Ubc Medicine Preclinical Gi Curriculum

Front 1

As food passes along the GI tract, it crosses 3 significant junctions in the histology of the mucosal epithelium. What are these 3 junctions?

Back 1

1. Esophagogastric junction (AKA the Z line) 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.

Front 2

What different epithelial cells are found lining the stomach and its gastric pits?

Back 2

-- 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.

Front 3

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?

Back 3

-- CV: MI, angina, pericarditis, aortic dissection, ruptured aortic aneurism -- Other: pneumonia, musculoskeletal. Pain during contraction of abdominal muscles, such as during a sit-up, is indicative of a muscle problem.

Front 4

What are the myenteric and submucosal plexuses?

Back 4

These two ganglionated plexuses make up the enteric nervous system, a component of the autonomic nervous system that regulates GI movement patterns, secretions, and sensations. 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.

Front 5

Interstitial Cells of Cajal act as 'pacemakers' for GI smooth muscle cells. What pattern of action potential do ICC cause?

Back 5

ICC set up 'slow wave' action potentials in smooth muscle (AKA Basic Electrical Rhythm). Slow wave action potentials determine the frequency of some types of intestinal motility patterns, such as peristalsis. Slow waves vary from their normal pattern or rate in some conditions, such as diarrhea.

Front 6

There are 4 main types of motility patterns in the GI system. Which type is impaired in gastroesophageal reflux disease?

Back 6

The 4 main types of motility patterns are: 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.

Front 7

Esophageal manometry (AKA tonometry) measures the pressure applied by esophageal muscles. For what esophageal motor disorder does manometry provide a definitive diagnosis?

Back 7

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.

Front 8

Describe the steps in primary peristalsis of the esophagus (ie. swallowing.)

Back 8

"1. Conscious desire to swallow activates the ""swallowing centre"" in the brain. 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."

Front 9

How does primary peristalsis differ from secondary peristalsis, in the esophagus?

Back 9

1. One is consciously activated, the other is a reflex activated by distention of the esophagus. 2. One can occur even if the sensory pathways are damaged, the other is initiated by sensation. 3. One is a continuation of the oropharyngeal phase of swallowing, the other can occur by itself. 4. One is for swallowing food, the other is for clearing food remnants and refluxed gastric juice.

Front 10

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?

Back 10

Some substances, such as pharmaceuticals, can irritate or damage the esophageal mucosa. Bisphosphonates, a class of drug used in the treatment of osteoporosis, can cause life-threatening esophageal perforations.

Front 11

Chronic alcohol abuse is a risk-factor for esophagogastric varices, among many other GI and non-GI conditions. Name 5 physical exam signs that may indicate chronic alcohol abuse.

Back 11

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.However, the Px may be normal despite the presence of alcoholism.

Front 12

Nausea and vomiting is a common complaint in hospital and outpatient settings. What are some associated symptoms that can help determine the cause of N/V?

Back 12

-- 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)

Front 13

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.

Back 13

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.

Front 14

The pancreas forms from a ventral bud and a dorsal bud, which fuse together. Which pancreatic duct corresponds with each pancreatic bud?

Back 14

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.

Front 15

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.

Back 15

-- 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.)

Front 16

What are the 5 regions of the stomach?

Back 16

1. Cardia: the portion adjoining the esophagus; involved in hiatus hernia 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

Front 17

What are the different parts of the duodenum?

Back 17

1st (superior) part: pyloric orifice to neck of the gallbladder; intraperitoneal; location for most duodenal ulcers. 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.

Front 18

What is the main blood supply of the foregut?

Back 18

The celiac trunk arises from the aorta and branches into: -- 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.

Front 19

What is the autonomic innervation of the upper GI tract?

Back 19

-- Sym. N.S.: T5-9 via the greater splanchnic nerve. -- 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.

Front 20

What is McBurney's point?

Back 20

McBurney's point, one third of the way from the ASIS to the umbilicus, is a landmark for the typical location of the appendix.

Front 21

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

Back 21

Virchow's node is a palpable medial-left-supraclavicular node, suggesting cancer spreading via the thoracic duct. Sister Mary Joseph nodules are are palpable periumbilical nodules. Either may indicate metastatic GI cancer. Rarely, cancer of the stomach can metastasise to the left axillary node (Irish's node.)

Front 22

What are 6 exocrine secretions of the stomach?

Back 22

1. HCl 2. Pepsinogen 3. Gastric lipase 4. Intrinsic factor (important for absorbing Vit B12) 5. Mucus 6. Bicarbonate (sets up a protective pH gradient in the mucus layer)

Front 23

What are the functions of gastric acid?

Back 23

1. Acts as a bacteriostatic agent 2. Transforms pepsinogen into active pepsin 3. Denatures proteins 4. Facilitates absorption of iron, calcium, and vitamin B12

Front 24

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.

Back 24

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

Front 25

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?

Back 25

1. The cephalic phase originates in the brain and is transmitted to the stomach via the vagus nerve. It is triggered by the thought, smell, sight, and taste of food. 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.

Front 26

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?

Back 26

Somatostatin-containing D Cells in the antrum detect a pH <3.0, and release somatostatin locally which inhibits gastrin secretion by G cells. Somatostatin serves several different functions throughout the body, as an endocrine or paracrine hormone. Its synthetic analogue, octreotide is used in several different conditions, such as carcinoid tumour.

Front 27

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?

Back 27

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 7. Conservative measures: Elevate head of the bed, discontinue NSAIDs, change of diet, smoking cessation.

Front 28

How effective are H2 receptor antagonists and PPIs at reducing acid secretion?

Back 28

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.

Front 29

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?

Back 29

-- Hot as a hare (hyperthermia)-- Blind as a Bat (dilated pupils) -- 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)

Front 30

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

Back 30

Some medications, such as oral iron supplements, or the anti-fungal ketoconazole, are dependant on the acidic pH of the stomach for proper absorption. Antacids, PPIs, and antihistamines that increase pH can decrease (or, in some cases, increase) medication and nutrient absorption.

Front 31

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

Back 31

5-15% of cases are resistant to therapies. 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.)

Front 32

Dimenhydrinate (Gravol), scopolamine, and ondansetron are all commonly used in treatment of N/V. How do their indications differ?

Back 32

-- Dimenhydrinate (antihistamine): Tx of vertigo and motion sickness. -- 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.

Front 33

What are some red flags in a gastrointestinal history?

Back 33

-- Change in appetite or unintentional wgt loss. -- Fever. -- Dysphagia. -- N/V. -- Abdominal pain or distension. -- Jaundice. -- Significant bleeding (upper or lower GI).

Front 34

What is dyspepsia?

Back 34

Dyspepsia (AKA indigestion) is an upper-abdominal feeling of discomfort, bloating, or feeling of fullness. It may be accompanied by Sx of heartburn, belching, or N/V. When no organic cause for the dyspepsia can be found, such as PUD, dyspepsia is classified as functional dyspepsia, and may be due to a dysmotility of the enteric nervous system.

Front 35

What is rebound tenderness?

Back 35

When the peritoneum is inflamed, it is painful when there is movement (or direct pressure.) To elicit rebound tenderness, press gently into the abdomen, then release suddenly; pain that is worse on release is rebound tenderness. The pain may be felt remotely from where you were pressing; for example in Rovsing's sign of appendicitis, rebound tenderness is felt in the RLQ after releasing pressure in the LLQ.

Front 36

GERD is often diagnosed clinically, based on symptom Hx and relief follwing a trial of pharmacotherapy. What are the clinical features of GERD?

Back 36

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.

Front 37

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?

Back 37

" 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."

Front 38

Most of the esophagus is surrounded by adventitia rather than serosa. What implications does this have in esophageal carcinoma?

