Comprehensive GI and Liver Notes

Algorithm for Diagnosis

• Start with the abnormality.

• Determine potential causes.

• Proceed with diagnostics.

• Organized approach for objective evaluation.

• Understand testing and alignment with suspected conditions.

GI Tract Overview

• GI starts with the mouth.

• Swallowing is a complex neuromuscular activity.

• Neurologic damage (e.g., stroke patients) can impair swallowing.

• Swallowing involves muscles in:

  • Oral cavity

  • Pharynx

  • Larynx

  • Esophagus

• Organized activity of multiple cranial nerves is required.

Swallowing Phases

• Oral (mouth)

• Pharyngeal (pharynx)

• Esophageal

• Involves digestion and motility (neuromuscular activity).

• Solids and liquids share common phases (pharyngeal, esophageal).

• Oral phase differs for solids vs. liquids, especially with cranial nerve/facial anomalies.

Complications of Dysphagia

• Nutrient deficiency and dehydration.

• Increased risk for choking and aspiration pneumonia.

• Anxiety.

Causes of Dysphagia

• Developmental errors (congenital).

• Obstruction (strictures, sphincters).

• Reflux.

• Diverticulum (outpouching of weakened muscle wall).

• Malignancies (esophagus, stomach, mouth, head/neck tumors).

Cleft Lip and Palate

• Common congenital defects (multifactorial).

• Diagnosed prenatally or postnatally.

• Failure of maxillary processes to fuse during the 4th-12th week of gestation.

• Creates opening between oral and nasal cavity.

• Size is variable.

• Signs/symptoms vary based on defect size and associated defects.

• Cleft lip can be unilateral or bilateral.

Complications with Infants

• Intact palate is needed to compress nipple for feeding.

• Difficulty drawing breast milk or formula due to defect.

• Require special feeders until palate repair.

• Growth needs close monitoring; drives earlier repair.

• Reflux is common.

• Vomiting can be dramatic due to oral/nasal cavity defect.

• May need NG or G tube until closure.

• Speech problems due to tongue's inability to hit roof of mouth for phonation.

• Ear infections are common due to eustachian tube dysfunction (shorter, straighter in infants).

• Risk for hearing issues/deficits due to recurrent ear infections and eardrum damage.

• Dental issues due to defect/disruption in gum line.

Timing of Repair

• Between 8-18 months depending on the patient.

• Based on growth, dental formation, and phonation.

Iatrogenic Dysphagia

• Surgeries involving tongue, vocal cords, pharynx, esophagus.

• Radiation can cause stenosis or strictures.

• Medications (doxycycline, alendronate, NSAIDs).

Functional Dysphagia

• Strokes and brain stem lesions.

• Polio, esophageal dysfunction, neurologic disorders, developmental delay.

• Increased risk for choking, aspiration, growth issues.

Esophageal Varices

• Complication of portal hypertension (abnormally high blood pressure in portal venous system).

• Associated with advanced liver disease (cirrhosis, liver failure).

• Impedance/obstruction of hepatic blood flow.

• Varices are dilated, dysfunctional vessels with large amounts of blood collecting in them.

• Rupture of esophageal varices is life-threatening.

• Treatment: Minnesota tube (balloon) to tamponade the esophagus and stop bleeding.

  • The tube applies opposing pressure to reduce the flow of blood to the varices to prevent further bleeding.

Peptic Ulcer Disease (PUD)

• Lesions affecting stomach lining and duodenum.

• Vary in severity

• Due to imbalance between destruction and protective mechanisms.

• H. pylori commonly associated with duodenal ulcers.

• Duodenal ulcers:

  • Epigastric pain, relieved by eating

• Gastric ulcers:

  • Less frequent, more concerning due to rupture/bleed.

  • Associated with malignancies and NSAID use.

  • May worsen with eating, while duodenal ulcers usually feel better.

• Risks: male sex, advancing age, NSAIDs, H. pylori, gastric tumors, diet, exercise, alcohol.

• Symptoms:

  • Epigastric/abdominal pain, cramping, heartburn, indigestion, nausea, vomiting.

• Can mimic symptoms of myocardial infarction (MI).

