What are these 3 junctions?

2. Gastroduodenal junction 

3. Anorectal junction (AKA dentate line) 

-- Histological junctions may be sites of precancerous metaplasia, especially when the environment is very different on either side, as it is across the Z line.

-- Surface Mucous cells are found throughout the stomach.
-- Gastric pits (AKA Oxyntic glands) are home to Parietal cells, Chief (AKA Peptic) cells, Mucous Neck cells and Paracrine cells.
-- Pyloric glands are home to G cells, which have an endocrine function: producing gastrin.

Acute pain due to pathology in the upper GI tract is sometimes localised to the epigastric or retrosternal areas.
What are some non-GI causes that should be considered for a patient with acute pain in those areas?

The myenteric (Auerbach's) plexus lies between the outer longitudinal and inner circular muscle layers of the muscularis externa, and the submucosal (Meissner's) plexus lies between the muscularis externa and the submucosa.

What pattern of action potential do ICC cause?

There are 4 main types of motility patterns in the GI system.

Which type is impaired in gastroesophageal reflux disease?

1. Tonic contraction (sphincters)

2. Rhythmic segmentation (mixing)

3. Oscillatory (Pendular) movements (mixing)

4. Peristalsis (movement of lumen contents)

-- In GERD, tonic contraction of the LES is impaired, usually by prolonged or more frequent TLESRs (transient lower esophageal sphincter relaxations.) Other etiologies, such as low basal LES tone in scleroderma, are possible.

Esophageal manometry (AKA tonometry) measures the pressure applied by esophageal muscles.

For what esophageal motor disorder does manometry provide a definitive diagnosis?

In achalasia, inflammatory degeneration of the esophageal myenteric plexus causes an increase in LES pressure, aperistalsis, and incomplete reflex relaxation of the LES during swallowing.

2. The swallowing centre coordinates the muscles of swallowing via the "nucleus ambiguous" (which innervates esophageal striated muscle) and the "dorsal motor nucleus of the vagus nerve" (which innervates smooth muscle). Both of these muscle coordination centres are in the brainstem.

2a. The nucleus ambiguous sequentially activates the striated muscle in the upper esophagus.

2b.  The dorsal motor nucleus continues the swallowing contractions by activating a peristaltic pattern in the esophageal myenteric plexus

3. The wave of contractions (ie. swallowing) traverses the esophagus in 9-10 seconds.

2. One can occur even if the sensory pathways are damaged, the other is initiated by sensation.

When swallowing (AKA deglutition) is impaired, which is common inelderly Pts, swallowed substances can linger in a patient's esophagus.

What are possible negative consequences of this prolonged contact with the esophageal mucosa?

Name 5 physical exam signs that may indicate chronic alcohol abuse.

Most signs of alcoholism are actually signs of significant damage to the liver: Asterixis, palmar erythema, bilateral gynecomastia, parotid enlargment, tremulousness, Dupuytren's contractures, hepatomegaly or a nobbly hard liver, splenomegaly, ascites, caput medusa, jaundice, rhinophyma (bulbous ruddy nose), telangiectasias, peripheral neuropathy, finger clubbing.

What are some associated symptoms that can help determine the cause of N/V?

-- Abdominal pain points to a GI cause, although a MI is also a possibility. 

-- Pain relief by vomiting indicates a GI obstruction or GERD, while pain that is not relieved can indicate an MI, pancreatitis, hepatitis, gallbladder Dz, or infectious gastroenteritis. 

-- Associated Sx such as headache or dizzyness indicates a central nervous system disorder, such as increased intracranial pressure, migraine, or a vestibular problem. 

-- Painless N/V can be due to a wide variety of causes, such as drugs and toxins, pregnancy, gastroparesis, and various metabolic disorders (eg. acidosis, hyperkalemia, hypercalcemia, uremia) 

Polyhydramnios can occur in a fetus that is unable to swallow and then absorb amniotic fluid.

Name 3 congenital malformations of the upper GI tract that may present with polyhydramnios due to impaired GI absorption.

1. Atresia of the esophagus

2. Hypertrophic pyloric stenosis

3. Duodenal atresia

-- If you suspect these conditions in a neonate who isn't feeding properly, the details of how the neonate is vomiting may allow differentiation, eg. by the force of the vomiting ('projectile vomiting') or the presence of bile in the vomitus.

The pancreas forms from a ventral bud and a dorsal bud, which fuse together.

Which pancreatic duct corresponds with each pancreatic bud?

The ventral bud, which forms in conjunction with the bile duct, forms the main pancreatic duct. The dorsal bud, which makes up most of the pancreas, forms the accesory duct.

As organs form and rotate in the dorsal & ventral mesogastrium of an embryo, they partition the mesogastrium into a variety of ligaments and peritoneal structures.

Name the ligament derivatives of the ventral mesogastrium.

-- The falciform ligament connects the liver to the anterior wall.

-- Together, the hepatogastric ligament and hepatoduodenal ligament form the lesser omentum, connecting the liver to the stomach and first part of the duodenum.

-- The free border of the lesser omentum marks the epiploic foramen (AKA the foramen of Winslow,) which connects the lesser sac behind the stomach to the rest of the peritoneal cavity (AKA the greater sac.) 

2. Fundus: the dome-shaped upper portion, to the left of the cardia 

3. Body (Corpus): the largest region of the stomach

4. Antrum: the distal narrowing; has a thicker circular layer of muscularis

5. Pylorus: thick circular muscularis forms the pyloric sphincter at the gastroduodenal junction

2nd (descending) part: superior duodenal flexure to the inferior flexure; contains the major (and minor) duodenal ampulla, the transition to the midgut. 

3rd (horizontal or inferior) part: the longest section, crossing several structures such as the aorta, IVC, and vertebral column. 