Back 38

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.

Front 39

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

Back 39

-- Dysphagia (initially intermittent with solids) is the cardinal Sx. Odynophagia, anorexia, regurgitation and wgt loss may also occur. -- Sx of GERD, esp. w adenocarcinoma. -- Cough can be from tracheal involvement or aspiration, or due to related GERD. -- Back or chest pain indicates local invasion. -- hematemesis or hemoptemesis may be massive as a result of tumor invasion of vasculature; FOB may be positive for smaller bleeds.

Front 40

What is the trend in prevalence of H. pylori infection?

Back 40

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.

Front 41

What disorders does H. pylori cause?

Back 41

-- Chronic gastritis. -- gastric and duodenal ulcers. -- gastric adenocarcinoma. -- MALT B-cell lymphomas.

Front 42

Testing for H pylori is indicated in active PUD, past Hx of peptic ulcer, or gastric MALT lymphoma. What investigations can you do to confirm the presence of H. pylori?

Back 42

-- 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.

Front 43

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?

Back 43

Pts who have Barrett's esophagus should be monitored with esophagogastroscopy (no dysplasia: every 3-5y; low-grade: 6-12mo; high-grade, w/o eradication therapy: every 3mo).

Front 44

What is the risk of malignant transformation in Barrett's esophagus?

Back 44

Prior to dysplasia, 0.4% per year. Roughly 6% per year for high-grade dysplasia. Up to 10% of GERD pts have developed Barrett's by the time they seek medical care.

Front 45

What are indications for gastroscopy in GERD?

Back 45

Pts who present with GERD for the first time should be scoped to: -- r/o conditions that mimic reflux (eg. cancer, PUD, infective esophagitis). -- distinguish btwn esophagitis, and non-esophagitis reflux. -- Dx presence of Barrett's.

Front 46

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

Back 46

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%). -- Epistaxis (nose bleed) and coagulopathy should also be considered when thinking of UGI bleeds.

Front 47

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.

Back 47

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).

Front 48

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?

Back 48

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).

Front 49

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

Back 49

-- 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.

Front 50

NSAIDs like ibuprofen are used in a wide variety of conditions, eg. as pain relief for arthritis, but often cause peptic ulcer disease or upper GI bleeds. What are some therapies that can be used to decrease the risk of side effects from NSAIDs, and what are indications for their use?

Back 50

-- 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.)

Front 51

What is the function of the pancreas?

Back 51

Endocrine: Islets of Langerhans are the only sources for glucagon and insulin. Islets also secrete somatostatin, one of the hormones controlling gastrointestinal activity. 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.

Front 52

Jaundice is common in newborns, affecting 60%. Is it something to worry about?

Back 52

Normal physiologic jaundice, due to replacement of fetal hemoglobin, mostly occurs between the 2nd to 7th day of life. Jaundice in the first 24 hours, persistent jaundice after 7-10 days, or jaundice with excessive unconjugated bilirubin must be investigated.

Front 53

What are 3 conditions you should think of if a Pt has intermittent abdo pain precipitated by eating?

Back 53

-- Obstruction (gastric outlet, small bowel). -- Pancreatitis. -- Ischemic bowel.

Front 54

What are some possible pathologies indicated by unusual stool colour?

Back 54

-- Green: Rapid transit, such as with some forms of diarrhea, may prevent bile from being digested. -- 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.

Front 55

Lactose intolerance (lactase deficiency) is a common maldigestion syndrome (ie it is an impairment of nutrient hydrolysis.) What is the clinical presentation of lactose intolerance?

Back 55

Chronic watery diarrhea or loose stool, abdominal pain, and bloating associated with dietary intake.

Front 56

What are the rules of 2s for Meckel's diverticulum? (There are 6 of 'em)

Back 56

-- 2% of population. -- 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).

Front 57

"What is meant by ""failure to thrive""?"

Back 57

Failure to thrive is used in pediatrics when a Pt's weight is not growing at a sufficient rate; definitions vary, but the 5th percentile is often used.

Front 58

Pancreatic exocrine proteins can be classified as amylolytic, lipolytic, proteolytic, or nuclease. Name one member of each.

Back 58

-- Amylolytic: alpha-amylase. -- Lipolytic: lipase, procolipase, cholesterolesterase, prophospholipase A2. -- Proteases: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases A & B. -- Nucleases: ribonuclease, deoxyribonuclease.

Front 59

How are pancreatic zymogens activated?

Back 59

In the duodenum, the brush border enzyme enteropeptidase cleaves a portion off of trypsinogen, leaving trypsin. Trypsin then activates the zymogens (including trypsinogen, causing positive feedback) by cleaving off portions

Front 60

A small amount of trypsinogen can spontaneously cleave to active trypsin within the pancreas. Normally, protective proteins prevent the trypsin from activating zymogens within the pancreas, which could lead to autodigestion. How do these protective mechanisms fail in hereditary pancreatitis?

Back 60

2 proteins prevent trypsin from prematurely activating other enzymes; PSTI (Pancreatic Secretory Trypsin Inhibitor) binds to and inhibits trypsin, while CTRC (chymotrypsin C) cleaves and inactivates. In hereditary pancreatitis, a mutation can occur in either of these protective proteins, or can occur in trypsin at their binding sites.

Front 61

In the intestinal phase of pancreatic secreation, secretin and cholecystokinin (CCK) stimulate the pancreas in response to chyme entering the duodenum. What are the effects of secretin and CCK?

Back 61

Secretin is released by the duodenum in response to a low pH of <4.5. It primarily acts on duct cells to secrete sodium bicarbonate solution. 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.

Front 62

Enterocytes are responsible for absorbing nutrients from the intestinal lumen. What are the 4 mechanisms of transcellular transport across an enterocyte's cell membrane?

Back 62

1. Passive diffusion: Some lipid-soluble nutrients, such as small-chain fatty acids and fat-soluble vitamins, can diffuse directly. 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.

Front 63

The ileum may be removed as part of the treatment of some diseases, such as Crohn's Dz. What effects on absorption of nutrients could resection of the ileum have?

Back 63

Vit B12 deficiency is possible, since it is only absorbed in the ileum. Bile salt reabsorption would be impaired. If only a small portion (< 100 cm) of the ileum is removed, the unabsorbed bile salts cause a watery diarrhea by retaining water through the large intestine. If >100 cm of ileum are removed, enterohepatic circulation is impaired enough that bile salt deficiency develops, impairing the ability to form micelles to digest and absorb lipids. Loss of surface area is also a factor decreasing lipid absorption. Steatorrhea (fatty diarrhea) develops.

Front 64

The digestion and absorption of lipids is complex because of their insolubility. What are 6 steps in lipid digestion and absorption?

Back 64

1. Emulsification: Dietary proteins, bile salts, and free fatty acids help disperse lipids into smaller droplets. 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.

Front 65

The embryological gut is divided into foregut, midgut, and hindgut based on which parts are supplied by the celiac artery, superior mesenteric artery, and inferior mesenteric artery. What are the derivatives of the midgut and hindgut?

Back 65

Midgut: Small intestine, except a portion of the duodenum; cecum; appendix; ascending colon; proximal 1/2 to 2/3 of transverse colon. Hindgut: Left 1/2 to 1/3 of transverse colon; descending and sigmoid colon; rectum; superior portion of anal canal.

Front 66

The rapidly growing midgut protudes into the umbilical cord during development, forming a physiological umbilical hernia. How does the midgut rotate during ths stage of development?

Back 66

During protrusion, 90 degrees CCW. At 10 weeks, the midgut returns and rotates a further 180 degrees CCW, forming the transverse and ascending colon. Malrotations occur in 1/500 live births; volvulus can be a life-threatening complication, presenting with bilious vomiting in infants. Nonrotation (left-sided colon) can be fairly benign, but reversed rotation causes the transverse colon to lie posterior to the superior mesenteric artery, possibly causing blockage.

