GI/Hepatic Flashcards

1
Q

Obese people and butilycholinesterase and ECF

A

Morbidly obese patients have both an increase in butyrylcholinesterase activity and extracellular fluid volume.

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2
Q

Usual dosage of sux:

A

1.0 mg/kg

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3
Q

The pathophysiology of ischemia-reperfusion injury is complex, however one of the mechanisms is thought to be:

A

disruption of the sodium potassium pumps secondary to decreased adenosine triphosphate and glycogen.

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4
Q

Liver transplantation is divided into which 3 phases?

A

Liver transplantation is often divided into three phases – preanhepatic, anhepatic, and neohepatic.

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5
Q

Tell me about the preanhepatic stage:

A

The preanhepatic stage begins with incision and ends with cross-clamping of the major vessels of the liver (portal vein, hepatic artery, inferior vena cava, or hepatic vein).

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6
Q

The anhepatic stage of liver transplantation:

A

The anhepatic stage starts with cross clamping and continues until anastomosis are made and perfusion restarts – in other words from occlusion of vascular inflow to start of graft reperfusion.

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7
Q

The neohepatic stage of liver transplantation:

A

The neohepatic phase begins with unclamping of the portal vein when reperfusion of the donor liver starts and continues during hepatic artery, biliary duct anastomosis, and abdominal closure.

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8
Q

When it comes to liver transplants; what is post reperfusion syndrome? When does it happen?

A

Postreperfusion syndrome typically happens within the first five minutes after reperfusion and consists of systemic hypotension and pulmonary hypertension. although the cause is unknown, electrolytes, acidosis, hypothermia, emboli, and vasoactive substances have all been implicated

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9
Q

Breakdown the reperfusion injury with Na/K+ pumps:

What fails and why? Whats the consequence? What happens to vascular permeability?

A

Depletion of adenosine triphosphate (ATP) and glycogen cause sodium-potassium pump failure which will in turn cause altered ion gradients across the cellular membrane. The consequence is extracellular sodium ions moving into cells leading to swelling. At the same time, vascular permeability is increased since cyclic adenosine monophosphate levels and adenylate cyclase activity is decreased.

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10
Q

What test can you use to know if an end stage liver disease patient is in DIC?

A

Factor VIII activity is helpful in discriminating between these conditions because factor VIII is consumed in DIC and factor VIII (8) levels are normal or elevated in liver disease. Coagulopathy due to end-stage liver disease without concomitant DIC will show a normal or elevated factor VIII level.

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11
Q

What does PTX look like in an intubated patient?

A

Pneumothorax would present with sudden hypoxemia and increased peak inspiratory pressures. If a tension pneumothorax develops, complete cardiovascular collapse may occur.

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12
Q

How does capnothorax look in an intubated patient? what is it? How is it treated?

A

Capnothorax is caused by carbon dioxide diffusion into the intrapleural space. Capnothorax will present with increasing end tidal carbon dioxide concentration and increased mean airway pressure. Capnothorax usually resolves WIThOUT insertion of a chest tube because the carbon dioxide is rapidly absorbed once pneumoperitoneum is released.

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13
Q

When pneumoperitoneum for laparoscopic surgery is intitiated, what happens as far as venous return from compressed blood vessels in splanchnic vasculature?

A

When pneumoperitoneum is initiated, an increase in venous return from compressed blood vessels in the splanchnic vasculature leads to an increased preload and cardiac output.
*KIM that venous return may decrase

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14
Q

CO2 and its effect during laparoscopic surgery. What would a CO2 embolus look like? What would you hear on auscultation of precordium? What about end tidal?

A

Most carbon dioxide that enters the circulation will not cause any effect because it is very soluble and will be excreted through the lungs. Large embolus may occur, presenting as profound hypotension, cyanosis, arrhythmias, and/or asystole. A grinding murmur may be heard on auscultation of the precordium and end-tidal carbon dioxide suddenly increases followed by acute decrease secondary to cardiovascular collapse.

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15
Q

An otherwise healthy patient undergoing laparoscopic surgery under general endotracheal anesthesia develops asystole with abdominal insufflation. Why?

A

Stretching of the peritoneum can result in a big vagal response.

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16
Q

Types of jaundice:

A

pre-hepatic, intra-hepatic, and post-hepatic categories.

17
Q

Causes behind pre-hepatic jaundice:

A

PRE-HEPATIC (MOST COMMON) causes include any increase in unconjugated (indirect) bilirubin and can be from hemolysis or resolution of a hematoma.

Hemolysis can be a consequence of a transfusion reaction or shearing forces placed upon RBCs by intravascular devices such as cardiopulmonary bypass, intra-aortic balloon pump, or extracorporeal membrane oxygenation. Pain, fever, or chills around the time of red blood cell transfusion, coupled with dark urine, suggest a transfusion reaction as the cause of jaundice. Erythrocyte breakdown occurs in patients with internal bleeding and subsequent resorption of the extravasated blood. Surgical trauma patients who have multiple injuries to muscle and soft tissue may be at particular risk

18
Q

Causes behind intra-hepatic jaundice:

A

INTRAHEPATIC — Multiple insults in the perioperative period can lead to hepatocellular or canalicular dysfunction. These include profound and prolonged hypotension, total parenteral nutrition, hypoxia, ischemia, drugs, newly acquired viral hepatitis, and sepsis.

19
Q

Causes of post-hepatic jaundice:

A

POSTHEPATIC — Biliary obstruction related to choledocholithiasis, biliary stricture, or bile leaks are some of the most common causes of postoperative jaundice in patients undergoing abdominal surgery. These patients would present with elevated conjugated (direct) bilirubin levels.