4th (ascending) part: suspended by the musculofibrous ligament of Treitz, the duodenojejunal flexure marks the end of the duodenum. 

-- L. gastric a.: Supplies the lesser curvature and lower esophagus.

-- Common hepatic a.: Supplies the liver, gallbladder, pylorus, duodenum, and head of the pancreas via its branches, the hepatic a. proper and the gastroduodenal a.

-- Splenic a.: Supplies the spleen, greater curvature, and tail of the pancreas.

-- Para. N.S.: via the vagus nerve (cranial n. X.) A vagotomy (resection of the vagus n.) is an option in surgical treatment of intractable peptic ulcer Dz. 

What are Virchow's node and Sister Mary Joseph's nodule?

2. Pepsinogen 

3. Gastric lipase 

5. Mucus 

6. Bicarbonate (sets up a protective pH gradient in the mucus layer)

2. Transforms pepsinogen into active pepsin

3. Denatures proteins

4. Facilitates absorption of iron, calcium, and vitamin B12

NSAIDs inhibit the formation of prostaglandins by cyclooxygenase, causing gastric side effects.

Name at least 3 protective effects of PGs on the gastric mucosal barrier.

1. Inhibit acid secretion

2. Stimulate mucus and bicarb secretion

3. Enhance synthesis of surface-active phospholipids

4. Prevent surface epithelial cell exfoliation

5. Increase mucosal blood flow

There are 3 stimulatory phases that prepare the stomach for a meal by increasing gastric secretion: The cephalic, gastric, and intestinal phases. 

What are the different triggers that initiate these phases?

2. The gastric phase is triggered by: buffering of pH by food; digestion products directly stimulating gastric cells (eg. parietal cells, G cells); distension; local reflexes.

3. The intestinal phase is triggered by the presence of nutrients (eg amino acids) in the duodenum.

There are 3 inhibitory phases that prevent gastric secretion when it is innappropriate:  The cephalic, gastric, and intestinal phases. 

What hormones are involved in the gastric phase of inhibition of gastric secretion?

Gastric acid is a factor in several disorders, such as functional dyspepsia, gastritis, Zollinger-Ellison syndrome, and others. What are some pharmaceutical strategies to deal with gastric acid?

1. Buffer with an antacid. 

2. Inhibit stimulation of parietal cells, eg. w/ H2 receptor antagonists (antihistamines such as ranitidine (AKA Zantac)) 

3. Directly inhibit H+ secretion w/ PPIs (Proton Pump Inhibitors) such as omeprazole (AKA Losec) 

4. Stimulate mucus production w/ a PG analog, such as misoprostal (AKA Cytotec) 

5. Coat the mucosa with a protective barrier, such as sucralfate or bismuth subsalicylate 

6. Increase the tone of the LES and speed gastric emptying w/ a prokinetic, such as metoclopramide 

H2 antagonists achieve a 70% reduction in daily acid secretion, while PPIs reduce acid 80-95%. FYI: PPIs act irreversibly on proton pumps, but they can only affect active pumps; therefore, timing the dose at 30-60 minutes before a meal maximises effectiveness. Because H2 antagonists are cheaper than PPIs, BC Pharmacare usually requires a trial with an H2 antagonist before approving PPIs.

As the parasympathetic nervous system (via the vagus n.) is important in stimulating acid secretion, anticholinergics have in the past been used in PUD Tx; however, the side effects of anticholinergics are very unfavorable. Anticholinergic effects may be encountered in several areas of medicine, such as an overdose of tricyclic antidepressants. What mnemonic can help you remember anticholinergic effect symptoms?

-- Hot as a hare (hyperthermia)

-- Dry as a bone (dry skin)

-- Red as a beet (vasodilation)

-- Mad as a hatter (agitation/hallucinations)

-- The bowel and bladder lose their tone and the heart goes on alone (ileus, urinary retention, tachycardia)

How can antacids such as calcium carbonate interfere with the absorption of other drugs?

What proportion of cases are resistant to the standard therapy for H. pylori eradication?

Standard care usually starts with triple therapy: PPI + clarithromycin + amoxicillin or metronidazole. Quadruple therapy is 2nd-line: PPI + bismuth + tetracycline + metronidazole (Quadruple therapy may be used to initiate Tx, eg. if pt has recently been exposed to 1st-line antibiotics.)

Dimenhydrinate (Gravol), scopolamine, and ondansetron are all commonly used in treatment of N/V. 

How do their indications differ?

-- Scopolamine (anticholinergic): Tx of motion sickness, chemo-induced N/V, and preoperatively (also for its amnestic and sedative effects).

-- Ondansetron (5-HT3 (serotonin) antagonist): Prevention and Tx of chemo- and radiation-induced N/V, prevention and Tx of post-op N/V.

-- Many other medications are also used in Tx of N/V, such as cannabinoids.

-- Fever.

-- Dysphagia.

-- N/V.

-- Abdominal pain or distension.

-- Jaundice.

-- Significant bleeding (upper or lower GI).

GERD is often diagnosed clinically, based on symptom Hx and relief follwing a trial of pharmacotherapy. 

What are the clinical features of GERD?

Heartburn and acid regurgitation are the typical Sx, and together are 80% sensitive and specific for GERD. Other esophageal Sx are bitter regurgitation, frequent belching, or senstion of a lump in the throat. Non-esophageal Sx may occur, such as a chronic cough, sore throat, voice changes or dental erosions, but these have low sensitivity and specificity. 

24h ambulatory pH monitoring is the most accurate test for GERD, as it allows correlation of pH with Sx, but is rarely required.

Dysphagia may occur due to structural blockages, neuromuscular disorders, or nervous system lesions. 

What are 2 key questions you can ask to differentiate the cause of dysphagia?

