Hepatitis – A to E

Hepatitis is an inflammation of the liver commonly caused by viral infections. but other infections, toxic substances (e.g. alcohol, certain drugs), and autoimmune diseases can also cause hepatitis. Hepatitis can be self-limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer.

There are 5 main hepatitis viruses, referred to as types A, B, C, D and E. Types B and C especially lead to chronic disease in a majority of affected people and, together, are the most common cause of liver cirrhosis and cancer.

Hepatitis A and E are typically caused by ingestion of food or water contaminated by the virus from faecal matter. Hepatitis B, C and D usually occur as a result of parenteral contact (contact with infected body fluids). Common modes of transmission for these viruses include receipt of contaminated blood or blood products, invasive medical procedures using contaminated equipment and for hepatitis B transmission from mother to baby at birth, from family member to child, and also by sexual contact.

Acute infections may be asymptomatic or associated with Jaundice, Dark urine, Fatigue, Nausea and abdominal pain.

Hepatitis A Virus Infections are in many cases mild, with most people making a full recovery and remaining immune from further HAV infections. Hepatitis B Virus spreads mainly through parenteral route and as a Sexually Transmitted Disease(STD). Safe and effective vaccines are available to prevent HBV.

There is no vaccine for Hepatitis C Virus and it mainly spreads through blood and blood products. It can also be an STD, though rarely.

Hepatitis D virus infects only those people who are already affected by HBV. The dual infection of HDV and HBV can result in a more serious disease and worse outcome. Hepatitis B vaccines provide protection from HDV infection.

HEV is a common cause of hepatitis outbreaks in developing parts of the world and is increasingly recognized as an important cause of disease in developed countries. Safe and effective vaccines to prevent HEV infection have been developed but are not widely available.

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Systemic Schlerosis


Synonyms: scleroderma, progressive systemic sclerosis, CREST syndrome

Systemic sclerosis (SS) is an autoimmune connective tissue disease characterised by changes in the texture and appearance of the skin due to increased collagen production.

Characteristics of systemic sclerosis include essential vasomotor disturbances; fibrosis; subsequent atrophy of the skin, subcutaneous tissue, muscles, and internal organs (eg, alimentary tract, lungs, heart, kidney, CNS); and immunologic disturbances accompany these findings.

It is called CREST Syndrome because it includes calcinosis, Raynaud’s phenomenon, oesophagal dysmotility, sclerodactyly, telangiectasia.


The autoimmune dysfunction leads to increased collagen deposits and changes in intercellular matrix.There will be fibrosis in the tissues. Different factors, including genetic, environmental, vascular, autoimmunologic, and microchimeric factors are involved in systemic sclerosis pathogenesis.


Clinical examination of the lesions along with symptomatology is sufficient for diagnosis. The presence of autoantibodies and occasionally biopsy may be needed for diagnosis.


There is no cure for scleroderma, though symptomatic treatment for softening the skin and reducing inflammation may be helpful. Some patients may benefit from exposure to heat.
Topical treatment by NSAID do not alter the disease course but may improve pain and ulceration.

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Fever of Unknown Origin (FUO)

Synonyms: Pyrexia of unknown origin (PUO), ‘febris e causa ignota(febris E.C.I.)’
FUO is a condition in which the patient has an elevated temperature (fever) but despite investigations by a physician no explanation has been found.


In 1961 Petersdorf and Beeson suggested the following criteria:

  • Fever higher than 38.3 °C (101 °F) on several occasions
  • Persisting without diagnosis for at least 3 weeks
  • At least 1 week’s investigation in hospital

A new definition which includes the outpatient setting (which reflects current medical practice) is broader, stipulating:

  • 3 outpatient visits or
  • 3 days in the hospital without elucidation of a cause or
  • 1 week of “intelligent and invasive” ambulatory investigation.

Classic FUO

Classic FUO includes the original classification by Petersdorf and Beeson. It can be due to

  • infections (e.g. abscesses, endocarditis, tuberculosis, and complicated urinary tract infections),
  • neoplasms (e.g. lymphomas, leukemias),
  • connective tissue diseases (e.g. temporal arteritis and polymyalgia rheumatica, Still’s disease, systemic lupus erythematosus, and rheumatoid arthritis),
  • miscellaneous disorders (e.g. alcoholic hepatitis, granulomatous conditions), and
  • undiagnosed conditions.

