Ascites

Color

ClearTurbidBloodyMilkyBrown + bilirubin>40Opalescent
CirrhosisInfectionHCC, traumatic tapping, cirrhosis, malignancy, Tuberculous peritonitisCirrhosis, malignancyRuptured gallbladder, perforated duodenal ulcer
Between turbid and milky

Lab data

Low Glucose- Infection, malignancy, bowel perforation

High LDH- Infection, malignancy, bowel perforation

High amylase- Pancreatitis, bowel perforation

Malignant ascites- Peritoneal carcinomatosis, liver metastasis, HCC, lymphoma


SAAG<1.1- Pancreatitis, serositis, Nephrotic syndrome, Peritoneal carcinomatosis, peritoneal tuberculosis, ruptured viscus

SAAG>1.1- Cirrhosis, Alcoholic hepatitis, Massive hepatic metastases, Heart failure/constrictive pericarditis, Budd-Chiari syndrome, Portal vein thrombosis, Idiopathic portal fibrosis


1.Spontaneous bacterial peritonitis

Diagnostic- Neutrophil>250, LDH<225, Glucose>50, Total protein<1

Treatment- Cefotaxime(2g q8h)

2.Bowel perforation, secondary bacterial peritonitis

Diagnostic- Neutrophil>250 + 2/3(Total protein>1, Glucose<50, LDH> 225)

Treatment- Piperacillin-tazobactam, cefoxitin, ampicillin+metronidazole+cirpofloxacin


*Portal hypertension- Portal vein>=13mm, SMV/Splenic vein>=11mm, splenomegaly>12cm

*Heart failure→  Protein>2.5, cirrhosis→ Protein<2.5


Lab of liver test

ALT- Less amount in liver, 47hrs half life, periportal zone, 100% in cytoplasm, injury>necrosis

AST- Large amount in liver, 17hrs half life, central zone, 80% in mitochondria, 20% in cytoplasm, necrosis>injury

AST/ALT<1- Chronic hepatitis, late stage of acute hepatits, obstructive jaundice, cholangitis, NAFLD

AST/ALT>1- Hypoxia, liver cirrohosis, acute hepatitis, alcoholic hepatitis

ALK-P(<100)- Bile canalicular membrane, Rise→ abnormal in alimentary, liver, kidney, placenta, bone

GGT(<60)- Bile duct epithelial cell, Rise→ Cholangiocarcinoma, CBD stone, DM, drug, PBC, PSC, alcohol

Bilirubin- Direct(0.2)(Albumin bound half-life 17 days), Indirect(1.0)(Half-life 4 hrs)

Conjugated hyperbilirubinemia- Dubin-Johnson’s syndrome, Rotor’s syndrome, viral or drug induced hepatitis, intrahepatic cholestasis (Sepsis, post-op, PBC, sex hormone, erythromycin), extrahepatic biliary obstruction(CBD stone, cholangiocarcinoma, pancreatic cancer)

Unconjugated hyperbilirubinemia-  hemolysis(ABO, Rh, spherocytosis, G6PD, sickle cell, thalassemia, streptomycin, Vitamin K), non-hemolysis(hematoma, polycythemia, cystic fibrosis), conjugation↓(breast milk, hypothyroidism, Gilbert, Crigler-Najjar)

Ileus

1.Mechanical

a)Small intestine- adhesion, hernia, gallstone ileus, intussusception

b)Large intestine- tumor, volvulus, fecal impaction

High location- vomiting, intermittent colic pain

Middle location- crescendo colic pain

Low location- fullness, feculent vomiting

PE- high-pitch hyperactive bowel sound, metallic sound, borborygm

X-ray- Fixed bowel gas, stack of coin sign, air-fluid levels, String of beads sign, pneumobilia(gallstone ileus), bent-inner tube sign

2.Paralytic

Etiology- Peritonitis, surgery, shock, sepsis, hypokalaemia, acetylcholine antagonist, morphine

X-ray- Bowel gas constantly changing

Gastric ulcer

Etiology- NSAID, H.pylori

Characteristic- 5% maglinant, hemorrhage was common

Corpus predominant gastritisAntral predominant gastritis
HP, NSAIDHP
Not related to GERDRelated to GERD
Pain after mealsPain before meals

Diagnosis- Endoscopy(a least 6 biopsy to exclude malignancy), barium examination(commonly located at lesser curvature, radiation of gastric mucosal showed benign lesion)

Treatment- Like Peptic ulcer, but harder to treat

Peptic ulcer

Forward- Related with MAG, DAG, MALToma

Risk factor- H.pylori, NSAID/aspirin, stress, gastrinoma, blood group O, HLA-B5, smoking, CRF, liver cirrhosis, hyperparathyroidism, COPD, systemic mastocytosis, renal transplantation

Presentation- Pain before meals and in the middle of the night , sudden breakthrough pain(perforation), hematemesis(bleeding), vomiting(gastric outlet obstruction)

Modified Johnson classification

TypeSiteEtiology
I (60%)Lesser curvatureMucosa damage
II (15%)gastric body + duodenumHCL↑
III (20%)PrepyloricHCL↑
IV (<10%)EC junctionMucosa damage
V (5%)any locationNSAID, aspirin

Diagnosis- Invasive(histologic, culture, rapid urease test), non-invasive(urease breath test, serum antibody, stool antigen)

Treatment 

1.H.pylori regimen

PPI+Clarithromycin+Metronidazole/amoxicillin for 14 days, Bismuth+PPI+Tetracycline+metronidazole