1. "Do you have trouble starting swallowing, such as choking or nasal regurgitation?" Indicates a problem in the oropharyngeal phase of swallowing, commonly of neurological origin. A sensation of food sticking in the throat is indicative of a problem in the esophageal phase. 

2. "Do you have trouble with solids, liquids, or both?" Solid food sticking in the esophagus indicates mechanical obstruction, such as a carcinoma or stricture, while both sticking indicates a neuromuscular disorder such as achalasia. 

-- Other important questions include progression Vs. intermittency; assoc. Sx such as regurgitation, heartburn, change in voice, odynophagia, weight loss, etc; past Hx of GERD, strokes, neuromuscular disorders; use of antacids and other remedies.

Most of the esophagus is surrounded by adventitia rather than serosa. 

What implications does this have in esophageal carcinoma?

Cancers are able to invade to adjacent structures more easily via an adventitia rather than through a layer of serosa. This is one factor in why esophageal carcinoma typically has a poor prognosis; another is that the cancer is often asymptomatic until late in the course of disease.

What are some possible presentations in a patient with esophageal carcinoma?

-- Sx of GERD, esp. w adenocarcinoma.

-- hematemesis or hemoptemesis may be massive as a result of tumor invasion of vasculature; FOB may be positive for smaller bleeds.

H. pylori infection is becoming less common due to antibiotic Tx and sanitation improvement. H. pylori associated Dz, such as PUD, is expected to become less common as well.

-- gastric and duodenal ulcers.

-- gastric adenocarcinoma.

-- MALT  B-cell lymphomas.

-- biopsy histology (endoscopic).

-- biopsy urease test (endoscopic, can be rapid).

-- urea breath testing (noninvasive, also useful to confirm eradication).

-- serology (ELISA to detect IgG).

-- stool antigen assay (also useful to confirm eradication).

-- NB: Many false negatives may occur if PPI Tx, or other heartburn medications have been used. Testing protocols may require abstaining from heartburn medication for up to 2 weeks.

In the West, adenocarcinoma of the distal 3rd of the esophagus is the most common esophageal cancer, and Barrett's esophagus is the most important risk factor. 

How can a patient be monitored for the development of esophageal Ca?

-- r/o  conditions that mimic reflux (eg. cancer, PUD, infective esophagitis).

-- distinguish btwn esophagitis, and non-esophagitis reflux.

-- Dx presence of Barrett's.

What are the 4 most common causes of upper GI bleeding?

1. Peptic Ulcer Dz (55%).

2. Esophogastric varices (14%). 

3. Arteriovenous malformations (6%).

4. Mallory-Weiss tears (5%).

5. Tumours (4%).

6. Erosions (4%).

7. Other causes (12%). 

An upper GI bleed can present with a variety of Sx. 

Order the following in decreasing amount of blood lost: coffee ground emesis, fecal occult blood, hematemesis, melena, hematochezia.

1. Hematochezia (red, maroon, or clotted blood in the stool) is usually indicative of a lower GI bleed (eg hemmorhoids), but can occur in a massive upper GI hemmorhage. 

2. Hematemesis is the vomiting of blood. 

3. Coffee ground emesis is a hematemesis of a smaller bleed, (or of swallowed blood,) where the blood is partially digested. 

4. Melena is dark tarry stools containing blood. 

5. Fecal occult blood is only detectable with laboratory tests of the feces. 

-- Other presentations of an upper GI bleed can include iron deficiency anemia, and uremia (due to protein overload from digesting blood).

You are on your Emerge rotation, treating a patient w/ CC of vomiting several cups of blood. 

What are some key components in your initial management of this patient?

1. Assess and maintain stability: ABC, signs of shock (HR, RR, BP +/- orthostatic changes, capillary refill, urine output;) IV fluids, transfusions, admit to ICU or consult surgery if unable to stabilise.

2. Hx & Px to point towards etiology.

3. Labs: CBC, blood type and cross-match, platelets, PT, PTT, electrolytes, BUN, Cr, LFT.

4. Keep NPO.

5. GI consult: Endoscopy for diagnosis, rebleed risk assessment, and possible intervention (eg. thermal coagulation).

6. IV PPI, especially if ulcer is suspected; IV octreotide if esophageal varices suspected (causes splanchnic vasoconstriction).

If endoscopy confirms that a peptic ulcer is failing to heal with medical management, what are some possible next steps in investigation and treatment?

-- Biosy the ulcer to assess for malignancy. Even if biopsies are negative, a gastric ulcer may be due to a primary gastric lymphoma or adenocarcinoma; continued failure to heal after 12 weeks of medical Tx is an indication for surgery. 

-- Refractory duodenal ulcers have a much lower risk of malignancy, but require exclusion of acid hypersecretion. 

-- Continued complications of PUD such as bleeding or perforation are an indication for surgery. 

-- Persistent or occult H. pylori infection may occur; assess factors such as patient compliance, antibiotic resistance, and the possibility of false-negative H. pylori tests. 

What are some therapies that can be used to decrease the risk of side effects from NSAIDs, and what are indications for their use?

-- If possible, lower NSAID dose or replace with an alternative such as acetaminophen. 

-- Combine with a cytoprotective agent, such as misoprostol or a PPI. 

-- Enteric coatings and IV dosing can avoid the direct erosive effects of NSAIDs on the gastric mucosa, but do not decrease incidence of ulceration. 

-- Indications for a cytoprotective adjunct are: Previous ulcers or upper GI bleed; high doses of NSAIDs; concurrent corticosteroid use; advanced age; presence of cardiovascular disease (which can decrease gastric blood supply.)

Exocrine: The pancreas supplies bicarbonate to neutralise chyme, and is the most important source of digestive enzymes (mostly synthesised and stored as inactive precursors.) Key enzymes include pancreatic amylase, pancreatic lipase, trypsin, chymotrypsin, and carboxypeptidase. 