Nosocomial FUO

Nosocomial FUO is defined as fever occurring on several occasions in a patient who has been hospitalized for at least 24 hours and has not manifested an obvious source of infection that could have been present before admission.

Immune-deficient FUO

Immune-deficient FUO, also known as neutropenic FUO, is defined as recurrent fever in a patient whose neutrophil count is 500 per mm3 or less and who has been assessed for three days without establishing an etiology for the fever.

HIV-associated FUO

HIV-associated FUO is defined as recurrent fevers over a four-week period in an outpatient or for three days in a hospitalized patient with HIV infection.


Diagnosis is based on exclusion, ie, by ruling out the causes one by one. Environmental factors and family history is also taken into consideration.


Unless the patient is acutely ill, no therapy should be started before the cause has been found unless there is neutropoenia. This is because non-specific therapy is rarely effective and mostly delays diagnosis.

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Crohn’s Disease

Crohn’s disease is a type of chronic inflammatory bowel disease (IBD) that may affect any part of the gastrointestinal tract.
Synonyms: Crohn’s Syndrome, Regional enteritis, Chronic Ileitis
Causes: Exact cause unknown
It is thought to be caused by a combination of genetic factors, immunological factors, and environmental causes.

Clinical Features

Signs and symptoms often include abdominal pain, diarrhea, fever, and weight loss. Extra-gastrointestinal tract symptoms may include anemia, skin rashes, arthritis, inflammation of the eye, and fatigue. Bowel obstruction is also common.


It is thought to be a disease where the immune system attacks the cells of the Intestinal tract. But it is not an autoimmune disease as the trigger for the immune system is environmental due to some bacterial infections.
A transmural pattern of inflammation – the inflammation spanning the entire depth of the intestinal wall is seen. Ulceration is an outcome seen in the highly active disease. There is usually an abrupt transition between unaffected tissue and the ulcer—a characteristic sign known as skip lesions.
There is infiltration of the mucosa by leukocytes especially mononuclear cells.
There is weakened mucosal layer and inability to clear bacteria from the intestinal walls, and microorganisms are taking advantage of this.


Symptomatology along with family history are crucial in diagnosis.
A colonoscopy showing signs of ulcers, inflammation, or bleeding along the mucosal layers is approximately 70% effective in diagnosing the disease. During a colonoscopy, biopsies of the colon are often taken to confirm the diagnosis. Multinucleated giant cells is a common finding in the lesions of Crohn’s disease.


About 10% to 20% of people with Crohn’s disease have at least one other family member who also has the disease and it is also common in some ethnic groups(Jews, Caucasians). It is thought to be due to one or other abnormality in about 70 pairs of genes leading to increased susceptibility.
Increased intake of animal proteins, milk etc are associated with Crohn’s disease and it is more prevalent in industrialized areas. Smoking also is considered as a contributory etiology.
Crohn’s disease can be categorized by the specific tract region involved. The ileum is the most affected part. Ileocolic Crohn’s accounts for fifty percent of cases. Crohn’s ileitis, manifest in the ileum only, accounts for thirty percent of cases, while Crohn’s colitis, of the large intestine, accounts for the remaining twenty percent of cases and may be particularly difficult to distinguish from ulcerative colitis.


There is no specific treatment. Lifestyle modification with reduced stress may be helpful in reducing Crohn’s. Dietary modification to eat lesser amounts at frequent intervals and avoiding animal proteins may be advised. Acute symptoms are controlled by medication if needed.


Crohn’s is an incurable chronic condition characterized by periodic remission and relapse. There is a rare possibility for intestinal cancers in some patients.

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Ramsay Hunt Syndrome

Three different conditions, first described by Ramsay Hunt, are called by the same name – Ramsay Hunt Syndrome.
Most important one is Ramsay Hunt cerebellar syndrome, is a rare form of cerebellar degeneration which involves myoclonic epilepsy, progressive ataxia, tremor, and a dementing process.