Front 67

What is the difference between gastroschisis, congenital omphalocele, and umbilical hernias?

Back 67

-- Gastroschisis (1/2000 live births) is the free extrusion of intestine into the amniotic cavity, due to incomplete closure of lateral folds. -- 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.

Front 68

Most neoplasms of the stomach are epithelial (adenocarcinoma) in origin, such as intestinal carcinoma, diffuse carcinoma (AKA linitis plastica,) and cancer of the cardia. What are some risk factors for gastric cancers?

Back 68

-- H. pylori. -- Pernicious anemia. -- Chronic atrophic gastritis. -- Smoking. -- EtOH. -- Smoked foods, foods preserved with nitrites and nitrates. -- Previous partial gastrectomy.

Front 69

What is the pathogenesis of Celiac Dz? What ages might Celiac Dz present?

Back 69

1. The mucosa is primed by a previous trigger, such as an adenovirus. 2. Gliadin (from gluten) derived peptides are presented by HLA class II molecules to helper T cells. 3. Activated Th 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.

Front 70

What are some clinical features of Celiac Dz?

Back 70

-- In children: Failure to thrive, malabsorption. -- 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.

Front 71

Malabsorption may occur due to problems in the lumenal phase, the mucosal phase, or the transport phase of digestion and absorption. What are some types of problems in the lumenal phase?

Back 71

1. Reduced nutrient availability, eg. due to cofactor deficiency in pernicious anemia, or nutrient consumption in bacterial overgrowth. 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.)

Front 72

If a patient presents with Sx such as chronic diarrhea and abdominal syndromes, weight loss and fatigue, you may suspect malabsorption. What are some baseline lab tests that could suggest malabsorption?

Back 72

CBC, folate, B12, Fe status, albumin, prealbumin, transferrin, Ca, phosphate, Mg. Depending on the Pt presentation, serum carotene & INR/PTT may also be useful bloodwork.

Front 73

As you continue to work-up malabsorption, specialised tests may investigate fat, carb, & B12 malabsorption. Name a test for each nutrient.

Back 73

-- Fat: Quantitative stool fat (eg. over 72 hr); Sudan III stain; 14C triolein breath test (yields radio-labeled CO2). -- 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.

Front 74

Nausea and vomiting can be distressing Sx for patients. What are some red flag warning signs in N/V?

Back 74

-- Focal neurological Sx, worse when supine (increased ICP) suggest a central cause. -- 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.

Front 75

Several different extra-abdominal signs can be present with abdominal disease. What are some things to look for?

Back 75

-- Chronic liver Dz: Jaundice, spider angiomata, palmar erythema, finger clubbing, gynecomastia, parotid enlargement, testicular atrophy, asterixis. -- IBD: Iritis, skin rash, arthritis, leg ulcers -- Chronic blood loss from GI Dz may produce signs of anemia, such as pallor.

Front 76

What is Grey-Turner's sign?

Back 76

Ecchymoses on the abdomen and flanks that occurs without trauma due to massive retroperitoneal bleeding (eg pancreatitis, strangulated bowel, bleeding from abscess.)

Front 77

Abdominal pain may be described as visceral or parietal. What is the difference?

Back 77

-- Visceral is pain of the organs, eg due to distension, forceful contraction, ischemia. It is poorly localised (often midline,) may be described as ache, burn, or cramp, and the Pt is often restless (colicky.) Nausea, sweating, pallor may be present. -- 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.

Front 78

Acute diarrhea is common in toddlers, and doesn't always require medical attention. What are some indications for medical examination of acute diarrhea in this population?

Back 78

-- Age <6 mo. -- Fever. -- Visible blood in stool. -- Frequent, substantial volume diarrhea. -- Signs of dehydration. -- Change in mental status.

Front 79

Diarrhea and vomiting raise worries of dehydration, especially in children. Name at least 4 signs to look for.

Back 79

1. Dry mucous membrane. 2. Depressed fontanelle. 3. Altered skin turgour. 4. Sunken eyes. 5. Tachycardia. 6. Decreased BP. 7. Decreased capillary refill. 8. Cool extremities. 9. Lethargy.

Front 80

P-BIND is a useful mnemonic for organising aspects of a pediatric Hx. What does it stand for?

Back 80

"-- Prenatal: Maternal illnesses (eg DM, HTN), drug exposures, complications (eg polyhydramnios.) -- 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.)"

Front 81

What are the I GET SMASHED causes of acute pancreatitis?

Back 81

-- Idiopathic. -- 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).

Front 82

What do serum amylase and serum lipase tell you about a Pt with suspected acute pancreatitis?

Back 82

Amylase and lipase will be elevated for 3-5 days in acute pancreatitis. Lipase is more specific, but both can be caused by other abdominal Dz, such as biliary Dz, bowel obstruct/ischemia, penetrating ulcers, peritonitis, chronic liver Dz, aneurysm, or ruptured ectopic pregnancy. Some non-abdo causes, such as renal failure, can also cause elevations; serum amylase >5x normal is almost always pancreatitis or renal Dz.

Front 83

Pain is the key symptom in acute pancreatitis. What are some characteristics to look for?

Back 83

L: Epigastric/upper abdomen. 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.

Front 84

How does the pain of chronic pancreatitis differ from acute?

Back 84

Pain is usually less intense; initially episodic then more severe. Pain may be worse after eating. 10% Pts are painless. Pain control is an important aspect of Tx of chronic pancreatitis and often requires narcotics, which can cause its own problems since alcoholism is the most common cause of chronic pancreatitis.

Front 85

What Dz presents w the following endoscopic & biopsy findings? Gross and microcopic loss of villi; elogated crypts; inflammatory cells in lamina propria; lymphocytes in surface epithelium.

Back 85

Celiac sprue

Front 86

What imaging is useful for investigating Dz of the pancreas?

Back 86

-- US is best for the biliary tree (67% sens, 100% spec) and gives some info on the pancreas (eg. dilated ducts). -- 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.

Front 87

Jaundice is a symptom in a variety of blood, liver, and biliary diseases. Why is painless jaundice considered an ominous sign?

Back 87

Painless ( or w vague, constant epigastric pain) jaundice is a common clinical feature of pancreatic cancer. Pancreatic Ca is usually incurable and terminal. Determine if the jaundice is due to an obstructive cause. Courvoisier's sign (palpable nontender gallbladder) may be helpful, it is present in 33% of Pts w pancreatic carcinoma.

Front 88

Supportive Tx is the basis for mild-moderate acute pancreatitis care. What are 5 goals of supportive therapy?

Back 88

1: Hemodynamic stability (eg IV fluids.) 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.)

Front 89

The late stages of chronic pancreatitis occur in 15% of Pts, when >90% of pancreatic function is lost. What complications may you see in them?

Back 89

-- Malabsorption syndrome (need digestive enzyme supplementation.) -- Steatorrhea. -- Diabetes. -- Jaundice. -- Weight loss. -- Ascites. -- GI bleed.

Front 90

If someone comes to your ER complaining of abdominal pain, what life-threatening causes do you want to rule out ASAP?

Back 90

-- CVS: MI, aortic dissection, ruptured AAA -- Gynecologic: ectopic pregnancy -- GI: perforated viscus, hepatic/splenic injury, ischemic bowel

Front 91

The Rome III criteria are: >= 12/52 in the last year of abdo discomfort/pain w 2 of 3: -- Relief w defecation. -- Change in freq of stool. -- Change in consistency of stool. What syndrome is diagnosed by these criteria?

