GI/Hepatic

Question 1

when can Peripheral Parenteral Nutrition be given? What are the indications (absolute) and relative indications for TPN?

Answer 1

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

Question 2

what serum level has the highest prediction value for perioperative outcomes for patients on TPN?

Answer 2

albumin

Question 3

patient has surgery. how much elevation does AST/ALT need to happen for further investigation/concern?

Answer 3

>2x normal

Question 4

GGT can be elevated with what disease processes?

Answer 4

liver, kidney, and heart dz

Question 5

what are risk factors for postoperative liver dysfunction?

Answer 5

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.

Question 6

Can TPN affect bilirubin?

Answer 6

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.

Question 7

what is crigler-najjar syndrome?

Answer 7

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.

Question 8

what is Gilbert’s syndrome?

Answer 8

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.

Question 9

elemental tube feeds are bad and increase length of stay and mortality?

Answer 9

true

Question 10

what alterations occurs to fat mass, lean body weight, cardiac output, and extracellular volume in obesity?

Answer 10

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.

Question 11

how much blood flow does the liver receive?

Answer 11

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.

Question 12

how does the hepatic arterial buffer response work?

Answer 12

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.

Question 13

what does volatile agents do to hepatic blood flow?

Answer 13

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.

Question 14

you are trying to decide if coagulopathy is due to DIC vs ESLD..what factor should you look at?

Answer 14

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.

Question 15

what is the half life of plasma albumin?

what is a good marker of liver disease?

Answer 15

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).

Question 16

what is the leading cause of perioperative mortality in the morbidly obese/

Answer 16

Bottom Line: The leading cause of perioperative mortality in the morbidly obese population is deep vein thrombosis leading to a pulmonary embolism.

Question 17

what is STOP_BANG?

Answer 17

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?

Question 18

is OSA associated with postoperative morbidity or mortality?

Answer 18

morbidity

Question 19

how does acute liver failure cause hepatic encephalopathy?

Answer 19

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.

Question 20

you have a morbidly obese patient…should you dose opioids based on total or lean body weight?

Answer 20

lean body weight for opioids

Question 21

what are reasons for postoperative jaundice?

Answer 21

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.

Question 22

what is the amplitude and frequency of the eeg during general anesthesia? what happens to the emg?

Answer 22

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

Question 23

what is the GCS?

Answer 23

Question 24

what is congenital myasthenic syndrome?

Answer 24

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.

Question 25

what is the neurotransmitter, receptor and response (hyperpolarization vs depolarization) for parasympathetic stimulation of heart?

Answer 25

Question 26

what are unique features of the parasympathetic pathway? long pre or post ganglion?

Answer 26

The autonomic nervous system is divided into two subsystems: the parasympathetic nervous system and the sympathetic nervous system. The parasympathetic nervous system is associated with the maintenance needs of the body, including gastrointestinal and genitourinary function, although it has several roles beyond that systemically. The parasympathetic system originates from cranial nerves in the midbrain and medulla (cranial nerves III, VII, IX, and X) as well as the sacral region (segments 2 through 4). Approximately 75% of all parasympathetic activity is transmitted via the vagus nerve (cranial nerve X), including fibers to the heart, tracheobronchial tree, spleen, kidney, liver, and gastrointestinal tract with the exception of the distal colon and rectum. The structure of the parasympathetic system consists of long preganglionic neurons that synapse with short postganglionic neurons in ganglia that are near or within the tissues being targeted. The postganglionic neurons then project short distances onto tissues. This differs from the sympathetic system, in which pre- and postganglionic nerves synapse in ganglia adjacent to the spinal cord.

Acetylcholine is the neurotransmitter utilized by the parasympathetic system at both pre- and postganglionic receptors, thus the nerves in the parasympathetic system are referred to as “cholinergic.” There are two classes of receptors utilized in the parasympathetic system: muscarinic and nicotinic. Muscarinic receptors are G-protein-coupled and there are five subtypes (M1-M5). Muscarinic receptors are present on peripheral visceral organs (i.e. gastrointestinal tract) and the heart, blood vessels, bronchial tree, eye, urinary bladder (detrusor, trigone, and sphincter), and salivary and sweat glands. Given the protein-coupled nature of muscarinic receptors, their activation causes a cascade that takes place over several seconds to minutes and also persists for several seconds to minutes. Nicotinic receptors are ligand-gated ion channels found in both the parasympathetic and sympathetic ganglia, as well as at the neuromuscular junction of skeletal muscle. While acetylcholine acts indeterminately on the two types of receptors, antagonists can be used to specifically target muscarinic or nicotinic receptors.

Question 27

should high dose steroids be given in TBI?

Answer 27

no. shown to increase mortality

Question 28

what is the most cost effective, accurate and reliable way to monitor ICP?

Answer 28

ventriculostomy catheter

Question 29

An intubated 19-year-old man with a traumatic brain injury suddenly suffers an acute increase in intracranial pressure. Which of the following is the BESTinitial treatment option?

Answer 29

increase respiratory rate

Question 30

hich of the following is MOST LIKELY responsible for the ST-T changes observed on ECG after subarachnoid hemorrhage?

Answer 30

catecholamine release causing subendocardial ischemia

Question 31

what is hypokalemic periodic paralysis? what would cause it? what is the inheritance pattern?

