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Complications of Cirrhosis

Portal hypertension Coagulopathy

Gastroesophageal varices Factor deficiency
Portal hypertensive gastropathy Fibrinolysis
Splenomegaly, hypersplenism Thrombocytopenia
Ascites Bone disease
Spontaneous bacterial peritonitis Osteopenia
Hepatorenal syndrome Osteoporosis
Type 1 Osteomalacia
Type 2 Hematologic abnormalities
Hepatic encephalopathy Anemia
Hepatopulmonary syndrome Hemolysis
Portopulmonary hypertension Thrombocytopenia
Malnutrition Neutropenia

Portal Hypertension → increased intrahepatic resistantto the passage of blood flow through liver d/t cirrhosis and regenerative nodules
→increased splanchnic blod flow secondaryto vasodilationwithin the splanchnic vascular bed

Portal vein formed by union of the sup mesenteric and splenic veins →pressure within it = 5-8mmhg normally
As portal pressure rises above 10-12mmhg→the main sites of collateral(gastero-esophageal j(x),rectum lt renal vein,diaphragm,
retroperitonium, ant abd wallvia umbilical vein) dilates. (PORTOSYSTEMIC SHUNT)

OGj(x) are superficial in position→tend to rupture

Rectal varices are found in 30% of pts.

1.Classification of Portal Hypertension(based on site of obstruction)

Prehepatic(blockage of the portal vein b4 liver)

Portal vein thrombosis
Splenic vein thrombosis
Massive splenomegaly (Banti's syndrome)
Hepatic(d/t distortion of d liver architecture)
Congenital hepatic fibrosis
Cirrhosis—many causes
Alcoholic hepatitis
Hepatic sinusoidal obstruction (venoocclusive
Posthepatic(venous blockage outside the liver)
Budd-Chiari syndrome
Inferior vena caval webs
Cardiac causes
Restrictive cardiomyopathy
Constrictive pericarditis
Severe congestive heart failure
Hepatic Encephalopathy/portosystemic encephalopathy
-neuropsychiatric syndrome 2˚ chronic liver Dz
-personality d/o of personality, mood, and intellect w reversal of normal sleep rhythm
-pts is irritable, confused, disoriented, sow slurred speech
-general features of N&V ,weakness
-hyperreflexia, increased tone

-Typically in pts w adv cirrhosis and jaundice
-low urine output w low urinary NA+ conc
-almost normal renal histology
-mechanism is similar to hat producing ascites
-Extreme vasodilation d/t NO → extreme ↓ in effective blood volume ad hypotension→activetea renin angiotensin system→rise
plama rennin and aldosteron,NA and vasopressin leading to vasoconstriction of the renal vasculature →↑ preglomerular vascular
resistant →causing blood flow to be directed away from the renal cortex→ reduce GFR and plasma rennin remain high, salt and water
retention occur w reabsorption of sodium from the renal tubules

-defined as hypoxaemia w adv liver ds
-intrapulmonaryvascular dilatation w no evidence of primary pulmonary dz
-features of: clubbing,spider naevi, cyanosis
-no resp Sx unless severe—develop dyspneaon standing
-TTE shows intrapulmonary shunting
-ABG- confirmof arterial O2 desaturation.

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