GIT Flashcards
1
Q
What is diverticulosis?
A
Inner layer of colon bulges through the focal area of weakness in the colon wall due to increased intraluminal pressure
2
Q
Where is the most common location for diverticulosis?
A
Sigmoid colon
3
Q
What are the clinical features of diverticulosis?
A
Usually asymptomatic, but can present with vague LLQ discomfort, bloating, constipation/diarrhea
4
Q
How is diverticulosis diagnosed?
A
Barium enema is the test of choice, but it is usually discovered during annual screening with colonscopy
5
Q
What are the complications of diverticulosis?
A
Painless rectal bleeding
Diverticulitis
6
Q
What is diverticulitis?
A
Feces become impacted in the diverticulum, leading to erosion and micro-perforation. AKA left sided appendicitis
7
Q
What are the clinical features of diverticulitis?
A
Fever, LLQ pain and leukocytosis
8
Q
What are the diagnostic tests for diverticulitis?
A
CT scan with oral and IV contrast
KUB or abdominal radiographs
(Barium enema and colonoscopy are contraindicated due to risk of perforation)
9
Q
How is diverticulitis managed?
A
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
10
Q
What are the complications of diverticulitis?
A
Abscess formation
Colovesical fistula
Obstruction
Free colonic perforation
11
Q
What is acute Liver failure?
A
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.
12
Q
What are the most common causes of acute liver failure?
A
Acetaminophen, hepatitis A, B, C, D, and E
13
Q
What are the 3 components that are required to diagnose acute liver failure?
A
Encephalopathy
INR > 1.5
Elevated liver enzymes (ALT and AST)
14
Q
How is acute liver failure managed?
A
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
15
Q
What is cirrhosis?
A
Chronic liver disease characterized by fibrosis, disruption of the liver architecture, and widespread nodules in the liver
16
Q
What are the two events that occur as a result of the distortion of the liver anatomy in cirrhosis?
A
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
17
Q
What are the causes of cirrhosis?
A
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
18
Q
What are the classical signs of chronic liver disease?
A
Ascites Varices Gynecomastia, testicular atrophy Palmar erythema, spider angiomas on skin Hemorrhoids Caput Medusa
19
Q
What are the complications of cirrhosis?
A
Portal hypertension Varices Ascites Hepatic encephalopathy Hepatorenal syndrome Spontaneous bacterial peritonitis Hyperestrinism Coagulopathy
20
Q
How are varices managed?
A
- 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)
21
Q
What diagnostic test is done in ascites?
A
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.
22
Q
How is ascites treated?
A
Low sodium diet and diuretics
Therapeutic paracentesis
Peritoneovenous shunt or TIPS to reduce portal HTN
23
Q
What is the most common toxic metabolite that causes hepatic encephalopathy?
A
Ammonia
24
Q
What are the clinical features of hepatic encephalopathy?
A
Decreased mental function, confusion, poor concentration, coma
Asterixis “flapping tremor”
Rigidity, hyperreflexia
Fetor hepaticus
25
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
26
What are the etiological agents that cause spontaneous bacterial peritonitis?
E. Coli
Klebsiella
Streptococcus pneumoniae
27
What are the clinical features of spontaneous bacterial peritonitis?
```
Abdominal pain
Fever
Vomiting
Rebound tenderness
May lead to sepsis
```
28
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)
29
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
30
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.
31
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)
32
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
33
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)
34
What are the signs of acute liver failure?
```
Coagulopathy
Jaundice
Hypoglycemia
Hepatic encephalopathy
Infection
Elevated LFT values
Any complication associated with cirrhosis
```
35
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.
36
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.
37
What are the complications of hemochromatosis?
```
Cirrhosis
Cardiomyopathy
Arthritis
Diabetes mellitus
Hypogonadism
Hypothyroidism
Hyperpigmentation of the skin
```
38
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.
39
How is hemochromatosis treated?
By performing repeated phlebotomies (TOC), defroxamine can be used, treat any complications, consider liver transplantation in advanced stages (it is not curative because it is a disease of the gut and transplantation won’t solve the problem of excessive absorption)
40
What is Budd-Chiari Syndrome?
A liver disease caused by occlusion of hepatic venous outflow, which leads to hepatic congestion and subsequent microvascular ischemia with gradual development of portal HTN and progressive deterioration of liver function. The clinical features resembles those of cirrhosis such as hepatomegaly, ascites, abdominal pain (RUQ), jaundice, variceal bleeding.
41
What are the causes of Budd-Chiari Syndrome.