Back 91

Irritable Bowel Syndrome is a functional bowel Dz characterised by abnormal motility: alternating constipation and diarrhea, flatulence, and lower abdo distension and pain. IBS is less likely in the presence of Red Flag S/Sx, and can be mimicked by other Dz, such as Giardiosis, lactose intolerance, Crohn's, & Celiac. The etiology of IBS is unclear, but stress is a factor.

Front 92

Malnourishment is common in hospitalised Pts. What 5 general outcomes will be worsened by malnourishment?

Back 92

1. Impaired growth and development. 2. Poor resistance to infections. 3. Decreased wound healing. 4. Increased length of stay. 5. Poor clinical outcomes: increased morbidity and mortality.

Front 93

The nutritional requirments of hospitalised Pts are different from the general population. How can you estimate how much energy is needed?

Back 93

Indirect calorimetry, measuring CO2 output, is the gold standard; more often, equations are used to estimate requirments based on activity factors, stress factors, and wgt. Different equations are available, such as the Frankenfield eq for trauma and sepsis Pts. Pts recovering from burns are an example of a where sepcail attention to nutrition is needed, since they have a high need.

Front 94

What proportions of calories do dietary macronutrients take in a normal diet?

Back 94

-- Carbs: 45%-65% (Plus fibre: F 25g/d, M 38g/d) -- 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

Front 95

What is the 4:2:1 rule of thumb for IV fluid maintenance in a NPO (non per orum) Pt?

Back 95

-- 4 mL/kg/h for first 10 kg -- 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

Front 96

What nutrient deficiency may be present in an alcoholic who presents w opthalmoplegia, nystagmus, ataxia, loss of recent memory, & confusion?

Back 96

Thiamine (Vit B1) deficiency can cause Wernicke's encepalopathy (confusion, ataxia, gaze abnormalities), and Korsakoff's psychosis (permanent impairment of formation of new memories, +/- confabulation)

Front 97

Marasmus and Kwashiorkor are nutritional deficiency syndromes seen in extremely poor or famine/war-tron countries. Is it likely that you'll see these syndromes in Canada?

Back 97

Marasmus (calorie & protein deficiency) is seen in end-stage Ca and anorexia nervosa. Kwashiorkor (protein deficiency) is less likely to be seen.

Front 98

The body shifts from the short-term to the long-term starvation response after glycogen stores are depleted. What changes occur in metabolism at this time?

Back 98

-- Decreased glucose oxidation and basal metabolism. -- Much more lipolysis and ketogenesis. -- Small increase in protein catabolism (protein sparing.)

Front 99

In refeeding syndrome, nutrient intake after prolonged starvation causes insulin secretion and switch to anabolism, in turn causing shifts in fluids and lytes (causing hypokalemia, hypomagnesemia, hypophosphatemia, thiamine def, & edema). When treating a Pt at risk (eg due to uncontrolled diabetes, malabsorptive diseases), what are the rules for nutrition support?

Back 99

-- Start low, go slow: 20 Cal/kg/d (<50% of needs) for first 3 days. -- Supplement phosphate, minimise Na, total fluid < 1L/d. -- Monitor lytes and cardiac status closely.

Front 100

A gluten-free diet is the mainstay of treatment of Celiac Dz. What are 5 possibilities to consider if a Celiac Pt has a poor response to a gluten-free diet?

Back 100

1. Incorrect Dx. 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).

Front 101

What is the function of the large intestine?

Back 101

Primarily absorption of H2O, and formation/storage of feces. In ileostomy and colostomy Pts, dietary modifications are targeted more at maintaining patency of the stoma and improving lifestyle (eg by reducing flatulence) rather than nutritional concerns from loss of colon surface area.

Front 102

Inflammatory diarrhea is a form of diarrhea characterised by loose to watery stool, often with mucus, pus, or blood. Cramping, fever and other Sx are present. What can cause acute inflammatory diarrhea?

Back 102

"-- IBD (Inflammatory Bowel Dz) such as Ulcerative Colitis or Crohn's Dz. -- Ischemic bowel. -- NSAIDs. -- Infectious: ""Your Stools Smell Extremely Crappy"" --> Yersinia enterocolitica, Shigella, Salmonella, E. coli (EHEC O157:H7), E. histolytica, Campylobacter, C. difficile."

Front 103

Na-K-ATPase is located on the basal membrane of enterocytes throughout the intestine, providing a driving force for the absorption of Na. What are 4 channels for absorbing Na in the apical membrane?

Back 103

1. Na+ transport coupled to organic solutes (glucose, galactose, AA), mostly in the jejunum, also illeum. 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.

Front 104

The NKCC1 transporter symports Na, K, & 2Cl into a cell at its basal membrane. What cell is this transporter found in, and what is the function of this transporter?

Back 104

NKCC1 is found in crypt cell basal membranse, and is part of the the cellular machinary (along with the CFTR Cl- channel, NaK-ATPase, and K channels) used to pump Cl- into the crypt lumen, causing Na+ and H2O to follow. Crypts secrete fluid for several purposes, such as maintiaining the fluidity of the intestinal lumen, or dilution of injurious substances (eg toxins). Cholera toxin causes an increase in cAMP, an intracellular regulator of the Cl- pumping machinery, causing massive secretory diarrhea.

Front 105

The pathophysiology of diarrhea can be broadly divided into deficiencies of absorption, and abnormally increased secretion. With diarrhea due to absorption problems, diarrhea stops w fasting. How can absorptive defficiencies be further subdivided?

Back 105

1. Inhibited or defective enterocytes. Eg heat-stable enterotoxin from E. coli causes diarrhea mainly by inhibiting NaCl absorption. 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.

Front 106

The pathophysiology of diarrhea can be broadly divided into deficiencies of absorption, and abnormally increased secretion. With secretory diarrheas, diarrhea continues despite fasting. How can varieties of increased secretion be further subdivided?

Back 106

1. Increased secretion due to crypt hyperplasia (more secretory cells). Crypt hyperplasia is commonly seen in the histology of Celiac sprue biopsies. 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.

Front 107

AXR (abdo plain film) is a quick and easy imaging technique for abdominal (inc. retroperitoneal) problems. What is one systematic approach to AXRs and other imaging?

Back 107

IT's Free For ABDO -- 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.

Front 108

Appendicitis occurs in 6% of the population, and can be life-threatening. What is the pathogenesis of appendicitis?

Back 108

Luminal obstruction --> bacterial overgrowth --> inflamm/swelling --> incr. pressure --> local ischemia --> gangrene/perforation --> abscess or peritonitis

Front 109

CT scan has a high accuracy for appendicitis and can investigate a DDx, but has disadvantages such as availability, delay & radiation. Diagnostic scoring systems, such as the modified Alvarado Score, can guide Tx of suspected appendicits. What are the 7 factors considered in the modified Alvarado Score?

Back 109

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.)

Front 110

Erect upright and supine are common Pt positions for AXRs. LLD (Left Lateral Decubitus) is another common AXR position, what is it useful for?

Back 110

LLD is useful for showing air in the peritoneum (pneumoperitoneum) sensitively, between the liver and abdo wall. Air indicates perforated viscus, although it also occurs in some benign conditions and remains in the peritoneum for up to 10d postoperatively. Followup imaging w a soluble GI tract contrast agent allows the perforation to be localised.

Front 111

Dilated bowel is a common finding in GI radiology. What are four basic causes?

Back 111

1. Obstruction: Peristalsis continues against an obstruction (eg Ca, impacted feces) causing lumen dilation. 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.

Front 112

What is the 3,6,9 rule of thumb?

