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SRNA3CoExisting > Liver, GI, and Biliary Diseases > Flashcards

Liver, GI, and Biliary Diseases Flashcards

1
Q

• Liver receives

A

25 -30% of the cardiac output

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2
Q

The Hepatic plexus is innervated by:

A

Sympathetic nerve fibers from T6-T11

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3
Q

Parasympathetic fibers from the

A

right and left vagus and right phrenic nerves.

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4
Q

Blood-cleansing function

A

(Kupffer Cells).

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5
Q

Major Physiologic Functions of the Liver

A
  1. Blood reservoir (up to 300 mls).
  2. Blood-cleansing function (Kupffer Cells).
  3. Metabolic functions
    • Metabolism of fat, carbohydrates, and
    proteins
  4. Drug metabolism
    • Production of plasma proteins, albumin,
    and plasma cholinesterases
  5. Bile formation/excretion
  6. Bilirubin Excretion
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6
Q

Check for liver function

A

PT/INR

Bilirubin

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7
Q

ALT

A

Does not measure liver function

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8
Q

Total bilirubin normal

A

<1mg/dl
>3mg scleral icterus
>4 mg overt jaundice

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9
Q

Alanine aminotransferase (ALT) is a

A

cytoplasmic enzyme highly specific to the liver.

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10
Q

Aspartate aminotransferase (AST) is an

A

enzyme that exists in hepatic and extrahepatic tissues

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11
Q

Most important enzymes

A

ALT

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12
Q
  • When both liver enzymes are elevated, ALT/AST ratio is considered:
  • < 1 =
A

nonalcoholic steato-hepatitis (NASH) (non-alcohol fatty liver)

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13
Q

• When both liver enzymes are elevated, ALT/AST ratio is considered:• 2 to 4 =

A

alcoholic liver disease

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14
Q

Portal vein is

A

Bigger than portal artery

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15
Q

Albumin • Synthesized

A

exclusively by hepatocytes

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16
Q

Severe impairment of the synthetic

A

capacity of the liver

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17
Q

• INR•

A

Correlated to liver dysfunction • Reliable predictive value for survival of patients c/ liver disease
• Impairment of the hepatic synthetic function of coagulation factors.

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18
Q

Direct correlation with liver dysfunction

A

INR

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19
Q

Risk for surgery

A

Screen INR

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20
Q

Acute Cholecystitis

A

Obstruction of the cystic duct or common bile duct by a

gallstone causes acute inflammation of the gall bladder

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21
Q

90% of gallstones are composed of

A

cholesterol, due to “Western diet”

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22
Q

Signs and symptoms of Acute cholecystitis

A
  • Nausea and vomiting
  • Fever
  • Abdominal pain
  • RUQ tenderness
• Severe mid-epigastric pain that moves to the RUQ and
radiates to the back = biliary colic
• Murphy’s sign
• Dark urine
• Scleral icterus
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23
Q

Treatment of Acute Cholecystitis

A
  • IV fluids, opioids for pain, antibiotics for leukocytosis
  • Laparoscopic cholecystectomy
  • 5% of “lap choles” convert to open because inflammation obscures the anatomy
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24
Q

Anesthesia considerations Immediate ↓ in venous return and cardiac output ➔ ↑ MAP and systemic vascular
resistance
• Opioid induced sphincter of Oddi spasm occurs in less than 3% of patients
• Treated c/ glucagon, naloxone, or nitroglycerin

A

• Insufflation ➔ ↑ intra-abdominal pressure ➔interferes c/ ventilation and venous return, can result in bradycardia (glycopyrrolate vs atropine)

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25
Q

Anesthesia considerations Insufflation

A

• Insufflation ➔ ↑ intra-abdominal pressure ➔interferes c/ ventilation and venous return, can result in bradycardia (glycopyrrolate vs atropine)

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26
Q

Anesthesia considerations:• Reverse Trendelenburg

A

can help c/ BP and SVR

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27
Q

Anesthesia considerations: Opioid induced

A

sphincter of Oddi spasm occurs in less than 3% of patient

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28
Q

Sphincter of Oddi spasms treated with

A

Treated c/ glucagon, naloxone, or nitroglycerin

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29
Q

Choledocholithiasis

A

Gallstones present in the common bile
duct• Signs and symptoms: cholangitis • Fever, shaking chills, jaundice, RUQ pain • Serum bilirubin and alkaline phosphatase
are sharply ↑ (distinguishing this
condition from ureterolithiasis and acute
intermittent porphyria)

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30
Q

Choledocholithiasis

A

Gallstones present in the common bile duct•

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31
Q

Choledocholithiasis Signs and symptoms:

A

cholangitis • Fever, shaking chills, jaundice, RUQ pain •

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32
Q

Biliary colic

A

Pain moves from mid-epigastric

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33
Q

Bilirubin and alk phosp

A

Serum bilirubin and alkaline phosphatase are sharply ↑ (distinguishing this condition from ureterolithiasis and acute intermittent porphyria)

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34
Q

WHat is Hepatitis?

