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Anesthesia 101 > ITE GI/Hepatic > Flashcards

ITE GI/Hepatic Flashcards

1
Q

Mechanism of ischemia-reperfusion injury is thought to be d/t ______

A

disruption of sodium potassium pumps secondary to lack of ATP

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2
Q

3 phases of liver transplantation

A
  1. preanhepatic
  2. anhepatic
  3. neohepatic
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3
Q

Preanhepatic stage of liver transplant begins with incision and ends with______

A

cross-clamping of major vessels of liver (portal vein, hepatic a, IVC or hepatic v)

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4
Q

Serum ____ levels are the strongest predictor of perioperative outcomes in pts receiving TPN

A

albumin

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5
Q

Acute _____ during abdominal insufflation may result in a huge vagal response (bradycardia, brady arrhythmias, asystole)

A

stretching of the peritoneum

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6
Q

INR following donor hepatectomy peaks on postop day ___ and returns to normal by day ___. This indicates they at an anticoagulated state compared to others post op.

A

1-3, 5

- risk of epidural hematoma periop

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7
Q

Lipid emulsions are an important component of TPN bc _______ is the predominant energy producing pathway states of stress (sepsis, burns, surgery)

A

lipid oxidation

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8
Q

Nutritional support via enteral or parenteral routes should be given to all pts who are not expected to resume PO intake w/in ____ days post op

A

7 days

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9
Q

Absolute indications for TPN

A
  1. short bowel syndrome
  2. SBO
  3. Active GI bleed
  4. Pseudo obstruction w/ complete intolerance to food
  5. High output enteric cutaneous fistulas
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10
Q

Hepatorenal syndrome in a cirrotic pt w/ ascites has a risk of 40% at 5 years. It is caused by _____

A

portal HTN and resultant reduction in renal perfusion

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11
Q

Type 1 vs Type 2 Hepatorenal syndrome

A

Type 1: acute rapid renal failure w/ precipitating cause (SBP, sepsis, surgery)

Type 2: insidious onset of RF as a result of portal HTN

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12
Q

Portopulmonary HTN definition

A 
pulmonary HTN (25 mmHg at rest, 30 mmHg during exercise) 
in a pt w/ portal HTN w/ no other known cause
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13
Q

Hepatopulmonary syndrome triad

A
  1. Liver dysfunction
  2. unexplained hypoxia
  3. Intrapulmonary vascular dilations (IPVDs)
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14
Q

Plasma albumin has a half life of ___

A

3 weeks
- acute decreases in liver fxn may not cause decrease in serum albumin [ ]

*PTT is a better marker of liver fxn

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15
Q

AST:ALT of ___ is common in alcoholic liver disease and ____ in nonalcoholic steatohepatitis

A

2-4

<1

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16
Q

(AST/ALT) is specific to hepatic origin

A

ALT

- think L for liver

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17
Q

Morbidly obese pts have an increase in _____ and ____, which can decrease the duration of action of succinylcholine and require larger doses

A

butyrylcholinesterase (pseudocholinesterase)

Extracellular fluid volume

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18
Q

Medications that should be calculated based on TBW

A

maintenance gtt of propofol

Succinylcholine

Neostigmine

Sugammadex

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19
Q

Medications that should be calculated based on lean body weight

A

thiopental
induction dose propofol
fentanyl, alfentanil, remifentanyl
Etomidate

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20
Q

Medications that should be calculated based on IBW

A

rocuronium
vecuronium
pancuronium

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21
Q

Advance liver disease, what happens to:

  • platelets
  • VWF
  • coagulation factors
  • PT/INR
A
  • platelets: decrease
  • VWF: increase
  • coagulation factors: decrease (most are synth in liver)
  • INR: increase

*thrombocytopenia is a well known feature of cirrhosis

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22
Q

2,3- DPG levels (increase/decrease) in cirrhotic pts, shifting the hgb dissociation curve to the (right/left)

A

increase

right

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23
Q

Alvimopan is a ____ receptor antagonist that (does/does not) cross the BBB

A

mu-receptor antagonist

  • combats opioid activity in gut
  • allows opioid activity in the CNS
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24
Q

Loperamide is a ____ used to slow gut motility and manage diarrhea

A

mu receptor agonist

- does not penetrate BBB

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25
Q

Why is using lean body weight for med dosing sometimes ideal?

