Cholestasis can be suspected when there is an elevation of both 5'-nucleotidase and ALP enzymes. With a few exceptions, the optimal test for cholestasis would be elevations of serum bile acid levels. However, this is not normally available in most clinical settings. The gamma-glutamyl transferase (GGT) enzyme was previously thought to be helpful in confirming a hepatic source of ALP; however, GGT elevations lack the necessary specificity to be a useful confirmatory test for ALP. Normally GGT and ALP are anchored to membranes of hepatocytes and are released in small amounts in hepatocellular damage. In cholestasis, synthesis of these enzymes is induced and they are made soluble. GGT is elevated because it leaks out from the bile duct cells due to pressure from inside bile ducts.

In a later stage of cholestasis AST, ALT and bilirubin may be elevated due to liver damage as a secondary effect of cholestasis.

Extrahepatic cholestasis can usually be treated by surgery.

Pruritis in cholestatic jaundice is treated by Antihistamines, Ursodeoxycholic Acid, Phenobarbital

Chronic liver diseases like chronic hepatitis, chronic alcohol abuse or chronic toxic liver disease may cause

- liver failure and hepatorenal syndrome

- fibrosis and cirrhosis of liver

Cirrhosis may also occur in primary biliary cirrhosis. Rarely, cirrhosis is congenital.

This remains a challenge in clinical practice due to a lack of reliable markers. Many other conditions lead to similar clinical as well as pathological pictures. To diagnose hepatotoxicity, a causal relationship between the use of the toxin or drug and subsequent liver damage has to be established, but might be difficult, especially when idiosyncratic reaction is suspected. Simultaneous use of multiple drugs may add to the complexity. As in acetaminophen toxicity, well established, dose-dependent, pharmacological hepatotoxicity is easier to spot. Several clinical scales such as CIOMS/RUCAM scale and Maria and Victorino criteria have been proposed to establish causal relationship between offending drug and liver damage. CIOMS/RUCAM scale involves a scoring system that categorizes the suspicion into "definite or highly probable" (score > 8), “probable” (score 6-8), “possible” (score 3-5), “unlikely” (score 1-2) and “excluded” (score ≤ 0). In clinical practice, physicians put more emphasis on the presence or absence of similarity between the biochemical profile of the patient and known biochemical profile of the suspected toxicity (e.g., cholestatic damage in amoxycillin-clauvonic acid ).

Hepatic adenoma is usually detected by imaging, typically an ultrasound or CT, as a hyperenhancing liver nodule. Given that several liver tumors appear similarly on these imaging modalities, a multi-phase contrast-enhanced imaging study such as CT or MRI may be used to provide more information. The significance of making a specific diagnosis is that, unlike other benign liver tumors such as hemangioma and focal nodular hyperplasia, hepatic adenomas have a small but meaningful risk of progressing into a malignancy. Although imaging provides supportive information, a definitive diagnosis of hepatic adenoma requires biopsy of the tissue.

Hepatic doppler ultrasound is typically utilized to confirm or suggest the diagnosis. Most common findings on liver doppler ultrasound include increased phasicity of portal veins with eventual development of portal flow reversal. The liver is usually enlarged but maintained normal echogenicity. A liver biopsy is required for a definitive diagnosis.

Liver haemangiomas are typically hyperechoic on ultrasound though may occasionally be hypoechoic; ultrasound is not diagnostic. Computed tomography (CT), magnetic resonance imaging (MRI) or single-photon emission computed tomography (SPECT) using autologous labelled Red Blood Cells (RBC) with Tc-99m is diagnostic. Biopsy is avoided due to the risk of haemorrhage.

Hepatic haemangiomas can occur as part of a clinical syndrome, for example Klippel-Trenaunay-Weber syndrome, Osler–Weber–Rendu syndrome and Von Hippel-Lindau syndrome.

The condition is usually congenital, but sporadic cases have also been reported. It may be associated with other congenital defects, commonly with autosomal recessive polycystic kidney disease, the most severe form of PKD. Some suggest that these two conditions are one disorder with different presentation.

Embryogenically, congenital hepatic fibrosis is due to malformation of the duct plate, a round structure appearing in the eighth week of gestation that is formed by primitive hepatocytes, which differentiate into cholangiocytes. Congenital hepatic fibrosis usually presents in adolescent or young adulthood, but onset of signs and symptoms can range from early childhood through mid-life. Clinical features may vary but commonly include Cholangitis, hepatomegaly and signs of portal hypertension.

Malignant neoplasm of liver and intrahepatic bile ducts. The most frequent forms are metastatic malignant neoplasm of liver)

- liver cell carcinoma

- hepatocellular carcinoma

- hepatoma

- cholangiocarcinoma

- hepatoblastoma

- angiosarcoma of liver

- Kupffer cell sarcoma

- other sarcomas of liver

Benign neoplasm of liver include hepatic hemangiomas, hepatic adenomas, and focal nodular hyperplasia (FNH).

1)positive tuberclin test

2)chest radiograph

3)CT scan

4)cytology/biopsy (FNAC)

5)AFB staining

6)mycobacterial culture

Aspiration pneumonia is typically caused by aspiration of bacteria from the oral cavity into the lungs, and does not result in the formation of granulomas. However, granulomas may form when food particles or other particulate substances like pill fragments are aspirated into the lungs. Patients typically aspirate food because they have esophageal, gastric or neurologic problems. Intake of drugs that depress neurologic function may also lead to aspiration. The resultant granulomas are typically found around the airways (bronchioles) and are often accompanied by foreign-body-type multinucleated giant cells, acute inflammation or organizing pneumonia. The finding of food particles in lung biopsies is diagnostic.

