutaneous Larva migrans?
-----------------------------------------------
1. secondary bacterial infection, usually with Streptococcus pyogenes, may lead to cellulitis.
2. Allergic reactions may occur.
What is the treatment of Cutaneous Larva migrans?
---------------------------------------------------------
The condition is usually self-limiting.
The intense itchiness and risk for infection may require treatment.
Invasive treatment:
---------------------
1.liquid nitrogen cryotherapy for progressive end of larval burrow.
2.electrocautery
Medication:
----------------
1.Thiabendazole
Thiabendazole is the best medication
Topical application is used for early, localized lesions.
The oral route is preferred for widespread lesions or unsuccessful topical treatment.
2.Mebendazole (Vermox)
Broad-spectrum anthelmintic that inhibits microtubule assembly and irreversibly blocks glucose uptake, thereby depleting the parasites' glycogen stores.
Other effective treatments include
3.albendazole,
4.ivermectin.
In most cases there is decreased itchiness within 24-48 hours and lesions resolve in 1 week.
5.Antibiotics are given if there are secondary bacterial superinfections.
6.Antihistamines are given for severe itchiness
What is the prognosis of Cutaneous Larva migrans ?
----------------------------------------------------
The prognosis is excellent.
This is a self-limiting disease.
Humans are accidental hosts and the larva usually dies within 4-8 weeks.
The lesions usually will disappear within 8 weeks to 1 year depending on complications.
What are the Preventive measures taken for Cutaneous Larva migrans ?
-----------------------------------------------------------------------------
Travellers to tropical regions and pet owners should be made aware of this condition.
Prevention is by avoiding direct skin contact with possible faecally contaminated soil.
Friday, October 24, 2008
A Simple Guide to Folliculitis
A Simple Guide to Folliculitis
----------------------------------------------
What is Folliculitis?
------------------------------------
Folliculitis is a bacterial infection of the skin hair follicle.
Who is at risk from Folliculitis?
---------------------------------------
People of all ages are affected .
It is more common in diabetes and people with low immune system.
What are the causes of Folliculitis?
--------------------------------------------------
1.The cause is infection of bacteria such as Staphylococcus aureus.
2.Poor skin hygiene
3.Skin damaged by eczema and dermatitis
4.Nasal transport of Staphylococcus aureus.
5.May complicate diabetes and low immune system patients like leukemia.
What are Signs and symptoms of Folliculitis?
---------------------------------------------
Symptoms:
1.Occurs at root of a hair follicle
2.superficial pustule or nodule
3.May become chronic at beard area.
4.May be painful
How is the diagnosis of Folliculitis made?
--------------------------------------------------------
1.pustule at root of hair.
2.Skin scraping for microscopic examination, culture and sensitivity.
3.Blood count.
What are the complications of Folliculitis?
-----------------------------------------------
1.Fungal infection
2.furuncle or carbuncle which are bigger and deeper areas of infection.
What is the treatment of Folliculitis?
------------------------------------
A. Skin hygiene
--------------------------
1. clean skin with antiseptic.
2. avoid scratching the skin
3. avoid plaster and poultices
4. cover with gauze after skin injury
B. Medicines:
-----------------
1. topical antibacterials such as bacitracin, neomycin, gentamycin, tetracycline creams
2. Oral Antibiotics may be given if necessary.
3. Complicated conditions such as carbuncles may require surgical debridement.
What is the prognosis of Folliculitis ?
------------------------------------------
Generally good to excellent but may recur.
Prompt treatment is important to prevent complication
What are the Preventive measures taken for Folliculitis?
--------------------------------------------------------
1.Good skin hygiene
2.Healthy lifestyle with balanced diet and adequate sleep.
3.Avoid scratching of skin
4.Use clean razors for shaving
5.Avoid plasters and poultices.
Thursday, October 23, 2008
A Simple Guide to Prickly Heat
A Simple Guide to Prickly Heat
----------------------------------------------
What is Prickly Heat?
------------------------------------
Prickly Heat(also known as miliaria) is a common non contagious disease which appears as acute itchy red rash on the body due to retained sweat.
Who is at risk from Prickly Heat?
---------------------------------------
People of all ages are affected but it is more common in children and infants due to their underdeveloped sweat glands.
It is more common in hot and humid conditions.
What are the types of Prickly Heat?
----------------------------------------------
I.Miliaria crystallina-
minute superficial vesicular lesions that normally do not cause any symptoms
2.Miliaria rubra -
deeper layer inflammatory lesions causing the typical appearance of redness (hence rubra) and larger blister-like lesions.
There is intense itching with a lack of sweating to affected areas.
This is the most common form of prickly heat.
3.Miliaria profunda-
the most severe form of miliaria due to the rapid spread and severe burning sensations.
The obstruction is deep in the structure of the sweat gland resulting in the sweat to leak between the superficial and deep layers of the skin.
The rash occurs within hours of an activity provoking sweating and disappear within hours when the stimulus for the sweating is removed.
The risk of heat exhaustion is higher.
What are the causes of Prickly Heat?
--------------------------------------------------
The cause is the result of the keratin or dead skin cells or bacteria such as Staphylococcus epidermidis of the skin blocking the sweat ducts.
The occluded sweat ducts ruptures when sweating occur and the sweat form an intraepidermal vesicle which leads to irritation(prickly sensation) and itchiness.
Secondary infection may occurs from invasion of staphalococcus.
What are Signs and symptoms of Prickly Heat?
---------------------------------------------
Symptoms:
1.Occurs in humid hot weather
2.Small red papulovesicular rashes
3.Occurs on the face, neck, under the breasts, trunk, under the scrotum, skin folds, behind knee and antecubital fossa.
4.Usually very itchy
5.Rash usually presents with prickly sensation
How is the diagnosis of Prickly Heat made?
--------------------------------------------------------
1.Symptoms and signs of small rashes occuring in hot humid condition with itchiness and prickly sensation
2.Skin scraping for microscopic examination.
What are the complications of Prickly Heat?
-----------------------------------------------
1.Fungal infection
2.bacterial infection
What is the treatment of Prickly Heat?
--------------------------------------------------
A. Cool Environment
--------------------------
1. air-conditioned environment
2. avoid heat and sweat-inducing activities
3. avoid occlusive clothing,
4. take frequent cool showers.
B. Medicines:
-----------------
1. topical antibacterials may reduce the symptoms in miliaria rubra
2. anti-itch preparations such as calamine or menthol preparations
3. topical steroid creams,
4. Avoid oil based preparations because they increase blockage to the sweat glands.
5. Oral Antibiotics may be given if there is secondary infection.
6. Oral antihistamines may be given if itch is troublesome.
7. VItamin C or A in high dosages have not been found to be effective
What is the prognosis of Prickly Heat ?
------------------------------------------
Generally good to excellent but may recur.
Environmental factors like humidty and heat should be avoided.
What are the Preventive measures taken for Prickly Heat ?
--------------------------------------------------------
1.Good skin hygiene
2.Healthy lifestyle with balanced diet and adequate sleep.
3.Wear light clothing
4.Reduce sweating (use air conditioner)
5.Frequent showers should help
6.Avoid heat and humidity.
----------------------------------------------
What is Prickly Heat?
------------------------------------
Prickly Heat(also known as miliaria) is a common non contagious disease which appears as acute itchy red rash on the body due to retained sweat.
Who is at risk from Prickly Heat?
---------------------------------------
People of all ages are affected but it is more common in children and infants due to their underdeveloped sweat glands.
It is more common in hot and humid conditions.
What are the types of Prickly Heat?
----------------------------------------------
I.Miliaria crystallina-
minute superficial vesicular lesions that normally do not cause any symptoms
2.Miliaria rubra -
deeper layer inflammatory lesions causing the typical appearance of redness (hence rubra) and larger blister-like lesions.
There is intense itching with a lack of sweating to affected areas.
This is the most common form of prickly heat.
3.Miliaria profunda-
the most severe form of miliaria due to the rapid spread and severe burning sensations.
The obstruction is deep in the structure of the sweat gland resulting in the sweat to leak between the superficial and deep layers of the skin.
The rash occurs within hours of an activity provoking sweating and disappear within hours when the stimulus for the sweating is removed.
The risk of heat exhaustion is higher.
What are the causes of Prickly Heat?
--------------------------------------------------
The cause is the result of the keratin or dead skin cells or bacteria such as Staphylococcus epidermidis of the skin blocking the sweat ducts.
The occluded sweat ducts ruptures when sweating occur and the sweat form an intraepidermal vesicle which leads to irritation(prickly sensation) and itchiness.
Secondary infection may occurs from invasion of staphalococcus.
What are Signs and symptoms of Prickly Heat?
---------------------------------------------
Symptoms:
1.Occurs in humid hot weather
2.Small red papulovesicular rashes
3.Occurs on the face, neck, under the breasts, trunk, under the scrotum, skin folds, behind knee and antecubital fossa.
4.Usually very itchy
5.Rash usually presents with prickly sensation
How is the diagnosis of Prickly Heat made?
--------------------------------------------------------
1.Symptoms and signs of small rashes occuring in hot humid condition with itchiness and prickly sensation
2.Skin scraping for microscopic examination.
What are the complications of Prickly Heat?
-----------------------------------------------
1.Fungal infection
2.bacterial infection
What is the treatment of Prickly Heat?
--------------------------------------------------
A. Cool Environment
--------------------------
1. air-conditioned environment
2. avoid heat and sweat-inducing activities
3. avoid occlusive clothing,
4. take frequent cool showers.
B. Medicines:
-----------------
1. topical antibacterials may reduce the symptoms in miliaria rubra
2. anti-itch preparations such as calamine or menthol preparations
3. topical steroid creams,
4. Avoid oil based preparations because they increase blockage to the sweat glands.
5. Oral Antibiotics may be given if there is secondary infection.
6. Oral antihistamines may be given if itch is troublesome.
7. VItamin C or A in high dosages have not been found to be effective
What is the prognosis of Prickly Heat ?