```
Hypercoagulable states
Myeloproliferative disorders (polycythemia vera)
Pregnancy
Chronic inflammatory diseases
Infection
Various cancers
Trauma
Idiopathic
```
42
How is Budd-Chiari Syndrome diagnosed?
By hepatic venography and serum ascites albumin gradient > 1.1 g/dL
43
How is Budd-Chiari Syndrome managed?
Medical therapy is usually unsatisfactory, surgery is eventually necessary in most cases (balloon angioplasty with stent placement in inferior vena cava, portacaval shunts) and liver transplantation if cirrhosis is present.
44
What are the clinical findings of cholestasis?
```
Jaundice
Grey stools
Dark urine
Pruritus
Elevated serum alkaline phosphatase (ALP)
Elevated serum cholesterol
Skin xanthomas
Malabsorption of fats and fat-soluble vitamins
```
45
What are the causes of conjugated hyperbilirubinemia?
-Decreased intrahepatic excretion of bilirubin:
Hepatocellular disease (viral or alcoholic hepatitis, cirrhosis)
Inherited disorders (Dublin-Johnson syndrome, Rotor syndrome)
Drug induced (OCPs)
PBC
PSC
```
-Extrahepatic biliary obstruction:
Gallstones
Carcinoma of the head of the pancreas
Cholangiocarcinoma
Periampullary tumors
Extrahepatic biliary atresia
```
46
What are the causes of unconjugated hyperbilirubinemia?
-Excess production as in hemolytic anemia
-Reduced hepatic intake or impaired conjugation:
Gilbert syndrome (decreased hepatic UDP glucuronyl transferase activity
Drugs ( sulfonamides, penicillin, rifampin, radiocontrast agents)
Crigler-Najjar syndrome (Type 1 complete absence and type 2 reduced activity)
Physiological jaundice of newborn
Diffuse liver disease
47
What are the causes of elevated ALT or AST in asymptomatic patients?
```
Autoimmune hepatitis
Hepatitis B
Hepatitis C
Drugs or toxins
Ethanol
Fatty liver
Growths (tumors)
Hemodynamic disorders
Iron (hemochromatosis)
Copper (Wilson disease)
AAT deficiency
```
48
When is ALP elevated and how can we confirm that the elevation is hepatic in origin?
Alkaline phosphatase is elevated when there is obstruction to the bile flow and is confirmed by the elevation of GGT
49
How are LFTs classified?
Cholestatic: ALP and GGT
Hepatocellular: ALT and AST
50
What is acute cholecystitis?
Obstruction of the cystic duct induced acute inflammation of the gallbladder wall.
51
What are the signs and symptoms of acute cholecystitis?
```
Signs:
RUQ tenderness, rebound tenderness in RUQ
Murphy sign
Hypoactive bowel sound
Low grade fever, leukocytosis
```
Symptoms:
Epigastric or RUQ pain that may radiate to shoulder or scapula
Nausea and vomiting, anorexia
52
How is acute cholecystitis diagnosed?
RUQ ultrasound (TOC): showing thickened gallbladder wall, peri hole cystic fluid, distended gallbladder, and presence of stones
CT scan: more sensitive in identifying complications
HIDA scan: used if US is inconclusive; a dye is injected an it should fill biliary tree, cystic duct and gallbladder; if all are visualized then normal and acute cholecystitis can be ruled out, but a positive HIDA scan means that gall bladder is not visualized.
53
How is acute cholecystitis managed?
Admit and start conservative measures with IV fluids, NPO, IV antibiotics (ciprofloxacin + metronidazole), analgesics, correction of electrolyte abnormalities.
Cholecystectomy
If patient unfit for surgery percutaneous cholecystostomy tube placement to drain gallbladder.
54
What are the complications of cholecystitis?
```
Gangrenous cholecystitis
Perforation of gallbladder
Emphysematous cholecystitis
Cholecystoenteric fistula with gallstone ileus
Empyema of gallbladder
```
55
What is cholangitis?
Infection of biliary tract secondary to obstruction, which leads to biliary stasis and bacterial overgrowth. It is potentially life threatening and requires emergency treatment
56
What are the causes of cholangitis?
Choledocholithiasis, pancreatic and biliary neoplasm, postoperative strictures, invasive procedures such as an ERCP or PTC and choledochal cysts
57
What are the clinical features of cholangitis?
Charcot triad: RUQ pain, jaundice, and fever
Reynolds pentad: Charcot triad + septic shock and altered mental status
58
How is cholangitis diagnosed?