A

It is most correlated to cardiac output

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26
Q

Medications that use total body weigh

A

fentanyl
sufentanil
propofol maintenance
thiopental

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27
Q

Morbidly obese pts have an (increase/decrease) cardiac output

A

increase

- alters elimination and delivery to kidney and liver

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28
Q

Morbidly obese pts have an (increase/decrease) hepatic clearance

A

no change

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29
Q

in the brain, ____ are the primary cell that metabolizes ammonia. These cells convert ammonia to _____, which acts as an osmotic agent, pulling water into the _____, and resulting in cerebral edema

A

astrocytes
glutamine
astrocytes

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30
Q

Acute hepatic encephalopathy is physiologically d/t ______ and ______

A

increase ammonia –> fluid shift -> swelling of the astrocytes –> cerebral edema

profound cerebral vasodilation from loss of autoregulation

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31
Q

Acute liver failure mortality is worse in (hyperacute/acute/subacute) liver failure

A

acute (8-28days) following liver injury

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32
Q

(acidemia/alkalemia) increases the diffusion of ammonia across the BBB and can worsen or precipitate hepatic encephalopathy in pts with chromic liver disease

A

alkalemia

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33
Q

____ is the most common medication used for both prophylaxis and tx of hepatic encephalopathy

A

lactulose

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34
Q

Effects of enteric feeds:

  • Gluconeogenesis
  • lipolysis
  • insulin secretion
A
  • Gluconeogenesis: decrease
  • lipolysis: decreases
  • insulin secretion: increase

*enteric feeds do not enter gluconeogenesis pathway,
whereas non-enteric feeds do enter gluconeogenesis pathway

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35
Q

______ is used by rapidly dividing cells and is a precursor of nucleotides. It is often decreased in states of stress.

A

Glutamine

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36
Q

(Hyper/Hypo)albuminemia leads to small bowel wall edema, which leads to diarrhea and malabsorption.

A

hypoalbuminemia

37
Q

In pts with end stage liver disease, _________ can be useful in identifying the cause of a coagulation disorder

A

Factor VIII

  • consumed in DIC
  • normal or elevated in liver disease
38
Q

Elevated D-Dimer is specific to DIC because _____

A

it indicates activation of both coagulation and fibrinolysis

39
Q

Levels associated with DIC

  • fibrinogen
  • Factor VIII
  • D Dimer
A
  • fibrinogen: low
  • Factor VIII: low
  • D Dimer: high
40
Q

Why are elevated AST/ALT levels (less than 2x normal) elevated in post op period?

A

asymptomatic preop elevations in liver enzymes

Liver disease

Surgery (blood transfusions)

41
Q

Neohepatic stage of liver transplantation

A

reperfusion of the graft through the portal vein

- stage with greatest degree of physiologic derangements

42
Q

Why is the neohepatic stage of liver transplantation associated with the most physiologic derrangements (postreperfusion syndrome)?

A

Large K and H+ load to central circulation
- severe and dangerous cardiac arrhythmias

*aggressively tx with calcium bicarb, insulin

43
Q

Hypocalcemia effects on QRS and PR interval

A

narrow QRS and reduction on PR interval

44
Q

QRS changes seen with marked hypothermia

A

J wave

- notch in downward portion of the R wave

45
Q

Common anesthesia drugs in pts with or high risk for pancreatitis

A

propofol

46
Q

droperidol MOA

aprepitant (emend) MOA

A

antidopaminergic
- prevent PONV

NK1 receptor antagonist

47
Q

Propofol infusion syndrome sx

A
  1. metabolic acidosis
  2. rhabdo
  3. CHF
  4. bradycardia
48
Q

Peripheral TPN can only be administered with a max fluid osm of 750. In order to provide adequate calorites with such low osm, ______ must be used

