GI/Hepatic Flashcards
(39 cards)
when can Peripheral Parenteral Nutrition be given? What are the indications (absolute) and relative indications for TPN?
Solutions with osmolarity greater than 750 mOsm/L cannot be given peripherally. Hence, PPN must be administered in much higher volumes at a lower osmolarity. The use of PPN also requires constant checking of the intravenous sites for any signs of phlebitis or extravasation. So people with heart failure shouldn’t get PPN bc it requires higher volumes. Absolute indications for TPN Short bowel syndrome Small bowel obstruction Active gastrointestinal bleeding Pseudo-obstruction with complete intolerance to food High-output enteric-cutaneous fistulas (unless a feeding tube can be passed distal to the fistula) Relative indications for TPN Non-healing moderate-output enteric-cutaneous fistulas Need for bowel rest such as during acute radiation enteritis and inflammatory bowel disease (IBD) flare-ups Intra-abdominal sepsis leading to ileus and abdominal distention Chylothorax unresponsive to a medium-chain triglyceride diet Other situations when the enteral route does not provide adequate nutrition
what serum level has the highest prediction value for perioperative outcomes for patients on TPN?
albumin
patient has surgery. how much elevation does AST/ALT need to happen for further investigation/concern?
>2x normal
GGT can be elevated with what disease processes?
liver, kidney, and heart dz
what are risk factors for postoperative liver dysfunction?
Postoperative hepatic dysfunction can be due to a variety of causes including asymptomatic preoperative elevations in liver enzymes, liver disease such as hepatitis or cirrhosis, and surgical factors including blood transfusion(abdominal surgeries -stomach, liver, biliary tract and heart surgery). If AST and ALT are elevated greater than two times the normal limit and sustained elevation occurs, further investigation is warranted.
Can TPN affect bilirubin?
Total parenteral nutrition (TPN) is a common cause of jaundice in patients, mostly due to cholestasis and biliary sludge, but also possibly due to cellular necrosis. About a third of acutely ill patients in the ICU have been seen to have elevations in bilirubin.
what is crigler-najjar syndrome?
Crigler-Najjar is a rare hereditary form of severe unconjugated hyperbilirubinemia that is diagnosed in the first few days of life, and definitive treatment is liver transplantation.
what is Gilbert’s syndrome?
Gilbert syndrome is a type of inherited autosomal dominant unconjugated hyperbilirubinemia. The primary defect is in the glucuronosyltransferase enzyme which is responsible for the conjugation of bilirubin. Bilirubin levels are usually below 5 mg/dL but can increase two to threefold with fasting, illness or stress. In this patient with no prior history of jaundice, Gilbert syndrome is an unlikely cause as she most likely would have known about this syndrome.
elemental tube feeds are bad and increase length of stay and mortality?
true
what alterations occurs to fat mass, lean body weight, cardiac output, and extracellular volume in obesity?
Alterations of medication dosing in morbidly obese patients must take into account the physiologic changes that accompany the disease. Most important are an increase in the fat mass, lean body weight, extracellular fluid volume, and cardiac output.
how much blood flow does the liver receive?
At rest, the liver receives about 25% of the heart’s total cardiac output and uses about 20% of the body’s oxygen consumption. The portal vein, acting as a capacitance vessel, supplies about 75% of the blood while the hepatic artery supplies the remaining 25%. The hepatic artery and the portal vein each provide about half of its oxygen supply.
how does the hepatic arterial buffer response work?
The hepatic arterial buffer response (HABR) is the main regulator of hepatic blood flow (HBF). With this system, a drop in hepatic portal venous flow (PBF) causes a subsequent increase in hepatic arterial blood flow, and an increase in PBF causes a decrease in hepatic artery blood flow. When PBF decreases, adenosine builds up in the liver causing hepatic artery dilation. Conversely, when PBF increases, adenosine is washed out causing the arterial constriction and continued constant HBF. If the portal venous flow decreases by more than 50%, the HABR may be unable to fully compensate and HBF may decrease. Factors reducing HBF include hypotension, decreased cardiac output, angiotensin II, pain, hypoxemia, and various anesthetics.
what does volatile agents do to hepatic blood flow?