RUQ US (initial study)
Lab findings: hyperbilirubinemia, leukocytosis, mild elevation in serum transaminases
Cholangiography (PTC or ERCP):
Do not perform during acute phase, but it is the definitive test
If duct system is dilated perform PTC
If duct system is normal perform ERCP
59
How is cholangitis managed?
Close monitoring of hemodynamics, BP, and urine output
IV antibiotics and IV fluids
Decompress CBD
60
What is the most serious and dreaded complication of acute cholangitis?
Hepatic abscess
61
What is primary sclerosing cholangitis?
A chronic idiopathic progressive disease of intrahepatic and/or extraheptic bile ducts characterized by thickening of bile duct walls and narrowing of their lumens; leading to cirrhosis, portal HTN, and liver failure. It is strongly associated with ulcerative colitis
62
How is PSC diagnosed?
ERCP and PTC are TOC that will show multiple areas of bead-like stricturing and bead-like dilatations of intra- and extrahepatic ducts.
Lab tests will show cholestatic LFTs ( elevated ALP and GGT)
63
How is PSC managed?
```
Liver transplantation (curative)
ERCP with stent placement if dominant stricture causes cholestasis
Cholestyramine for symptomatic relief
```
64
What is primary biliary cholangitis?
It is an autoimmune chronic and progressive cholestatic liver disease characterized by destruction of intrahepatic bile ducts with portal inflammation and scarring
65
What are the clinical features of PBC?
```
Fatigue
Pruritus (early in course of disease)
Jaundice (late in course of disease)
RUQ discomfort
Xanthomata and xanthelasmata
Osteoporosis
Portal HTN
```
66
How is PBC diagnosed?
```
Lab findings:
Cholestatic LFTs (elevated ALP)
Positive antimitochondiral antibodies
Elevated cholesterol, HDL
Elevated IgM
Liver biopsy (to confirm)
Abdominal US or CT scan (to rule out biliary obstruction)
```
67
How is PBC managed?
```
Symptomatic:
Cholestyramine (for pruritus)
Calcium, bisphosphonates, vitamin D (for osteoporosis)
Ursodeoxycholic acid
Liver transplantation (curative)
```
68
What is acute pancreatitis?
Inflammation of the pancreas resulting from prematurely activated pancreatic digestive enzymes that invoke pancreatic tissue autodigestion.
69
What are the causes of acute pancreatitis?
```
Gallstones (MCC)
Ethanol (MCC)
Trauma (MCC in children)
Steroids
Mumps, coxsackievirus B
Autoimmune pancreatitis
Scorpion stings
Hyperlipidemia, hypercalcemia, hyperparathyroidism
ERCP
Drugs (sulfonamides, thiazide diuretics, furosemide, estrogens, HIV meds)
```
70
What are the clinical features of acute pancreatitis?
Symptoms:
Epigastric abdominal pain that may radiate to the back
Nausea and vomiting, anorexia
Signs:
Low grade fever, tachycardia, hypotension, leukocytosis
Epigastric tenderness, abdominal distention
Decreased or absent bowel sounds that indicate paralytic ileus
Grey Turner sign, Cullen sign and fox sign (these are seen with hemorrhagic pancreatitis)
71
How is acute pancreatitis diagnosed?
Lab studies:
Serum lipase and amylase (enough to diagnose acute pancreatitis)
LFTs (to identify the cause)
Hyperglycemia, hypoxemia, and leukocytosis
Abdominal radiograph (helpful in ruling out other diagnoses)
Abdominal ultrasound (help in identifying cause and useful for follow up)
CT scan of abdomen
72
What are the complications of acute pancreatitis?
```
Pancreatic necrosis
Pancreatic pseudocyst
Hemorrhagic pancreatitis
Adult respiratory distress syndrome
Pancreatic ascites/pleural effusion
Ascending cholangitis
Pancreatic abscess
```
73
How is mild acute pancreatitis managed?
```
NPO
IV fluids (balanced crystalloids)
Pain control
Nasogastric tube
Cholecystectomy and early ERCP if gallstone pancreatitis
```
74
How is severe acute pancreatitis managed?
Admit to ICU
Early enteral nutrition through nasojejunal tube
Prophylactic antibiotics if >30% of pancreas necrosed
75
What is chronic pancreatitis?
Persistent or continuing inflammation of the pancreas, with fibrotic tissue replacing pancreatic parenchyma, and alteration of pancreatic ducts eventually results in irreversible destruction of the pancreas.
76
What is the most common cause of chronic pancreatitis?
Chronic alcoholism
77
How is chronic pancreatitis diagnosed?
