FUNDUS FLUORESCEIN ANGIOGRAPHY treatment details

Fundus flourescein angiography (FFA) is a valuable
tool in the diagnosis and management of a large number of fundus disorders.
Basically, FFA gives information by allowing the examiner to study the changes, produced by various fundus disorders, in the flow of fluorescein dye along the vasculature of the retina and choroid. Indications. It is indicated in many disorders of ocular fundus, viz., (1) Diabetic retinopathy (2) Vascu-lar occlusions; (3) Eales’ disease. (4) Central serous retinopathy, (5) Cystoid macular oedema.
Technique.

The technique of FFA comprises of rapidly injecting 5 ml of 10 per cent solution of sterile sodium fluorescein dye in the antecubital vein and taking serial photographs (with fundus camera) of the fundus of the patient who is seated with pupils fully dilated. The fundus camera has a mechanism to use blue light (420-490 nm wavelength) for exciting the fluorescein present in blood vessels and to use yellow-green filter for receiving the fluorescent light (510-530 nm wavelength) back for photography.
The first photograph is taken after 5 seconds, then every second for next 20 seconds and every 3-5 seconds for next one minute. The last pictures are taken after 10 minutes.
Complications. FFA is comparatively a safe procedure. Minor side effects include : discoloration of skin and urine, mild nausea and rarely vomiting. Anaphylaxis or cardiorespiratory problems are extremly rare. However, a syringe filled with dexamethasone and antihistaminic drug along with other measures should be kept ready to deal with such catastrophy.
Phase of angiogram. Normal angiogram consists of following overlapping phases:
1.  Pre-arterial phase. Since the dye reaches the choroidal circulation 1 second earlier than the retinal arteries, therefore in this stage choroidal circulation is filling, without any dye in retinal arteries.
2.  Arterial phase. It starts 1 second after prearterial phase and lasts until the retinal arterioles are completely filled.

involves the complete filling of retinal arterioles and capillaries with a laminar flow along the retinal veins
4. Venous phase. In this phase veins are filling and arterioles are emptying. This phase can be subdivided into early, mid, and late venous phase.
Abnormalities detected by FFA. In the blood fluorescein is readily bound to the albumin. Normally the dye remains confined to the intravascular space due to the barriers formed by the tight junctions between the endothelial cells of retinal capillaries (in-ler blood-retinal barrier) and that between the pig-nent epithelial cells (outer blood retinal barrier).
In diseased states abnormalities in the form of lyperfluorescence and hypofluorescence may be letected on FFA. !. Hyperfluorescence. The causes are :
a)   A window defect in RPE due to atrophy shows background choroidal fluorescence.
b)  Pooling of dye under detached RPE.
c)  Pooling of dye under sensory retina after breakdown of the outer blood-retinal barrier as
occurs in central serous retinopathy (CSR).
i) Leakage of dye into the neurosensory retina due to a breakdown in inner blood-retinal barrier e.g. as seen in cystoid macular edema (CME).
e) Leakage of dye from the choroidal or retinal neovascularization e.g. as seen in cases of proliferative diabetic retinopathy, and subretinal neovascular membrane in age-related macular degeneration.

(f)   Staining i.e. long retention of dye by some tissues e.g. as seen in the presence of drusen.
(g)   Leakage of dye from optic nerve head as seen in papilledema.
2. Hypofluorescence. The causes are:
(a)   Blockage of background fluorescence due to abnormal deposits on retina e.g. as seen due to the presence of retinal haemorrhage, hard exudates and pigmented clumps.
(b)   Occlusion of retinal or choroidal vasculature, e.g. as seen in central retinal artery occlusion and occlusion of capillaries in diabetic retinopathy.
(c)   Loss of vasculature as occurs in patients with choroideremia and myopic degeneration.

Jaundice in Children-Different types and Symptoms

Jaundice means yellow discoloration of the skin, mucous membrane and sclera due to elevation of bilirubin level in the blood. Intensity of jaundice depends on the amount of free bilirubin circulating in the blood which can easily diffuse into the tissues. Jaundice should be distinguished from yellow coloration of the skin due to hypercarotenemia. In the latter condition sclera does not become yellow.

Regurgitant jaundice (conjugated hyperbilirubinemia)
1.  Hepatocellular jaundice.
(a)   Viral hepatitis A and B
(b)   Toxic injury to the liver-antibiotics, drugs, poisons.
(c)    Infestations: malaria, bilharzia.
(d)   Cirrhosis of the liver
(e)   Infections:  Infectious mononucleosis.
2.   Cholestatic jaundice.
(a)   Due to drug reaction to chlorpromazine, methyl testosterone, isoniazid and rifampicin.
(b)   Dubin Johnson syndrome (chronic benign conjugated hyperbilirubinemia with deposition of melanin like pigment in the liver; autosomal recessive inheritance, no mechanical obstruction of duct); Rotor syndrome (Like Dubin Johnson; no pigment in the liver).

