UBC Med Preclinical GI Curriculum Flashcards

1
Q

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

What are these 3 junctions?

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the myenteric and submucosal plexuses?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Interstitial Cells of Cajal act as ‘pacemakers’ for GI smooth muscle cells.

What pattern of action potential do ICC cause?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A
  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.
    1. The nucleus ambiguous sequentially activates the striated muscle in the upper esophagus
    2. 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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.

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

Which pancreatic duct corresponds with each pancreatic bud?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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.

A
  • 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.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 5 regions of the stomach?

A
  1. Cardia: the portion adjoining the esophagus; involved in hiatus hernia
  2. Fundus: the domeshaped 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the different parts of the duodenum?

A
  1. 1st (superior) part: pyloric orifice to neck of the gallbladder; intraperitoneal; location for most duodenal ulcers.
  2. 2nd (descending) part: superior duodenal flexure to the inferior flexure; contains the major (and minor) duodenal ampulla, the transition to the midgut.
  3. 3rd (horizontal or inferior) part: the longest section, crossing several structures such as the aorta, IVC, and vertebral column.
  4. 4th (ascending) part: suspended by the musculofibrous ligament of Treitz, the duodenojejunal flexure marks the end of the duodenum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the main blood supply of the foregut?

A

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the autonomic innervation of the upper GI tract?

A
  • 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is McBurney’s point?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are 6 exocrine secretions of the stomach?

A
  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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the functions of gastric acid?

A
  1. Acts as a bacteriostatic agent
  2. Transforms pepsinogen into active pepsin
  3. Denatures proteins
  4. Facilitates absorption of iron, calcium, and vitamin B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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.

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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?

A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

How do their indications differ?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are some red flags in a gastrointestinal history?

A
  • Change in appetite or unintentional wgt loss.
  • Fever.
  • Dysphagia.
  • N/V.
  • Abdominal pain or distension.
  • Jaundice.
  • Significant bleeding (upper or lower GI).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is dyspepsia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is rebound tenderness?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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

What are the clinical features of GERD?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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?

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

What implications does this have in esophageal carcinoma?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

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

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What disorders does H. pylori cause?

A
  • Chronic gastritis.
  • Gastric and duodenal ulcers.
  • Gastric adenocarcinoma.
  • MALT B-cell lymphomas.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

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?

A
  • 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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?

A

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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

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

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are indications for gastroscopy in GERD?

A

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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

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

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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.

A
  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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

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?

A
  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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

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?

A
  • 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.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the function of the pancreas?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Jaundice is common in newborns, affecting 60%.

Is it something to worry about?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

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

A
  • Obstruction (gastric outlet, small bowel).
  • Pancreatitis.
  • Ischemic bowel.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are some possible pathologies indicated by unusual stool colour?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

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?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

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

A
  • 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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is meant by “failure to thrive”?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pancreatic exocrine proteins can be classified as amylolytic, lipolytic, proteolytic, or nuclease.

Name one member of each.

A
  • Amylolytic: alpha-amylase.
  • Lipolytic: lipase, procolipase, cholesterolesterase, prophospholipase A2.
  • Proteases: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases A & B.
  • Nucleases: ribonuclease, deoxyribonuclease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How are pancreatic zymogens activated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Enterocytes are responsible for absorbing nutrients from the intestinal lumen.

What are the 4 mechanisms of transcellular transport across an enterocyte’s cell membrane?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

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?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

The digestion and absorption of lipids is complex because of their insolubility.

What are 6 steps in lipid digestion and absorption?

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

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?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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?

A
  • H. pylori.
  • Pernicious anemia.
  • Chronic atrophic gastritis.
  • Smoking.
  • EtOH.
  • Smoked foods, foods preserved with nitrites and nitrates.
  • Previous partial gastrectomy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the pathogenesis of Celiac Dz?

What ages might Celiac Dz present?

A
  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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are some clinical features of Celiac Dz?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

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?