-- Pancreatitis.

-- Ischemic bowel.

-- Light, white, or clay-coloured: A lack of bile and bilirubin in the stool may indicate bile duct obstruction as a cause of jaundice.

-- Black: Upper GI bleed.

-- Red: Lower GI bleed.

-- Dietary sources can also colour the stools: Green leafy vegetables, iron supplements, black licorice, beets, artificial food colouring.

-- 2:1 M:F ratio.

-- Symptomatic in 2% of cases.

-- Found within 2 feet of the ileocecal valve.

-- 2 inches in diameter & length.

-- 2 types of ectopic tissue (gastric, pancreatic).

-- Lipolytic: lipase, procolipase, cholesterolesterase, prophospholipase A₂.

-- Proteases: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases A & B.

-- Nucleases: ribonuclease, deoxyribonuclease.

CCK is released by the duodenum in response to amino acids and free fatty acids. In the pancreas, it stimulates enzyme secretion by acinar cells.

2. Facilitated diffusion: Eg. fructose diffuses down its chemical gradient through the GLUT5 transporter.

3. Active transport: Most sugars, amino acids, peptides, and bile salts are actively transported. Na⁺ is often the driving force (secondary active transport.) 

4. Pinocytosis: This is an important route for proteins and lipids. 

2. Micellar solubilisation: Bile salts breakup the emulsion into small micelles, which are water-soluble.

3. Hydrolysis: Lipases cleaves some triacyl glycerides into free fatty acids and mono- & diacyl glycerides. Other lypolytic enzymes hydrolyse phospholipids and cholesterol esters. 

4. Absorption: Digestion products dissociate from micelles and cross the enterocyte membrane. Most lipid absorption occurs in the jejunum and ilium. 

5. Re-synthesis of triglycerides and phospholipids: The endoplasmic reticulum reforms the lipids and packages them with apolipoproteins to form chylomicrons.

6. Chylomicrons are exocytosed into the central lacteal of the villus, enter the lymphatic circulation, eventually distributing lipids to tissues and liver.

Hindgut:  Left 1/2 to 1/3 of transverse colon; descending and sigmoid colon; rectum; superior portion of anal canal. 

-- An omphalocele (1/5000) is a persitent protrusion of the intestine and peritoneum into the umbilical cord, covered by amnion, due to failure of reduction of the physiological umbilical hernia. 

-- An umbilical hernia (2-14%) ia a reprotrusion of intestines, covered by skin, through a defect in the peritoneum and fascia of the abdominal wall. Often spontaneously repairs by age 5.

What are some risk factors for gastric cancers?

-- Pernicious anemia.

-- Chronic atrophic gastritis.

-- Smoking.

-- EtOH.

-- Smoked foods, foods preserved with nitrites and nitrates.

-- Previous partial gastrectomy.

2. Gliadin (from gluten) derived peptides are presented by HLA class II molecules to helper T cells.

3. Activated T_h cells lead to invasion of mucosa by cytotoxic T cells and other lymphocytes.

4. Enterocytes are damaged.

-- Because the sensitisation involves exposure to an external agent, the virus, Celiac Dz can present any time from infancy to elderly. Peak presentation is in infancy, when cereals are introduced.

-- In adults: Diarrhea, steatorrhea, weight loss, bloating & gas.

-- As the Dz is usually more severe in proximal bowel, deficiencies of Fe, Ca and folic acid are more likely than B₁₂. Presentation may include conditions such as anemia, osteoporosis, neuropathies.

2. Impaired fat solubilisation due to bile salt deficiency. Presents w steatorrhea, deficiencies of fat-soluble vitamins.

3. Defective nutrient hydrolysis due to pancreatic insufficiency (eg. CF), inadequate mixing (eg. post resection), rapid transit (eg. hyperthyroid.)

Depending on the Pt presentation, serum carotene & INR/PTT may also be useful bloodwork.

-- Carbs: Hydrogen breath test (lactose digested by bacteria yields H₂); D-xylose absorptive area test.

-- B₁₂: Schilling test - Part 1: radiolabeled Vit B₁₂ PO, low urine levels confirms malabsorption; Part 2: labeled B₁₂ bound to intrinsic factor, normalised urine levels confirms intrinsic factor deficiency (pernicious anemia.)

-- Because of deficiencies in sensitivity or specificity, or difficulty of the test, the above tests are rarely done, but are part of the curriculum. Clinically, transglutaminase serology, imaging, and Tx trial w pancreatic enzymes are useful since Celiac Dz and pancreatic insuficiency are common causes of steatorrhea.

-- Pain migrating to RLQ suggests appendicitis.

-- Abdominal distention, feculent or bilious vomitus suggest obstruction.

-- Severe epigastric pain could be pancreatitis.

-- Decreased LOC and severe dehydration.

-- IBD: Iritis, skin rash,  arthritis, leg ulcers

-- Chronic blood loss from GI Dz may produce signs of anemia, such as pallor.

-- Parietal pain is typically persistent and severe, a result of inflammation, and more accurately localised due to the rich innervation of the parietal peritoneum. Parietal pain is exacerbated by movements, such as coughs, so the Pt lies still.

-- The classic presentation of appendicitis, migrating from the umbilical area to the RLQ, possibly developing psoas and other signs, shows the progression from visceral pain to parietal.

-- Fever.

-- Visible blood in stool.

-- Frequent, substantial volume diarrhea.

-- Signs of dehydration.

-- Change in mental status.

2. Depressed fontanelle.

3. Altered skin turgour.

4. Sunken eyes.

5. Tachycardia.

6. Decreased BP.

7. Decreased capillary refill.

8. Cool extremities.

9. Lethargy.

-- Birth: Gestational age, birth wgt, mode of delivery, complications (eg asphyxiation), 1st meconium, prolonged stay.