Aemolytic jaundice
(a)   Hereditary spherocytosis.
(b)   Sickle cell anemia.
(c)   Thalassemia.
(d)   Drug induced hemolytic anemia in patients with G 6-PD deficiency.
(e)   Acute acquired hemolytic anemia.
Hepatocellular jaundice
Unconjugated bilirubin level in the blood is elevated due to impaired uptake, defective transport and diminished glucuronation of the bile by the damaged hepatic cell. Conjugated bilirubin level also rises due to the blockage of canaliculi by the thick bile and obstruction due to the inflammatory cells around the cholangioles. Altered permeability of the liver cells and rupture of the canaliculi also contribute to the elevation of the level of conjugated bilirubin.
Thus in hepatocellular jaundice, serum levels of both the conjugated and unconjugated bilirubin are elevated and bilirubin is excreted in the urine. The excretion of urobilinogen in the feces is reduced because less bile passes into the gut. A part of the urobilinogen (or stercobilinogen) is absorbed in the portal circulation but liver is unable to excrete it and therefore it is excreted mostly in the urine. As the illness becomes severe and the obstruction becomes almost complete, the bilirubin cannot be excreted into the gut. Consequently no urobilinogen is formed and absorbed from the gut. Therefore at this stage urobilinogen disappears from the urine in complete obstruction or at the peak of the disease process.

Cholestatic jaundice
Cholestatic jaundice occurs following drug reaction to chlorpromazine, methyl testosterone and isonicotinic acid hydrazide and rifampicin. The jaundice in Dubin Johnson and Rotor syndromes is also cholestatic. The defect is due to the functional disturbances in the transport of bilirubin across the liver cells.
Obstructive jaundice
Following obstruction of the bile duct, the conjugated bilirubin escapes into the circulation. This may be due to (1) rupture of the distended canaliculi into the hepatic sinusoids or lymph spaces, (2) through leaks in the canals of Hering which connect the bile canaliculi with the terminal bile ducts and (3) in the blood through the parenchymal cells. Later, hepatocellular damage may occur as a result of marked increase in the level of unconjugated bilirubin.
Complete obstruction of the extrahepatic biliary system is uncommon in children. Cholecystitis and gall bladder calculi rarely present in childhood. Partial intermittent obstruction due to cystic dilatation of a part or whole of the common bile duct may occur due to partial obstruction or neuromuscular incoordination of the ampulla of Vater.
Large cyst of the bile duct is called choledochal cyst.
Patient presents with a mass in the right upper quadrant of

Hepatomegaly-Liver enlargement- Symptoms ,Causes and different types

Palpability of liver does not always indicate enlargement.It only reflects the relation of the liver to adjacent structures.In normal children,liver is palpable 1 cm below the costal margin and in Infants it may be felt up to 2 cm below the rib margin.

Besides the size and shape of the liver, consistency and character of the surface and palpable margin should be evaluated for the assessment of hepatomegaly. Liver should be examined for tenderness and also auscultated for any murmurs. The upper border of the liver should be defined by percussion. Abdomen should be palpated for other masses or enlargement of the spleen.
Pathogenesis of liver enlargement. The liver may be enlarged due to any of the following causes:
(a) Inflammation
(b) Fatty infiltration
(c) Kupffer’s cell hyperplasia
(d) Congestion
(e) Cellular infiltration and
(f) Storage of metabolites

CAUSES OF LARGE LIVER

Newborn
Infections, (a) Intrauterine infection e.g., toxoplasmosis, cytomegalic inclusion disease, congenital syphilis., (b) septicemia, and (c) neonatal hepatitis including viral hepatitis.
Cellular infiltration. Erythroblastosis fetalis.
Hepatobiliary obstruction.   Biliary atresia.
Congestive cardiac failure.
Alpha-1-anti trypsin deficiency.
Infants and children
1.  Benign hypertrophy. Periportal round cell infiltration following viral infections of upper respiratory tract. The liver regresses in 6 to 8 weeks.
2.  Fatty infiltration. Kwashiorkor, Reye’s syndrome, tetracycline toxicity, tuberculosis, diabetes mellitus, cystic fibrosis and galactosemia.
3.   Inflammatory processes. (i) Intrauterine and intrapartum infection, (ii) hepatitis, (iii) infectious mononucleosis, (iv) parasitic infestations (visceral larva migrans, amebic hepatitis), (v) pyogenic or amebic abscess of liver, cholangitis (vi) toxins and (vii) drugs.
4.   Cellular infiltration. (i) Leukemia and lymphomas (ii) neoplasms-primary (hepatoblastoma, hemangioendothelioma), (iii) secondaries to Wilms’ tumor and neuroblastoma and (iv) histiocytosis (Letterer-Siwe disease).
5.   Storage disorders (Metabolic). (i) Glycogen storage disease, (ii) galactosemia, (iii) mucopolysaccharidoses, (iv) lipidosis (Gaucher, Niemann Pick, gangliosidosis M). (v) amyloidosis, (vi) alpha-1-anritrypsin deficiency, (vii) hepatic porphyria, (viii) cystinosis and (ix) hemosiderosis, Wilson disease, cystinosis and tyrosinosis.
6.    Congestion. (i) Congestive cardiac failure, (ii) pericarditis, (iii) Budd Chiari syndrome (thrombosis of hepatic vein) and (iv) veno-occlusive disease of the liver.
7.   Kupffer’s cell hyperplasia. Granulomatous hepatitis as in tuberculosis and sarcoidosis.
8.  Miscellaneous. Cirrhosis of liver—Indian Childhood cirrhosis, congenital cysts and hydatid cyst.

