Intermediate: GI

Question 1

How do NSAIDs lead to ulcers?

Answer 1

Mucous is secreted by the stomach by mucous neck cells (which also secrete HCO3- and pepsinogen). Prostaglandins increase production of bicarb and mucous which protect the stomach from the corrosive effects of HCl and pepsin allowing an environment for H. pylori to further damage the mucosal barrier leading to ulceration. NSAIDs sharply decrease production of prostaglandins and will therefore lead to decreased protection.

Question 2

Which of the following is NOT considered an increased risk factor for gastric ulceration?

A. Significant burn
B. Coagulopathy
C. Prolonged mechanical ventilation
D. Lumbar epidural steroid injection (LESI)
E. Continuous intrathecal morphine

Answer 2

E: Continuous intrathecal morphine.
There are very few things that anesthesiologists do that directly increase the risk of gastritis, the closest being LESI with the steroid component being a small risk factor for gastric ulcer (far less common than those mentioned before). Intrathecal morphine does not increase the risk of GI bleeding.

Question 3

Diarrhea ABG (acute) 
Oversimplification of gap and non Gap
What type of non gap acidosis has increased K?

Answer 3

What you need to know is that diarrhea causes a non-gap metabolic acidosis with hypokalaemia. You should also know that non-gap acidoses are associated with increased Cl- (hence no anion gap)

A gap is associated with an accumulation of acid; whereas nongap is associated with loss of bicarb (gross oversimplification)…

Only RTA type IV (aldosterone deficiency/ resistance) where K+ is retained.

Question 4

An 80 year old man with cholecystitis presents with ST elevations and undergoes emergency coronary artery bypass grafting (CABG). Two days later, the patient is on aortic balloon pump (AoBP) and levophed gtt. The surgeon tells you that he is concerned of impending sepsis and gangrene (of the gallbladder) and wants to take the patient to the OR now for cholecystectomy. Currently there is no evidence for sepsis. Your plan is:

A. Take the patient to the OR immediately
B. Suggest that percutaneous drainage be performed in interventional radiology (IR)
C. Delay surgery until the AoBP is removed
D. Delay surgery until the patient is stab

Answer 4

B: Suggest that percutaneous drainage be performed in interventional radiology (IR)

Percutenous drainage is an excellent temporizing measure for non-necrotic cholecystitis and sometimes the only safe answer in necrotic gall bladder disease.

Also, for completeness sake, AoBP has two main advantages for cardiogenic shock: afterload reduction and increased aortic diastolic pressure (for coronary perfusion pressure). Classically in sepsis, systemic vascular resistance is low and AoBP does not address this. In some (many) cases of severe sepsis myocardial depression with reduced sytolic function is seen (FYI). I bet you didn’t expect to learn all of this on the GI section!

Question 5

T/F

Answer 5

Cholinergics like neostigmine (parasympathetic: rest & digest) increase the strength of LES contraction while anicholinergics do the opposite.

True

Question 6

Which meds reduce LES tone?

Answer 6

Other medications that reduce LES tone are:Volatile anesthetics, opioids, propofol, thiopental, some B-blockers, tricyclic antidepressants, glucagon

Question 7

What do these do to LES tone?

propranolol, H2 antagonists, non depolarizing muscle relaxants

Answer 7

propranolol, H2 antagonists, non depolarizing muscle relaxants

Nothing!!

Question 8

NPO guidelines

Answer 8

NPO guidelines for clear liquids (water, soda, juice without pulp, black coffee) is 2 hours; breast milk is 4 hours; non-human milk and formula is 6 hours; a light meal is 6 hours; and heavy meals are 8 hours.

Question 9

Why does pain caused delayed gastric emptying?

Which of the following comorbidities of diabetes is delayed gastric emptying most strongly associated with:

A. Autonomic neuropathy
B. Peripheral neuropathy
C. HbA1c
D. Duration of disease
E. Post-prandial glucose (absolute number)

Answer 9

A-autonomic neuropathy

Take a moment and think about how the GI tract is innervated: parasympathetic moves things along and sympathetic does the opposite. Now it makes sense why this is true (true meaning based on one small study!). Also in this context, it makes sense why trauma, pain (especially abdominal), and labor are associated with delayed gastric emptying too. This last sentence you definitely need to know for the boards.

