UBC Med Preclinical GI Curriculum Flashcards

Question

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?

Answer 1

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.

Answer 2

Somatostatin-containing D Cells in the antrum detect a pH 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.

Answer 3

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.

Answer 4

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.

Answer 5

* 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)

Answer 6

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.

Answer 7

5-15% of cases are resistant to therapies. **Standard** care usually starts with **triple therapy**: PPI + clarithromycin + amoxicillin or metronidazole. **Quadruple therapy is 2ndline**: PPI + bismuth + tetracycline + metronidazole (Quadruple therapy may be used to initiate Tx, eg. if pt has recently been exposed to 1st-line antibiotics.)

Answer 8

* **Dimenhydrinate (antihistamine)**: Tx of vertigo and motion sickness. * **Scopolamine (anticholinergic)**: Tx of motion sickness, chemoinduced 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.

Answer 9

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

Answer 10

**Dyspepsia** (AKA **indigestion**) is an upperabdominal 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.

Answer 11

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.

Answer 12

**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.

Answer 13

1. **"Do you have trouble starting swallowing, such as choking or nasal regurgitation?"** 1. 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?"** 1. 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.

Answer 14

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.

Answer 15

* **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.

Answer 16

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.

Answer 17

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

Answer 18

* 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.

Answer 19

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

Answer 20

* 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.

Answer 21

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.

Answer 22

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.

Answer 23

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).

Answer 24

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).

Answer 25

* 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.

Answer 26

* 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.)

Answer 27

**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**.

Answer 28

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.

Answer 29

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

Answer 30

* **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.

Answer 31

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

Answer 32

* 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).

Answer 33

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.

Answer 34

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

Answer 35

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

Answer 36

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.

Answer 37

**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.

Answer 38

1. **Passive diffusion**: Some lipid-soluble nutrients, such as small-chain fatty acids and fat-soluble vitamins, can diffuse directly. 2. **Facilitated diffusio**n: 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.

Answer 39

* 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.

Answer 40

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.

Answer 41

**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.

Answer 42

* 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.

Answer 43

* **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.

Answer 44

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

Answer 45

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.

Answer 46

* 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.

Answer 47

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.)

Answer 48

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.

Answer 49

* **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.

Answer 50

* 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.

Answer 51

* **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.

Answer 52

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

Answer 53

* **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.

Answer 54

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

Answer 55

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.

Answer 56

* **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.)

Answer 57

* 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).

Answer 58

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.

Answer 59

* **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.

Answer 60

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.

Answer 61

Celiac sprue

Answer 62

* **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.

Answer 63

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.

Answer 64

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.)

Answer 65

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

Answer 66

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

Answer 67

**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.

Answer 68

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.

Answer 69

**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 where special attention to nutrition is needed, since they have a high need.

Answer 70

* **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

Answer 71

* **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

Answer 72

**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)

Answer 73

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

Answer 74

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

Answer 75

* 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.

Answer 76

1. Incorrect Dx. 2. Diet nonadherence. 3. Concurrent Dz, eg. pancreatic insufficiency. 4. Development of intestinal lymphoma (enteropathy associated T-cells). 5. Diffuse intestinal ulceration (precursor to lymphoma).

Answer 77

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.

Answer 78

* **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.

Answer 79

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** absorption 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.

Answer 80

* NKCC1 is found in **crypt cell basal membranes**, 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.

Answer 81

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.

Answer 82

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

Answer 83

**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.

Answer 84

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

Answer 85

1. Tenderness in the R iliac fossa (2 points). 2. Migratory R iliac fossa pain (1 point). 3. Rebound tenderness in the R iliac fossa (1 point). 4. N/V (1 point). 5. Fever \>37.5 (1 point). 6. Anorexia (1 point). 7. Leukocytosis (2 points). 8. 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.)

Answer 86

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.

Answer 87

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.

Answer 88

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

Answer 89

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.

Answer 90

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

Answer 91

**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.

Answer 92

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.

Answer 93

* **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.

Answer 94

* **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.

Answer 95

**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.

Answer 96

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

Answer 97

* 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.

Answer 98

**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]

Answer 99

* 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.

Answer 100

* **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

Answer 101

* 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 emphasize 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.

Answer 102

* **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.

Answer 103

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.

Answer 104

* **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

Answer 105

* **Rheum**: 15-20% peripheral arthritis; 10% ankylosing spondylitis * Hepatobiliary: 10-35% cholelithiasis; 1-5% primary sclerosing cholangitis * **Derm**: up to 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

Answer 106

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.

