Define cirrhosis
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cirrhosis definition pathophysiology etiology
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Cirrhosis
Cirrhosis is the end-stage result of chronic hepatic injury, characterized by diffuse replacement of normal liver architecture with fibrous scar tissue and structurally abnormal regenerative nodules. This irreversible remodeling disrupts the liver's vascular and functional architecture.
Pathophysiology
Repeated or sustained liver injury activates hepatic stellate cells, which transdifferentiate into myofibroblasts and deposit excess collagen (primarily types I and III) throughout the hepatic parenchyma. The result is:
- Bridging fibrosis connecting portal tracts and central veins
- Regenerative nodules — islands of hepatocytes attempting to compensate, but disorganized
- Distortion of the sinusoidal microcirculation, raising intrahepatic resistance
- Portal hypertension — elevated pressure in the portal venous system, driving most of the major complications
Etiology (Common Causes)
| Cause | Examples |
|---|---|
| Alcoholic liver disease | Chronic excessive alcohol use |
| Chronic viral hepatitis | Hepatitis B, Hepatitis C |
| Metabolic-associated steatotic liver disease (MASLD) | Formerly NAFLD/NASH; associated with obesity, DM2 |
| Autoimmune | Autoimmune hepatitis, primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) |
| Genetic/metabolic | Wilson disease, hereditary hemochromatosis, alpha-1 antitrypsin deficiency |
| Biliary obstruction | Chronic biliary stricture, secondary biliary cirrhosis |
| Drugs/toxins | Methotrexate, amiodarone |
| Cryptogenic | No identifiable cause (~10%) |
Clinical Stages
| Stage | Description |
|---|---|
| Compensated | Fibrosis present but liver function maintained; often asymptomatic; may have spider angiomata, palmar erythema, or mild splenomegaly |
| Decompensated | Overt complications develop; 1-year mortality rises sharply |
Complications (Decompensation Events)
- Ascites — most common decompensating event; results from portal hypertension + sodium retention
- Variceal hemorrhage — from portosystemic collaterals (esophageal/gastric varices)
- Hepatic encephalopathy (HE) — impaired ammonia metabolism → neuropsychiatric dysfunction
- Spontaneous bacterial peritonitis (SBP) — infection of ascitic fluid
- Hepatorenal syndrome (HRS) — functional renal failure due to renal vasoconstriction
- Hepatocellular carcinoma (HCC) — major long-term risk, particularly with viral or metabolic etiology
- Hyperdynamic circulation — decreased systemic vascular resistance, low arterial BP, increased cardiac output (noted in decompensated patients)
Diagnosis
- Labs: elevated bilirubin, low albumin, prolonged PT/INR, thrombocytopenia, elevated AST/ALT (though may normalize in advanced disease)
- Imaging: US/CT/MRI showing nodular liver, splenomegaly, ascites, varices
- Elastography (FibroScan): non-invasive assessment of liver stiffness
- Liver biopsy: gold standard for staging fibrosis (METAVIR F4 = cirrhosis), though not always required
- Scoring systems: Child-Pugh score, MELD score (Model for End-Stage Liver Disease) — used to assess severity and transplant priority
Cirrhosis is largely irreversible once established, though removing the causative agent (e.g., viral cure with direct-acting antivirals, alcohol cessation) can stabilize disease and, in select cases, lead to partial regression of fibrosis. Liver transplantation remains the only definitive treatment for end-stage disease.
Active ingredient in saheli tablet
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Saheli tablet active ingredient centchroman contraceptive
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The active ingredient in Saheli tablet is Centchroman (also known as Ormeloxifene).
Key Facts
| Property | Detail |
|---|---|
| Drug name | Centchroman / Ormeloxifene |
| Drug class | Selective Estrogen Receptor Modulator (SERM) |
| Brand name | Saheli (marketed by HLL Lifecare / Hindustan Latex) |
| Dose per tablet | 30 mg |
| Developed by | Central Drug Research Institute (CDRI), Lucknow, India |
Mechanism of Action
Centchroman is a non-steroidal, non-hormonal contraceptive. It works by:
- Asynchrony between ovulation and uterine receptivity — it accelerates transport of the fertilized ovum through the fallopian tube while simultaneously delaying endometrial maturation, making implantation impossible.
- Acts as an estrogen antagonist in the uterus but has weak estrogenic effects elsewhere, so it does not suppress ovulation in most cycles.
Dosing Schedule
- First 3 months: One tablet twice a week (every 3–4 days)
- After 3 months: One tablet once a week
Advantages
- Non-hormonal — does not disrupt the hypothalamic-pituitary-ovarian axis
- Suitable for women who cannot use estrogen-containing pills (e.g., those with hypertension, diabetes, lactating women)
- Reversible contraception with rapid return of fertility on discontinuation
- Efficacy: ~98–99% with correct use
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