Question 10

Hi premeds-do they prevent aspiration? What about bicitra and h2 blockers for pH? Metoclopramide and gastric volume?

Answer 10

None of the GI premeds have been shown to reduce the risks of aspiration, with the same going for NGTs and nonparticulate antacids (bicitra). H2 blocker and PPIs have been proven to increase gastric pH and reduce volume and metoclopramide has been proven to reduce gastric volume; but neither of these benefits have been proven to translate to a clinical benefit

Question 11

Can NGT prevent aspiration?

Answer 11

NGTs can interrupt the lower esophageal sphincter (LES) (as well as the upper ES) and there is some evidence that NGTs can facilitate regurgitation (around the tube). It should also be noted that reducing the size of the NGT does not appear to help.

Question 12

LMA has been shown to do what to LES and pH?

Answer 12

There are numerous small studies suggesting that LMA use decreases LES tone, some studies showing more reflux (especially when the LMA is in place during emergence), and even a decreased (not increased) pH. What hasn’t been shown is if any of this has any clinical relevance.

Question 13

Which of the following is most important for a patient with Zenker’s diverticulum?

A. Strict adherence to NPO guidelines
B. Preoperative antacids
C. Preoperative H2 blockade
D. Preoperative metoclopramide
E. Preoperative nasogastric tube (NGT)

Explain each

Answer 13

The correct answer is: A: Strict adherence to NPO guidelines

Zenker’s diverticulum is an abnormal pouch formed in the pharynx over time, typically seen in older patients causing aspiration pneumonias and dysphagia. Food bits get stuck in the pouch and are released. The mucus produced by the pouch is alkaline so H2 blockers will not help. Metoclopramide does not work on the diverticulum. NGTs can get stuck and perforate the diverticulum. NPO guidelines should be adhered to, as retained food after meals is common.

Question 14

Propranolol decreases portal pressure by which mechanism:

A. Causing portal vein vasodilatation
B. Causing portal vein vasoconstriction
C. Causing hepatic artery vasodilatation
D. Causing hepatic artery vasoconstriction

Answer 14

D: Causing hepatic artery vasoconstriction

Hepatic blood flow has (about) 30% contribution from the hepatic artery and the remaining 70% comes from the portal vein. The hepatic artery has alpha -1 receptors that constrict the hepatic artery and beta-2 and dopa-1 vasodilation effects on the hepatic artery. The net effect of beta blocking is to reduce hepatitc artery vasodilation thus reducing total hepatic blood flow.

Next we think about portal pressures. Portal pressures are elevated because of liver congestion. The portal vein does not have B-2 receptors and B-blockers do not affect the portal vein directly. However, by reducing hepatic artery flow to the liver, hepatic congestion is reduced and over time portal pressures decrease.

This is one of the reasons patients with portal hypertension might be on a non-selective Beta-Blocker such as propanolol.

Unrelated (but related): Even though the hepatic artery supplies only 25-30% of the blood, it supplies half of the liver’s oxygen needs.

Question 15

Which clotting factors are NOT made in the liver? Explain weird wording about factor 8

Answer 15

Most of the clotting factors are made in the liver (MM is wrong BTW), with notable exceptions being Factor III (Tissue Factor) and vWB, which are made in the endothelium, and factor VIII. Factor VIII is made by a variety of endothelial tissues as well as the liver sinusoidal cells. Factor VII has the shortest half-life of these factors and is why the PT (test of the extrinsic pathway, see haematology section) is the best test for liver synthetic function (transaminases more specifically mark damage not synthetic function).

If the question was which of the following are made by the liver, you might add factor VIII, unless it said which of the following are made “exclusively” by the liver, then the answer would be the same. Thank goodness the ABA would never want to trick you like that….yea right!

Question 16

Which of the following are NOT expected to result from portal hypertension (PTH):

A. Esophageal varicies
B. Splenomegaly
C. Hyperdynamic circulation
D. Spontaneous bacterial peritonitis
E. Cirrhosis

Answer 16

E: Cirrhosis

Cirrhosis occurs following chronic injury to liver tissue leading to areas of necrosis, regeneration, and fibrosis which obstructs hepatic blood flow causing congestion and PTH.

