GI Accessory organs Flashcards
Prehepatic Jaundice
Overproduction of unconjugated bilirubin from excess RBC breakdown and the liver cannot keep up
- High unconjugated (indirect)
- Decreased hct
Hepatic jaundice
Liver inability to take, conjugate and conjugae bilirubin. Conjugated will leak out of hepatocytes.
Occurs in hepatitis and Cirrhosis
- High unconjugated + conjugated
- High LFT
- Dark urine
Post hepatic jaundice
Failure to reach duodenum
- Intrahepatic - swelling or fibrosis
- Extrahepatic - cholestitis, gallstones, pancreatic cancer
- High conjugated (direct) bilirubin
- Dark urine
- Steatorrhea - pale coloured stool
- High cholesterol
- Accumulation of bile salts in skin = pruritis
- Vit K deficiency
Viral hepatitis
Infection of liver causing damage from cytotoxic cytokines and NK cells that destroy the infected hepatocytes. Chronic infection leads to scarring then cirrhosis
1) Hepatitis A
- Fecal oral route
- Poor hygiene, handling of food, sanitation, crowded places
- Diagnosed by HAV-specific antibodies, PCR test
2) Hepatitis B
- Higher pravelence
- Blood and body fluids
3) Hepatitic C
- Liver damage, through blood
- No vaccination
Viral hepatitis clinical manifestations
- RUQ pain = liver enlargement
- Fatigue, myalgia, arthralgia, malaise, anorexia, fever
- Jaundice
Chronic can lead to liver scarring, cirrhosis and failure, with more risk to develop cancer
NAFLD = non alcoholic fatty liver disease
Ranges from simple to severe cirrhosis
Accumulation of fat in the liver cells without alcohol, usually in obesity or DM2
Often adymptomatic
Toxic/Drug induced hepatitis
Symetic posison (e.g. gold, carbon tetrachloride) or those converted in liver to toxic live Tylenol or alcohol
Liver necrosis can occur in 2-3 days
Liver Cirrhosis
Irreversible fibrosis and conversion of liver to abnormal nodules - caused by viral hepatitis B&C, NAFLD, toxic/drug, autoimmune
Excessive alcohol is leading cause
Hepatocyte dyfunction as inadequate blood flow occurs
Complication - portal HTN, varices, ascites/edema, HE, coaguabulity, billary obstruction, hepatorenal syndrome, bacterial peritonitis
Portal hypertension
Structural change where the hepatic portal vein becomes obstructed, causing backup of blood into spleen = Splenomegaly, thombocytopenia due to trapping plateltys and WBC
- Signs of bleeding/bruising
Varices made as collateral circulation
Varices
Created to bypass the liver.
Distended and tortuous collateral veins that are fragile, commonly in esophagus, abdomen or hemorrhoidal
- Cause hematemesis or melena
- Esophageal burst commonly causing life threatening GI bleeds
Ascites/edema
Accumulation of fluid in abdomen due to portal HTNN, more hepatic lymph, less albumin (liver makes albumin!! so less oncotic pressure), hyperaldosteronism (liver breaks down aldosterone)
= Abdomen distention, dependent edema, weight gain, hypokalemia
Hepatic Encephalopathy
i) Ammonia rich blood shunted past liver due to collateral veins/varices
ii) Dysfunctional hepatocytes cannot convert it into urea
= sleep disturbances, coma, asterixis, fetor hepaticus (neurotoxic)
Coagulopathy/anemia
Pancytopenia due to
- Portal HTN causing splenomegaly and trapping it
- Clotting factor not produced in liver
- Unable to excrete bile for vitamin K absorption
- Esophageal varices = bleeding/hemorrhage
Other manifestations of cirhosis
i) Jaundice - Hepatic jaundice as intrahepatic damage - mix of conjugated and unconjugated
ii) Infections - portal HTN so bypass filtering ingested bacteria
iii) Hepatorenal syndrome - sudden decrease in urine, high BUN/creatinine
iv) Hormonal - steroid hormones not broken (aldosterone, estrogen, etc)= water retention, testiculat atrophy, gynecomastia, amonrrhea, spider angioma, palmar erythema, abnormal hair growth
iv) Drug toxicity - elevated levels of drugs = toxic
Gallbladder
RUQ - Concentrates bile products by liver
- Bile made up water, bile salts, cholesterol and bilirubin