Answer 31

Hypokalemic periodic paralysis is a muscle membrane channelopathy characterized by transient episodes of weakness in the limbs and trunk, typically sparing the respiratory muscles. Attacks are precipitated by a fall in serum potassium that can be produced by strenuous exercise, ingestion of carbohydrates, sodium rich foods, or the infusion of glucose and insulin.

The condition is caused by an autosomal dominant mutation in two skeletal muscle membrane cation channels. Hypokalemic periodic paralysis is the most common form of periodic paralysis.

Potassium supplementation can alleviate or shorten attacks.

The condition is diagnosed by EMG, muscle biopsy, and DNA testing. Treatment revolves around avoidance of precipitants. Patients should eat small, regular meals with low carbohydrate content. Some may take oral potassium to alleviate or shorten attacks.

Question 32

Which of the following perioperative interventions is MOST likely to decrease the incidence of hoarseness following cervical spine surgery?

Question 33

what should map be held at for neuro (spinal) shock?

anesthetic management?

Answer 33

It is recommended that mean arterial pressure be maintained greater than 85 mmHg for the first seven days following injury.

When emergency surgery is required following spinal cord injury, anesthetic management can alter outcomes. Often outcome is improved when mean arterial blood pressure is maintained greater than 85 mmHg and arterial oxygen tension is above 100 mmHg. Additionally, normoglycemia and oxygen delivery should be optimized.

Question 34

A 19-year-old woman with a history of anxiety and depression presents for urgent open reduction and internal fixation of a distal radius fracture sustained following a ground-level fall without evidence of head trauma. On arrival, the patient is hyperthermic, tachycardic, hypertensive, and is clenching her jaw. She is apparently disinhibited, is adamant that she is in no pain, and there is a concern for drug intoxication. Which of the following agents is MOST LIKELY to be found on this patient’s urine toxicology screen?

Answer 34

3,4-Methylenedioxymethamphetamine (MDMA), also known as “ecstasy”, is a commonly abused party drug that has no clear medical indication. MDMA interacts with the serotonergic and dopaminergic transport systems, resulting in increased concentrations of both of these neurotransmitters within their relevant synaptic junctions. When combined with a serotonin reuptake inhibitor which is first-line for the treatment of anxiety and depression, this drug can cause a potentially fatal serotonin syndrome that presents as hypertension, hyperthermia, and tachycardia.

Question 35

mac effects of acute alcohol intoxication?

chronic alcohol intoxication?

Answer 35

Alcohol has well documented and described chronic and acute effects. Patients with alcoholism can be at risk for delirium tremens, which results from the life-threatening withdrawal of the GABA-agonism that alcohol provides. This acute withdrawal can result in autonomic instability and potentially fatal seizure activity. These patients also tend to have a host of hepatic and cardiac disease related to their alcohol abuse. Acute intoxication with alcohol can have a similar effect on an anesthetic as benzodiazepines and a lower MAC requirement, keeping in mind that the patient likely has a full stomach following alcohol ingestion. Chronic alcohol abuse without acute intoxication may cause an increased anesthetic requirement.

Question 36

what are effects (MOA) of cocaine?

what are effects of amphetamines?

Answer 36

Cocaine is among the most common illicit substance in drug-related deaths (not including alcohol and opioids) and accounts for around 30% of drug-related emergency room admissions. Cocaine acts by inhibiting the reuptake of serotonin, norepinephrine, and dopamine, and consequently can cause an increase in blood pressure, heart rate, and body temperature. If cocaine toxicity is suspected in the perioperative period, it is essential that alpha-adrenergic blockade is instituted prior to beta-adrenergic blockade given the risk of precipitating a life-threatening hypertensive crisis. Amphetamines have a similar clinical effect as cocaine, and consequently should be treated similarly if acute intoxication is suspected in the perioperative period. MDMA is a form of amphetamine that is described above. All of these agents will tend to increase anesthetic requirements around the time of surgery in addition to their other effects.

Question 37

tell me about myasthenia gravis? sensitive to ndnmb and succinylcholine?

tell me about lambert eaton?

Answer 37

Myasthenia gravis is caused by antibodies against acetylcholine receptor (80%) or a receptor-associated protein, muscle-specific tyrosine kinase (MuSK-Ab) (10%). It worsens with exercise, muscle pain is uncommon, deep tendon reflexes are normal, and autonomic instability is not a feature. Most commonly it starts as ocular or bulbar weakness although when it progresses it can involve the limbs (mostly arms). Patients are very sensitive to nondepolarizing neuromuscular blocking agents but resistant to succinylcholine. All in all, a low preoperative vital capacity (often defined as < 2.9 L) has been one of the factors most strongly associated with the need for postoperative mechanical ventilation, whereas the predictive ability of factors like disease duration or pyridostigmine dosage has been inconsistent across studies.

Lambert-Eaton myasthenic syndrome (LEMS) is caused by antibodies against P/Q-type voltage-gated calcium channels. It improves with exercise, muscle pain is common, has decreased deep tendon reflexes, and autonomic dysfunction. Most commonly it starts as weakness in proximal legs, although it can sometimes involve bulbar muscles (and rarely ocular muscles). Patients are very sensitive to both non-depolarizing neuromuscular blocking agents and succinylcholine. Mnemonic: lambs are sensitive animals.