Question 17

ORAL BOARDS ALERT

A 45 year old alcoholic man is hospitalized for lumbar spine injury following a motor vehicle accident with cauda equina syndrome requires emergency surgery. He is short of breath in the supine position due to a large abdominal mass of ascites. He was scheduled to have a paracentesis this week for symptom improvement. Which of the following is the next best step prior to surgery:

A. Large volume paracentesis (LVP) with 1:1 ratio of ascetic volume removed to gram of albumin administered IV
B. LVP with 1:1 ratio of ascitic volume to colloid volume administered IV
C. LVP with 10-20 cc of 25% albumin administered IV for every liter of ascitic volume removed
D. LVP with 50-100 cc of 5% albumin administered IV for every liter of ascitic volume removed
E. Emergency transjugular intrahepatic portosystemic shunt (TIPS)

Answer 17

C: LVP with 10-20 cc of 25% albumin administered IV for every liter of ascitic volume removed

Of the following “LVP with 10-20 cc of 25% albumin administered IV for every liter of ascitic volume removed” is the best (as it has been described and is a common protocol). LVP for this patient would be important, as the patient not only has to lay flat but will also be prone. Abdominal contents can impede ventilation (restrictive lung disease), reduce functional reserve volume (FRC), and lead to increased paravetebral bleeding in the prone position. LVP can quickly and safely reduce abdominal mass. In some patients haemodynamic instability can occur following LVP due to intravascular depletion (due to rapid accumulation of ascites), so albumin is commonly given to ameliorate this response. Without the use of a volume expander, increased creatinine and electrolyte abnormalities are more common when more than 6 L are evacuated. The use of 25% albumin allows small intravascular volumes of albumin to be administered. Answer”LVP with 50-100 cc of 5% albumin administered IV for every liter of ascitic volume removed” would also be acceptable as it is the same total amount of albumin, but involve a larger volume. Answer “LVP with 1:1 ratio of ascitic volume to colloid volume administered IV” would require huge amounts of intravascular volume that would not be tolerated (5-8L paracentesis is common, leading to 5-8 liters given IV). Typically 5 g of albumin (not 1g as in answer A) is given per liter of ascites is removed (100 cc of 25% albumin would cover a 5L paracentesis). TIPS can be used for the chronic management of ascites, but has not shown superiority in clinical trials to LVP; reserving it for other complications of portal hypertension, such as varices. Preoperative LVP is a frequent topic on oral boards.

Question 18

What measurements are a part of the child Pugh score?

Answer 18

Child-it’s easy as A, B, P, C, E
The Child-Pugh score uses plasma albumin, bilirubin, PT or INR, as well as clinical judgment of ascites and encephalopathy. Child’s score C (A-C) is the most severe and associated with high perioperative mortality.

That c is clinical judgement of ascites and encephalopathy
With children, you have to have good judgement

Question 19

What does meld score use?

Answer 19

The MELD score only utilizes laboratory data (bilirubin, creatinine, and INR).

Question 20

Can hepatic encephalopathy occur with normal plasma ammonia level?

Answer 20

It can, but it’s rare

Question 21

Hepatopulmonary syndrome? And how can you know if it’s a shunt?

Answer 21

The patient has evidence of pulmonary shunt, that being minimal increase in arterial paO2 despite increased FiO2. Decreased ability of the liver to clear vasodilating substances (probably also causing systemic endothelial dysfunction) leads to arterial-venous shunts within the pulmonary circulation. Paradoxically, the hypoxaemia is worsened by being in the upright position (orthodeoxia). Approximately a 35% shunt is required for the patient to have essentially no response to 100% oxygen delivery

Question 22

The best (most proven) treatment for hepatopulmonary syndrome is:

A. Octreotide gtt
B. Somatostatin gtt
C. Nitric oxide
D. Intrapulmonary arterial banding
E. Liver transplant

Answer 22

E: Liver transplant

Hepatopulmonary syndrome resolves (essentially completely) following successful liver transplantation in most (~80%+) cases. Somatostatin, and its more potent synthetic peptide cousin octreotide can be used to improve hepatopulmonary syndrome, but results have been inconsistent and evidence is lacking for efficacy. Nitric oxide may be one of the final common pathways that uncleared vasodilating substances used to produce the syndrome (see GI20), so administering more would probably only worsen the syndrome. AV shunting occurs with small vessels throughout the lung and banding a pulmonary artery would not likely help.