• Diagnosis:

  • History and physical exam

  • Upper GI x-ray

  • EGD

  • Serum H. pylori

  • H. pylori

  • Breath test

  • Stool analysis for H. pylori

  • Occult blood test

  • Cardiac enzymes (to rule out MI): troponin and CK-MB should be negligible.

• Complications: GI hemorrhage, obstruction, perforation, peritonitis.

• Treatment/management:

  • Bland diet

  • Identify triggers

  • Antibiotics for H. pylori

  • Surgical repair for perforation/peritonitis

  • Prophylactic meds: H_2 blockers and PPIs

Important points on PPIs and H2 Blockers

• Critical illness can be a risk factor for gastritis and GI bleeding, so they are frequently part of ICU bundles.

• For routine patients who don't need it long-term, try to wean them off due to potential for adverse effects.

• Coming off PPIs is important due to link to osteoporosis and pathologic fractures.

• H2 blockers are implicated in bacterial overgrowth due to acid suppression, which normally aids in reducing bacteria. Therefore, the use of H2 blockers, if not needed, allows bacterial overgrowth.

• In the NICU, H_2 blockers may cause necrotizing enterocolitis in preterm infants.

Mesenteric Vascular Insufficiency

• Rare but an emergent condition.

• Occlusive/nonocclusive obstruction to venous or arterial blood flow in the mesenteric region.

• Most common in elderly patients.

• Acute mesenteric ischemia: mucosal blood flow disruption to large and the small intestine.

• Can affect celiac, superior mesenteric, or inferior mesenteric arteries.

• Vasopressors can cause this due to vasoconstriction (epinephrine).

• Symptoms: Abdominal pain, bloody stools, acute onset.

• Diagnosis: Lactic acid level (high in decreased perfusion to the gut).

Liver Function

• Metabolizes carbohydrates, proteins, fats

• Synthesizes glucose, protein, cholesterol, triglycerides, and clotting factors

• True liver failure results in a change in homeostasis

• Impacts primary hemostasis, coagulation, and fibrinolysis

• Stores micronutrients

• Detoxifies

• Maintains intravascular volume through albumin

• Produces bile

• Inactivates and prepares hormones for excretion

• Removes old erythrocytes

• Converts fatty acids to ketones

Cirrhosis

• Can cause liver failure

• Portal hypertension

• Ascites

• Jaundice (erythrocytes don't get recycled properly)

• Varicosities

• Enlarged organs

• Hyperlipidemia or hypoglycemia can result

• Toxins and bile accumulation

• Clay-colored stools

• Dark urine

• Feminization and irregular menses

• Causes: hepatitis, chronic alcohol

• Diagnosis: based on history and physical.

  • Liver biopsy shows cirrhosis careful on FULMINANT liver failure due to high chance of bleeding.

  • Abdominal X-ray shows a large liver

  • Liver enzyme panel: at the beginning, transaminases will be elevated. True liver failure the transaminases will drop due to hepatocyte death.

  • Clotting studies evaluation will help with diagnosis.

  • Stool exam for occult blood

Cirrhosis Complications:

• Anorexia, nausea, vomiting

• Fetor hepaticus

• Hepatic encephalopathy from bilirubin and pneumonia accumulation (and other toxins)

• Heme, thrombocytopenia, anemia, and coag disorders

• Hepatorenal syndrome

  • High pressure in the liver -> impacts the kidneys (dysfunction in the RAS system in aldosterone) which leads to issues associated with higher pressures and pre-renal conditions

• Integumentary, jaundice, spider angiomas, palmar erythema (hormones)

• Cardiomyopathy

• Periphreal edema

• Portal hypertension, anorectal varices

• Hyperbilirubinemia and hyponatremia

• Treatment:

  • First, minimize the harm compounded by the issue

    • Avoiding drugs and or hepatotoxic meds

    • Watching for nutritional imbalances and metabolic dysfunction.

    • Bile acid binding agents for cirrhosis ascites or edema fluid restriction

    • Low-sodium, diets, diuretics, paracentesis, and shunts

    • Surgically implanted shunt if needed

    • Give Lactulose to promote ammonia excretion in the stool or rifaximin which will help supress

    • The intestinal flora with decreases ammonia production

Gallbladder Disorders

• The liver makes bile, and this then gets stored in the gallbladder until needed. If the gallbladder stores the liver bile in preparation to breakdown the digested material.