EVALUATION OF THE HEPATIC ENLARGEMENT

Assess if the liver is just palpable or is actually enlarged. Determine if the enlargement is due to organic causes and also the nature and severity of the illness responsible for it.
A good medical history, intelligent interpretation of the associated clinical manifestation and judicious use of laboratory investigations and ultrasonography are helpful in arriving at a correct diagnosis in most cases of hepatic enlargement. The following points may help in diagnosis.
Age of the patient. Age of onset of the illness limits the etiological possibilities.
Geographic factors. Indian childhood cirrhosis is common in children of Indian extraction. Thalassemia is more frequent in North West India, Bengal, Indochina, Sri Lanka and persons of Mediterranean extraction. Veno-occlusive disease is observed in Jamaica and West Indies. It has been recently reported from Afghanistan and some parts of central India.
Associated clinical manifestations which aid in diagnosis of hepatomegaly
Protein-energy malnutrition. There is fatty infiltration of the liver.
Jaundice. Intrauterine infections, septicemia, neonatal hepatitis, viral hepatitis, biliary atresia and Indian childhood cirrhosis in terminal stages present with jaundice.
Engorged neck veins and raised jugular venous pressure.

Constrictive Pericarditis
Skin rash. Histiocytosis.
Microcephaly or hydrocephaly. Intrauterine infections like toxoplasmosis and cytomegalic inclusion disease.
Eyes. Cataract and mental retardation with hepatosplenomegaly suggest galactosemia.
Presence of Kayser-Fleischer ring over the cornea indicates Wilson     disease.         Hazy     cornea     is     seen     in
Mucopolysaccharidosis type 1.
Neurological manifestations. Wilson disease may present with neurological manifestations.
Skeletal changes of rickets may be observed in cystinosis and tyrosinosis.
Mental retardation. Patients with galactosemia may show gross mental retardation.

How did Sonam kapoor loss her weight?

The weight loss of  Sonam kapoor is pretty famous in the bollywood Industry.Sonam kapoor recently revealed the secrets which she followed to bring down her weight.Sonam studied in a boarding school in Singapore and she had no plans in entering the movie industry that  didn’t care her diet and had junk foods.Sonam kapoor had a weight of 86 kilos once.She was a real fatty girl at that time.later Sonam decided to put down her weight and according to sonam,her mother was a great help to her in bringing down her weight.Sonam Aimed a target of reducing 35 kg and she somewhat achieved it.And How was she able to achieve that?what was the secret of her

weight loss?

What Diet did Sonam Kapoor follow?

Sonam Kapoor once decided to bring down her weight,completely avoided junk foods and Chocolates,and ice cream.She had six small meals a day.oatmeal and fruits was the breakfast. After the work out She had brown bread with egg whites. Afterwards, it was a protein shake with juice. Lunch consisted of  dal, sabzi, one ragi roti, salad and a small piece of fish(chicken rarely) Evening diet consisted of  high-fibre crackers with egg whites. As dinner Sonam had Soup,Salad and a piece of chicken or fish.And She lost 35 kilos in No time! She also had warm water in the morning with some honey in it.And she always avoided Salt and Sugar.

What was Sonam Kapoor’s activities for the weight loss?

She did a bunch of activities like dancing,Walking and Swimming.She practiced Kathak and according to sonam kapoor ,kathak dancing  can bring down lots of weight and can put on beautiful curves to your body.Sonam also practiced Power Yoga and Artistic Yoga , that whatever excess fat  had,she could easily burn it off!

Try these tips from Sonam Kapoor,so that you can also bring down your weight.As many think weight loss or reducing fat, is not that big deal if you have mind for that