------------------------------------------
Generally good to excellent but may recur.
Environmental factors like humidty and heat should be avoided.
What are the Preventive measures taken for Prickly Heat ?
--------------------------------------------------------
1.Good skin hygiene
2.Healthy lifestyle with balanced diet and adequate sleep.
3.Wear light clothing
4.Reduce sweating (use air conditioner)
5.Frequent showers should help
6.Avoid heat and humidity.
Wednesday, October 22, 2008
A Simple Guide to Osteogenesis Imperfecta
A Simple Guide to Osteogenesis Imperfecta
--------------------------------------------
What is Osteogenesis Imperfecta(also known as Brittle Bones)?
---------------------------------------------------------------------
Osteogenesis imperfecta (OI) is an inherited disorder of the connective tissue resulting in imperfect bone formation and hence causing fractures in childhood.
It also causes fractures in adults.
Who is at risk of Osteogenesis Imperfecta?
-----------------------------------------------
Osteogenesis Imperfecta is a congenital condition affecting 2 forms of genetic disorder:
1.autosomal dominant - usually milder with frequent fractures
2.autosomal recessive - usually more severe and can lead to early death
Therefore there is always a family history of fractures of children in the family.
usually resulting from abnormalities of the genes that control the production of a protein called ; it has nothing to do with the calcium part of bone, which is what shows up on X-rays
What causes Osteogenesis Imperfecta?
----------------------------------
Osteogenesis Imperfecta is a condition resulting from impaired maturation of the collagen fibres or synthesis of abnormal collagen.
Collagen is the main protein in bone and is necessary for the bone to form strong bone matrix.
The abnormal collagen results in soft fragile bones, ligamentous laxity and thin sclera.
In the autosomal dominant form of Osteogenesis Imperfecta, the condition can be passed from one generation to the next.
Sometime the cause is a new genetic mutation which results in the Osteogenesis Imperfecta.
There is no previous history of Osteogenesis Imperfecta.
This has been seen in IVF of frozen egg from mothers trying for a pregnancy.
What are the symptoms of Osteogenesis Imperfecta?
-------------------------------------------------
Symptoms:
---------------
1.fractures is the most common symptom especially in newborns.
Multiple fractures may occur easily in the newborns and pose a danger to life.
As the child grow older the risk of fractures decreases especially after puberty.
2.lax joints
3.eyes conjunctiva(white)may be blue or grey.
4.teeth may be discoloured and fragile.
5.increased liability to bruising due to the abnormal collagen in the lining of small blood vessels.
6.Deafness is due to problems in the small bones in the middle ear which may be fractured or deformed so that sound waves cannot be transmitted easily to the inner ear
7.Hernias are due to poor formation of collagen fibres or abnormal collagen in the muscles.
8.Excessive sweating or intolerance of heat - the cause of this is unknown.
9.Dwarfism and structural abnormalities may occur due to basic defect and frequent fractures
10.Mental development is not affected
How do you made the diagnosis of Osteogenesis Imperfecta?
-------------------------------------------------
Diagnosis of Osteogenesis Imperfecta is often based on
1. history and pattern of fractures
2. blue or gray whites of the eyes.
3.X-rays in severe cases -shows previous fractures and deformities
The bones may appear demineralised .
4.wormian bones are additional small bones seen in the sutures between the scalp bones.
They occur in 50% cases of Osteogenesis Imperfecta.
5.Specialised test for diagnosis of Osteogenesis Imperfecta involve taking a small piece of skin, culturing the cells and chemically examining the collagen produced.
6.Another specialized test uses a blood sample to search for mutations of the genes coding for the collagen of bone.
What are the complications of Osteogenesis Imperfecta?
-------------------------------------------------------
The complications of Osteogenesis Imperfecta are:
1. multiple frequent fractures of the bone,
2. deformities of the bone and body
3. death in newborns from multiple fractures
What is the treatment of Osteogenesis Imperfecta?
-------------------------------------------------------
1.Good treatment of fractures to make sure that the bones healed without deformities.
Immobilization of fractures can lead to the loss of bone so early mobilization of the patient is important.
2.Surgical use of fixed or telescopic metal rods inserted into the shafts of bones can prevent appreciable deformity.
3.occupational therapy is important in preventing falls especially with handrails and other adaptation to the home.
4.no drug treatment including growth hormone have been effective.
Various bisphosphonate drugs trials are in progress.
There has encouraging evidence of their effectiveness in some patients.
5.Women with Osteogenesis Imperfecta may try Hormone Replacement Therapy(HRT) at menopause since HRT has been know to improve the bone structure and also prevent heart attacks.
However there is a very small risk of breast cancer.
In the case of Osteogenesis Imperfecta ,the advantages of HRT may be greater than the disadvantages as the chances of fractures is higher after the menopause.
6.Stopping smoking is important because smoking diminishes the bone by up to 5 per cent, thus increasing the risk of fractures.
What is the prognosis of Osteogenesis Imperfecta?
----------------------------------------
Prognosis depends on the severity of Osteogenesis Imperfecta.
In very severe cases, death within several years
In less severe cases, multiple and frequent fractures may occur followed by deformities.
--------------------------------------------
What is Osteogenesis Imperfecta(also known as Brittle Bones)?
---------------------------------------------------------------------
Osteogenesis imperfecta (OI) is an inherited disorder of the connective tissue resulting in imperfect bone formation and hence causing fractures in childhood.
It also causes fractures in adults.
Who is at risk of Osteogenesis Imperfecta?
-----------------------------------------------
Osteogenesis Imperfecta is a congenital condition affecting 2 forms of genetic disorder:
1.autosomal dominant - usually milder with frequent fractures
2.autosomal recessive - usually more severe and can lead to early death
Therefore there is always a family history of fractures of children in the family.
usually resulting from abnormalities of the genes that control the production of a protein called ; it has nothing to do with the calcium part of bone, which is what shows up on X-rays
What causes Osteogenesis Imperfecta?
----------------------------------
Osteogenesis Imperfecta is a condition resulting from impaired maturation of the collagen fibres or synthesis of abnormal collagen.
Collagen is the main protein in bone and is necessary for the bone to form strong bone matrix.
The abnormal collagen results in soft fragile bones, ligamentous laxity and thin sclera.
In the autosomal dominant form of Osteogenesis Imperfecta, the condition can be passed from one generation to the next.
Sometime the cause is a new genetic mutation which results in the Osteogenesis Imperfecta.
There is no previous history of Osteogenesis Imperfecta.
This has been seen in IVF of frozen egg from mothers trying for a pregnancy.
What are the symptoms of Osteogenesis Imperfecta?
-------------------------------------------------
Symptoms:
---------------
1.fractures is the most common symptom especially in newborns.
Multiple fractures may occur easily in the newborns and pose a danger to life.
As the child grow older the risk of fractures decreases especially after puberty.
2.lax joints
3.eyes conjunctiva(white)may be blue or grey.
4.teeth may be discoloured and fragile.
5.increased liability to bruising due to the abnormal collagen in the lining of small blood vessels.
6.Deafness is due to problems in the small bones in the middle ear which may be fractured or deformed so that sound waves cannot be transmitted easily to the inner ear
7.Hernias are due to poor formation of collagen fibres or abnormal collagen in the muscles.
8.Excessive sweating or intolerance of heat - the cause of this is unknown.
9.Dwarfism and structural abnormalities may occur due to basic defect and frequent fractures
10.Mental development is not affected
How do you made the diagnosis of Osteogenesis Imperfecta?
-------------------------------------------------
Diagnosis of Osteogenesis Imperfecta is often based on
1. history and pattern of fractures
2. blue or gray whites of the eyes.
3.X-rays in severe cases -shows previous fractures and deformities
The bones may appear demineralised .
4.wormian bones are additional small bones seen in the sutures between the scalp bones.
They occur in 50% cases of Osteogenesis Imperfecta.
5.Specialised test for diagnosis of Osteogenesis Imperfecta involve taking a small piece of skin, culturing the cells and chemically examining the collagen produced.
6.Another specialized test uses a blood sample to search for mutations of the genes coding for the collagen of bone.
What are the complications of Osteogenesis Imperfecta?
-------------------------------------------------------
The complications of Osteogenesis Imperfecta are:
1. multiple frequent fractures of the bone,
2. deformities of the bone and body
3. death in newborns from multiple fractures
What is the treatment of Osteogenesis Imperfecta?
-------------------------------------------------------
1.Good treatment of fractures to make sure that the bones healed without deformities.
Immobilization of fractures can lead to the loss of bone so early mobilization of the patient is important.
2.Surgical use of fixed or telescopic metal rods inserted into the shafts of bones can prevent appreciable deformity.
3.occupational therapy is important in preventing falls especially with handrails and other adaptation to the home.
4.no drug treatment including growth hormone have been effective.
Various bisphosphonate drugs trials are in progress.
There has encouraging evidence of their effectiveness in some patients.
5.Women with Osteogenesis Imperfecta may try Hormone Replacement Therapy(HRT) at menopause since HRT has been know to improve the bone structure and also prevent heart attacks.
However there is a very small risk of breast cancer.
In the case of Osteogenesis Imperfecta ,the advantages of HRT may be greater than the disadvantages as the chances of fractures is higher after the menopause.
6.Stopping smoking is important because smoking diminishes the bone by up to 5 per cent, thus increasing the risk of fractures.
What is the prognosis of Osteogenesis Imperfecta?
----------------------------------------
Prognosis depends on the severity of Osteogenesis Imperfecta.
In very severe cases, death within several years
In less severe cases, multiple and frequent fractures may occur followed by deformities.
Tuesday, October 21, 2008
A Simple Guide to Gynecomastia
A Simple Guide to Gynecomastia
----------------------------------------
What is Gynecomastia?
----------------------------
Gynecomastia is unilateral or bilateral enlargement in the glandular tissue of the breast in males.
What causes Gynecomastia?
---------------------------------
The causes of gynecomastia is not completely clear.