Back 112

Useful for detecting dilated bowel on abdominal imaging; maximum normal diameters for small int., large int., and cecum: 3cm, 6cm, 9cm

Front 113

An O&P (Ova & Parasite) test of stool may be indicated in Pts who have severe diarrhea, or mild-moderate diarrhea for >5/7. What are 6 risk factors for infxn by GI parasites?

Back 113

1. Travel or immigration from an endemic area. 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.

Front 114

What are 6 different ways C diff infxn can manifest? (mildest to worst)

Back 114

1. Asymptomatic carriage. 2. Mild diarrhea. 3. Severe diarrhea. 4. Pseudomembranous colitis. 5. Perforation. 6. Toxic megacolon.

Front 115

Are alcohol hand sanitisers effective against C diff?

Back 115

No, C diff is able to form endospores that survive dessication, heat, and toxins such as alcohol. Proper hand washing and barrier methods are necessary when interacting w Pts who are infected w C diff.

Front 116

A Pt presents to you with CC soft-stool diarrhea q6/7, 7+ small-volume episodes/d, fever 38.5, urgency, lower abdo cramping & tenesmus. FamHx & extra-intestinal signs are negative for IBD. The Pt recently had dinner made by an aunt who was ill with 'stomach pains.' Palpation elicits lower abdo tenderness. Hx and Px otherwise unremarkable (eg no diet changes, meds, travel, etc.) What might you do next for this Pt?

Back 116

-- This Pt meets both the frequency/duration and the fever criteria for severe diarrhea. Symptoms, despite having no blood, pus or mucus in the stool, point towards inflammatory diarrhea rather than the watery, large-volume of noninflammatory; presence of RBCs and WBCs in stool would help confirm this impression. Hx points to infectious cause. 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. 3. Antimotility (eg loperamide, codeine) agents are contraindicated in inflammatory diarrhea; consider bismuth subsalicylate for some diarrheal relief, acetaminophen for analgesia & antifever. 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.

Front 117

A stool S&C tests for the most common reportable causes of bacterial diarrhea: Campy, Salmonella, Shigella, & E.coli. What are some abx options to treat these infections? (Note: Some labs include Yersina, Vibrio, Aeromonas &/or Pleisomonas in their standard S&C.)

Back 117

-- Campylobacter: Erythromycin. -- 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.

Front 118

What uncommon infections of the esophagus or intestines should be worried about in Pts w HIV/AIDS, leukemia, or transplants?

Back 118

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

Front 119

What endoscopic finding is decribed by the following? -- 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.

Back 119

Pseudomembranous colitis is almost diagnostic for C diff. C diff toxins disrupt mucosal cytoskeleton, forming ulcers. Ulcers allow exudation of serum proteins, mucus, and inflammatory cells, manifesting as the pseudomembrane. Pseudomembranes don't occur in 10-20%, and biopsy may be needed. 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.

Front 120

What syndromes make up IBD? (Inflammatory Bowel Dz)

Back 120

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

Front 121

What are some clinico-pathologic features of UC?

Back 121

-- Starts in rectum and spreads proximally. -- 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.

Front 122

How much does UC increase the risk of CRC? (ColoRectal Cancer)

Back 122

Risk is increased: Overall risk of Ca complicating UC is 5%; risk is highest in long-standing and extensive UC, with an incidence ratio of 7.0. Monitoring for Ca is an important part of UC care. The risk of CRC in Crohn's is likely similar, but there is not a clear consensus. [UpToDate]

Front 123

What are some clinico-pathologic features of Crohn's Dz?

Back 123

"-- 85% of cases involved the terminal ileum. -- 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."

Front 124

Constipation is a common complaint, especially in older adults, the institutionalised, and as a side-effect of opioids and anti-cholinergics. It is important to treat and prevent constipation, as it could develop into fecal impaction. What pharmaceutical options are available?

Back 124

-- Bulk laxatives (eg metamucil): Dietary fibre (eg prunes) is preferrable; avoid these in debilitated patients with low fluid intake, as these can form a 'glue'. -- 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

Front 125

What conservative/lifestyle changes can you reccommend to Pts suffering from constipation?

Back 125

-- 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.-- In Pts at increased risk of constipation, such as high-dose opioid analgesics for palliative care, it is important to emphasise preventing constipation, not just waiting for it to become a problem. Prescribe a laxative, and ensure a pro-peristaltic agent such as Senokot is taken if the Pt goes a day or two w/o a BM.

Front 126

What is the difference between diverticulosis and diverticulitis?

Back 126

-- Diverticulosis is the simple herniation of colonic mucosa, ie the presence of diverticula. >80% never symptomatic. -- 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.

Front 127

How does a right-sided colon tumour present differently from a left-sided tumour?

Back 127

Because the feces is much more liquid in the proximal colon, a right-sided tumour is less likely to present with the obstruction, abdominal pain, and change in bowel habits that a left-sided tumour might. Hematochezia or melena is less likely in right-sided than rectosigmoid tumours, but development of iron deficiency anemia due to longstanding occult blood loss is more likely for right sided tumours.

Front 128

In BC, the lifetime risk of developing CRC is 7%, dying of CRC 3.4%. What is the screening protocol for CRC?

Back 128

-- Average risk, asymptomatic Pts: FOB every 1-2 years for age 50-75, continue to age 85 if Pt will benefit. A colonoscopy every 10y is an alternative screen. -- 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

Front 129

Up to 33% of IBD Pts have at least one extraintestinal manifestation of IBD. What are some more common ones?

Back 129

-- Rheum: 15-20% peripheral arthritis; 10% ankylosing spondylitis -- 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

Front 130

Uveitis (inflammation of the part of the eye that includes the iris) in IBD may occur during remission, or after bowel resection. Prompt Tx w systemic glucocorticoids is key to avoid scarring and visual impairment. What are some Sx of uveitis?

Back 130

Ocular pain, photophobia, blurred vision, headache. In contrast, episcleritis of the eye is a benign disorder that presents w mild Sx of ocular burning, and can be treated topically.

Front 131

Incidence of IBD has been increasing over the past few decades. Which of the causative factors of IBD is responsible for this trend?

Back 131

Trick question! Despite being described for 100 yrs, we don't know the cause of IBD. The consensus is that there is dysregulation of mucosal immune function, possibly responding to the normal intestinal flora. Many genetic risk loci have been found. Risk factors for IBD include: FamHx, Jewish, Caucasian (more-so northern European), urban.

Front 132

What are 5 goals of Tx in IBD?

Back 132

1. Induction of steroid-free clinical remission. 2. Achieve mucosal healing. 3. Ameliorate complications. 4. Maintain remission. 5. Prevent colon Ca.

Front 133

What anti-inflammatory class of drugsis the mainstay Tx for UC and Crohn's?

Back 133

5-ASA (5-aminosalicylic acid); 2 different compounds are available, sulfasalazine and mesalazine. Dual Tx, oral and enema delivery, is better than oral alone.

Front 134

Systemic corticosteroids are used in the Tx of many chronic inflammatory disorders, but they have a high rate of side effects. IBD Tx can avoid these SEs to some extent by using budesonide, a steroid that acts topically on the intestinal mucosa with little absorption. What are some of the SEs of corticosteroids?

Back 134

-- Short-term: Night sweats, increased appetite, adrenal insufficiency, impaired glucose metabolism. -- Long-term: Cushing's syndrome (abnormal fat deposition, fatigability, hirsutism, ...), cataracts, glaucoma, osteoporosis, HTN, growth supression, immunosupression, and more

Front 135

Hereditary Nonpolyposis Colon Cancer (HNPCC) is an autosomal dominant genetic disorder, caused by mutations in mismatch repair genes. Despite being named for colon Ca, it also commonly causes Ca in other organs. Name at least 3 of those organs.