Question 23

ORAL BOARDS ALERT!

Explain hepatorenal syndrome. Does giving volume help?

Answer 23

Never say the words “hepatorenal syndrome,” on the boards unless you have an idea of what it means. Hepatorenal syndrome is essentially a pre-renal condition, likely due to decreased intravascular tone leading to the “perception (of the kidney)” of inadequate volume status. More likely, the splanchnic system is severely vasodilated and the renal arteries are vasoconstricted.

Unlike normal pre-renal states, administration of intravenous volume does not improve the disease course and only leads to volume overload. Kidney biopsies of patients with hepatorenal syndrome are essentially normal and the syndrome can be reversed with liver transplant. Diagnosis is essentially one of exclusion after other causes of renal failure have been ruled out. Hepatorenal syndrome is often rapidly fatal (< 1 month), although a slower insidious form is also possible.

Question 24

A man with severe liver disease is undergoing abdominal surgery under general anesthesia with use of vecuronium for muscle relaxation. Which of the following is the best strategy of use of vecuronium for this patient:

Answer 24

The reasoning is that patients with severe liver disease have increased volume of distribution (for hydrophilic drugs such as muscle relaxants) requiring a larger initial dose to take effect. Subsequent doses; however should be reduced due to decreased liver metabolism of the drug. Cisatracurium, which relies of Hoffman degradation, completely independent of the liver, would probably be answered best with response “Both initial and maintenance doses should be increased.”

Question 25

In the setting of general anesthesia, hepatic blood flow generally:

A. Does not change
B. Increase
C. Decreases

Answer 25

Decreases

Hepatic blood flow generally decreases with both neuraxial and general anesthesia, without any clinical significance. This is due to increased vasodilatation and decreased MAP.

Question 26

A 50 year old woman with a history of IV drug use, alcoholism, and idiopathic pulmonary arterial hypertension (IPAH) presents with hepatosplenomegally, ascites, peripheral oedema, and increased jugular venous pulse (JVP). Three months prior the patient was asymptomatic and none of the above findings were documented on her outpatient chart. Which of the following would be the most likely finding:

A. Severely cirrhotic liver on biopsy
B. Dilated inferior vena cava (IVC) on echocardiogram
C. Left ventricular (LV) dysfunction on echocardiogram
D. HIV positive status
E. Acute tubular necrosis (ATN) on renal biopsy

Answer 26

The patient has IPAH (also referred to as primary pulmonary hypertension) with right-sided congestive heart failure, which has lead to congestive liver disease. Other evidence of right heart failure is peripheral oedema and elevated JVP. IPAH can progress both rapidly and insidiously, and is generally without effective (or definitive) treatment. Cirrhosis (answer a) is less likely the cause as the symptoms have rapidly become worsened and high-output cardiac failure (generally) slowly develops and worsens. LV failure is unlikely given a preexisting diagnosis of IPAH, which requires the lack of LV dysfunction causing the pulmonary hypertension.

Question 27

Halothane hepatitis may occur how?

Answer 27

It may occur through an autoimmune mechanism

Repeat exposure (especially when chronologically spaced close together), obesity, and middle age females seem to be at increased risk. The etiology is uncertain but probably results from metabolites of halothane and/or autoimmune mechanisms. Halothane is extensively metabolized by the liver relative to other volatile agents (20% vs 2% for sevoflurane). Hepatic failure is typically quick and fatal more than 50% of the time.

Question 28

A 50 year old alcoholic man with cirrhosis is hospitalized and diagnosed with “high cardiac output heart failure.”