A
  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.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

As you continue to work-up malabsorption, specialised tests may investigate fat, carb, & B12 malabsorption.

Name a test for each nutrient.

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Nausea and vomiting can be distressing Sx for patients.

What are some red flag warning signs in N/V?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Several different extra-abdominal signs can be present with abdominal disease.

What are some things to look for?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is Grey-Turner’s sign?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Abdominal pain may be described as visceral or parietal.

What is the difference?

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

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?

A
  • Age <6 mo.
  • Fever.
  • Visible blood in stool.
  • Frequent, substantial volume diarrhea.
  • Signs of dehydration.
  • Change in mental status.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Diarrhea and vomiting raise worries of dehydration, especially in children.

Name at least 4 signs to look for.

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

P-BIND is a useful mnemonic for organising aspects of a pediatric Hx.

What does it stand for?

A
  • 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.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the I GET SMASHED causes of acute pancreatitis?

A
  • 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).
82
Q

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

A

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.

83
Q

Pain is the key symptom in acute pancreatitis.

What are some characteristics to look for?

A
  • 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.
84
Q

How does the pain of chronic pancreatitis differ from acute?

A

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.

85
Q

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.

A

Celiac sprue

86
Q

What imaging is useful for investigating Dz of the pancreas?

A
  • 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.
87
Q

Jaundice is a symptom in a variety of blood, liver, and biliary diseases.

Why is painless jaundice considered an ominous sign?

A

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.

88
Q

Supportive Tx is the basis for mild moderate acute pancreatitis care.

What are 5 goals of supportive therapy?

A
  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.)
89
Q

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?

A
  • Malabsorption syndrome (need digestive enzyme supplementation.)
  • Steatorrhea.
  • Diabetes.
  • Jaundice.
  • Weight loss.
  • Ascites.
  • GI bleed.
90
Q

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

A
  • CVS: MI, aortic dissection, ruptured AAA
  • Gynecologic: ectopic pregnancy
  • GI: perforated viscus,hepatic/splenic injury, ischemic bowel
91
Q

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?

A

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.

92
Q

Malnourishment is common in hospitalised Pts.

What 5 general outcomes will be worsened by malnourishment?

A
  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.
93
Q

The nutritional requirments of hospitalised Pts are different from the general population.

How can you estimate how much energy is needed?

A

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.

94
Q

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

A
  • 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
95
Q

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

A
  • 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
96
Q

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

A

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)

97
Q

Marasmus and Kwashiorkor are nutritional deficiency syndromes seen in extremely poor or famine/war-torn countries.

Is it likely that you’ll see these syndromes in Canada?

A

Marasmus (calorie & protein deficiency) is seen in end-stage Ca and anorexia nervosa.

Kwashiorkor (protein deficiency) is less likely to be seen.

98
Q

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?

A
  • Decreased glucose oxidation and basal metabolism.
  • Much more lipolysis and ketogenesis.
  • Small increase in protein catabolism (protein sparing.)
99
Q

In refeeding syndrome, nutrient intake after prolonged starvation causes insulin secretion and switch to anabolism, in turn causing shifts in fluids and electrolytes (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?

A
  • 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.
100
Q

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?

A
  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).
101
Q

What is the function of the large intestine?

A

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.

102
Q

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?

A
  • 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.
103
Q

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?

A
  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.
104
Q

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?

A
  • 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.
105
Q

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 deficiencies be further subdivided?

A
  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.

106
Q

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?

A
  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.
107
Q

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?

A

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.
108
Q

Appendicitis occurs in 6% of the population, and can be lifethreatening.

What is the pathogenesis of appendicitis?

A

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

109
Q

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?

A
  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.)
110
Q

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

A

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.

111
Q

Dilated bowel is a common finding in GI radiology.

What are four basic causes?

A
  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.
112
Q

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

A

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

113
Q

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?

A
  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.
114
Q

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

A
  1. Asymptomatic carriage.
  2. Mild diarrhea.
  3. Severe diarrhea
  4. Pseudomembranous colitis.
  5. Perforation.
  6. Toxic megacolon.
115
Q

Are alcohol hand sanitisers effective against C diff?