-- Immunisations: Up to date? Why not?

-- Nutrition: Breast Vs formula, recent changes, incorporating solids, food "allergies."

-- Development: Wgt & Hgt, milestones (fine motor, gross motor, language, social), adaptive abilities (feeding, toileting, dressing.)

-- Gallstones - 45%.

-- Ethanol - 35%.

-- Tumours.

-- Scorpions.

-- Microbio (bacterial, viral, parasites).

-- Autoimmune.

-- Surgery/trauma (eg ERCP, blunt abd trauma).

-- Hyperlipidemia, Hypercalcemia.

-- Emboli or ischemia.

-- Drugs/toxins (eg azathioprine, estrogen).

O: May be assoc w EtOH abuse, biliary colic, drugs, trauma, ERCP, viral infxn, or Fam HX.

P: 3 phases: local inflam + necrosis; systemic inflam, esp lungs; local complications 2 wks after (abscess, sepsis).

Q: Often severe.

R: May radiate to back.

S: Possibly N/V, restlesness, jaundice, fever/tachy, guarding, ileus.

T: Steady.

-- CT w contrast is most useful for Dx and prognosis, showing only viable tissue; also for calcifications and other signs.

-- ERCP, MRCP, and MRI may be useful in uncertain etiologies. 

-- AXR is quick and easy, may show calcifications or dilated proximal jejunum.

2: Analgesia.

3: Oxygen (eg in ICU).

4: Stop progression (rest pancreas by NG suction, NJ feeding, TPN, etc.)

5: Treat local and systemic complications (eg Tx of infxn w imipenem, cephalosporins.)

-- Steatorrhea.

-- Diabetes.

-- Jaundice.

-- Weight loss.

-- Ascites.

-- GI bleed.

-- Gynecologic: ectopic pregnancy

-- GI: perforated viscus, hepatic/splenic injury, ischemic bowel

-- Relief w defecation.

-- Change in freq of stool.

-- Change in consistency of stool.

What syndrome is diagnosed by these criteria?

2. Poor resistance to infections.

3. Decreased wound healing.

4. Increased length of stay.

5. Poor clinical outcomes: increased morbidity and mortality.

-- Fat: 20%-35% (<10% saturated fat)

-- Protein: 10%-35% (11 essential AA)

-- Adjustments may be needed, such as low carb/high fat for intubated Pts to minimise CO₂ production

-- 2 mL/kg/h second 10kg

-- 1 mL/kg/h remaining wgt >20kg

-- This rule applies to crystalloid solutions only; 

-- Increased requirements in: fever, sweating, GI losses, adrenal insufficiency, hyperventilation, polyuric renal Dz

-- Decreased reqs in CHF, SIADH, anuria/oliguria, humid atmospheres

-- Much more lipolysis and ketogenesis.

-- Small increase in protein catabolism (protein sparing.)

-- Supplement phosphate, minimise Na, total fluid < 1L/d.

-- Monitor lytes and cardiac status closely.

2. Diet non-adherence.

3. Concurrent Dz, eg. pancreatic insufficiency.

4. Development of intestinal lymphoma (enteropathy associated T-cells).

5. Diffuse intestinal ulceration (precursor to lymphoma).

-- Ischemic bowel.

-- NSAIDs.

-- Infectious: "Your Stools Smell Extremely Crappy" --> Yersinia enterocolitica, Shigella, Salmonella, E. coli (EHEC O157:H7), E. histolytica, Campylobacter, C. difficile.

2. Na⁺-H⁺ exchanger; bicarbonate-rich chyme in the duodenum and jejunum stimulates Na absorption.

3. Neutral, coupled NaCl absoroption is impaired in some diarrheas. In the ileum and proximal colon Na-H exchange is paired with an apical Cl-HCO₃ exchanger. 

4. Epithelial Na⁺ channels (ENaCs) are imprtant in the distal colon & rectum, as they can transport against large concentration gradients, driving H₂O absorption. Aldosterone enhances this transport, while amiloride inhibits.

-- Passive transport of Na thru tight junctions is also an important process, both for absorption and secretion.

2. Presence of osmotically-active agents. Eg overuse of MgOH or too much sorbitol intake can cause an osmotic diarrhea.

3. Decreased mucosal contact time. This can be due to rapid motility, as in IBS, or due to lost mucosa, as in resection.

Diarrheas don't necessarily fit into a single category, such as for lactase deficiency. But thinking about the pathological processes behind a diarrhea can help guide Pt education and Tx with drugs or diet changes. 

2. Increased secretory activity of normal gastrointestinal cells.

2.a. Toxins, such as from Vibrio cholerae, can directly act on secretory pathways.

2.b. Neuroendocrine tumours release secretion-stimulating hormones into the bloodstream, eg VIPoma, Gastrinoma, or carcinoid syndrome.

3. Inflammation associated secretions: Inflammatory cytokines can induce secretion directly, and also cause mucosal destruction and increased permeability allowing transudation of fluid. Enterocyte destruction or inactivation is significant in inflammatory processes, so decreased absorption is also a factor in inflammatory diarrheas.

-- Identification: Date, name, Pt#, age, type of study.

-- Technical factors: Good coverage, appropriate penetration, Pt is oriented properly for the type of view.

-- Free fluid in the peritoneum.

-- Foreign bodies, eg G-tubes, swallowed magnets.

-- Air: Common but possibly pathological when in the GI lumen, usually pathological elsewhere.

-- Bowel wall thickening may be seen in inflammation (colitis), hypoproteinemia, submucosal hemmorrhage, but is common and nonspecific.

-- Densities: Check the bones, look for calcifications, r/o AAA.

-- Organs: Kx2, L, GB, St, Sp, P, UB, & psoas shadow. Organs are much better visualised w CT.