Question 1/2:

Which of the following are most likely findings on echocardiogram:

A. Structurally normal heart
B. Left ventricular hypertrophy
C. Left ventricular dilation
D. Right ventricular dilation
E. Mitral regurgitation

Answer 28

A: Structurally normal heart

Another example of knowing what you are talking about when you say something. High output failure has an increased cardiac output and the heart is, in fact, doing its job appropriately. Due to vasodilation, there is hypoperfusion of organs, including the kidney in which salt and fluid retention occur. In the setting of portal hypertension, the salt/ fluid retention supplies a never-ending volume source for ascites.

Question 29

A 50 year old alcoholic man with cirrhosis is hospitalized and diagnosed with “high cardiac output heart failure.”

Question 2/2:

Which of the following are the most likely findings on pulmonary catheter readings:

A. CO 7.5, SVR 1300, PAPs 25/15
B. CO 7.7, SVR 500, PAPs 15/5
C. CO 7.5, SVR 500, PAPs 35/ 18
D. CO 7.5, SVR 1300, PAPs 15/5

And tell me the normal values for these readings as well

Answer 29

C: CO 7.5, SVR 500, PAPs 35/ 18

You cannot do enough PA catheter readings (and ABG readings) in preparing for the boards. In high output failure one would expect a high cardiac output (CO), low systemic vascular resistance (SVR) due to systemic vasodilation, and a mildly increased pulmonary artery pressure (PAP) due to high flows through a fixed area. Notice you need to know normal values for the boards (as well as real life).

CO: 5 L/min

CI: 3 L/min/m^2

Stroke volume: 70 cc

Stroke volume index: 40 cc/m^2

SVR: 1000 dyn*sec/cm^5

PVRL 200 dyn*sec/cm^5

PAPs: 25/15 (often lower in truly normal people who don’t need swans)

Question 30

Liver transplant phases:

Answer 30

Pre-anhepatic, Anhepatic, and Neohepatic.

Question 31

Explain pre-anhepatic phase of liver transplant:

Answer 31

The preanhepatic phase consists of surgical dissection and is essentially like any other large abdominal case on a patient with liver failure. The anhepatic phase begins by cross-clamping the IVC (above and below the liver), the portal vein and hepatic artery, and common bile duct. After being clamped, each is transected and the liver is removed. A new liver with a new IVC portion is anastomosed in its place.

Question 32

Explain venovenous bypass:

Answer 32

Venovenous bypass diverts blood from the IVC (below the liver) to the upper circulation, usually the axiallary vein. It preserves preload and decreases the acidic shower associated with release of cross clamp after the new liver is transplanted.

Question 33

The first major test to see how the anhepatic phase will go is:
And what do you do if it’s not going so well?

Answer 33

IVC cross-clamp where preload is greatly decreased. Patients with greater collateral venous circulations (especially children who have adapted generally tolerate cross-clamp better). This patient had a very poor result which could be due to numerous factors; but the two most likely are under-resuscitation prior to cross-clamp and too great a proportion of preload interrupted. Answer “Unclamp, check abg, haemoglobin (hb), electrolytes, volume status and administer fluids” is most correct, as you would ensure the patient is ‘optimized’ for cross clamp removal and treat as needed.

Question 34

Following re-anastomosis of a new liver the IVC cross clamp is released leading to first bradycardia with PVCs then ventricular fibrillation. The patient was successfully defibrillated but has persistent ventricular bradycardia and is being transcutaneously paced. What is the most likely etiology:

A. Hypocalcaemia
B. Alkalaemia
C. Hypernatraemia
D. Hyperkalaemia
E. Hypomagnesaemia

Answer 34

D: Hyperkalaemia

Of the available options, hyperkalaemia is most likely. Release of cross clamp is associated with a large acid load and shower unmetabolized, vasodilating substances which decrease contractility and preload. In addition to this, quite predictably, is a large potassium load from the new liver as well as from the associated acidaemia. Acidaemia should be treated with sodium bicarbonate and hyperventilation and hyperkalaemia should be addressed with calcium administration, insulin, and normalizing the pH (as acidaemia causes a release of intracellular potassium).