It is believed to be caused by an imbalance of sex hormones especially during puberty.
A.Hormonal:
----------------------
1.In male babies the painless swelling of the breast may occur due to the effects of the mother's female hormones.
The swelling usually subsides after a few weeks.
2.At Puberty for boys the development of breasts is due to the increased ratio of free estradiol to free testesterone.
In most cases the breasts may disappear after 1 year.
3.Some cases of Gynecomastia may be due to ingestion of female hormones injected into chicken and ducks
B.Genetic
---------------------
Some cases of male hypogonadism causing reduced testosterone.
C.Liver cirrhosis
---------------------
Failure of metabolism of circulating estrogens can increase the female hormones in the adults and cause Gynecomastia
D.Medications:
---------------------
a.Spironolactone
b.digoxin
c.cimetidine
d.maxolon
E.Tumors
----------------
Testicular or Pituitary Tumors may cause increased estrogen and reduced testesterone and hence increase the production of breasts.
What are the symptoms of Gynecomastia?
---------------------------------------------------
The Symptoms of Gynecomastia are:
1.Pain usually present in all cases except in babies
2.swelling of the breasts or the nipple area in males
Signs:
1.redness of the breast
2.swelling of the breast tissue
3.Local tenderness of swollen area
How is diagnosis of Gynecomastia confirmed?
----------------------------------------------
1. clinical features
2. Endocrine blood tests including HCG levels
3. Liver function tests
4.Ultrasound scan of the breasts
What is the treatment of Gynecomastia?
------------------------------------
1.treat underlying cause
2.Medications causing Gynecomastia should be stopped.
3.cosmetic surgery-liposuction, gland excision, reduction mammoplasty,
4.Tamoxifen if necessary
5.Radiation therapy may prevent gynecomastia in patients with prostate cancer prior to estrogen therapy.
What is the Prognosis of Gynecomastia?
------------------------------------
Most cases has good prognosis.
Aldolescent cases usually regress spontaneously.
Monday, October 20, 2008
A Simple Guide to Intermittent Claudication
A Simple Guide to Intermittent claudication
-----------------------------------------------------
What are Intermittent claudication?
---------------------------------------------
Intermittent claudication is a symptom of ischemic muscle pain usually in the calf muscles due to inadequate blood supply during exercise.
It is usually relieved by rest.
Who is at risk of Intermittent claudication?
-----------------------------------------------------------------
1.Age older than 65 years
2.men older than 50 years affected more than women.
3.smoking
What are the causes of Intermittent claudication?
-------------------------------------------------------
The causes of intermittent claudication are:
1.vascular intermittent claudication caused by peripheral arterial disease(atherosclerosis)- most common cause
2.Neurogenic intermittent claudication caused by spinal canal stenosis.
What are the symptoms of Intermittent claudication?
----------------------------------------------
The symptoms and signs are:
1.Pain in the leg especially when walking a certain distance, disappear after rest, recur again after walking
2.Paraesthesia or numbness of the leg
3.Decrease in Pulse in the leg arteries(dorsalis pedis or posterior tibial arteries)
4.Decreased in temperature due to poorer blood flow
5.Pallor of the skin of leg when leg is raised upwards to 60 degrees
6.Redness of the skin when limb is placed downwards
7.Cyanosis if blood supply to the leg is compromised
8.Atrophic changes like loss of hair
9.Bruits may be heard where the arteries are narrowed
10.Paralysis of leg if condition worsen
What are the investigations needed in assessment of Intermittent claudication?
-------------------------------------------------------------------------------------
The type, size, location and depth of the arterial narrowing in the legs can be determined:
1.Ultrasound (non-invasive)
2.Arteriography where a dye is injected into the artery to determine the areas of narrowing.
What is the treatment for Intermittent claudication?
-------------------------------------------
In patients who smoke, smoking cessation is the most effective treatment. Exercise can improve symptoms as do Surgery is only indicated in severe cases with limb-threatening ischemia or lifestyle-limiting claudication. The vascular surgeon will perform an . Low molecular weight heparin (LMWH), oral anticoagulants (warfarin), vitamin E or chelation therapy is not effective.
A. Healthy lifestyle
--------------------------
1. Stop smoking in smokers.
2. Reduce weight in the obese
3. Exercise to improve blood flow can improve symptoms
4. Foot hygiene and appropriate chiropody
B.Medical treatment:
-------------------------
medication to control the
1.lipid profile - reduction of fats will reduce arteriosclerosis eg. statins
2.diabetes - reduction of blood sugar to normal reduce the risk of diabetic arteriosclerosis
3.hypertension - hypertensive drugs has been found particularly useful in the treatmeent of hypertension and intermittent claudication:
Angiotensin converting enzyme (ACE) inhibitors,'
beta-blockers,
4.blood clotting
antiplatelet agents (ASA and clopidogrel),
5.vasodilators
pentoxifylline
cilostazol ( PDE3 inhibitor)
C. Surgical treatment:
---------------------------
1.endarterectomy of leg arteries
2.arterial bypass of localised areas of obstruction
3.Sympathectomy may help in some resistant cases.
What is the prognosis for Intermittent claudication?
------------------------------------------------------
If treated early, prognosis is fair.
Surgical treatment is only needed if progressive gangrene develops.
How can Intermittent claudication be prevented?
-----------------------------------------------------
1.Stop smoking
2.Reduce weight
3.Exercise
4.Aviod prolonged walking
5.Put your feet up when sitting
-----------------------------------------------------
What are Intermittent claudication?
---------------------------------------------
Intermittent claudication is a symptom of ischemic muscle pain usually in the calf muscles due to inadequate blood supply during exercise.
It is usually relieved by rest.
Who is at risk of Intermittent claudication?
-----------------------------------------------------------------
1.Age older than 65 years
2.men older than 50 years affected more than women.
3.smoking
What are the causes of Intermittent claudication?
-------------------------------------------------------
The causes of intermittent claudication are:
1.vascular intermittent claudication caused by peripheral arterial disease(atherosclerosis)- most common cause
2.Neurogenic intermittent claudication caused by spinal canal stenosis.
What are the symptoms of Intermittent claudication?
----------------------------------------------
The symptoms and signs are:
1.Pain in the leg especially when walking a certain distance, disappear after rest, recur again after walking
2.Paraesthesia or numbness of the leg
3.Decrease in Pulse in the leg arteries(dorsalis pedis or posterior tibial arteries)
4.Decreased in temperature due to poorer blood flow
5.Pallor of the skin of leg when leg is raised upwards to 60 degrees
6.Redness of the skin when limb is placed downwards
7.Cyanosis if blood supply to the leg is compromised
8.Atrophic changes like loss of hair
9.Bruits may be heard where the arteries are narrowed
10.Paralysis of leg if condition worsen
What are the investigations needed in assessment of Intermittent claudication?
-------------------------------------------------------------------------------------
The type, size, location and depth of the arterial narrowing in the legs can be determined:
1.Ultrasound (non-invasive)
2.Arteriography where a dye is injected into the artery to determine the areas of narrowing.
What is the treatment for Intermittent claudication?
-------------------------------------------
In patients who smoke, smoking cessation is the most effective treatment. Exercise can improve symptoms as do Surgery is only indicated in severe cases with limb-threatening ischemia or lifestyle-limiting claudication. The vascular surgeon will perform an . Low molecular weight heparin (LMWH), oral anticoagulants (warfarin), vitamin E or chelation therapy is not effective.
A. Healthy lifestyle
--------------------------
1. Stop smoking in smokers.
2. Reduce weight in the obese
3. Exercise to improve blood flow can improve symptoms
4. Foot hygiene and appropriate chiropody
B.Medical treatment:
-------------------------
medication to control the
1.lipid profile - reduction of fats will reduce arteriosclerosis eg. statins
2.diabetes - reduction of blood sugar to normal reduce the risk of diabetic arteriosclerosis
3.hypertension - hypertensive drugs has been found particularly useful in the treatmeent of hypertension and intermittent claudication:
Angiotensin converting enzyme (ACE) inhibitors,'
beta-blockers,
4.blood clotting
antiplatelet agents (ASA and clopidogrel),
5.vasodilators
pentoxifylline
cilostazol ( PDE3 inhibitor)
C. Surgical treatment:
---------------------------
1.endarterectomy of leg arteries
2.arterial bypass of localised areas of obstruction
3.Sympathectomy may help in some resistant cases.
What is the prognosis for Intermittent claudication?
------------------------------------------------------
If treated early, prognosis is fair.
Surgical treatment is only needed if progressive gangrene develops.
How can Intermittent claudication be prevented?
-----------------------------------------------------
1.Stop smoking
2.Reduce weight
3.Exercise
4.Aviod prolonged walking
5.Put your feet up when sitting
Wednesday, October 15, 2008
A Simple Guide To Atrial Fibrillation II
A Simple Guide To Atrial Fibrillation II
--------------------------------------------------------
What is the Complications of Atrial Fibrillation?
------------------------------------------------------
1.fibrosis of the atria
2.Enlarged atria and heart
3.Thrombosis to the brain(stroke),
intestines(ischemia),
fingers and toe(ischemia or gangrene)
What is the Treatment of Atrial Fibrillation?
------------------------------------------------------
The treatment of atrial fibrillation is aimed at
1.regulating the heart beat and rhythm- digoxin, dilatrend, betablockers
2.preventing blood clots to be thrown out in the blood stream -anticoagulants
3.In cases of uncontrolled tachycardia, immediate cardioversion may be done.
Regulating the heart beat:
----------------------------
a.rate control
Rate control is by drugs to reduce the heart rate to 60 to 100 bpm without changing to a regular rhythm.
The medications work by blocking the AV node reducing the electrical impulses to the ventricles.
1.Beta blockers such as metoprolol, atenolol, bisoprolol
2.Cardiac glycosides ( digoxin)
3.Calcium channel blockers (i.e. diltiazem or verapamil)
4.amiodarone has AV node blocking effects which can be used when other agents are contraindicated (eg.hypotension).
b.rhythm control
Rhythm control work to restore the regular heart rhythm and maintain it with drugs.