1. Tenderness in the R illiac fossa (2 points).

2. Migratory R illiac fossa pain (1 point).

3. Rebound tenderness in the R illiac fossa (1 point).

4. N/V (1 point).

5. Fever >37.5 (1 point).

6. Anorexia (1 point).

7. Leukocytosis (2 points).

-- Scores of 7-9 indicate a high clinical suspicion of appendicitis, and can merit immediate appendectomy for males, diagnostic laparoscopy for females (gynecological DDx decreases chance of appendicitis.) 

2. Ileus: Non- or hypomotile bowel becomes flaccid and stretched, acting as a nonmechanical obstruction.

3. Malabsorption: Decreased absorption in the small intestine causes increased fluid load and dilation of the colon.

4. Infarct/ischemia: Dead, dying bowel is weaker and nonmotile.

2. Consumption of unsafe food or water.

3. Swimming in unsafe water.

4. Children attending daycare.

5. Sexual practices that can cause exposure.

6. Prolonged diarrhea >2/52.

2. Mild diarrhea.

3. Severe diarrhea.

4. Pseudomembranous colitis.

5. Perforation.

6. Toxic megacolon.

1. Maintenance of fluid and electrolytes, usually orally.

2. Labs: Stool C&S (Culture & Sensitivity), C diff. Viral antigen (eg norovirus) testing may be indicated if an outbreak is suspected.

4. Consider empiric abx; Pt is stable w marginally severe diarrhea, but other factors such as Pt anxiety, planned travel or other life situations may factor. 

5. Treat (or further investigate) according to C&S results, f/u.

(Note: Some labs include Yersina, Vibrio, Aeromonas &/or Pleisomonas in their standard S&C.)

-- Shigella: TMP-SMZ, a floroquinolone (eg Cipro), ceftriaxone, nalidixic acid, azithromycin.

-- Salmonella spp (non-typhi): Tx not recommended unless immunocompromised or meets other condition (eg valvular heart Dz); TMP-SMZ, a floroquinolone, or ceftriaxone.

-- ETEC, EPEC, & EIEC: TMP-SMZ, a floroquinolone, or ceftriaxone.

-- EHEC: Role of abx is unclear; may increase risk of HUS (hemolytic uremic syndrome) especially in younger Pts. Stop empiric abx, and offer supportive Tx and monitoring.

-- Diarrheal: Cryptosporidium parvum, Mycobacterium avium complex. Salmonella infections are more likely to progress to bacteremia in immunocompromised Pts, and C diff is more common.

-- Yellow or cream-coloured exudates, firmly adherent to mucosal surfaces

-- Exudate starts in superficial intercryptal mucosa, enlarges to form dilated crypt mouths.

-- Lesions may be scattered, or confluent over the entire mucosa.

Sigmoidoscopy (or colonoscopy) may be useful to Dx C diff cases in some situations:

-- High clinical suspicion w neg labs.

-- Prompt Dx needed.

-- Failure to respond to abx.

-- Atypical presentation, w ileus or minimal diarrhea.

-- Crohn's Dz.

-- Indeterminate colitis (full workup shows features of both UC & Crohn's.)

-- Continuous Dz, no skip areas.

-- Mucosal-based Dz, no transmural spread (except in fulminant colitis).

-- Muscular strictures.

-- Remissions and relapses.

-- Advanced Dz may spread as far as 3 cm into the terminal ileum.

The risk of CRC in Crohn's is likely similar, but there is not a clear consensus. [UpToDate]

-- Patchy, discontinuous inflammation.

-- Can involve any part of the GI tract: "From gum to bum."

-- Transmural inflammation (through the entire thickness of the intestinal wall.)

-- Fibrous strictures and/or fistulae may occur.

-- Lubricant laxatives (mineral oil): Avoid, especially for chronic use, as it decreases absorption of fat soluble vitamins; can be used as enema.

-- Osmotics (eg lactulose, polyethylene glycol): PEG is well tolerated.

-- Stool softener (eg docusate): Prevents the need to strain against hard stools.

-- Stimulant (eg senna): Affects electrolyte transport across the mucosa, and enhances motility. 

-- Other types: Peripheral opioid antagonists, serotonin agonists

-- Diet: Lots of fluid and fibre, eg prunes, if possible; some foods (eg cheese, steak) agravate constipation.

-- Attempts at pooping 30-60m after a meal to take advantage of the gastrocolic reflex.

-- Do not delay the urge to have a BM.

-- Be in a proper sitting position (eg avoid bedpans).

-- Avoid excessive straining.

-- Taper laxatives if discontinuing.

-- Diverticulitis is the inflammation of a diverticulum; it presents w some similarities to appendicitis, except in the LLQ. CT scan is most sensitive to Dx.

-- Significant FamHx risk, asymptomatic Pts: Colonoscopy every 5 years starting age 40, or 10 yrs younger than age of youngest affected relative. Use FOB or other modalities only if Pt declines colonoscopy or colonoscopy is unable to be completed. Hereditary syndromes such as FAP and HNPCC have special requirements.

-- IBD of significant duration: Colonoscopy every 1-2y w multiple biospies to detect dysplasia.

-- For more info see http://www.bcguidelines.ca

-- Hepatobiliary: 10-35% cholelithiasis; 1-5% primary sclerosing cholangitis

-- Derm: upto 15% erythema nodosum, assoc w arthritis; 1-12% Pyoderma gangrenosum, may present before IBD.

-- Urologic: upto 20% (higher after ileal resection) calculi: unabosrbed bile salts bind lumenal Ca²⁺ which would have otherwise bound to oxalate. Unbound oxalate is absorbed to a greater degree, leading to the formation of calcium oxalate ureteral stones.