Synonyms: dyssynergia cerebellaris myoclonica, dyssynergia cerebellaris progressiva, dentatorubral degeneration, Ramsay Hunt syndrome (RHS) type 1
Cause: the impairment of a regulatory mechanism between cerebellar and brainstem nuclei.
Treatment: Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms.

Ramsay Hunt syndrome type 2 is the reactivation of herpes zoster in the geniculate ganglion. It has a variable presentation which may include a lower motor neuron lesion of the facial nerve, deafness, vertigo, and pain.
Synonyms: herpes zoster oticus, geniculate neuralgia, nervus intermedius neuralgia, zoster sine herpete(when without rashes)

Clinical Features

A triad of ipsilateral facial paralysis, ear pain, and vesicles on the face, on the ear, or in the ear is the typical presentation.
Taste loss on the front of the tongue, dry eyes and mouth is a classical presentation with tinnitus, hearing loss, and vertigo in some cases when the Vestibulocochlear nerve is affected.


After initial infection, varicella-zoster virus lies dormant in nerve cells, where it is kept in check by the immune system. During an illness that suppresses the immune system, the virus travels to the end of the nerve cell, where it causes the symptoms.
Ramsay Hunt syndrome is thought to be the cause of as many as 20% of clinically diagnosed cases of Bell palsy.

Prevention & Treatment

Shingles can be prevented by immunizing against the causal virus, varicella zoster. Treatment with the steroid prednisone and the antiviral drug acyclovir is prevalent though controversial as some studies report only 22% effectiveness in recovery from paralysis and have no effect on hearing loss.

Ramsay Hunt syndrome type 3 is a less commonly referenced condition, an occupationally induced neuropathy of the deep palmar branch of the ulnar nerve. It is also called Hunt’s disease or Artisan’s palsy.

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Infectious Mononucleosis

Synonyms: Mono, Kissing Disease, Glandular Fever, Pfeiffer’s disease, Filatov’s disease.
Causative Organism: Epstein–Barr virus (EBV) -90%, Human Cytomegalovirus (CMV)

Infectious mononucleosis is recognized as a clinical syndrome consisting of fever, pharyngitis, and adenopathy.


EBV is transmitted through intimate contact with body secretions, especially saliva.
The first site of infection is pharyngeal epithelial cells followed by B-Lymphocytes.Circulating B cells spread the infection throughout the entire reticular endothelial system (RES), ie, liver, spleen, and peripheral lymph nodes. The host immune response involves cytotoxic T cells against infected B lymphocytes, resulting in enlarged, atypical lymphocytes (Downey cells).Lymphocytosis observed in the RES is caused by a proliferation of EBV-infected B lymphocytes. Pharyngitis observed in EBV infectious mononucleosis is caused by the proliferation of EBV-infected B lymphocytes in the lymphatic tissue of the oropharynx.


The most commonly used diagnostic criterion is the presence of 50% lymphocytes with at least 10% atypical lymphocytes (large, irregular nuclei), while the person also has a fever, pharyngitis, and swollen lymph nodes. Only half of the patients presenting with the symptoms held by mononucleosis and a positive heterophile antibody test (the monospot test) meet the entire set of criteria.


Most cases of EBV infectious mononucleosis are subclinical, and the only manifestation of EBV infection is a positive serological test. Mortality and morbidity rates due to uncomplicated primary EBV infectious mononucleosis are low.

Splenic rupture may be the initial presentation of EBV mononucleosis and such cases have high mortality. Hepatic necrosis caused by extensive EBV proliferation in the RES of the liver is the usual cause of death in affected males. EBV is the main cause of malignant B-cell lymphomas in patients receiving organ transplants.

Patients with EBV infection who present clinically with infectious mononucleosis invariably experience accompanying fatigue. Fatigue may resolve gradually in 3 months in most of the cases.


Infectious mononucleosis is generally self-limiting, so only symptomatic or supportive treatments are used.


CNS Complications: meningitis, encephalitis, hemiplegia, Guillain–Barré syndrome, and transverse myelitis.
Haematological: Anaemia and thrombocytopenia.
Jaundice and rarely hepatitis
Upper airway obstruction from enlarged tonsils
Splenic rupture
Cancers of lymphatic tissue

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