The anti-arrhythmic medications makes the heart tissue less excitable.
These medications are often used in concert with electrical cardioversion.
Prevention of blood clots in blood stream:
--------------------------------------------
Anticoagulation with drugs as below reduce the risk of blood clots being thrown out from the heart and blocking the passage of blood in the arteries of the heart or brain
1.aspirin
2.clopidogrel in those who are allergic to aspirin
3.warfarin or similar drugs.
4.heparin intravenously prevents blood clotting in urgent cases.
Cardioversion
---------------------
Cardioversion is the conversion of an abnormal heartbeat to a normal heartbeat using electrical or chemical means
1.Electrical cardioversion restores the heart rhythm by appying a DC electrical shock to the heart.
2.Chemical cardioversion uses medicine such as amiodarone, dronedarone, procainamide, ibutilide, propafenone or flecainide.
Cardioversion should not be done unless adequate anticoagulation has been given to patients for 48 hours.
There is a relapse rate of 1% following cardioversion.
3.Catheter ablation
It is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker Another method involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate.This method do not need a pacemaker.
4. Radiofrequency ablation uses radiofrequency energy to remove abnormal electrical pathways in heart tissue.
5. laser, cryothermy and high intensity ultrasound has been use to eliminate the responsible heart tissue causing the irregular heart beats.
Surgical Maze procedure
----------------------------
A series of incisions is made in the atriain a maze-like pattern.
This block abnormal electrical circuits that AF requires.
Minimaze surgery is a minimally invasive cardiac surgery that do not require a median sternotomy or cardiopulmonary bypass.
Laser, cryothermy, radiofrequency, or acoustic energy are used to destroy atrial tissue near the pulmonary veins and and other ablations to mimic the maze.
What is the prognosis of Atrial Fibrillation?
---------------------------------------------------
Most cases of patients treated with rate control and cardioversion with ablation has excellent prognosis, usually better than those with rhthym control.
Recurrence may recur especially if there is an underlying condition which cannot be cured.
What are the prevention measures for Atrial Fibrillation?
--------------------------------------------------------------
Rest and a healthy lifestyle may help to prevent an onset or recurrence of atrial fibrillation.
Avoid stress and anxiety.
--------------------------------------------------------
What is the Complications of Atrial Fibrillation?
------------------------------------------------------
1.fibrosis of the atria
2.Enlarged atria and heart
3.Thrombosis to the brain(stroke),
intestines(ischemia),
fingers and toe(ischemia or gangrene)
What is the Treatment of Atrial Fibrillation?
------------------------------------------------------
The treatment of atrial fibrillation is aimed at
1.regulating the heart beat and rhythm- digoxin, dilatrend, betablockers
2.preventing blood clots to be thrown out in the blood stream -anticoagulants
3.In cases of uncontrolled tachycardia, immediate cardioversion may be done.
Regulating the heart beat:
----------------------------
a.rate control
Rate control is by drugs to reduce the heart rate to 60 to 100 bpm without changing to a regular rhythm.
The medications work by blocking the AV node reducing the electrical impulses to the ventricles.
1.Beta blockers such as metoprolol, atenolol, bisoprolol
2.Cardiac glycosides ( digoxin)
3.Calcium channel blockers (i.e. diltiazem or verapamil)
4.amiodarone has AV node blocking effects which can be used when other agents are contraindicated (eg.hypotension).
b.rhythm control
Rhythm control work to restore the regular heart rhythm and maintain it with drugs.
The anti-arrhythmic medications makes the heart tissue less excitable.
These medications are often used in concert with electrical cardioversion.
Prevention of blood clots in blood stream:
--------------------------------------------
Anticoagulation with drugs as below reduce the risk of blood clots being thrown out from the heart and blocking the passage of blood in the arteries of the heart or brain
1.aspirin
2.clopidogrel in those who are allergic to aspirin
3.warfarin or similar drugs.
4.heparin intravenously prevents blood clotting in urgent cases.
Cardioversion
---------------------
Cardioversion is the conversion of an abnormal heartbeat to a normal heartbeat using electrical or chemical means
1.Electrical cardioversion restores the heart rhythm by appying a DC electrical shock to the heart.
2.Chemical cardioversion uses medicine such as amiodarone, dronedarone, procainamide, ibutilide, propafenone or flecainide.
Cardioversion should not be done unless adequate anticoagulation has been given to patients for 48 hours.
There is a relapse rate of 1% following cardioversion.
3.Catheter ablation
It is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker Another method involves ablating groups of cells near the pulmonary veins where atrial fibrillation is thought to originate.This method do not need a pacemaker.
4. Radiofrequency ablation uses radiofrequency energy to remove abnormal electrical pathways in heart tissue.
5. laser, cryothermy and high intensity ultrasound has been use to eliminate the responsible heart tissue causing the irregular heart beats.
Surgical Maze procedure
----------------------------
A series of incisions is made in the atriain a maze-like pattern.
This block abnormal electrical circuits that AF requires.
Minimaze surgery is a minimally invasive cardiac surgery that do not require a median sternotomy or cardiopulmonary bypass.
Laser, cryothermy, radiofrequency, or acoustic energy are used to destroy atrial tissue near the pulmonary veins and and other ablations to mimic the maze.
What is the prognosis of Atrial Fibrillation?
---------------------------------------------------
Most cases of patients treated with rate control and cardioversion with ablation has excellent prognosis, usually better than those with rhthym control.
Recurrence may recur especially if there is an underlying condition which cannot be cured.
What are the prevention measures for Atrial Fibrillation?
--------------------------------------------------------------
Rest and a healthy lifestyle may help to prevent an onset or recurrence of atrial fibrillation.
Avoid stress and anxiety.
Monday, October 13, 2008
A Simple Guide to Atrial Fibrillation I
A Simple Guide to Atrial Fibrillation I
------------------------------------------------
What is Atrial Fibrillation?
---------------------------------
Atrial Fibrillation is a heart condition where the disordered electrical impulses of the atrial muscle leads to irregular electrical impulses to the ventricular heart muscles resulting in irregular heart beats.
Who is at risk of Atrial Fibrillation?
-----------------------------------------
1.Age: 8% of people over 80 has AF
2.family history of AF increases risk by 30%.
What is the cause of Atrial Fibrillation?
---------------------------------------------------
Atrial Fibrillation is caused by underlying heart conditions such as:
1.Primary heart diseases:
a.coronary artery disease
b.mitral stenosis
c.mitral regurgitation
d.hypertrophic cardiomyopathy
e.pericarditis
f.congenital heart disease
g.previous heart surgery
2.Hypertension (High blood pressure)
3.Lung diseases such as
a.pneumonia,
b.lung cancer,
c.pulmonary embolism,
d.sarcoidosis
4.Excessive alcohol consumption
5.Hyperthyroidism
What are the Symptoms of Atrial Fibrillation?
------------------------------------------------------------
Atrial fibrillation often do not present with symptoms.
When they do the symptoms are generally non -life threatening:
Symptoms:
-----------
1.fast heartbeat or palpitations
2.Breathlessness
3.fainting
4.chest pain
Signs:
--------------
1.Pulse is fast and irregular in rhythm and strength
2.Angina pectoris(pain over heart area)
3.Congestive cardiac failure with ankle swelling and breathlessness
4.exercise intolerance
5.Abnormal ECG reading with absent P waves and irregular rhythm
6.Underlying heart disease such as hypertension, pericarditis, valvular disease of heart,
7.Underlying systemic disease such as hyperthyroidism, diabetes, stroke
How is diagnosis of Atrial Fibrillation made?
-------------------------------------------------------
1. History and physical examination
Palpitations, atrial fibrillation episodes
2. Blood tests:
renal function and electrolytes,
thyroid hormones, thyroid-stimulating hormone,
blood count.
Where there is chest pain,
blood cardiac enzymes and
coagulation tests are also done
3.Electrocardiogram
a.absence of P waves,
b.irregularity of R-R interval due to irregular conduction of impulses
4.Echocardiography
transthoracic echocardiogram is done in newly diagnosed AF to detect
valvular heart disease ,
left and right atrial size,
left ventricular size and function,
peak right ventricular pressure ,
presence of left ventricular hypertrophy
pericardial disease
5. Chest X-ray
chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested,
6.Transesophageal echocardiogram
transesophageal echocardiogram (TEE) is done to detect thrombus formation
7.Ambulatory holter monitoring
A holter monitor is a heart monitor which can be worn by the patient to check the heart rate and heart rhythm for 24 hours.
It can detect presence of AF.
8.Exercise stress testing
A threadmill test can gauge the heart rate in response to exertion.
------------------------------------------------
What is Atrial Fibrillation?
---------------------------------
Atrial Fibrillation is a heart condition where the disordered electrical impulses of the atrial muscle leads to irregular electrical impulses to the ventricular heart muscles resulting in irregular heart beats.
Who is at risk of Atrial Fibrillation?
-----------------------------------------
1.Age: 8% of people over 80 has AF
2.family history of AF increases risk by 30%.
What is the cause of Atrial Fibrillation?
---------------------------------------------------
Atrial Fibrillation is caused by underlying heart conditions such as:
1.Primary heart diseases:
a.coronary artery disease
b.mitral stenosis
c.mitral regurgitation
d.hypertrophic cardiomyopathy
e.pericarditis
f.congenital heart disease
g.previous heart surgery
2.Hypertension (High blood pressure)
3.Lung diseases such as
a.pneumonia,
b.lung cancer,
c.pulmonary embolism,
d.sarcoidosis
4.Excessive alcohol consumption
5.Hyperthyroidism
What are the Symptoms of Atrial Fibrillation?
------------------------------------------------------------
Atrial fibrillation often do not present with symptoms.