-- Ocular (1-10%): Conjunctivitis, uveitis/irits, episcleritis 

2. Achieve mucosal healing.

3. Ameliorate complications.

4. Maintain remission.

5. Prevent colon Ca.

-- Long-term: Cushing's syndrome (abnormal fat deposition, fatigability, hirsutism, ...), cataracts, glaucoma, osteoporosis, HTN, growth supression, immunosupression, and more

2. Bruits may be heard over arteries (renal, illiac, aorta). Renal artery stenosis, heard as a bruit, may explain HTN.

3. Rarely, you may hear a soft IVC venous hum, or hepatic or splenic friction rubs.

4. "Nonauscultory stethoscope palpation" may be helpful in fussy children.

-- General: Is patient in distress, lying comfortably, can they push out or suck in their abdomen, or cough, w/o pain.

-- Umbilicus: contour, inflammation, bulges.

-- Contour: shape, symmetry, local bulges, bulging flanks.

-- Peristalsis: Can be visible in intestinal obstruction, or normally in the thin.

-- Pulsations: Normal aortic pulsation is frequently visible.

-- Flatus (gas) - causes a tympanic percussion note

-- Fluid (ascites)

-- Fetus

-- Frickin' big mass (tumour)

-- Tympany usually predominates in the GI tract, with scattered areas of dullness from fluid and feces. Dullness in both flanks indicates further testing for ascites. 

-- Percussion is used in special tests, eg. detecting an enlarged spleen, shifting dullness of ascites, and CVA (costovertebral angle) tenderness of pyelonephritis.

-- Castell's sign: Percuss the lowest intercostal space in the left anterior axillary line; this is normally tympanic. With an enlarged spleen, the spleen will descend into this area during deep inspiration as it is pushed by the diaphragm; listen for a change from tympany after asking the pt to take a deep breath.

-- Palpation: Similar to palpating for an enlarged liver, lift the posterior costal margin with your left hand while deeply palpating with your right, while the patient takes deep breaths.

2. Deep palpation to delineate abdominal (or pelvic) masses.

3. Feel for the lower edge and texture of the liver, and feel for the gallbaldder, urinary blader, fetus, or spleen if indicated.

4. Bimanual palpation or ballottment of the kidneys.

5. Assessing for an aortic aneurism.

-- GU: ureteral calculi, pyelonephritis, gynecological

-- MSK: Abdominal wall hematoma, psoas abscess

2. 2+ generations involved. 

3. 1+ CRC before age 50

4. FAP (Familial Adenomatous Polyposis) is excluded

2. Palpate the walls of the anus, note sphincter tone. Pain during the exam is present if there is a thrombosed hemmorhoid, abscess or fistula-in-ano.  

3. Use bidigital palpation with the thumb on the perineal skin if palpating for an abscess. 

4. Advance the finger past the anorectal junction. Palpate the anterior wall: Prostate, seminal vesicles, and retrovesical pouch in men; the cervix (+/- retroflexed uterus) and retrouterine pouch in women.

5. Palpate the lateral and posterior walls, the sacrum and the coccyx.

-- increase fibre intake.

-- apply topical anesthetics & glucocorticoids.

-- sitz baths.

-- stool softeners for constipated Pts. 

-- Chronic fissures (>6 wks) may need Tx to decrease anal canal resting tone: eg. nitroglycerin ointment, Botox. Surgical Tx has a risk of causing incontinence.

2. Metabolic conversion of carbohydrates, amino acids, and lipids into fuel substrates that may be released into circulation for uptake in brain and other tissues.

3. Synthesis of most plasma proteins

4. Synthesis of porphyrins

5. Detoxification and excretion of metabolic wastes

6. Metabolism and elimination of drugs, hormones and toxins

7. Production of bile

8. Hematopoesis (in embryo, fetus, or erythropoietic disorders)

-- Portal tracts and thin interlobular septae separate the classic hepatic lobules.

-- Hepatic stellate cells: Involved in fibrosis by laying down extra-cellular matrix.

-- Portal lobule: Triangle, w central veins at corners and bile ductule (in triad) at centre; represents drainage of bile. 

-- Portal acinus: Diamond, w triads at equator and central veins at pole; separated into an equatorial region (Periportal: good oxygen supply but more exposed to toxins/viruses from portal veins and bile-backup from blockage) and into a polar region (Perivenular: poorer oxygen supply, thus first to be damaged by reduced perfusion, excess lipids or alcohol.)

-- Transection or damage to the common ducts is a potentially life-threatening complication of cholecystectomy.  

Other tests may be indicated by Hx, Px, or the initial lab results, such as CXR, ECG, B₁₂, ANA, HepC, HepB, TB, Lyme Dz serology.

-- Acute viral hepatitis (A, B, rarely C)

-- Acute drug toxicity (eg acetaminophen overdose, or therapeutic doses taken during heavy EtOH consumption.)

-- Ischemic liver injury, eg post prolonged hypotension.

Alcoholic hepatitis alone typically does not much exceed 250 IU/L. Even higher levels of AST or ALT > 5000 IU/L also goes against viral hepatitis as a cause.

II. Asterixis, lethargy, drowsiness, disorientation.

III. Rousable stupor, hyperactive reflexes, extensor plantar responses.

IV. Coma (response to painful stimuli only.)

-- Compensated, continue EtOH consumpion: 5 year survival 70%.

-- Decompensated, continue EtOH consumpion: 5 year survival 30%.

-- Educating a patient about the risks of continued EtOH abuse may cause move them from the pre-contemplative to the contemplative or preparative states in the process of changing behaviour.

2. Diabetes.

-- Transferrin saturation has >90% sensitivity; <45% saturation is N, the criteria used to indicate hemochromatosis varies  between sources, from >50% to >60%, with >80% being diagnostic.

-- Serum iron: Measured as part of determining transferrin sat, the more useful measure for iron overload.

Liver biopsy and genetic testing may be part of a further workup when the screening labs are positive.