Back 135

Uterus (endometrial Ca), ovaries, stomach, small bowel, hepatobiliary, ureter. Consider investigating for HNPCC in a Pt who presents w/ CRC if they have a past Hx of cancer in one of these organs.

Front 136

In the abdominal physical exam, what is auscultation used for?

Back 136

"1. Normal bowel sounds (""borborygmi"") transmit well, and can be confirmed listening in the RLQ or elsewhere. Increased sounds may indicate diarrhea or early intestinal obstruction; decreased or absent sounds may indicate ileus or peritonits. High-pitched tinkling suggests intestinal fluid and air under tension; intestinal obstruction is possible if heard coinciding with an abdominal cramp. 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."

Front 137

Step 1 in an abdominal exam is inspection. What are things to note in inspection of the abdomen?

Back 137

-- General: Is patient in distress, lying comfortably, can they push out or suck in their abdomen, or cough, w/o pain.-- Skin: Scars, striae (old, silver OR pink-purple?), dilated veins, rashes and lesions. -- 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.

Front 138

When inspecting an abdomen, it is important to note if it is scaphoid, flat or protuberant. What are the 5 F's for protuberant abdomens?

Back 138

-- Fat (most common) -- Flatus (gas) - causes a tympanic percussion note -- Fluid (ascites) -- Fetus -- Frickin' big mass (tumour)

Front 139

Percussion of the abdomen typically comes after inspection and auscultation. What can be found with percussion?

Back 139

-- Firstly, pain upon percussion is a good indication of peritonitis, and can give you warning to proceed carefully when palpating. -- 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 can detect (or delineate the borders of) organs or masses, such as an enlarged liver, distended bladder, or pelvic mass. -- Percussion is used in special tests, eg. detecting an enlarged spleen, shifting dullness of ascites, and CVA (costovertebral angle) tenderness of pyelonephritis.

Front 140

What physical exam techniques can be used to detect an enlarged spleen?

Back 140

-- Percussion in Traube's space: Traube's space is the left lower axillary area; an enlarged spleen displaces the gastric bubble in this area, causing a mid-axillary dull note (or anterior-axillary with greater enlargment), while a normal spleen is located posteriorly. -- 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.

Front 141

What steps are part of palpation of the abdomen?

Back 141

1. Light papation for tenderness and rigidity, and masses located w/in the abdo wall. 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.

Front 142

For which of stress incontinence, urge incontinence, and overflow incontinence might you detect an enlarged urinary bladder on physical exam?

Back 142

In overflow incontinence, detrusor contractions are insufficient to overcome urethral resistance, eg due to an enlarged prostate. The bladder is typically large, even after an effort to void.

Front 143

What are some non-GI causes of lower abdominal pain to consider in your DDx?

Back 143

-- CV: Leaking abdominal aortic aneurism -- GU: ureteral calculi, pyelonephritis, gynecological -- MSK: Abdominal wall hematoma, psoas abscess

Front 144

What are some gynecological causes of abdominal pain?

Back 144

Ectopic pregnancy, pelvic inflammatory Dz, endometriosis, tubo-ovarian abscess, adnexal torsion, mittleschmertz.

Front 145

Colon Ca is the third most comon cause of cancer death. The majority of cases are sporadic, even if there is a family history; the Amsterdam Criteria is used for clinical Dx of HNPCC, the most common familial CRC. What are the 4 criteria?

Back 145

1. 3 relatives w CRC, one of whom is a first degree relative of the other two. 2. 2+ generations involved. 3. 1+ CRC before age 50 4. FAP (Familial Adenomatous Polyposis) is excluded

Front 146

The ano-rectal examination allows examination of the anus and walls of the rectum, adjacent internal organs, and lower peritoneal contents. How is it done?

Back 146

1. Use lube, place the pad of the finger on the anal sphincter, exert gentle pressure until the sphincter relaxes. 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. -- Abnormal findings include: Masses, narrowed lumen, a rectal (Blumer) shelf, impacted feces, and blood.

Front 147

What is the most common cause of fecal incontinence?

Back 147

Obstetric injury to the pelvic floor (eg levator ani tears, pudendal nerve stretching), during delivery or while carrying the fetus. Other causes include congenital abnormalities (eg imperforate anus,) trauma, or rectal prolapse.

Front 148

Anal fissues can occur at all ages, and are the most common cause of rectal bleeding in infancy. They are associated w constipation, diarrhea, perianal trauma, Crohn's, and infectious causes. If you find an anal fissure in a patient, what Tx would you recommend?

Back 148

Conservative Tx will heal most fissures: -- 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.

Front 149

What are hemmorhoids?

Back 149

With constipation and straining, the hemmorhoidal cushions (normal vascular structures that prevent damage to the sphincter muscle) become enlarged and can prolapse out of the anal canal.

Front 150

Aside from diverticulitis, how else can a symptomatic diverticulum present?

Back 150

Painless rectal bleeding, 30-50% being massive enough to threaten hemodynamic stability. 80% will stop spontaneously, with a 30% risk of rebleed within the next few weeks. Much more rare is diverticular colitis, w diarrhea, abdo pain, tenesmus, and hematochezia.

Front 151

What are the 8 functions of the liver?

Back 151

1. Storage of nutrients: glycogen, triglycerides, vitamins and trace metals 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)

Front 152

The stroma is connective tissue that supports the functional hepatocytes of the liver. What makes up the hepatic stroma?

Back 152

-- The Glisson capsule, a thin external capsule. -- Portal tracts and thin interlobular septae separate the classic hepatic lobules. -- Hepatic stellate cells: Involved in fibrosis by laying down extra-cellular matrix.

Front 153

The liver parenchyma can be divided into separate units based on function: the classic lobule, the portal lobule, and the portal acinus. What do these functional units represent?

Back 153

-- Classic lobule: 6-sided, w triads at the corner and central vein; represents drainage of arterial and portal blood. -- 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.)

Front 154

What is the pathway of bile in the body?

Back 154

-- Secreted by hepatocytes into canaliculi --> canals of Hering --> intrahepatic bile ductules --> interlobular bile ducts --> R & L hepatic ducts --> common hepatic duct (connecting to cystic duct from gall bladder) --> common bile duct (connecting w main pancreatic duct) --> to intestine via major duodenal papilla. -- Transection or damage to the common ducts is a potentially life-threatening complication of cholecystectomy.

Front 155

What are Kupffer cells?

Back 155

Kupffer cells are the liver's resident macrophages, and play an important role in clearing toxins and bacteria coming from the GI tract. In a technetium 99m scan, liver adenomas often show a defect because there are few Kupffer cells phagocytosing the radiomarker.

Front 156

Pruritis is a typical sign of cholestasis, tending to affect the extremities more. It may precede jaundice for a prolonged period (eg in primary biliary cirrhosis.) What complications can arise due to pruritis?

Back 156

Itching is a distressing symptom, causing a severe impact on quality of life for patients; excoriation can lead to scarring, secondary infection, and sepsis. Generalised pruritis can also arise due to chronic renal failure.

Front 157

A patient who complains of long-standing fatigue may have a GI cause, such as malabsorption or occult blood loss, but fatigue can occur due to processes in many other body systems. What screening tests could you order when working up a CC of fatigue?

Back 157

Labs: CBC+diff, lytes, BUN, Cr, ESR, glucose, TSH, ferritin, albumin, LFT (AST, ALT, ALP), UA would make a good start. 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.

Front 158

What nutirents are stored in the liver?

Back 158

Glycogen, triglycerides, B12, folate & Vit A, iron & copper

Front 159

Bile is made up of bile salts (cholesterol derivatives,) electrolytes, phospholipids, proteins, cholesterol, and bilirubin. What effect does the drug cholestyramine have on bile salts?