A

Higher fluid volumes

- not tolerated well in certain populations

49
Q

STOP BANG score identifies pts with ____

A

severe OSA
- 6

Snore
Tired
Observed
Pressure (blood)
BMI >35
Age >50
Neck circ >40
Gender M
50
Q

The __________ is the major regulator of the hepatic blood supply. Represents the ability of hepatic artery to adjust its flow in response to changes in portal venous flow. The major substance for this system is _______

A

hepatic arterial buffer system

adenosine

51
Q

How does adenosine affect portal venous blood flow (more vs less)

A

adenosine

  • less adenosine (good portal v blood flow): hepatic a vasoconstriction
  • More adenosine (poor portal v blood flow): hepatic artery dilation to maintain stable oxygen delivery
52
Q

Explain the RASS system

A

Angiotensinogen is produced by the liver
- converted to Angiotensin I by renin

Angiotensin I is converted to angiotensin II by ACE (lungs)

Angiotensin II is a potent vasoconstrictor and stimulates the secretion of both aldosterone and ADH (salt and water retention)

53
Q

At rest, the liver receives __% of the hearts total cardiac output and __% of the body’s oxygen consumption

A

25%

  • portal vein supplies 75%
  • hepatic a supplies 25%

20%

54
Q

Explain the hepatic arterial buffer response and how it regulates hepatic blood flow

A

A drop in hepatic portal blood flow (PBF) -> adenosine builds up in liver -> hepatic artery dilation -> increase in hepatic arterial blood flow -> increase PBF

55
Q

Leading cause of periop mortality in morbidly obese

A

DVT leading to PE

- consider periop ac

56
Q

Opioid dosing should be based on (TBW/LBW)

A

LBW

- if TBW, concerns for post op opioid induced ventilatory depression

57
Q

Postpyloric feeds decrease the risk of (pneumonia/aspiration)

A

PNA

*does not decrease risk of aspiration

58
Q

Compared to orogastric tubes, NGT are associated with increased risk of ____ and ____ when used for long times

A

sinusitis

otitis media

59
Q

Why does TPN commonly cause jaundice and elevated bili levels in pts?

A

Cholestasis and biliary sludge

- Poss cellular necrosis

60
Q

3 main categories of post-op jaundice

A
  1. overproduction or underexcretion of bilirubin
  2. direct hepatocellular injury
  3. extrahepatic obstruction
61
Q

Common causes of overproduction of bilirubin

A
  1. hemolysis from blood transfusions (10% of RBCs transfused)
  2. hematoma reabsorption
  3. drug associated hemolysis
62
Q

Most common periop drugs implicated in immune related hemolytic anemia

A

acetaminophen, insulin

63
Q

Crigler-Najar is a form of severe (conjugated/unconjugated) hyperbilirubinemia, and is diagnosed (early/later) on in life

A

unconjugated (indirect)

early

64
Q

Gilbert syndrome is an inherited autosomal dominant (conjugated/unconjugated) hyperbilirubinemia, where the primary defect is the _____ enzyme, which is responsible for conjugation of bilirubin. Bilirubin levels are usually below ___ mg/dL

A

unconjugated (indirect)

glucuronosyltransferase

5

65
Q

Safe anesthetic drug to use in pts at high risk of hepatic encephalopathy.

A

Propofol

  • minimally affects hepatic blood flow and oxygenation
  • allows a more rapid and predictable emergence form anesthesia
66
Q

TIPS procedure, the shunt is being placed between ____ and ____ circulations

A

portal, systemic

- effectively bypassing liver and the filtration it provides

67
Q

dexmedetomidine is metabolized by the ____.

A

liver

  • severe liver failure decreases clearance and prolongs therapeutic effect
  • may mask hepatic encephalopathy in pts at high risk
68
Q

Best marker for hepatic synthetic function

Most sensitive marker of hepatic dysfunction <24h

A

albumin (synth by liver)

PT

69
Q

Clotting factors in the extrinsic pathway and Vit K dependent clotting factors II, VII, IX, and X can be assessed with _____

A

PT

70
Q

(Prehepatic/Posthepatic) jaundice will show elevated unconjugated (indirect) hyperbilirubinemia

A

Prehepatic: increase unconjugated (indirect) bili

Posthepatic: inc conjugated (direct) bili

71
Q

Pts with Small bowel obstruction should have ____ placed prior to induction of anesthesia.