When they do the symptoms are generally non -life threatening:
Symptoms:
-----------
1.fast heartbeat or palpitations
2.Breathlessness
3.fainting
4.chest pain
Signs:
--------------
1.Pulse is fast and irregular in rhythm and strength
2.Angina pectoris(pain over heart area)
3.Congestive cardiac failure with ankle swelling and breathlessness
4.exercise intolerance
5.Abnormal ECG reading with absent P waves and irregular rhythm
6.Underlying heart disease such as hypertension, pericarditis, valvular disease of heart,
7.Underlying systemic disease such as hyperthyroidism, diabetes, stroke
How is diagnosis of Atrial Fibrillation made?
-------------------------------------------------------
1. History and physical examination
Palpitations, atrial fibrillation episodes
2. Blood tests:
renal function and electrolytes,
thyroid hormones, thyroid-stimulating hormone,
blood count.
Where there is chest pain,
blood cardiac enzymes and
coagulation tests are also done
3.Electrocardiogram
a.absence of P waves,
b.irregularity of R-R interval due to irregular conduction of impulses
4.Echocardiography
transthoracic echocardiogram is done in newly diagnosed AF to detect
valvular heart disease ,
left and right atrial size,
left ventricular size and function,
peak right ventricular pressure ,
presence of left ventricular hypertrophy
pericardial disease
5. Chest X-ray
chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested,
6.Transesophageal echocardiogram
transesophageal echocardiogram (TEE) is done to detect thrombus formation
7.Ambulatory holter monitoring
A holter monitor is a heart monitor which can be worn by the patient to check the heart rate and heart rhythm for 24 hours.
It can detect presence of AF.
8.Exercise stress testing
A threadmill test can gauge the heart rate in response to exertion.
Thursday, October 9, 2008
A Simple Guide to Osteomyelitis
A Simple Guide to Osteomyelitis
--------------------------------------
What is Osteomyelitis?
----------------------------
Osteomyelitis is an infection of the bone substance by pyogenic bacteria and fungus.
What causes Osteomyelitis?
----------------------------------
The most causes of Osteomyelitis is
1.Staphylococcus aureus bacteria(80%).
Other bacteria involved are:
2.Streptococci Group A & B
3.Enterobacter species including E.Coli
4.Haemophilus influenzae
5.Pneumococci
6.Serratia marcescens
Systemic mycotic (fungal) infections may also cause osteomyelitis.
1.Blastomyces dermatitidis
2.Coccidioides immitis.
In children,
-------------------
1.the long bones are usually affected in children.
2.Spread of bacteria occurs from the bloodstream from a skin boil, dental abscess, direct injury to the bone.
3.Acute osteomyelitis almost invariably occurs in children.
In adults
---------------
1.injury to the bone is the most common cause.
The bone injury is exposed to local infection in the skin or environment.
Staphylococcus aureus is the most common bacteria in osteomyelitis resulting from bone injury and infection.
Other bacteria such as Pseudomonas aeruginosa, E. coli, and Serratia marcescens, are also common.
2.The vertebrae and the pelvis are the bones most commonly affected in adults.
For osteomyelitis of the vertebral bodies,
50% are due to Staphylococcus aureus,
and the remaining 50%f are due to tuberculosis usually from the lungs.
3.Bone infection in adults are usually due to their lower resistance from
debilitation,
intravenous drug abuse,
infectious root-canal teeth,
other disease or drugs (e.g. immunosuppressive therapy).
What are the symptoms of Osteomyelitis?
-------------------------------------------------
Symptoms:
---------------
1.pain and swelling of the bone
2.fever
3.toxemia
Signs:
-----------
1.Hot tender bones
2.Throbbing pain of bones
3.Abscess and swelling
How do you made the diagnosis of Osteomyelitis?
-------------------------------------------------
Diagnosis of osteomyelitis is often based on:
1.radiologic results showing a translucent center with a ring of sclerosis(hardened bones)
2.Blood and bone cultures are normally required to identify the specific pathogen
What are the complications of Osteomyelitis?
-------------------------------------------------------
The complications of Osteomyelitis are:
1.fractures of the bone
2.amyloidosis
3.endocarditis
4.septicemia
What is the treatment of Osteomyelitis?
----------------------------------------
1.antibiotic therapy - usually as prolonged treatment lasting a matter of weeks or months.
2.Hyperbaric oxygen therapy has helped in the treatment of refractory osteomyelitis.
3.Immobilization of the bone affected(bed rest, plaster casts,splints)
4.Osteomyelitis may also need surgical debridement to remove pus and damaged bone tissues.
5.Severe cases may lead to the loss of a limb.
What is the prognosis of Osteomyelitis?
----------------------------------------
Prognosis depends on the rapidity of onset of treatment.
The faster the treatment the faster thee cure.
Otherwise the condition may become a chronic illness requiring multiple surgical procedures.
--------------------------------------
What is Osteomyelitis?
----------------------------
Osteomyelitis is an infection of the bone substance by pyogenic bacteria and fungus.
What causes Osteomyelitis?
----------------------------------
The most causes of Osteomyelitis is
1.Staphylococcus aureus bacteria(80%).
Other bacteria involved are:
2.Streptococci Group A & B
3.Enterobacter species including E.Coli
4.Haemophilus influenzae
5.Pneumococci
6.Serratia marcescens
Systemic mycotic (fungal) infections may also cause osteomyelitis.
1.Blastomyces dermatitidis
2.Coccidioides immitis.
In children,
-------------------
1.the long bones are usually affected in children.
2.Spread of bacteria occurs from the bloodstream from a skin boil, dental abscess, direct injury to the bone.
3.Acute osteomyelitis almost invariably occurs in children.
In adults
---------------
1.injury to the bone is the most common cause.
The bone injury is exposed to local infection in the skin or environment.
Staphylococcus aureus is the most common bacteria in osteomyelitis resulting from bone injury and infection.
Other bacteria such as Pseudomonas aeruginosa, E. coli, and Serratia marcescens, are also common.
2.The vertebrae and the pelvis are the bones most commonly affected in adults.
For osteomyelitis of the vertebral bodies,
50% are due to Staphylococcus aureus,
and the remaining 50%f are due to tuberculosis usually from the lungs.
3.Bone infection in adults are usually due to their lower resistance from
debilitation,
intravenous drug abuse,
infectious root-canal teeth,
other disease or drugs (e.g. immunosuppressive therapy).
What are the symptoms of Osteomyelitis?
-------------------------------------------------
Symptoms:
---------------
1.pain and swelling of the bone
2.fever
3.toxemia
Signs:
-----------
1.Hot tender bones
2.Throbbing pain of bones
3.Abscess and swelling
How do you made the diagnosis of Osteomyelitis?
-------------------------------------------------
Diagnosis of osteomyelitis is often based on:
1.radiologic results showing a translucent center with a ring of sclerosis(hardened bones)
2.Blood and bone cultures are normally required to identify the specific pathogen
What are the complications of Osteomyelitis?
-------------------------------------------------------
The complications of Osteomyelitis are:
1.fractures of the bone
2.amyloidosis
3.endocarditis
4.septicemia
What is the treatment of Osteomyelitis?
----------------------------------------
1.antibiotic therapy - usually as prolonged treatment lasting a matter of weeks or months.
2.Hyperbaric oxygen therapy has helped in the treatment of refractory osteomyelitis.
3.Immobilization of the bone affected(bed rest, plaster casts,splints)
4.Osteomyelitis may also need surgical debridement to remove pus and damaged bone tissues.
5.Severe cases may lead to the loss of a limb.
What is the prognosis of Osteomyelitis?
----------------------------------------
Prognosis depends on the rapidity of onset of treatment.
The faster the treatment the faster thee cure.
Otherwise the condition may become a chronic illness requiring multiple surgical procedures.
Monday, October 6, 2008
A Simple Guide to Systemic Lupus Erythematosis
A Simple Guide to Systemic Lupus Erythematosis
----------------------------------------------------
What is Systemic Lupus Erythematosis?
---------------------------------------
Systemic Lupus Erythematosis is a chronic multisystem autoimmune inflammatory disease which attacks the whole body.
It typically has a butterfly erythematous rash on the face.
It is not contagious.
Who is affected by Systemic Lupus Erythematosis?
---------------------------------------------------
Systemic Lupus Erythematosis is more common in women than in men(9:1 ratio)
Most cases begin at the age range of 15-45 years and occurs less frequently between the age of 45-70 years.
It occurs more frequently in blacks than in white people.
What is the Cause of Systemic Lupus Erythematosis?
-----------------------------------------------------
The exact cause of Systemic Lupus Erythematosis is not known.
1.It has been suggested that an autoimmune disease is the main cause of Systemic Lupus Erythematosis disease.
The antibodies produced by the body to fight germs starts to attack the body's own healthy tissue.
2.Psychological problems like stress and anxiety is not a cause of Systemic Lupus Erythematosis but has been known to trigger off the disease.
3.Some cases are induced by medications such as :
hydralazine
procainamide
penicillamine
isoniazid
What are the Symptoms and signs of Systemic Lupus Erythematosis?
-----------------------------------------------------------
The disease may be mild to severe.
There are also periods of remissions and activity.
During the active stage:
Systemic involvement:
-----------------------------
1.fever
2.anorexia
3.weakness
4.weight loss
5.Lymphadenopathy
Skin Mucosa Involvement:
-------------------------------
1.Typical butterfly erythrematous rash on the face
2.pleomorphic erythrematous and maculopapular lesions on the face, neck and extremeties.
3.Vasculitic nail bed and digital pulp lesions
4.Alopecia, petechiae, bullae, and mucous membrane lesions.