PSC antibody labs ANCA and ANA are less sensitive and specific, so ERCP and MRCP are used to confirm the Dx.

-- HBV (Acute or chronic): presence of virus: HBsAg; active replication: HBeAg, HBV-DNA; recent infection: anti-HBc IgM; previous exposure: anti-HBc; protective immunity: anit-HBs.

-- HCV (mostly Chronic): anti-HCV ELISA, PCR for HCV-RNA; assess Dz activity w LFT; assess liver fibrosis w Fibroscan (special US available in some centres.)

-- HEV (Acute): anti-HEV IgM, HEV PCR.

-- Neonates: almost 100% (but <10% with anti-HBV immunoglobulin prophylaxis.)

-- Children and immunosuppressed: intermediate risk. 

2. Cholestasis (eg amoxicillin/clavulanate).

3. Steatohepatitis and fibrosis (eg methotrexate).

4. Idiosyncratic/allergic injury; may be acute or chronic (eg nitrofurantoin, sulfa).

5. Granulomatous hepatitis (eg allopurinol).

-- Oral activated charcoal.

-- N-acetylcysteine IV (or PO): >95% effective if given w/in 10h, but should be given to all Pts regardless of time. This drug promotes hepatic glutathione synthesis, allowing excess acetaminophen to be metabolised to a benign glutathione adduct. The glutathione scavenger system is involved in inactivating many toxic metabolites.

-- Monitor in ICU of a hospital w a liver transplant program.

-- Ablation (EtOH, radiofrequency).

-- Chemoembolisation.

-- Liver transplant.

-- Tx options differ for metastasis; systemic chemotherapy may be an option if the met is susceptible.

-- Wilson's Dz

-- alpha₁-antitrypsin deficiency

-- Primary biliary cirrhosis

-- Idiopathic

-- To maintain the pressure gradient across gastrointestinal capillaries, arteries dilate; pressure increases cause increased transudation of protein-poor lymph from intestinal capillaries (which have tight junctions that don't permit proteins.)

-- When peritoneal lymphatic capacity is exceeded, fluid is sequestered in the abdomen as ascites; the renin-angiotensin-aldosterone system activates in response to the drop in effective circulating volume, retaining salt and water. The body develops a total salt/water overload.

-- Hypoalbuminemia, though not necessary for development of ascities, can contribute by decreasing intravascular osmotic pressure, changing the balance of Starling forces in favour of increased lymph production.

2. Renal failure.

3. Liver failure.

4. Carcinomatosis.

5. Chronic peritonitis.

-- Prehepatic: Hemolysis, neonatal jaundice

-- Hepatic: Hepatocellular diseases: Viral, Autoimmune, Drugs, Alcohol, Hemochromatosis, Wilson's Dz, etc.

-- Posthepatic: Biliary obstruction: Gallstones, Parasites, Malignancy

1. Potential Exposures:

-- Intermediate risk: Hemodialysis; Infant born to HCV Mom; Needle sticks.

-- Other risks include intranasal/inhaled drug use; higher-risk sex; tattooing, piercing, rituals.

2. Clinical clues possible for HCV:

LFTs; S/Sx of chronic liver Dz; substance dependancy; HBV or HIV infxn; Dz requiring multiple blood transfusions; unexplained renal impairment; Non-Hodgkin's Lymphoma; vasculitis (due to assoc. cryoglobulinemia). 

2. If anti-HCV positive, check HCV-RNA.

3. If HCV-RNA negative, consider other liver Dz if ALT is elevated; retest HCV-RNA and LFT in 6 months.

4. If HCV-RNA is positive, Pt has chronic HCV infection.

If you have diagnosed a patient to have chronic hepatitis, what are the next steps? (Asides from referral!)

1. Complete Px exam. 

2. Evaluate for other liver Dz (risk of rapid decline). 

3. Evaluate other viruses affecting liver health or potential Tx (eg. HIV). 

4. Assure immunity to HAV & HBV (check status, offer vaccines, confirm titres). 

5. Pt education.

6. Further evaluation of chronic infxn (risk factors, duration, liver labs, HCV load and genotype). 

7. If cirrhotic: HCC surveillance; annual influenza vaccine; pneumococcal vaccine. 

-- Pregnant women with chronic HCV have no change to routine care, unless the have cirrhosis.

-- Pregnant women with cirrhosis require referral to an expert in high-risk obstetrical care.

-- HCV positive moms can breastfeed as long as the nipples are not cracked or bleeding.

-- Children & adolescents do not require urgent care. Children rarely develop end-stage liver Dz.

-- Central obesity

-- Smoking

-- EtOH > 3 drinks/day

-- Co-infxn w HBV or HIV

-- Male-- Older age when infected (>40)

-- 20% of acute HCV infections will lead to recovery, 80% will persist.

-- Sexual activity is safe unless it involves trauma or higher risk sexual behaviours

-- Use condoms and dental dams in nonmonogamous relationships and for new sexual partners.

-- For HCV, there is currently no proven method to reduce the 5% risk of vertical transmission; transmission during breastfeeding is avoidable by monitoring the nipples for fissures.

-- Never donate blood, organs, semen, or tissues

-- Never share drug paraphernalia; discuss HCV status w drug using partners

-- No ASA or NSAIDs if possible

-- Acetaminophen, OCPs, and statins are safe to use

-- Ensure the care team is informed of any complementary/alternative therapies.

-- Keep in mind the possibility of changed liver metabolism affecting serum drug levels, and the increased possibility of drug interactions.

-- Clinical presentation: any S/Sx consistent w acute viral hepatitis, along with elvated ALT

-- Anti-HCV Ig present (becomes + at 4-12 weeks post-exposure) OR HCV-RNA positive (2-4 weeks)

-- Anti-HAV IgM negative AND Anti-HBc IgM negative