Back 159

Cholestyramine binds to bile salts, causing it to pass through the ileum unabsorbed, thus interfering with enterohepatic circulation. Cholestyramine is used to treat hypercholesterolemia, and has an off-label use in Tx of pruritis.

Front 160

ALT is normally <55 U/L, AST <38 U/L. What sorts of diseases are suggested by extremely elevated levels of >1000 IU/L?

Back 160

This level of aminotransferase enzymes indicates significant hepatocyte injury: -- 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.

Front 161

While doing your internal medicine rotation, you are part of the care team for a 15yo male who attempted suicide by ingesting a bottle of tylenol. He feels extremely guilty, and has developed a desire to deal with his mood troubles now that he has faced death. Late one evening, you note that his most recent labs show a significant decrease in his transaminases. Do you tell him the good news about his recovering liver?

Back 161

The decrease in transaminases can indicate fulminant liver failure, the death of hepatocytes, rather than their recovery. In acute liver Dz, it is also important to monitor other indicators of liver function, such as bilirubin and INR, and of course monitor patient status for hepatic encephalopathy.

Front 162

What do aminotransferase levels tell you about the level of fibrosis of the liver?

Back 162

Persistent elevations of liver enzymes, at 2-10 times normal levels, indicates chronic hepatitis, but provide no info about the degree of liver fibrosis. Levels can be normal in Pts with advanced but inactive cirrhosis.

Front 163

Hepatic encephalopathy is an acute neuropsychiatric syndrome due to liver Dz, caused by systemic toxins like ammonia and mercaptans. In acute failure, the problem is nonfunctioning hepatocytes, while in chronic failue, portal-systemic shunting allows bypass of liver filtration. Hepatic encephalopathy is precipitated by electrolyte disturbances, infection, drugs, nitrogen load, or a further deterioration in hepatic function. What are the 4 stages of hepatic encephalopathy?

Back 163

I. Apathy, restlessness, reverse sleep-wake cycle, slowed intellect, impaired computational abilities & handwriting. II. Asterixis, lethargy, drowsiness, disorientation. III. Rousable stupor, hyperactive reflexes, extensor plantar responses. IV. Coma (response to painful stimuli only.)

Front 164

Increases in the cholestatic enzymes (ALP & GGT) are useful as evidence of intra- and extrahepatic cholestatic Dz, or infiltrative liver Dz like hepatic amyloidosis. What else may increases indicate?

Back 164

ALP is also present in other tissues, such as placenta, fallopian tubes, and bone which has a large influence on serum levels. Increases can indicate high bone metabolic activity, particularly bone resoroption, eg bone tumours & mets, osteomalacia, or calcium-wasting kidney Dz (renal osteodystrophy.) GGT is specific to the liver; increases have been used as an indicator of alcohlism, but this measure is not specific.

Front 165

What is Gilbert syndrome?

Back 165

Gilbert is a common (3-7%) benign hepatic cause of high levels of unconjugated bilirubin. It is due to a genetic defect causing less efficient uptake of unconjugated bilirubin into hepatocytes.

Front 166

What diseases are the following laboratory measures used to investigate: ANA, AMA, ANCA, anti-smooth muscle antibody, anti-LKM and serum immunoglobulins?

Back 166

These self-antibodies (such as antinuclear Ab, antimitochondrial Ab) are used to investigate autoimmune diseases. Liver autoimmune Dz includes Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Primary Sclerosing Cholangitis. Some are used in the investigations of other autoimmune Dz, eg ANA for lupus; they are often lacking in specificity, and the entire clinical picture must be taken into account.

Front 167

People who drink heavily and abuse alcohol are at risk for hepatic steatosis, alcoholic hepatitis, and cirrhosis. Their risk of hepatocellular carcinoma also increases. What are the survival rates for Pts with compensated and decompensated cirrhosis?

Back 167

-- Compensated, stop EtOH consumpion: 5 year survival 90%. -- 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.

Front 168

NAFLD and NASH (NonAlcoholic SteatoHepatitis) are increasing in prevalence, and are now one of the most common causes of elevated liver blood tests, which may be the only evident abnormality. What are the risk factors for NAFLD and NASH?

Back 168

1. Obesity: NAFLD is found in 80% of obese Pts. 2. Diabetes. 3. Hypertriglyceridemia. 4. High fat/High fructose diets. -- Healthy diet, weight loss, exercise, and metabolic syndrome drugs are the treatment.

Front 169

Hemochromatosis is a common hereditary metabolic disorder that can lead to liver cirrhosis (as are Wilson Disease and alpha1-antitrypsin deficiency.) The clinical features of early hemochromatosis are nonspecific (eg arthralgia, fatigue, abdominal discomfort, impotence, dysthesias, glucose intolerance) and so screening labs are important when there is reason to suspect this Dz. What labs are used to screen for hereditary hemochromatosis?

Back 169

-- Serum ferritin is used as a measure of iron stores, but is often raised also as an acute phase reactant, eg in inflammation. -- 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.

Front 170

What is the prognosis for untreated autoimmune hepatitis?

Back 170

Very poor. ~50% die within 5y, most die within 10y of Dz onset. Severe initial presentation corellates w poorer outcome. Autoimmune hepatitis should be considered for any Pt who has acute hepatitis (fever, liver tenderness, jaundice) or acute liver failure (coagulopathy, jaundice) though it can also present as chronic hepatitis or cirrhosis.

Front 171

Primary biliary cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC) are similar in that both are progressive, autoimmune cholestatic Dz that can necessitate liver transplant; PBC affecting intrahepatic bile ducts, PSC affecting both intra- and extrahepatic ducts. How are they diagnosed?

Back 171

PBC has a very good blood test: Antimitochondrial antibody (AMA) is 90-95% sens 98% spec; biopsy can confirm. PSC antibody labs ANCA and ANA are less sensitive and specific, so ERCP and MRCP are used to confirm the Dx.

Front 172

What is quantitative phlebotomy?

Back 172

Old fashioned blood-letting q2/52 (phlebotomy every 2 weeks) is the treatment for hemochromatosis. Counting the number of 450mL phlebotomies required (~250mg Fe per session) to normalise labs gives a measure of iron overload, which may be ~10 times normal body iron of 3-4g. The calculated total body iron overload confirms the original diagnosis of hemochromatosis.

Front 173

What serologic tests are available to Dx viral hepatitis?

Back 173

-- HAV (Acute infxn): anti-HAV IgM. -- 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.

Front 174

What proportion of HBV exposures evolve into chronic hepatitis?

Back 174

-- Healthy adults: 1-5%. -- Neonates: almost 100% (but <10% with anti-HBV immunoglobulin prophylaxis.) -- Children and immunosuppressed: intermediate risk.

Front 175

What virus is described by the following: RNA-dependent RNA polymerases don't proofread, high mutation rate; 6 genotypes, w subtypes differing by up to 20%; quasispecies within the same individual differing by 1-3%.

Back 175

HCV is a highly mutable virus with high natural variation, which contributes to treatment resistance. Standard alpha-interferon + ribavarin Tx has only a 50-80% success rate, and requires 48 weeks of therapy for genotype 1, 24 weeks for genotypes 2 & 3 (1,2 & 3 common in BC.)

Front 176

What are 5 pathological mechanisms through which meds can cause liver disease?

Back 176

1. Biotransformation to reactive, damaging intermediates (eg acetaminophen). 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).

Front 177

Acetaminophen is the commonest cause of fulminant liver failure, about half of these cases due to therapeutic misadventure, not suicidal intent. What is used to Tx acetaminophen toxicity?

Back 177

-- gastric lavage/emesis < 2h after ingestion. -- 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.

Front 178

What is the most common malignancy found in the liver?