Musculoskeletal System:
---------------------------
1.Polyarthritis especially small joints of fingers
2.Arthritis milder and non erosive compared to rheumatoid arthritis
3.morning stiffness
4.muscle atrophy and weakness may occur
Eyes:
-----------
1.Retinal hemorrhages and exudates
2.Cytoid bodies
Lungs and Pleura:
-----------------------
1.Recurrent pleurisy
2.Pleural effusions - small
3.Pulmonary infiltrates
Cardiovascular
-----------------
1.Pericarditis
2.Endocarditis with vegetation on the mitral valve especially
Gastrointestinal
--------------------
1.Non specific nausea
2.Gastrointestinal ulcers, hemorrhage, necrosis
Renal
-------------
1.Focal membranous nephritis
2.Proliferative nephritis - deposit of autoimmune complexes on capillary walls give rise to typical wireloop changes and epithelial crescents in kidneys resulting in proteinuria, hematuria,and renal failure.
Central nervous system:
------------------------------
1.Lesions in the brain can cause mental disorders( dementia, psychosis,epilepsy), chores, cerebrovascular accidents,cranial nerve lesions.
2.Peripheral neuropathy of various types
Others:
-----------------
1.Thrombotic thrombocytopenic purpura
2.Sjogren's syndrome
How do you make the Diagnosis of Systemic Lupus Erythematosis?
------------------------------------------------------------
1.A history of facial butterfly rash, systemic symptoms
2.Blood for ESR, positive ANA(antnuclear Antibodies), LE cells
3.Full blood count for anemia, hemolytic anemia, neutopenia, thrombocytopenia, Coombs' test(usually positive)
4.Renal or skin biopsy
5.X- rays of the chest, abdomen and brain
6.MRI of brain, kidney,
What are the complications of Systemic Lupus Erythematosis?
-----------------------------------------------------------------
1.Severe Dermatitis with discoid lesions (maculopapular in nature)
2.Polyathritis with swelling of joints
3.Anemia
4.Pleural effusions
5.hemorrhage
6.Dementia
7.Renal failure
What is the treatment of Systemic Lupus Erythematosis?
--------------------------------------------------------------
There is no cure for SLE at the present moment.
Treatment is to relieve symptoms and prevent organs from deteriorating.
Patients with mild symptoms may not need any treatment.
Mild Cases:
---------------
1.short course of antiinflammatory medications such as NSAID or corticosteroids.
2.Rest and freedom from stress
Severe cases:
--------------------
Patients with serious illness which has affected their organ may require stronger medications:
1.high doses of corticosteroids intially intravenously, followed by oral medication whose dosage is reduced slowly to the minimum possible.
Corticosteroids are particularly helpful if internal organs are involved.
Side effects of corticosteroids include gastric problems, thinning of the bones, infection, facial puffiness, cataracts.
2.NSAIDs can reduce inflammation and pain especially in the musculoskeletal system.
Examples of NSAIDs include aspirin, ibuprofen, naproxen.
The side effects are stomach upset, abdominal pain, ulcers or GIT bleeding.
To reduce the side effects, NSAIDs are usually taken with food or H2 antagonist like cimetidine, ranitidine.
3.Antimalarial medication such as Hydroxychloroquine has been particularly effective for SLE patients with fatigue, skin, and joint disease.
Side effects include diarrhea, upset stomach, and eye pigment changes.
Eye pigment changes are rare, but require monitoring by an ophthalmologist
Other antimalarial drugs, such as chloroquine or quinacrine, are considered
4.Treatment for severe skin disease skin disease include dapsone and retinoic acid (Retin-A).
5.immunosuppressive medications are used for treating patients with more severe manifestations of SLE with damage to internal organ(s).
Examples of immunosuppressive medications include methotrexate, azathioprine (Imuran), cyclophosphamide, and cyclosporine .
Side effects are depression of blood cell counts and increased risks of infection and bleeding.
6. mycophenolate mofetil (Cellcept) is very effective in lupus with kidney disease.
It has been able to reverse active lupus kidney disease and maintain remission.
It's lower side effects made it more useful than immunosuppresive drugs.
7.plasmapheresis is used to remove antibodies and other immune substances from the blood to suppress immunity.
It has also help to to remove proteins (cryoglobulins) that can lead to vasculitis.
SLE patients with low platelet levels can have severe bleeding.
7.rituximab is an intravenously infused antibody that suppresses a particular white blood cell, the B cell, by reducing the number in the blood stream.
B cells play a central role in lupus activity, and when suppressed, the disease tends toward remission.
8.omega-3 fish oils could help patients with lupus by decreasing disease activity and possibly decreasing heart disease risk.
9.rest during periods of active disease
Poor sleep quality can cause fatigue in patients with SLE.
Sleep quality and the effect of underlying depression, lack of exercise can have an adverse effect on the health of SLE patients.
It is important to maintain muscle tone and range of motion in the joints.
10.Endstage kidney damage from SLE requires dialysis and/or a kidney transplant.
What is the prognosis of Systemic Lupus Erythematosis?
-------------------------------------------------------------
The prognosis depends on the severity of the disease
Severe cases with renal disease has poorer prognosis.
How is SLE prevented?
----------------------------
1.Adequate rest
2. Avoid stress
3. Avoid the sun and use sunscreen.
4.Healthy lifestyle with exercise prevents arthritis
----------------------------------------------------
What is Systemic Lupus Erythematosis?
---------------------------------------
Systemic Lupus Erythematosis is a chronic multisystem autoimmune inflammatory disease which attacks the whole body.
It typically has a butterfly erythematous rash on the face.
It is not contagious.
Who is affected by Systemic Lupus Erythematosis?
---------------------------------------------------
Systemic Lupus Erythematosis is more common in women than in men(9:1 ratio)
Most cases begin at the age range of 15-45 years and occurs less frequently between the age of 45-70 years.
It occurs more frequently in blacks than in white people.
What is the Cause of Systemic Lupus Erythematosis?
-----------------------------------------------------
The exact cause of Systemic Lupus Erythematosis is not known.
1.It has been suggested that an autoimmune disease is the main cause of Systemic Lupus Erythematosis disease.
The antibodies produced by the body to fight germs starts to attack the body's own healthy tissue.
2.Psychological problems like stress and anxiety is not a cause of Systemic Lupus Erythematosis but has been known to trigger off the disease.
3.Some cases are induced by medications such as :
hydralazine
procainamide
penicillamine
isoniazid
What are the Symptoms and signs of Systemic Lupus Erythematosis?
-----------------------------------------------------------
The disease may be mild to severe.
There are also periods of remissions and activity.
During the active stage:
Systemic involvement:
-----------------------------
1.fever
2.anorexia
3.weakness
4.weight loss
5.Lymphadenopathy
Skin Mucosa Involvement:
-------------------------------
1.Typical butterfly erythrematous rash on the face
2.pleomorphic erythrematous and maculopapular lesions on the face, neck and extremeties.
3.Vasculitic nail bed and digital pulp lesions
4.Alopecia, petechiae, bullae, and mucous membrane lesions.
Musculoskeletal System:
---------------------------
1.Polyarthritis especially small joints of fingers
2.Arthritis milder and non erosive compared to rheumatoid arthritis
3.morning stiffness
4.muscle atrophy and weakness may occur
Eyes:
-----------
1.Retinal hemorrhages and exudates
2.Cytoid bodies
Lungs and Pleura:
-----------------------
1.Recurrent pleurisy
2.Pleural effusions - small
3.Pulmonary infiltrates
Cardiovascular
-----------------
1.Pericarditis
2.Endocarditis with vegetation on the mitral valve especially
Gastrointestinal
--------------------
1.Non specific nausea
2.Gastrointestinal ulcers, hemorrhage, necrosis
Renal
-------------
1.Focal membranous nephritis
2.Proliferative nephritis - deposit of autoimmune complexes on capillary walls give rise to typical wireloop changes and epithelial crescents in kidneys resulting in proteinuria, hematuria,and renal failure.
Central nervous system:
------------------------------
1.Lesions in the brain can cause mental disorders( dementia, psychosis,epilepsy), chores, cerebrovascular accidents,cranial nerve lesions.
2.Peripheral neuropathy of various types
Others:
-----------------
1.Thrombotic thrombocytopenic purpura
2.Sjogren's syndrome
How do you make the Diagnosis of Systemic Lupus Erythematosis?
------------------------------------------------------------
1.A history of facial butterfly rash, systemic symptoms
2.Blood for ESR, positive ANA(antnuclear Antibodies), LE cells
3.Full blood count for anemia, hemolytic anemia, neutopenia, thrombocytopenia, Coombs' test(usually positive)
4.Renal or skin biopsy
5.X- rays of the chest, abdomen and brain
6.MRI of brain, kidney,
What are the complications of Systemic Lupus Erythematosis?
-----------------------------------------------------------------
1.Severe Dermatitis with discoid lesions (maculopapular in nature)
2.Polyathritis with swelling of joints
3.Anemia
4.Pleural effusions
5.hemorrhage
6.Dementia
7.Renal failure
What is the treatment of Systemic Lupus Erythematosis?
--------------------------------------------------------------
There is no cure for SLE at the present moment.
Treatment is to relieve symptoms and prevent organs from deteriorating.
Patients with mild symptoms may not need any treatment.
Mild Cases:
---------------
1.short course of antiinflammatory medications such as NSAID or corticosteroids.
2.Rest and freedom from stress
Severe cases:
--------------------
Patients with serious illness which has affected their organ may require stronger medications:
1.high doses of corticosteroids intially intravenously, followed by oral medication whose dosage is reduced slowly to the minimum possible.
Corticosteroids are particularly helpful if internal organs are involved.
Side effects of corticosteroids include gastric problems, thinning of the bones, infection, facial puffiness, cataracts.
2.NSAIDs can reduce inflammation and pain especially in the musculoskeletal system.
Examples of NSAIDs include aspirin, ibuprofen, naproxen.
The side effects are stomach upset, abdominal pain, ulcers or GIT bleeding.
To reduce the side effects, NSAIDs are usually taken with food or H2 antagonist like cimetidine, ranitidine.
3.Antimalarial medication such as Hydroxychloroquine has been particularly effective for SLE patients with fatigue, skin, and joint disease.
Side effects include diarrhea, upset stomach, and eye pigment changes.
