GIT Flashcards
What is diverticulosis?
Inner layer of colon bulges through the focal area of weakness in the colon wall due to increased intraluminal pressure
Where is the most common location for diverticulosis?
Sigmoid colon
What are the clinical features of diverticulosis?
Usually asymptomatic, but can present with vague LLQ discomfort, bloating, constipation/diarrhea
How is diverticulosis diagnosed?
Barium enema is the test of choice, but it is usually discovered during annual screening with colonscopy
What are the complications of diverticulosis?
Painless rectal bleeding
Diverticulitis
What is diverticulitis?
Feces become impacted in the diverticulum, leading to erosion and micro-perforation. AKA left sided appendicitis
What are the clinical features of diverticulitis?
Fever, LLQ pain and leukocytosis
What are the diagnostic tests for diverticulitis?
CT scan with oral and IV contrast
KUB or abdominal radiographs
(Barium enema and colonoscopy are contraindicated due to risk of perforation)
How is diverticulitis managed?
If uncomplicated: IV abx (ciprofloxacin + metronidazole) for 7-10 days, NPO, IV fluids. If symptoms persist for 3-4 days then resection of involved segment by surgery may be necessary. If recurrent then surgery is recommended.
If complicated: surgery
What are the complications of diverticulitis?
Abscess formation
Colovesical fistula
Obstruction
Free colonic perforation
What is acute Liver failure?
Acute, severe liver injury with concurrent encephalopathy and impaired synthetic liver function and in order to diagnose, the patient must not have an underlying liver disease or cirrhosis prior to insult.
What are the most common causes of acute liver failure?
Acetaminophen, hepatitis A, B, C, D, and E
What are the 3 components that are required to diagnose acute liver failure?
Encephalopathy
INR > 1.5
Elevated liver enzymes (ALT and AST)
How is acute liver failure managed?
Close monitoring
Supportive care
Treat underlying cause
Neurological checks every 2 hours due to encephalopathy
Monitor ICP in patients with advancing encephalopathy and if elevated treat with mannitol
Liver transplantation
What is cirrhosis?
Chronic liver disease characterized by fibrosis, disruption of the liver architecture, and widespread nodules in the liver
What are the two events that occur as a result of the distortion of the liver anatomy in cirrhosis?
Portal hypertension: due to decreased blood flow through the liver, that leads to ascites, peripheral edema, splenomegaly and varicosity of veins (bleeding is the most life-threatening complication). TIPS can be used to lower portal pressure.
Hepatocellular failure: leads to impairment of biochemical functions
What are the causes of cirrhosis?
Alcoholic liver disease (MCC)
Chronic hepatitis B and C infections ( next MCC)
Nonalcoholic steatohepatitis
Drugs such as acetaminophen toxicity and methotrexate
Autoimmune hepatitis
Primary biliary cirrhosis, secondary biliary cirrhosis
Inherited metabolic disease such as hemochromatosis and Wilson disease
Hepatic congestion secondary to right-sided heart failure, constrictive pericarditis
AAT deficiency
Hepatic veno-occlusive disease
What are the classical signs of chronic liver disease?
Ascites Varices Gynecomastia, testicular atrophy Palmar erythema, spider angiomas on skin Hemorrhoids Caput Medusa
What are the complications of cirrhosis?
Portal hypertension Varices Ascites Hepatic encephalopathy Hepatorenal syndrome Spontaneous bacterial peritonitis Hyperestrinism Coagulopathy
How are varices managed?
- Hemodynamic stabilization
- IV antibiotics
- IV octreotide
- Once stabilized, perform endoscopy to diagnose and treat hemorrhage either with variceal ligation or sclerotherapy
- Give non selective beta-blockers (long-term therapy to prevent rebleeding)
What diagnostic test is done in ascites?
Paracentesis is done to determine whether it is due to portal hypertension or another process. It is examined for cell count, ascites albumin, gram stain and culture to rule out infection.
Serum ascites albumin gradient is measured, if > 1.1 g/dL then portal HTN is very likely, but if < 1.1 g/dL then less likely.
How is ascites treated?
Low sodium diet and diuretics
Therapeutic paracentesis
Peritoneovenous shunt or TIPS to reduce portal HTN
What is the most common toxic metabolite that causes hepatic encephalopathy?
Ammonia
What are the clinical features of hepatic encephalopathy?
Decreased mental function, confusion, poor concentration, coma
Asterixis “flapping tremor”
Rigidity, hyperreflexia
Fetor hepaticus
How is hepatic encephalopathy treated?
Lactulose to prevent absorption of ammonia
Rifaximin (abx) kills bowel flora to decrease ammonia production by intestinal bacteria
Limit protein in diet
What are the etiological agents that cause spontaneous bacterial peritonitis?
E. Coli
Klebsiella
Streptococcus pneumoniae
What are the clinical features of spontaneous bacterial peritonitis?
Abdominal pain Fever Vomiting Rebound tenderness May lead to sepsis
How is the diagnosis of spontaneous bacterial peritonitis established and managed?
Paracentesis and examination of ascitic fluid for WBCs ( especially PMNs > 250), gram stain with culture and sensitivity.
Treated with broad-spectrum antibiotics (ceftriaxone)
What is the treatment for cirrhosis?
Treat underlying cause
Avoid agents that cause injury to the liver such as acetaminophen
Manage any complication that arises due to cirrhosis
Liver transplantation is the only hope for a cure
What is Wilson disease?
It is an autosomal recessive disease of copper metabolism. Mutations in the ATP7B gene lead to impairment of copper excretion into bile. Therefore, copper accumulates in liver cells and as hepatocytes die copper leaks into plasma and accumulates in various organs including kidney, cornea, and brain.
What are the clinical features of Wilson Disease?
Liver disease (acute hepatitis, cirrhosis, and fulminant hepatic failure)
Kayser-Fleischer rings
CNS findings such as Parkinsonian symptoms, chorea, drooling, and incoordination
Renal involvement (aminoaciduria, nephrocalcinosis)
How is Wilson disease diagnosed?
Elevated aminotransferases, impaired synthesis of coagulation factors and albumin (hepatic disease)
Decreased serum ceruloplasmin levels
Liver biopsy is the best which will show significantly elevated copper concentration
How is Wilson disease managed?
D-penicillamine (chelating agents)
Zinc (prevents uptake of dietary copper)
Liver transplantation
Monitor (copper levels, urinary copper excretion, ceruloplasmin, and liver function, signs of liver or neurological disease)
What are the signs of acute liver failure?
Coagulopathy Jaundice Hypoglycemia Hepatic encephalopathy Infection Elevated LFT values Any complication associated with cirrhosis
What is hemochromatosis?
An autosomal recessive disease of iron absorption, in which excessive iron absorption in the intestine that leads to increased accumulation of iron in various organs such as liver, pancreas, heart, joints, skin, thyroid gland and hypothalamus. Over the years, fibrosis occurs secondary to hydroxyl free radicals that are generated by excess iron.
What are the clinical features of hemochromatosis?
Mostly asymptomatic and mildly elevated AST and ALT may be the only abnormality so obtain iron studies, if elevated order biopsy to confirm the diagnosis. Findings may include signs of involved organs.
What are the complications of hemochromatosis?
Cirrhosis Cardiomyopathy Arthritis Diabetes mellitus Hypogonadism Hypothyroidism Hyperpigmentation of the skin
How is hemochromatosis diagnosed?
By markedly elevated serum iron and serum ferritin (>1000), elevated iron saturation >50%, decreased TIBC, genetic testing for etiologies mutations ( gold standard), biopsy of the liver is the best as it will show elevated iron.