Back 178

In Western countries, metastases (usually multifocal) are more common than primary tumours such as hepatocellular carcinoma.

Front 179

Hemangiomas are the most common type of liver tumour (5-20% of pop.), are benign, and are usually asymptomatic. How can you Dx a liver mass as a hemangioma?

Back 179

Contrast imaging is best, either CT or MRI-Gd. It will show bright enhancement w centripetal progression (initial peripheral enhancement, delayed venous emptying); US will show a homogenous hyperechoic mass. Avoid biopsy, as it may result in hemmorhage.

Front 180

What are the Tx options for hepatocellular carcinoma?

Back 180

-- Liver resection. -- Ablation (EtOH, radiofrequency). -- Chemoembolisation. -- Liver transplant. -- Tx options differ for metastasis; systemic chemotherapy may be an option if the met is susceptible.

Front 181

In some parts of the the world, hepatocellular carcinoma is the most common malignancy, where HBV is endemic. HCC is secondary to cirrhosis in most cases; what are some less common causes of cirrhosis?

Back 181

-- Chronic hepatic congestion: may be due to cardiac cirrhosis (eg due to right heart failure), or due to hepatic vein thrombosis (Budd-Chiari syndrome) -- Wilson's Dz -- alpha1-antitrypsin deficiency -- Primary biliary cirrhosis -- Idiopathic

Front 182

You have a Pt with a long history of hypothyroidism who has been stable on his medication for over a decade. With a targeted review-of-systems, you find he has complaints of cold-intolerance, weight gain, constipation, and generalised muscle aches that have slowly progressed over the part year. During your physical exam, you note thin hair and the smell of alcohol on his breath. What is the likely pathophysiology behind his symptoms?

Back 182

This patient shows signs and symptoms of hypothyroidism. This Pt has likely increased his alcohol intake, inducing quicker metabolism of thyroid replacement hormone, causing his medication to be subtherapeutic. Many drugs such as levothyroxin are metabolised in the liver, and certain drugs, foods, or herbal supplements can affect the number or efficiency of enzymes, in turn affecting drug levels. Warfarin, an inhibitor of coagulation factor synthesis, used in conditions such as atrial fibrillation to prevent clot formation, is an example of one important drug influenced by interactions of other drugs with the liver.

Front 183

Ascites is a symptom of late-stage liver cirrhosis. What are some pathophysiological mechanisms that cause ascites?

Back 183

-- Increased portal venous pressure causes transudation of a relatively protein-rich fluid from the liver, due to the fenestrated capillaries permittance of proteins to pass. -- 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.

Front 184

What are the 5 main causes of ascites?

Back 184

1. Heart failure. 2. Renal failure. 3. Liver failure. 4. Carcinomatosis. 5. Chronic peritonitis.

Front 185

How is ascites managed?

Back 185

Salt-restriction and diuretics are the cornerstones. Diuretics which counter mineralocorticoid activity, such as spironolactone, often in combination w loop diuretics such as furosemide are effective. Large volume paracentesis may be necessary, paired with administration of IV albumin to prevent ascitic fluid from reaccumulating rapidly.

Front 186

How can you test for an ascitic abdomen in the Px exam?

Back 186

"Bulging flanks (""puddle"" sign); test for a fluid wave; test for shifting dullness"

Front 187

How can liver cirrhosis lead to thrombocytopenia (low platelet numbers?)

Back 187

Cirrhosis causes portal hypertension, which causes splenic congestion, and eventually splenomegaly. The spleen acts as a storage organ for platelets, but when enlarged too many platelets are sequestered, and the Pt becomes thrombocytopenic.

Front 188

When investigating a Pt with jaundice, a useful approach is to separate causes into prehepatic, hepatic, and posthepatic. This allows you to think of the problem as production of too much bilirubin, a failure in processing/excreting bilirubin, or a failure in transporting the bilirubin to the intestines. Give an example Dz for prehepatic, hepatic, and posthepatic.

Back 188

Some examples: -- Prehepatic: Hemolysis, neonatal jaundice -- Hepatic: Hepatocellular diseases: Viral, Autoimmune, Drugs, Alcohol, Hemochromatosis, Wilson's Dz, etc. -- Posthepatic: Biliary obstruction: Gallstones, Parasites, Malignancy

Front 189

Define these terms: Cholecystitis, cholangitis, cholelithiasis, choledocolithiasis, biliary colic

Back 189

-- Cholecystitis: inflammation of gall bladder. -- Cholangitis: inflammation of one or more bile ducts. -- Cholelithiasis: presence of gallstones in gallbladder. -- Choledocolithiasis: presence of calculi in the gallbladder and common bile duct. -- Biliary colic: steady or intermittent ache in upper abdomen, usually under right side of rib cage.

Front 190

"What clinical sign is described by the following: ""A brief, involuntary lapse of the postural tone of a muscle, typically causing a flapping motion""?"

Back 190

Asterixis. Although asterixis is usually discussed as a flapping tremor of a fully extended wrist, it may also be seen in the tongue, foot, facial, or other skeletal muscles.

Front 191

Who should be screened for HCV?

Back 191

1. Potential Exposures:-- High risk: IDU (Injxn Drug Users); Incarcerated; Born, traveled or resided where HCV is common(esp. if received invasive medical care), or where healthcare practices are lax; Transfusion, blood products or organ transplant before 1992. -- 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).

Front 192

What are the steps in using labs to Dx chronic HCV infection? (A different algorithm is used if there has been an acute exposure.)

Back 192

1. Screen with test for anti-HCV (also consider LFT and HIV); even if negative, follow-up test for HCV-RNA if Pt is high risk or immunocompromised. 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.

Front 193

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

Back 193

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.

Front 194

What are 5 special clinical considerations for HCV?

Back 194

-- Some HCV Pts must be referred to HCV-experienced colleagues, eg HIV+, extra-hepatic HCV (eg renal failure, Non-Hodgkins Lymphoma). -- 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.

Front 195

Name at least 4 risk factors that may contribute to liver damage (ie fibrosis) in chronic HCV?

Back 195

-- Central obesity -- Smoking -- EtOH > 3 drinks/day -- Co-infxn w HBV or HIV -- Male -- Longer duration of infxn-- Older age when infected (>40)

Front 196

When discussing a person's disease with them, one of the important things to cover is their disease's prognosis. What are the possible outcomes of HCV infection?

Back 196

Educating a patient about their risks can be a useful motivator to change modifiable risk factors. -- 20% of acute HCV infections will lead to recovery, 80% will persist. -- Of the Pts that develop chronic HCV, 30% will have chronic, nonprogressive hepatitis (less likely if fibrosis risk factors are present); 40% will have variable progression; 30% will have severe progressive hepatitis. -- Of the Pts eligible for treatment, treatment will fail for 20-50%, and lead to a sustained response in 50-80%.

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What advice can you provide that can help a Pt to reduce the risks of transmission or re-infection of HCV?

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-- Never share sharp instruments/personal hygiene materials (eg razors, nailclipper, toothbrush) -- 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

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What medications should be reconsidered in liver cirrhosis?

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-- If possible, avoid benzodiazepines, aminoglycosides, and narcotics (including codeine) -- 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.

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You learn from a patient that they have RUQ discomfort, and malaise. You find out that he got pricked by a needle at work 3/52 ago; he is a bus driver, and he brushed a hand against a needle wedged between seats while he was cleaning out his bus. What are the criteria for diagnosing acute hepatitis C?

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Confirmed acute HCV must meet several criteria: -- 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

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What should you do if you diagnose acute hepatitis C infection in a Pt?

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Make an urgent referral to a colleague w experience in HCV management to start antivirals ASAP; success rates for viral clearance is much higher for treatments following acute HCV infection.