2.Sulcralfate– bind to ulcer up to 12hrs, 1g 1hr before meal and bedtime

3.Prostaglandin– misoprostol, 200ug qid, prevent ulcer caused by NSAID

4.PPI– Rabeprazole(20mg bid), lansoprazole(30mg bid), pantoprazole(40mg bid), esomeprazole(40mg qd), plateu reach at 4th day, became to normal after discontinuation over 3~5 days, duration 4~8weeks

5.H2 receptor antagonist- cimetidine(400mg qd)(antiandrogen, renal and hepatic, blood dyscrasia),ranitidine(150mg qd)(像cimetidine, 但副作用較少), famotidine(20mg qd)

6.Antacid– Al(constipation), Mg(diarrhea),Ca(milk alkali syndrome), 140mmol 1h and 3h after eating and bedtime

Complication- Bleeding, hematemesis, melana(60ml, 7days), perforation, obstruction

Stomach physiology

1.Vagus nerve→ M3 receptor→ Gq→ IP3/Ca→ H-K pump

2.G cells→ gastrin→ CCKb receptor→ Gq→ IP3/Ca→ H-K pump

3.G cells→ gastrin→ ECL cell→ Histamine→ H2 receptor→ Gs→ cAMP→ H-K pump

4.PGE→ Gi→ inhibit cAMP→ H-K pump

*Somatostatin– Inhibit ECL cells(secretes histamine), G cells

*Chief cell→ Pepsinogen I and II

*Parietal cell→ HCL, intrinsic factor

*Mucosal cell→ Mucus, pepsinogen II, bicarbonate

*D cell→ Somatostatin

Lower GI bleeding

Etiology: Anatomic (diverticulosis), vascular (angiodysplasia, ischemic, radiation-induced), inflammatory (infectious, inflammatory bowel disease), and neoplastic

Presentation: Hematochezia, normal BUN/Cre

Management

1.Fluid resuscitation

2.Blood transfusion- Young→ <7need transfusion, Old→ <9 need transfusion

Diagnostic: Early colonscopy- within 24 hrs

Imaging:

1.Radionuclide imaging– 0.1ml/min, use Tc-99m

Disadvantage: Need active bleeding

2.CT angiography– 0.3ml/min

Disadvantages: Need active bleeding, could not treat only for diagnosis, IV contrast

3.Angiography– 0.5ml/min

Advantages: could treat, no need bowel preparation

SOP: NG tube→ Colonscopy→ RBC scan

Upper GI bleeding

Presentation: Melena, coffee ground in NG tube, BUN/Cre>30

Etiology: Peptic ulcer, Aorto-enteric fistula, Angiodysplasia, varices, malignancy, Mallory-Weiss tear, anticoagulant

Treatment

1.Fluid resuscitation

2.Unstable→ Hct<9 need transfusion, stable→ Hct<7 need transfusion, If INR>2 or platelet count<50000 need FFP

3.Acid suppression- Esomeprazole 40 mg IV twice daily after an initial bolus of 80 mg IV

4.Prokinetic- Erythromycin(3 mg/kg IV over 30 minutes, 30 to 90 minutes prior to endoscopy)(promote gastric emptying)

5.Vasoactive agent- Octreotide IV bolus of 50 mcg, followed by a continuous infusion at a rate of 50 mcg/hr

6.Anti-platelet and anti-coagulant- maybe need to hold

Diagnostic: Early endoscopy- within 24 hrs

Risk stratification

1.Rockall score- >2/11, age, the presence of shock, comorbidity, diagnosis, and recent hemorrhage

2.Glasgow Blatchford score- >0/23, blood urea nitrogen, hemoglobin, systolic blood pressure, pulse, and the presence of melena, syncope, hepatic disease, and/or cardiac fail

Diarrhea

a)NPO improves→ Hypermotility, osmotic

b)NPO cannot improves→ Secretory, inflammatory

c)Fecal WBC/RBC(-)→ Secretory

d)Fecal WBC/RBC(+)→ Inflammatory

1.Osmotic

Mechanism- Absorption↓, non-absorbable material induces fluid secretion into intestine

Etiology- Magnesium oxide, Vitamin C, Mannitol, pancreas function↓, Lactulose, intestinal absorption↓, lactose intolerance, Bacteria↑

Lab- FOG>125

2.Secretory

Presentation- stool volume >1L/day

Etiology- Hyperthyroidism, Zollinger-Ellison syndrome, Villous adenoma, VIPoma, cholera, ETEC, C.difficile, rotavirus, congenital chloride diarrhea, colchicine, neuroblastoma

Lab- FOG<50

3.Inflammatory

Etiology- IBD, Yersinia, Campylobacter, Salmonella, Shigella, EHEC

Lab- CRP, ESR, fecal calprotectin

4. Hypermotility

Mechanism- Lack of absorption of the food due to increase movement of the bowel induces fluid secretion into intestine

Etiology- Salmonella, Campylobacter, C.difficile, IBD, celiac disease

*FOG=290-2(Na+K of stool)

1.Small bowel

Etilogy- Virus, E.coli, Klebsiella, perfringen, cholera, vibrio, giardia, cryptosporidium

Presentation- Watery, of large volume, abdominal cramping, bloating, and gas. Fever, occult blood/inflammatory cell rarely, PH<5.5

2.Large intestine

Etiology- Yersinia, shigella, salmonella, campylobacter, EHEC, difficile, entamoeba

Presentation- Frequent, regular, small volume, painful bowel movements. Fever and bloody or mucoid stools are common, and red blood cells and inflammatory cells,PH>5.5, serum WBC elevated