A

NGT awake pt

  • Decompress full stomach
  • risk of aspiration
72
Q

Nitrous oxide is contraindicated in SBO because _____

A

it causes distention of bowel by diffusing into air-filled spaces faster than nitrogen diffuses out
- 34x more soluble in blood than nitrogen

73
Q

Why is metoclopramide contraindicated in SBO even though it is an anti nausea medication?

A

Risk of bowel perf

Dopamine antagonist

  • increases gastric emptying
  • pro-motility agent
  • inc peristalsis
74
Q

The liver receives ___% of

total cardiac output

A

20-30%

75
Q

The hepatic artery provides __% of the blood flow to the liver, but __% of the oxygen supply to the liver.

The portal vein provides __% of the blood flow to the liver, but __% of the oxygen supply.

A

25%, 50%

75%, 50%

76
Q

Hepatic arterial buffer response (HABR)

- When the flow in the portal vein decreases, adenosine (increases/decreases)

A

increases
- Adenosine will accumulate -> decreases hepatic arteriolar resistance -> increase hepatic artery blood flow -> increases delivery of oxygenated blood via hepatic a.

  • HABR reaches its max effect when hepatic arterial flow is doubled.
  • adenosine is a rapidly metabolized vasodilating agent
77
Q

Hepatic arterial buffer response (HABR)

- When the flow in the portal vein increases, adenosine (increases/decreases)

A

decreases
- adenosine will be washed out from periportal regions -> increase hepatic arteriolar resistance and decrease hepatic arterial flow

  • adenosine is a rapidly metabolized vasodilating agent
78
Q

Which one carries more oxygenated blood to the liver, hepatic artery or portal vein?

A

Hepatic artery

79
Q

Things other than flow that affect the Hepatic arterial buffer response (HABR)

A
  1. oxygen tension
  2. pH (acid base status)
  3. stretch receptors and smooth muscle cells w/in hepatic vasculature
80
Q

Inhaled anesthetic most likely to cause liver injury?

A

Halothane and Chloroform

81
Q

Though rare, how do these gases cause liver injury?

  • Isoflurane
  • Desflurane
  • Sevoflurane
A
  • Isoflurane: production of reactive intermediates
  • Desflurane: Trifluoroacetic acid (TFA) reactive intermediates -> form immunogenic compounds
  • Sevoflurane: very low. Hexafluoroisopropanol (HFIP) -> does not accumulate and rapidly undergoes phase II biotransformation
82
Q

(Hyper/Hypo)magnesemia is associated with citrate intoxication

A

Hypomagnesemia

- Citrate chelates BOTH calcium and magnesium

83
Q

Two major types of postop liver injuries

A
  1. Mild injury from halogenated anesthetic

2. Immune mediated severe acute hepatitis w/ widespread necrosis

84
Q

Markers of cholestasis (3)

A
  1. 5’-nucleotidase
  2. y-glutamyl transpeptidase
  3. alk phos
    - nonspecific for hepatobiliary disease, may be derived from bone
85
Q

Alcoholic liver disease liver ratio

A

AST:ALT
2:4

86
Q

Why is PTT or INR a better marker of liver synthetic function?

A

bc of the short life of factor VII (4 hours)

  • The prothrombin test specifically evaluates the presence of factors VII, V, and X, prothrombin, and fibrinogen
87
Q

The (PTT) specifically evaluates the presence of factors _____

A

Factors XII, XI, IX, VIII

- intrinsic

88
Q

PT vs PTT, which one measures the integrity of the intrinsic and extrinsic system?

A

PT: extrinsic
PTT: intrinsic

89
Q

The prothrombin test (PTT) specifically evaluates the presence of factors _____

A

VII, V, and X, prothrombin, and fibrinogen
- extrinsic

*A prolonged prothrombin time (PT) indicates a deficiency in any of factors

Anesthesia 101 (38 decks)

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