Eye pigment changes are rare, but require monitoring by an ophthalmologist
Other antimalarial drugs, such as chloroquine or quinacrine, are considered
4.Treatment for severe skin disease skin disease include dapsone and retinoic acid (Retin-A).
5.immunosuppressive medications are used for treating patients with more severe manifestations of SLE with damage to internal organ(s).
Examples of immunosuppressive medications include methotrexate, azathioprine (Imuran), cyclophosphamide, and cyclosporine .
Side effects are depression of blood cell counts and increased risks of infection and bleeding.
6. mycophenolate mofetil (Cellcept) is very effective in lupus with kidney disease.
It has been able to reverse active lupus kidney disease and maintain remission.
It's lower side effects made it more useful than immunosuppresive drugs.
7.plasmapheresis is used to remove antibodies and other immune substances from the blood to suppress immunity.
It has also help to to remove proteins (cryoglobulins) that can lead to vasculitis.
SLE patients with low platelet levels can have severe bleeding.
7.rituximab is an intravenously infused antibody that suppresses a particular white blood cell, the B cell, by reducing the number in the blood stream.
B cells play a central role in lupus activity, and when suppressed, the disease tends toward remission.
8.omega-3 fish oils could help patients with lupus by decreasing disease activity and possibly decreasing heart disease risk.
9.rest during periods of active disease
Poor sleep quality can cause fatigue in patients with SLE.
Sleep quality and the effect of underlying depression, lack of exercise can have an adverse effect on the health of SLE patients.
It is important to maintain muscle tone and range of motion in the joints.
10.Endstage kidney damage from SLE requires dialysis and/or a kidney transplant.
What is the prognosis of Systemic Lupus Erythematosis?
-------------------------------------------------------------
The prognosis depends on the severity of the disease
Severe cases with renal disease has poorer prognosis.
How is SLE prevented?
----------------------------
1.Adequate rest
2. Avoid stress
3. Avoid the sun and use sunscreen.
4.Healthy lifestyle with exercise prevents arthritis
A Simple Guide to Acoustic neuroma
A Simple Guide to Acoustic neuroma
---------------------------------------------------
What are Acoustic neuroma ?
------------------------------------------------
Acoustic neuroma is a neurofibroma of the eight nerve.
Who are at risk of Acoustic neuroma?
-------------------------------------
1.Both sexes are equally affected.
2.Acoustic neuroma occurs more in the 50- 60 age group.
3.It forms 5-10% of the intracranial tumors in adults.
What are the different types of Acoustic neuroma?
--------------------------------------------------------
1.Neurofibroma I -
a. Unilateral acoustic neuroma usually
Bilateral acoustic neuromas are not common.
b. occurs in adult life,
c. the tumor involve the 8th nerve,
d. can involve any other cranial nerve or the spinal root.
e.Incidence is usually 90-95%
2.Neurofibroma II -
a. bilateral acoustic neuromas are common
b. occurs before the age of 21.
c. affects the entire nerve
d. autosomal dominant inheritance.
e. Incidence is about 5 to 10%.
What are the Causes of Acoustic neuroma?
------------------------------------------------------
Acoustic neuroma in the adult begins in the Schwann's cells of the vestibular portion of the 8th nerve inside the internal auditory canal.
The tumor grows slowly and can extend into the posterior fossa to occupy the space between the cerebellum and the pons.
Because of its location, it can also compress the 5th, 7th, and less often, the 9th and 10th cranial nerves.
If it grows larger, it may also compress the pons and lateral medulla of the brain, causing blockage of the cerebrospinal fluid and increased intracranial pressure.
What are the symptoms and signs of Acoustic neuroma?
-------------------------------------------------------
Symptoms:
--------------
1.unilateral hearing loss
2.tinnitus with unilateral high-pitched ringing sound
3.loss of sense of balance
4.vertigo
5.nausea and vomiting
6.altered gait
7.pressure in the ear
8.rarely headache and altered consciousness.
Signs:
-------------
1.unilateral facial weakness.
2.sensory impairment of the nerve
3.impairment of glandular secretions
4.loss of taste
5.loss of sensation in one side of the face and mouth
6.rarely altered gag or swallowing reflexes.
How are diagnosis of Acoustic neuroma made?
------------------------------------------------------------
1.Contrast-enhanced CT will detect almost all acoustic neuromas that are greater than 2.0 cm in diameter
2.MRI with gadolinium enhancement may show even smaller tumors
3.Audiology and vestibular tests are done to check for Nerve versus conduction hearing loss.
What is the Treatment of Acoustic neuroma?
-------------------------------------------
Treatment of acoustic neuroma is usually by surgery and radiotherapy.
Conservative treatment
--------------------------
In some cases because the neuroma grow so slowly, the tumor is monitored by annual MRI to see its growth.
This method is common among patients over 70 years old.
In rare cases, acoustical neuroma have been known to disappear spontaneously.
Acoustic neuroma may result in gradual hearing loss and tinnitus.
Surgery
-----------------
Surgical removal of acoustic neuroma usually involve microsurgery to remove the tumor.
The superior and inferior vestibular nerves are removed at surgery.
This effectively restores balance in the patient.
Radiation treatment
-----------------------
Radiotherapy using gamma knife radiosurgery or fractionated stereotactic radiotherapy does not remove the tumor but is able to slow or stop its growth.
What is the Prognosis of Acoustic neuroma?
-------------------------------------------
Prognosis is good in all early diagnosis and small tumors.
Large tumors may give rise to residual neurolgical damage even afer removal.
---------------------------------------------------
What are Acoustic neuroma ?
------------------------------------------------
Acoustic neuroma is a neurofibroma of the eight nerve.
Who are at risk of Acoustic neuroma?
-------------------------------------
1.Both sexes are equally affected.
2.Acoustic neuroma occurs more in the 50- 60 age group.
3.It forms 5-10% of the intracranial tumors in adults.
What are the different types of Acoustic neuroma?
--------------------------------------------------------
1.Neurofibroma I -
a. Unilateral acoustic neuroma usually
Bilateral acoustic neuromas are not common.
b. occurs in adult life,
c. the tumor involve the 8th nerve,
d. can involve any other cranial nerve or the spinal root.
e.Incidence is usually 90-95%
2.Neurofibroma II -
a. bilateral acoustic neuromas are common
b. occurs before the age of 21.
c. affects the entire nerve
d. autosomal dominant inheritance.
e. Incidence is about 5 to 10%.
What are the Causes of Acoustic neuroma?
------------------------------------------------------
Acoustic neuroma in the adult begins in the Schwann's cells of the vestibular portion of the 8th nerve inside the internal auditory canal.
The tumor grows slowly and can extend into the posterior fossa to occupy the space between the cerebellum and the pons.
Because of its location, it can also compress the 5th, 7th, and less often, the 9th and 10th cranial nerves.
If it grows larger, it may also compress the pons and lateral medulla of the brain, causing blockage of the cerebrospinal fluid and increased intracranial pressure.
What are the symptoms and signs of Acoustic neuroma?
-------------------------------------------------------
Symptoms:
--------------
1.unilateral hearing loss
2.tinnitus with unilateral high-pitched ringing sound
3.loss of sense of balance
4.vertigo
5.nausea and vomiting
6.altered gait
7.pressure in the ear
8.rarely headache and altered consciousness.
Signs:
-------------
1.unilateral facial weakness.
2.sensory impairment of the nerve
3.impairment of glandular secretions
4.loss of taste
5.loss of sensation in one side of the face and mouth
6.rarely altered gag or swallowing reflexes.
How are diagnosis of Acoustic neuroma made?
------------------------------------------------------------
1.Contrast-enhanced CT will detect almost all acoustic neuromas that are greater than 2.0 cm in diameter
2.MRI with gadolinium enhancement may show even smaller tumors
3.Audiology and vestibular tests are done to check for Nerve versus conduction hearing loss.
What is the Treatment of Acoustic neuroma?
-------------------------------------------
Treatment of acoustic neuroma is usually by surgery and radiotherapy.
Conservative treatment
--------------------------
In some cases because the neuroma grow so slowly, the tumor is monitored by annual MRI to see its growth.
This method is common among patients over 70 years old.
In rare cases, acoustical neuroma have been known to disappear spontaneously.
Acoustic neuroma may result in gradual hearing loss and tinnitus.
Surgery
-----------------
Surgical removal of acoustic neuroma usually involve microsurgery to remove the tumor.
The superior and inferior vestibular nerves are removed at surgery.
This effectively restores balance in the patient.
Radiation treatment
-----------------------
Radiotherapy using gamma knife radiosurgery or fractionated stereotactic radiotherapy does not remove the tumor but is able to slow or stop its growth.
What is the Prognosis of Acoustic neuroma?
-------------------------------------------
Prognosis is good in all early diagnosis and small tumors.
Large tumors may give rise to residual neurolgical damage even afer removal.
Friday, October 3, 2008
A Simple Guide to Glossitis
A Simple Guide to Glossitis
-----------------------------------
What is Glossitis?
---------------------------
Glossitis is an acute or chronic inflammatory disease of the tongue which can cause swelling of the tongue and change of colour of the tongue.
The finger like papilla on the surface of the tongue may be lost as a result leading to a smooth tongue.
What are the causes of Glossitis?
----------------------------------------
Bacterial Infections:
----------------------------
1.Gram positive bacteria such as Streptococcus and Staphphylococcus may be painful and lead to upper respiratory tract infection
2.Gram negative bacteria such as Klebsiella, E.coli, Pseudomonas, Mycobacteria(including tuberculosis), Legionaire's Disease,chlamydia
Viral infections:
------------------
Herpes simplex
Non-infectious:
----------------
1.Dryness of the mouth and low saliva in the mouth may allow bacteria to grow more readily.
2.Local dental abnormalities, rough edges of teeth ,ill fitting dental appliances, or other trauma to the tongue
3.Tongue Piercings
4.irritants such as tobacco, alcohol, hot foods, and spicy food.
5.Sensitivity to toothpaste, mouthwash, breath fresheners,and dental material
6.Allergies to dyes in candy or preservatives in food.