A

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.

116
Q

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?

A

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.
117
Q

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.)

A
  • 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.
118
Q

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

A
  • 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.
119
Q

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.
A

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.
120
Q

What syndromes make up IBD? (Inflammatory Bowel Dz)

A
  • Ulcerative Colitis (UC).
  • Crohn’s Dz.
  • Indeterminate colitis (full workup shows features of both UC & Crohn’s.)
121
Q

What are some clinico-pathologic features of ulcerative colitis?

A
  • 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.
122
Q

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

A

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]
123
Q

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

A
  • 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.
124
Q

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?

A
  • 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
125
Q

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

A
  • 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.
126
Q

What is the difference between diverticulosis and diverticulitis?

A
  • 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.
127
Q

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

A

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.

128
Q

In BC, the lifetime risk of developing CRC is 7%, dying of CRC 3.4%.

What is the screening protocol for CRC?

A
  • 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
129
Q

Up to 33% of IBD Pts have at least one extraintestinal manifestation of IBD.

What are some more common ones?

A
  • 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
130
Q

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?

A

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.

131
Q

Incidence of IBD has been increasing over the past few decades.

Which of the causative factors of IBD is responsible for this trend?

A

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.

132
Q

What are 5 goals of Tx in IBD?

A
  1. Induction of steroid-free clinical remission.
  2. Achieve mucosal healing.
  3. Ameliorate complications.
  4. Maintain remission.
  5. Prevent colon Ca.
133
Q

What anti-inflammatory class of drugs is the mainstay Tx for UC and Crohn’s?

A

5-ASA (5-aminosalicylic acid)

2 different compounds are available, sulfasalazine and mesalazine. Dual Tx, oral and enema delivery, is better than oral alone.

134
Q

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?

A
  • 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
135
Q

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.

A

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.

136
Q

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

A
  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.
137
Q

Step 1 in an abdominal exam is inspection.

What are things to note in inspection of the abdomen?

A
  • 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.
138
Q

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?

A
  • Fat (most common)
  • Flatus (gas)
    • causes a tympanic percussion note
  • Fluid (ascites)
  • Fetus
  • Frickin’ big mass (tumour)
139
Q

Percussion of the abdomen typically comes after inspection and auscultation.

What can be found with percussion?

A
  • 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.
140
Q

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

A
  • 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.
141
Q

What steps are part of palpation of the abdomen?

A
  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.
142
Q

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

A

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.

143
Q

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

A
  • CV: Leaking abdominal aortic aneurism
  • GU: ureteral calculi, pyelonephritis, gynecological
  • MSK: Abdominal wall hematoma, psoas abscess
144
Q

What are some gynecological causes of abdominal pain?

A
  • Ectopic pregnancy
  • pelvic inflammatory Dz
  • endometriosis
  • tubo-ovarian abscess
  • adnexal torsion
  • mittleschmertz.
145
Q

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?

A
  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
146
Q

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?

A
  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.

147
Q

What is the most common cause of fecal incontinence?

A

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.

148
Q

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?

A

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.
149
Q

What are hemmorhoids?

A

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.

150
Q

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

A

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.

151
Q

What are the 8 functions of the liver?

A
  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)
152
Q

The stroma is connective tissue that supports the functional hepatocytes of the liver.

What makes up the hepatic stroma?

A
  • 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.
153
Q

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?

A
  • 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.)
154
Q

What is the pathway of bile in the body?

A

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.

155
Q

What are Kupffer cells?

A

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.

156
Q

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?

A

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.

157
Q

A patient who complains of longstanding 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?

A

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.

158
Q

What nutirents are stored in the liver?

A
  • Glycogen
  • triglycerides
  • vitamin B12
  • folate
  • Vit A
  • iron
  • copper
159
Q

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?

A

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.

160
Q

ALT is normally <55 U/L, AST <38 U/L.