• Left hepatic duct -> Right hepatic duct -> cystic duct -> Common hepatic duct

• If gallbladder stone is present in areas such as hepatic, then there is a high chance of jaundice presence due to the blockage of bile being not bale to drain from the liver. If gallbladder stone is present in the common bile duct then abdominal pain is more imminent.

  • Symptoms common in any gallbladder are abdomen pain due to inflammation etc.

  • Risk Factors: Advanced age, obesity, diet, weightloss, pregnancy, PN use, or hormone replacement

  • Obstructions can cause Gallbladder rupture if unaddressed. Fistula/Gangrene can happen + hepatitis pancreatitis and carcinoma

Manifestations of Gallbladder issues:

• Biliary colic

• abdominal distension, nausea vomiting Jaundice if located at liver

• Then there is the chance of gangreen, fever or leukocytosis issues.

Important Notes

• Diagnosis: History Physical, ULTRASOUND

• Treatment: ULTRASOUND

  • LowFat, diet meds to dissolve calculi, Antibiotics if present lithrotripsy to break it down, choledeochostony if theres gangrenous involved.

Pancreatitis

• Inflammmation of the pancreas due to autodigestion either acute or chronic.

• ACUTE: SUDDEN! Severe upper abdomen pain as well radiation issues and also position can help relief pain with naausea Low grade fever comes with this pain

• CHRONIC: Weightloss wihtout trying and also abdominal pain as well. Steatorhea occurs. Constipiation and flatulance occurs!

Serum Amalayse and Lipase will become abnormal.

• Other serum calcium, CBCs and liver enzymes are also useful with diagnostic as with analyzing stool.

• What comes with this? you need to rest the pancreas to quiet it and lower the potential of having autodigestion.

• Pancreatic enzyme and Supplements can also improve this function along with antiacids and a healthy diet to maintain the pancreas strength.

Lower GI tract

• Small intesting and nutrient absorption is the key to survival of most organisms.

• Cecum is where the small intensity ends where a cecal value works to slowly transit from the small to the large intensity. Important after ressection to have this otherwise there will be dumping

• Appendicitis is where all the infected pockets reside.

• Colon is to absorb water and electrolytes to eliminate wastes

• The rectum also helps to store feces for defecation.

Obstructions:

• Mechanical or Functional from foreign objects in the body! TUMORS ADHESIONS HERNIA INUSS SESEPTION FECAL IMPAC
  FUNCTINAL OBSTRCUTON: Paralytic ileus etc which is a temproary obs due to an internal factor like opiates etc.

Types of Ostruciton

• Paralytic: Neruologic impairment, surgery, chemicals etc.
  Intubated paitemnts could have duodena altaresia, help to decompress as there is much fluid

• Crowns disease/UC: Patcgy inflammation that includes the intestinal wall ulcerations that leads to thivk cell walls. These are bad because they have potential impacts on digestion

• Abdominal pain, cramping etc right lower quadrant
  Increased intesitnml motility to diarrhea in a patient. Consittapation also occurs

• UC inflammatory process affecting the rectum and colon. Triggered through cell acculmation with is damaged and has erosion. Watery diarrhea blood mucuso

Perionitis

• INflammation of the preitoneum. If hit muliple times can cause constriction with slowd peristalsis and translocation with bacterias.

SUDDENL, ABDO PAING PAIN DECREASED PERSISITLA SI and symptoms such as infection tachycardia for what can lead to infection like: chemical irritation like stones/bile spill appendicitis SBP or spontaneous bacterial peritonitius

• A ppendicyis againa causes inflamamtion usually because some foor fromm the diestive tract makes it self there and doesnt leabe.

Patient Lab Evaluation

• Looking at the AST, ALT , LACTIC acid LFT and looking at infection signs of CLOT IN LIVER, NECORITC TISSUE! LIVER ISSUE OR METABOLITC DISORDER! ALL OF THESE ARE LOOKED AT THEN YOU SEND THEM ALL, LFTs ARE TAKING PRIOR TO HLH GENETIC MUTATION, YOU SEE EVERYTHING ALL OVER THE PLAN THEN YOURE SCREWED!