7.Drug induced such as anticholinergics (cause dryness of mouth), certain blood-pressure medications (ACE inhibitors).
8.Mouth breathing
Systemic diseases:
--------------------
1.iron deficiency anemia, pernicious anemia and other B-vitamin deficiencies
2.Skin diseases such as oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris,
3.Systemic diseases such as syphilis, and others.
Genetic
---------------
Occasionally Glossitis may be inherited
What are Signs and symptoms of Glossitis?
---------------------------------------------
Symptoms:
1.Swelling of the tongue
2.Tongue color changes often dark red
3.Pale if caused by anemia.
4.Fiery red if due to vitamin B deficiency
5.Sore and tender tongue
6.Smooth tongue
7.Aphthous ulcers of the tongue
8. Swollen tongue resulting in difficulty with chewing, swallowing, or speaking.
This may require emergency treatment especially if breathing is compromised.
How is the diagnosis of Glossitis made?
------------------------------------------
1.Symptoms and signs of red, swollen and inflamed tongue
2.blood tests (complete blood count, ESR and blood culture)
3.Biopsy of the tongue in rare cases.
What are the complications of Glossitis?
-----------------------------------------------
1.difficulty in breathing and swallowing
2.cervical lymphadenitis - swelling of the neck lymph nodes
3.upper respiratory tract infection
What is the treatment of Glossitis?
------------------------------------
The Main treatment is to reduce inflammation.
1.Good oral hygiene
2.Attend to dental problems
3.Antibiotics and antifungal treatment depending on the organism found
4.Corticosteroids may be given to reduce inflammation
5.For mild cases, topical applications of steroid mouth rinses or creams that is not swallowed are used
6.Underlying causes such as Anemia and nutritional deficiencies must be treated, often by changes in diet or vitamin supplements
7.Avoid irritants such as hot or spicy foods, alcohol, and tobacco to minimize the discomfort.
8.hospitalization may be required if unless tongue swelling is is affecting breathing or swallowing.
What is the prognosis of Glossitis ?
------------------------------------------
Usually very good.
Recurrences are common
What are the Preventive measures taken for Glossitis ?
--------------------------------------------------------
1.Avoid smoking
2.Healthy lifestyle with balanced diet and exercise.
3.Regular cleaning of gums and teeth by brushing and flossing
4.Gargling of mouth after meals
5.Regular dental checkups
Thursday, October 2, 2008
A Simple Guide to Ichthyosis
A Simple Guide to Ichthyosis
----------------------------------------------
What is Ichthyosis?
------------------------------------
Ichthyosis is a rare non contagious disease of the keratin of the skin where there is reduction of sweat and sebaceous secretions.
The word Ichthus means fish.
So Ichthyosis means fish like appearance of the skin.
Who is at risk of Ichthyosis?
----------------------------------------------
a family history of ichthyosis
What are the causes of Ichthyosis?
--------------------------------------------------
Most forms of ichthyosis are due to:
A.genetic conditions:
------------------------
1.Ichthyosis vulgaris 95% -autosomal dominant
2.X-linked ichthyosis -sex linked recessive
3.Ichthyosis lamellaris - autosomal recessive usually in newborns
4.Harlequins Ichthyosis -autosomal recessive
5.Bullous Ichthyosis - autosomal dominant
B.Acquired Ichthyosis
----------------------
6.Ichthyosis acquisita occur in :
leprosy,
hypothyroidism,
lymphoma,
sarcoidosis,
Hodgkin disease
7.Xeroderma - is a mild form of ichthyosis, occurs in middle aged and older patients.
What are Signs and symptoms of Ichthyosis?
---------------------------------------------
Symptoms:
1.extensor surface of limbs covered with dry scales(rarely the whole body is covered).
2.axilla and antecubal fossa (elbows,armpits,groins,back of knee)not affected
3.Usually symptoms present in childhood but improve during puberty to becoming worst again in later life.
4.Rashes can be extremely itchy in xeroderma
5.The condition is worse in colder weather.
6.Hair may be thin and dry.
7.Nails are brittle and dry.
How is the diagnosis of Ichthyosis made?
--------------------------------------------------------
1.Appearance of the skin
2.Family history of Ichthyosis
2.Skin biopsy for microscopic examination.
What are the complications of Ichthyosis?
-----------------------------------------------
1.keratisis with corneal and ocular surface disease
2.Ectropion of eyelids due to dehydration
3.Deafness in a Keratitis-Ichthyosis-Deafness (KID)Disease
What is the treatment of Ichthyosis?
------------------------------------
There is no cure for Ichthyosis.
1.Symptomatic treatment with emolient creams such as petroleum jelly my help to hydrate the skin.
2.Itch may be controlled with antihistamines
3.Hydration with propylene glycol solution will help
4.Urea in emulsion creams has also help the dry skin
5.Topical or oral retinoic acid has brought some improvement to the skin.
6.Exposure to the sun may improve or worsen the condition.
What is the prognosis of Ichthyosis ?
------------------------------------------
It is a lifelong condition and need continuous treatment.
What are the Preventive measures taken for Ichthyosis ?
--------------------------------------------------------
There is no known preventive measure for ichthyosis
----------------------------------------------
What is Ichthyosis?
------------------------------------
Ichthyosis is a rare non contagious disease of the keratin of the skin where there is reduction of sweat and sebaceous secretions.
The word Ichthus means fish.
So Ichthyosis means fish like appearance of the skin.
Who is at risk of Ichthyosis?
----------------------------------------------
a family history of ichthyosis
What are the causes of Ichthyosis?
--------------------------------------------------
Most forms of ichthyosis are due to:
A.genetic conditions:
------------------------
1.Ichthyosis vulgaris 95% -autosomal dominant
2.X-linked ichthyosis -sex linked recessive
3.Ichthyosis lamellaris - autosomal recessive usually in newborns
4.Harlequins Ichthyosis -autosomal recessive
5.Bullous Ichthyosis - autosomal dominant
B.Acquired Ichthyosis
----------------------
6.Ichthyosis acquisita occur in :
leprosy,
hypothyroidism,
lymphoma,
sarcoidosis,
Hodgkin disease
7.Xeroderma - is a mild form of ichthyosis, occurs in middle aged and older patients.
What are Signs and symptoms of Ichthyosis?
---------------------------------------------
Symptoms:
1.extensor surface of limbs covered with dry scales(rarely the whole body is covered).
2.axilla and antecubal fossa (elbows,armpits,groins,back of knee)not affected
3.Usually symptoms present in childhood but improve during puberty to becoming worst again in later life.
4.Rashes can be extremely itchy in xeroderma
5.The condition is worse in colder weather.
6.Hair may be thin and dry.
7.Nails are brittle and dry.
How is the diagnosis of Ichthyosis made?
--------------------------------------------------------
1.Appearance of the skin
2.Family history of Ichthyosis
2.Skin biopsy for microscopic examination.
What are the complications of Ichthyosis?
-----------------------------------------------
1.keratisis with corneal and ocular surface disease
2.Ectropion of eyelids due to dehydration
3.Deafness in a Keratitis-Ichthyosis-Deafness (KID)Disease
What is the treatment of Ichthyosis?
------------------------------------
There is no cure for Ichthyosis.
1.Symptomatic treatment with emolient creams such as petroleum jelly my help to hydrate the skin.
2.Itch may be controlled with antihistamines
3.Hydration with propylene glycol solution will help
4.Urea in emulsion creams has also help the dry skin
5.Topical or oral retinoic acid has brought some improvement to the skin.
6.Exposure to the sun may improve or worsen the condition.
What is the prognosis of Ichthyosis ?
------------------------------------------
It is a lifelong condition and need continuous treatment.
What are the Preventive measures taken for Ichthyosis ?
--------------------------------------------------------
There is no known preventive measure for ichthyosis
Wednesday, October 1, 2008
A Simple Guide to Pityriasis Rosea
A Simple Guide to Pityriasis Rosea
----------------------------------------------
What is Pityriasis Rosea?
------------------------------------
Pityriasis Rosea is a common non contagious disease which appears as numerous patches of red rash on the trunk of the body.
Who is at risk of Pityriasis Rosea?
----------------------------------------------
All ages and both sex are affected but occurs more between 10 -35 years of age.
What are the causes of Pityriasis Rosea?
--------------------------------------------------
The cause is unknown but a viral infection is suspected to cause it.
What are Signs and symptoms of Pityriasis Rosea?
---------------------------------------------
Symptoms:
1.A single red large patch of rashes or herald patch usually occur 1-20 days on the body before the onset of numerous small patches.
2.sore throat may occur before the onset of rashes
3.Numerous Large patches of red oval-shaped rash on the body may occur on the chest, back and neck.
4. As the rashes subside on the body, they may spread to the groin and extremities like the legs and arms
5.Rashes can be extremely itchy
6.breathlessness
7.low-grade fever
8.headache
9.nausea
10.fatigue.
How is the diagnosis of Pityriasis Rosea made?
--------------------------------------------------------
1.Symptoms and signs of typical herald patch followed by other patches of rashes
2.Skin scraping for microscopic examination.
What are the complications of Pityriasis Rosea?
-----------------------------------------------
1.Fungal infection
2.bacterial infection
What is the treatment of Pityriasis Rosea?
------------------------------------
1.No treatment may be necessary as the illness is self limiting
2.Itch may be controlled with antihistamines
3.Corticosteroid (oral or cream) may help reduce severe itching and inflammation
4.Soap should be avoided because it irritate the skin.
5.Moisturizer is better because of the dry skin
6.UV therapy sometimes help
7.Antibiotics may be given if there is secondary infection.
What is the prognosis of Pityriasis Rosea ?
------------------------------------------
Generally excellent but may recur.
What are the Preventive measures taken for Pityriasis Rosea ?
--------------------------------------------------------
1.Good skin hygiene
2.Healthy lifestyle with balanced diet and adequate sleep.
3.Proper skin care of the body.
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