Question 35

You inform the family member of a patient with small bowel ischaemia who is to undergo emergency laparotomy in the setting of pancreatitis that the patient has a high risk for perioperative mortality because:

A. The patient’s BUN is now less than 5 mg/ dL
B. The patient’s blood glucose is less than 100 mg/dL
C. The patient is 25 years old
D. The patient’s serum calcium (Ca) is 7.0 mg/dL
E. The patient’s white blood count (WBC) is 6,000/uL

Answer 35

D: The patient’s serum calcium (Ca) is 7.0 mg/dL

What is important to understand is that hypoclcaemia in the setting of pancreatitis is a very bad sign as it is due to precipitation of Ca with fats degraded by the pancreatic enzymes. And this is also why Ca drops in severe fat embolism. And yet again, this is why Ca drops in rhabdomyolysis (precipitates with injured muscle)

Question 36

Advantage of enteral nutrition vs parenteral nutrition:

Answer 36

With disuse, the GI tract atrophies and can become increasingly permeable to bacteria that can translocate through the lumen causing infections. Furthermore, gut flora changes without EN due to changes in the immune system and decreased excretion of bile salts (which help control bacterial growth). Finally, in the absence of EN, the immunologic system of the gut (which is tremendous) changes in multiple ways such that less IgA is produced, T helper cells differentiate into forms more likely to excrete pro-inflammatory responses (accounting for increased SIRS in PN vs EN, supposedly). Better immune system with EN

Question 37

Transmission rates of the big 3:

Answer 37

Of the three viruses, HBV is most transmissible (reported as high as 40% but likely far lower), HCV averages about 2% and HIV is 0.3%. HBV vaccine is 90-95% effective.

Question 38

So, you get HCV from a needle stick-now what?

Answer 38

Most patients who have contracted HCV will develop asymptomatic chronic infections for years. About 1/5th of these patients will live long enough to develop cirrhosis (typically takes about 20-30 years or longer). Associated risk factors that speed progression is lack of treatment, alcohol, HIV coinfection, fatty liver, advanced age, and male gender.

Question 39

A healthcare worker sticks herself with a small bore hallow needle filled with a patient’s blood who has hepatitis C virus (HCV), hepatitis B virus (HBV), and human immunodeficiency virus (HIV).

Question 3/3:

Which of the following is appropriate care for the health care worker:

A. Start interferon therapy
B. Start antiviral therapy directed against HIV
C. Plasmapheresis
D. Vancomycin therapy

Answer 39

Start antiviral therapy directed against HIV

Pretty much everyone knows you need to start retroviral therapy after an HIV needle stick. Typically 2 agents are used with low viral loads and 3 agents are used for high viral loads. Interferon-2a therapy may reduce the risk of developing chronic HCV infection, but remains unproven. Plasmapharesis will not be effective in clearing the blood from the virus, and also remember that free floating virus is not the problem anyway

Question 40

Propofol gtt and TGs:

Answer 40

Triglycerides should be checked after two days of continuous propofol use, although it typically takes about a week to develop very high triglycerides.

Question 41

Explain Propofol infusion syndrome:

Answer 41

Pancreatic lipase breaks down triglycerides into free fatty acids that go onto produce a pro-inflammatory response leading to pancreatitis (in about 10% of these patients). Propofol infusion syndrome, is a related concept where propofol induces an inability of mitochondria to utilize fatty acids as a energy source, so that when free glucose and amino acid energy supplies are depleted (common in the critically ill), metabolic needs are initially met with lactic acidosis and eventually when all energy sources are depleted, necrosis develops

Question 42

Which of the following have the least effect on the sphincter of Oddi contraction:

A. Hydromorphone
B. Fentanyl
C. Morphine
D. Meperidine
E. Fentanyl and glucagon

Answer 42

E: Fentanyl and glucagon

Opioids cause constriction of the sphincter of Oddi and therefore is theorized to worsen (and in some animal studies to precipitate) pancreatitis and gall stone retention. In general, meperidine is considered to have the least effect (of those listed) and fentanyl to have a relatively strong effect. In the presence of glucagon, however; opioid’s effect on the sphincter of Oddi is greatly reduced. Mixed antagonist/antagonist opiods such as buprenorphine and various synthetic other opioids (tramadol), have even less effect than meperidine.