Intermediate: GI Flashcards
How do NSAIDs lead to ulcers?
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.
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
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.
Diarrhea ABG (acute) Oversimplification of gap and non Gap What type of non gap acidosis has increased K?
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.
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
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!
T/F
Cholinergics like neostigmine (parasympathetic: rest & digest) increase the strength of LES contraction while anicholinergics do the opposite.
True
Which meds reduce LES tone?
Other medications that reduce LES tone are:Volatile anesthetics, opioids, propofol, thiopental, some B-blockers, tricyclic antidepressants, glucagon
What do these do to LES tone?
propranolol, H2 antagonists, non depolarizing muscle relaxants
propranolol, H2 antagonists, non depolarizing muscle relaxants
Nothing!!
NPO guidelines
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.
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)
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.
Hi premeds-do they prevent aspiration? What about bicitra and h2 blockers for pH? Metoclopramide and gastric volume?
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
Can NGT prevent aspiration?
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.
LMA has been shown to do what to LES and pH?
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.
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
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.
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
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.
Which clotting factors are NOT made in the liver? Explain weird wording about factor 8
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!
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
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.
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)
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.
What measurements are a part of the child Pugh score?
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
What does meld score use?
The MELD score only utilizes laboratory data (bilirubin, creatinine, and INR).
Can hepatic encephalopathy occur with normal plasma ammonia level?
It can, but it’s rare
Hepatopulmonary syndrome? And how can you know if it’s a shunt?
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
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
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.
ORAL BOARDS ALERT!
Explain hepatorenal syndrome. Does giving volume help?
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.
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:
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.”