What sorts of diseases are suggested by extremely elevated levels of >1000 IU/L?

A

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.
161
Q

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?

A

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.

162
Q

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

A

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.

163
Q

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 failure, 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?

A
  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.)
164
Q

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?

A

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.

165
Q

What is Gilbert syndrome?

A

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.

166
Q

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

A

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.

167
Q

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?

A
  • 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.
168
Q

NAFLD (nonalcoholic fatty liver disease) and NASH (Nonalcoholic steatohepatitis) are increasing in prevalence, and are now one of the most common causes of elevated liverblood tests, which may be the only evident abnormality.

What are the risk factors for NAFLD and NASH?

A
  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.
169
Q

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?

A
  • 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.
170
Q

What is the prognosis for untreated autoimmune hepatitis?

A

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.
171
Q

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?

A

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.

172
Q

What is quantitative phlebotomy?

A

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.

173
Q

What serologic tests are available to Dx viral hepatitis?

A
  • 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.
174
Q

What proportion of HBV exposures evolve into chronic hepatitis?

A
  • Healthy adults: 1-5%.
  • Neonates: almost 100% (but <10% with anti- HBV immunoglobulin prophylaxis.)
  • Children and immunosuppressed: intermediate risk.
175
Q

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%.
A

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.)

176
Q

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

A
  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).
177
Q

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?

A
  • 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.
178
Q

What is the most common malignancy found in the liver?

A

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

179
Q

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?

A
  • 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.
180
Q

What are the Tx options for hepatocellular carcinoma?

A
  • Liver resection.
  • Ablation (EtOH, radiofrequency).
  • Chemoembolisation.
  • Liver transplan.
  • Tx options differ for metastasis; systemic chemotherapy may be an option if the met is susceptible.
181
Q

In some parts of the the world, hepatocellular carcinoma (HCC) 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?

A
  • 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
182
Q

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?

A

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.

183
Q

Ascites is a symptom of late-stage liver cirrhosis.

What are some pathophysiological mechanisms that cause ascites?

A
  • 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.
184
Q

What are the 5 main causes of ascites?

A
  1. Heart failure.
  2. Renal failure.
  3. Liver failure.
  4. Carcinomatosis.
  5. Chronic peritonitis.
185
Q

How is ascites managed?

A
  • 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.
186
Q

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

A
  • “Bulging flanks (“puddle” sign)
  • test for a fluid wave
  • test for shifting dullness
187
Q

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

A

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.

188
Q

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.

A
  • Prehepatic: Hemolysis, neonatal jaundice
  • Hepatic: Hepatocellular diseases: Viral, Autoimmune, Drugs, Alcohol, Hemochromatosis, Wilson’s Dz, etc.
  • Posthepatic: Biliary obstruction: Gallstones, Parasites, Malignancy
189
Q

Define these terms:

  • Cholecystitis
  • Cholangitis
  • Cholelithiasis
  • Choledocolithiasis
  • Biliary colic
A
  • 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.
190
Q

What clinical sign is described by the following:

A brief, involuntary lapse of the postural tone of a muscle, typically causing a flapping motion?

A

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.

191
Q

Who should be screened for HCV?

A
  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).
192
Q

What are the steps in using labs to Dx chronic HCV infection?

(A different algorithm is used if there has been an acute exposure.)

A
  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.
193
Q

If you have diagnosed a patient to have chronic hepatitis, what are the next steps?

(Asides from referral!)

A
  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.
194
Q

What are 5 special clinical considerations for HCV?

A
  • 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.
195
Q

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

A
  • Central obesity
  • Smoking
  • EtOH> 3 drinks/day
  • Co-infxn w HBV or HIV
  • Male
  • Longer duration of infxn
  • Older age when infected (>40)
196
Q

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?

A

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%.
197
Q

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

A
  • 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
198
Q

What medications should be reconsidered in liver cirrhosis?

A
  • 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.
199
Q

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?

A

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
200
Q

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

A

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.