CT scan is initial study of choice (but normal scan doesn’t rule it out)
Abdominal radiograph
ERCP (gold standard, but not routine)
Serum amylase and lipase are not elevated.
78
What features are diagnostic for chronic pancreatitis?
Chronic epigastric pain
Calcifications on plain abdominal films
Or
Classic triad: steatorrhea, diabetes mellitus, pancreatic calcification on plain films or CT scan
79
What are the complications of chronic pancreatitis?
```
Narcotic addiction
Diabetes mellitus
Malabsorption/steatorrhea
Pseudocyst formation
Pancreatic ductal dilation
CBD obstruction (if head of pancreas is fibrosed)
Vitamin B12 malabsorption
Effusions
Pancreatic carcinoma
```
80
How is chronic pancreatitis managed?
Narcotic analgesics for pain
NPO
Pancreatic enzymes (to decrease pancreatic secretions) and H2 blockers (to prevent degradation of pancreatic enzymes by gastric acid)
Insulin
Alcohol abstinence
Frequent, small-volume, low-fat meals
Surgery (pancreaticojejunostomy, pancreatic resection)
81
What are the causes of upper GI bleeding?
```
Peptic ulcer disease
Reflux esophagitis
Esophageal varices
Gastric varices
Gastric erosions, duodenitis
Mallory-Weiss tear
Hemobilia
Dieulafoy vascular malformation
Aortoenteric fistulas
Neoplasm
```
82
What are the causes of lower GI bleeding?
```
Diverticulosis
Angiodysplasia
IBD
Colorectal carcinoma (a lower GI bleed in patients over 40 is colon cancer until proven otherwise)
Colorectal adenomatous polyps
Ischemic colitis
Hemorrhoids, anal fissures
Small intestinal bleeding
```
83
What are the management steps in any patient with GI bleeding?
Resuscitation “ABCs) (stabilization) with IV fluids (2 large-bore IV lines or central line) and transfusion (blood is given regardless of Hb level because it may not drop during acute bleeding)
Risk stratification
Treatment depends on the cause/source of the bleed
84
What is achalasia?
Acquired motor disorder of esophageal smooth muscle in which the LES fails to completely relax with swallowing, and abnormal peristalsis of esophageal body replaces normal peristalsis.
85
What are the clinical features of achalasia?
Dysphagia (difficulty in swallowing solids and liquids)
Regurgitation
Chest pain
Weight loss
Recurrent pulmonary complications secondary to aspiration
86
How is achalasia diagnosed?
```
Barium swallow (bird’s beak)
Upper GI endoscopy
Manometry (to confirm the diagnosis)
```
87
How is achalasia managed?
Adaptive measures
Medical therapy:
-Antimuscarinic agents (usually unsatisfactory)
-Sublingual nitroglycerin, long-acting nitrates and calcium channel blockers (useful in early stage and for short-term treatment)
Injection of botulinum toxin
Forceful dilation:
Pneumatic balloon dilatation is most effective
Surgical:
Heller myotomy (circular muscle layer of LES is incised)
88
What is diffuse esophageal spasm?
Non-peristaltic spontaneous contraction of esophageal body, several segments of the esophagus contracts simultaneously and prevents appropriate advancement of food bolus, but in contrast to achalasia the sphincter function is normal
89
What are the clinical features of diffuse esophageal spasm?
Non cardiac chest pain that mimics angina and may radiate to the jaw, arms and back.
Dysphagia
90
How is diffuse esophageal spasm?
```
Esophageal manometry (diagnostic): simultaneous, multiphasic, repetitive contractions that occur after a swallow; sphincter response is normal
Upper GI barium swallow (corkscrew esophagus)
```
91
How is diffuse esophageal spasm managed?
There is no completely effective therapy
Medical treatment involves nitrates and calcium channel blockers
Esophagomyotomy
92
What are the types of hiatal hernias?
Sliding hiatal hernias (type 1): both the gastroesophageal junction and a portion of the stomach herniate into the thorax. A common and benign finding that is associated with GERD.
Paraesophageal hiatal hernia (types 2-4)
93
How is esophageal hiatal hernias diagnosed?
Barium upper GI series and upper endoscopy
94
How is esophageal hiatal hernias managed?
Type 1 are treated medically with antacids, small meals and elevation of the head after meals, but if there is no response then surgery (Nissen fundoplication) maybe required
Type 2-4 are treated with elective surgery
95
What are the complications of esophageal hiatal hernias?
- Complications of sliding hiatal hernias: GERD, reflux esophagitis and aspiration
- Complications of paraesophageal hernias: obstruction, hemorrhage, incarceration and strangulation