"Acute on chronic liver failure" is said to exist when someone with chronic liver disease develops features of liver failure. A number of underlying causes may precipitate this, such as alcohol misuse or infection. People with ACLF can be critically ill and require intensive care treatment, and occasionally a liver transplant. Mortality with treatment is 50%.

In most cases, liver function will return to normal if the offending drug is stopped early. Additionally, the patient may require supportive treatment. In acetaminophen toxicity, however, the initial insult can be fatal. Fulminant hepatic failure from drug-induced hepatotoxicity may require liver transplantation. In the past, glucocorticoids in allergic features and ursodeoxycholic acid in cholestatic cases had been used, but there is no good evidence to support their effectiveness.

An elevation in serum bilirubin level of more than 2 times ULN with associated transaminase rise is an ominous sign. This indicates severe hepatotoxicity and is likely to lead to mortality in 10% to 15% of patients, especially if the offending drug is not stopped (Hy's Law). This is because it requires significant damage to the liver to impair bilirubin excretion, hence minor impairment (in the absence of biliary obstruction or Gilbert syndrome) would not lead to jaundice. Other poor predictors of outcome are old age, female sex, high AST.

The granulomas of tuberculosis tend to contain necrosis ("caseating tubercules"), but non-necrotizing granulomas may also be present. Multinucleated giant cells with nuclei arranged like a horseshoe (Langhans giant cell) and foreign body giant cells are often present, but are not specific for tuberculosis. A definitive diagnosis of tuberculosis requires identification of the causative organism by microbiologic cultures.

Hepatic adenomas are related to glycogen storage diseases, type 1, as well as anabolic steroid use.

Primary diagnosis usually starts off with a thorough physical exam and evaluation of medical history. To further investigate, a dermoscope, a diagnostic tool, is used by the dermatologist to examine the skin using a magnified lens. A complete blood count (CBC) along with other blood tests can also be done to rule out any sort of other infections. Lastly, a skin biopsy test may be ordered to arrive at a definitive diagnosis. This pathological examination of the skin biopsy helps to arrive at the correct diagnosis via a fungal culture(mycology). The biopsy is put together with clinical and microscope findings and study of the special tissues if need be. The signs and symptoms of MG are similar to many other clinical conditions and therefore it is necessary to perform all of the additional tests in order for a physician to correctly rule out all other possible diagnoses.

Due to its overwhelming incidence on the gingiva, the condition is often associated with two other diseases, though not because they occur together. Instead, the three are associated with each other because they appear frequently on gingiva—peripheral giant cell granuloma and peripheral ossifying fibroma. Detailed analysis can be used to distinguish these conditions.

Granuloma annulare, microscopically, consists of dermal epithelioid histiocytes around a central zone of mucin - a so-called palisaded granuloma.

Inflammatory myofibroblastic tumours are diagnosed based on their appearance under the microscope, by pathologists. Medical imaging findings are non-specific.

Prognosis is usually good, however recurrence may happen with rate up to 16%. Presence of myxoid structures in the pyogenic granuloma may be the main cause of recurrence.

Although pyogenic granulomas are not infectious or malignant, treatment may be considered because of bleeding or ulceration. Frequently, pyogenic granulomas are treated with electrodesiccation (cauterization) and curettage (excision), though laser treatment using pulsed dye laser or CO laser is often effective.

Several reports have demonstrated the efficacy of topical application of the beta-adrenergic antagonist timolol in the treatment of pediatric pyogenic granuloma.

There is usually no treatment if the pyogenic granuloma occurs during pregnancy since the lesion may heal spontaneously. Recurrent bleeding in either oral or nasal lesions may necessitate excision and cauterization sooner, however. If aesthetics are a concern, then treatment may be pursued as well. Usually, only minor surgery may be needed, along with a dental cleaning for oral lesions to remove any calculus or other source of irritation. For nasal lesions, nose-picking should be discouraged.

The basis of management is to find and correct the underlying cause. Many times cats with EGC will respond to treatment with corticosteroids or to ciclosporin.

This large, atypical haemangioma of the liver may present with abdominal pain or fullness due to haemorrhage, thrombosis or mass effect. It may also lead to left ventricular volume overload and heart failure due to the increase in cardiac output which it causes. Further complications are Kasabach-Merritt syndrome, a form of consumptive coagulopathy due to thrombocytopaenia, and rupture.

The diagnosis is made clinically, and usually this is clear cut if the lesion is associated with the flange of a denture. Tissue biopsy is not usually indicated before removal of the lesion, since the excises surgical specimen is usually sent for histopathologic examination and the diagnosis is confirmed retrospectively. Rarely, incisional biopsy may be indicated to rule out neoplasia, e.g. in the presence of suspicious ulceration. The appearance may also be confused with pyogenic granuloma.

The excessive tissue is composed of cellular, inflamed fibrous connective tissue. The appearance of an epulis fissuratum microscopically is an overgrowth of cells from the fibrous connective tissue. The epithelial cells are usually hyperkeratotic and irregular, hyperplastic rete ridges are often seen.

The exact cause of Majocchi's granuloma is not well established however a dysfunctinoal immune system may be a causative factor. The first form of MG, the superficial perifollicular form occurs predominately on the legs of otherwise healthy young women who repeatedly shave their legs and develop hair follicle occlusions that directly or indirectly disrupt the follicle and allow for passive introduction of the organism into the dermis. Hence, the physical barrier of the skin is important because it prevents the penetration of microorganisms. Physical factors that play a major role in inhibiting dermal invasion include the interaction among keratin production, the rate of epidermal turnover, the degree of hydration and lipid composition of the stratum corneum, CO levels, and the presence or absence of hair. Keratin and/or necrotic material can also be introduced into the dermis with an infectious organism to further enhance the problem. In immunocompromised individuals, the use of topical corticosteroids may lead to a dermatophyte infection due to local immunosuppression.