Answer 107

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.

Answer 108

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

Answer 109

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

Answer 110

* **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

Answer 111

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.

Answer 112

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.

Answer 113

* **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.

Answer 114

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

Answer 115

* 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.

Answer 116

* **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.

Answer 117

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.

Answer 118

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.

Answer 119

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

Answer 120

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

Answer 121

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

Answer 122

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: 1. Prostate, seminal vesicles, and retrovesical pouch in men; 2. 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.

Answer 123

**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.

Answer 124

**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.

Answer 125

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.

Answer 126

**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.

Answer 127

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)

Answer 128

* 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.

Answer 129

* **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.)

Answer 130

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.

Answer 131

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.

Answer 132

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.

Answer 133

**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.

Answer 134

* Glycogen * triglycerides * vitamin B12 * folate * Vit A * iron * copper

Answer 135

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.

Answer 136

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.

Answer 137

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.

Answer 138

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.

Answer 139

1. Apathy, restlessness, reverse sleep-wake cycle, slowed intellect, impaired computational abilities & handwriting. 2. Asterixis, lethargy, drowsiness, disorientation. 3. Rousable stupor, hyperactive reflexes, extensor plantar responses. 4. Coma (response to painful stimuli only.)

Answer 140

**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 resorption, 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.

Answer 141

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.

Answer 142

These **self-antibodies** (such as anti-nuclear Ab, anti-mitochondrial 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.

Answer 143

* **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.

Answer 144

1. Obesity: NAFLD is found in 80% of obese Pts. 2. Diabetes. 3. Hypertriglyceridemia. 4. High fat/High fructose diets. 5. Healthy diet, weight loss, exercise, and metabolic syndrome drugs are the treatment.

Answer 145

* **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.

Answer 146

**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.

Answer 147

**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.

Answer 148

**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.

Answer 149

* **Hep A Virus** (Acute infxn): * anti-HAV IgM. * **Hep B Virus** (Acute or chronic): * presence of virus: HBsAg; * active replication: HBeAg, HBV-DNA; * recent infection: anti-HBc IgM; * previous exposure: anti- HBc; * protective immunity: anti-HBs. * **Hep C Virus** (mostly Chronic): * anti-HCV ELISA, PCR for HCVRNA; * assess Dz activity w LFT; * assess liver fibrosis w Fibroscan (special US available in some centres.) * **Hep E Virus** (Acute): * anti-HEV IgM, HEV PCR.

Answer 150

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

Answer 151

**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.)

Answer 152

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).

Answer 153

* 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.

Answer 154

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

Answer 155

* **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.

Answer 156

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

Answer 157

* 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

Answer 158

**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.

Answer 159

* 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.

Answer 160

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

Answer 161

* **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.

Answer 162

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

Answer 163

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.

Answer 164

* **Prehepatic**: Hemolysis, neonatal jaundice * **Hepatic**: _Hepatocellular diseases_: Viral, Autoimmune, Drugs, Alcohol, Hemochromatosis, Wilson's Dz, etc. * **Posthepatic**: _Biliary obstruction_: Gallstones, Parasites, Malignancy

Answer 165

* **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.

Answer 166

**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.

Answer 167

1. **Potential Exposures:** 1. _High risk_: 1. IDU (Injxn Drug Users); 2. Incarcerated; 3. Born, traveled or resided where HCV is common (esp. if received invasive medical care), or where healthcare practices are lax; 4. Transfusion, blood products or organ transplant before 1992. 2. _Intermediate risk_: 1. Hemodialysis; 2. Infant born to HCV Mom; 3. Needle sticks. 3. _Other risks_: 1. intranasal/inhaled drug use; 2. higher-risk sex; 3. tattooing, piercing, rituals. 2. **Clinical clues possible for HCV**: 1. LFTs; 2. S/Sx of chronic liver Dz; 3. substance dependancy; 4. HBV or HIV infxn; 5. Dz requiring multiple blood transfusions; 6. unexplained renal impairment; 7. Non-Hodgkin's Lymphoma; 8. vasculitis (due to assoc. cryoglobulinemia).

Answer 168

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.

Answer 169

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.

Answer 170

* 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.

Answer 171

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

Answer 172

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%.

Answer 173

* 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

Answer 174

* 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.

Answer 175

**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

Answer 176

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.

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UBC Med Preclinical GI Curriculum Flashcards

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