Propofol has been shown in experimental and human studies to increase hepatic blow flow and may have a beneficial effect on ischemic-reperfusion injury in patients undergoing liver surgery. Sevoflurane, isoflurane, and desflurane all decrease HBF by means of reduced cardiac output. Of these three, none have clearly been shown to be superior to the others in preserving HBF, although all three are better than enflurane and halothane. Some research has shown sevoflurane to have an ischemic-preconditioning effect on the liver similar to its effect on the heart. Xenon does not alter hepatic artery blood flow and may have no effect on HBF.
you are trying to decide if coagulopathy is due to DIC vs ESLD..what factor should you look at?
Coagulation test results in patients with severe liver disease may be similar to those in patients with DIC, although D-dimer levels may not be as high and platelet counts not as low. Factor VIII activity is helpful in discriminating between these conditions because factor VIII is consumed in DIC and factor VIII levels are normal or elevated in liver disease. So, unlike D-dimer and platelet count, factor VIII levels will not change in the same direction with these two disorders.
what is the half life of plasma albumin?
what is a good marker of liver disease?
Plasma albumin has a half-life of nearly 3 weeks. Because of this, acute decreases in liver synthetic function may not cause a decrease in serum albumin concentration for at least a few days. In addition, serum albumin may decrease due to conditions other than a poor hepatic synthetic function (e.g. renal losses).
On the other hand, prothrombin time (or INR) is a better marker of liver synthetic function and can provide timely information because of the short life of factor VII (approx 4 hours). Furthermore, prothrombin time provides prognostic information as well (together with the serum bilirubin and creatinine levels, it is used to calculate the MELD score).
what is the leading cause of perioperative mortality in the morbidly obese/
Bottom Line: The leading cause of perioperative mortality in the morbidly obese population is deep vein thrombosis leading to a pulmonary embolism.
what is STOP_BANG?
TrueLearn Insight : A STOP-BANG score of 4 has a sensitivity of 88% for identifying patients with severe OSA. Increasing the cutoff threshold to 6 increases the specificity for severe OSA, but with a lower sensitivity.
S = Snore – do you snore loud? T = Tired – do you feel tired no matter how many hours of sleep you get? O = Observed – have others observed you stop breathing during sleep? P = Pressure – are you being treated for high blood pressure? B = BMI – is your body mass index \> 35 kg/m2 A = Age – are you older than 50? N = Neck circumference – is the neck circumference \> 40 cm? G = Gender – is the patient a male?
is OSA associated with postoperative morbidity or mortality?
morbidity
how does acute liver failure cause hepatic encephalopathy?
Acute liver failure is defined as the presence of hepatic encephalopathy following a liver injury and can occur both in patients with and without underlying chronic liver disease. The primary cause of this encephalopathy is cerebral edema resulting from the conversion of ammonia to osmotically active glutamine within cerebral astrocytes, resulting in a fluid shift into the brain. Treatment is primarily supportive and is centered on decreasing the amount of circulating ammonia in the body.
you have a morbidly obese patient…should you dose opioids based on total or lean body weight?
lean body weight for opioids
what are reasons for postoperative jaundice?
PRE-HEPATIC 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.
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.
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.
what is the amplitude and frequency of the eeg during general anesthesia? what happens to the emg?
With increasing levels of anesthesia, there is a transition from the low-amplitude high-frequency pattern of wakefulness, to the high-amplitude slow-frequency EEG of NREM sleep.
minimal motor activity on EMG
what is the GCS?
what is congenital myasthenic syndrome?
Congenital myasthenic syndrome (CMS) is a set of rare genetically inherited disorders. Perioperative management needs to be developed on a case-by-case basis since they are not all the same. It is imperative to know the type and what protein or signaling pathway is defective to tailor treatment. CMS are not similar to other myasthenic like syndromes (Myasthenia gravis and lambert eaton which involve antibodies) and thus treatment is different.