A

Acute inflammation or swelling of the liver

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35
Q

Causes of Hepatitis

A

Causes: virus, drugs, or toxins

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36
Q

If unable to retract gallbladder due to ______

A

enlarged liver

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37
Q

Viral hepatitis:

A

A, B, C, D, E, Epstein-Barr virus, Cytomegalovirus

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38
Q

What about Hep C?

A

is the most virulent ➔ chronic hepatitis (40%) and cirrhosis ➔ endstage liver disease requiring liver transplantation

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39
Q

Meds that can cause Hepatitis

A

• Analgesics, anticonvulsants, antibiotics, antihypertensives, etc.

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40
Q

Acetaminophen overdose occurs when glutathione stores are

A

insufficient to conjugate toxic metabolites of the drug

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41
Q

CO2 in diaphragm

A

Shoulder pain

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42
Q

Ischemia in closed system

A

Compartment syndrome

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43
Q

Normal intraabdominal pressure

A

<15 mmHg

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44
Q

Increase Abdominal pressure

A

Bradycardia due to Vagal response

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45
Q

S/Sx:

A

dark urine, fatigue, anorexia, nausea, fever, emesis,

headache, abdominal discomfort, light-colored stools, pruritus

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46
Q

Enzyme MOST indicative of liver damage

A

ALT

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47
Q

If patient gets bradycardic

A

Tell surgeon

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48
Q

Cardiac thump

A

Hit chest or glucagon

Give epi

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49
Q

Dose of glucagon for spasm of sphincter oddi

A

1mg IVP

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50
Q

Acute Hepatitis
Anesthesia Considerations
•

A

Volatile gases produce mild, self-limiting postoperative liver dysfunction related to alterations in hepatic oxygen supply
• α glutathione-S-transferase (sensitive marker for hepatocellular damage) ↑ transiently after administration of isoflurane, desflurane, and sevoflurane

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51
Q

Acute Hepatitis

Anesthesia Considerations

A

• Vasoactive drugs can cause splanchnic
vasoconstriction leading to inadequate hepatic BF
and impaired hepatocyte oxygenation

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52
Q

Hepatitis (acute) ;One unit of PRBC =

A

250 mg of bilirubin, which can overwhelm someone c/ hepatic disease

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53
Q

Stent for choledocholithiasis

A

Need to be removed

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54
Q

Choledocholithiasis –>

A

NEVER DO MAC

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55
Q

Immune-Mediated Hepatotoxicity

Administration of volatile anesthetics (especially halothane) leads to

A

immune-mediated hepatotoxicity (IgG)

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56
Q

Immune-Mediated Hepatotoxicity

Administration of volatile anesthetics (especially halothane) leads to

A

immune-mediated hepatotoxicity (IgG)

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57
Q

Fluorinated volatile anesthetics (enflurane, isoflurane, and desflurane) form

A

trifluoroacetylated metabolites, which have a cross sensitivity c/ halothane; sevoflurane does NOT have this property.

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58
Q

Fluorinated volatile anesthetics (enflurane, isoflurane, and desflurane) form

A

trifluoroacetylated metabolites, which have a cross sensitivity c/ halothane; **sevoflurane does NOT have this property

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59
Q

Cirrhosis

• Definitive diagnosis: Percutaneous liver biopsy

A

• Excessive chronic alcohol ingestion, chronic viral
hepatitis, or a variety of other progressive liver
diseases ➔ Scarring of the liver

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60
Q

Scarring of the liver leads to

A

➔Disruption of normal liver architecture and

parenchymal nodules are regenerated

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61
Q

Symptoms Cirrhosis :

A

fatigue, malaise, palmar erythema, spider angiomata, gynecomastia,
testicular atrophy, portal hypertension,

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62
Q

Symptoms Cirrhosis :

A

fatigue, malaise, palmar erythema, spider angiomata, gynecomastia, testicular atrophy, portal hypertension,

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63
Q

Light colored stools in Hepatitis Why?

A

Because of the bilirubin

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64
Q

Viral Hepatitis leading to chronic liver diseases

A

Hepatitis C

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65
Q

Hepatitis Co infection B

A

B and D

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66
Q

Hepatitis CO infection C and

A

E

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67
Q

Complications of Cirrhosis : Portal hypertension

A

Portal hypertension (combined c/ hypoalbuminemia and ↑
ADH → ascites) = hallmark of end-stage cirrhosis, leads to
extensive collateral circulation
• Fibrotic degeneration in liver ↑ resistance to BF
• Propranolol ↓ portal venous pressure
—> Gastroesophageal varices (accounts for 1/3 of deaths due to cirrhosis)

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68
Q

After administration of Iso, des and sevo

A

Alpha glutathione-S elevated

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69
Q

Vasoactive drugs leads to

A

Hepatic artery vasoconstriction ( do not vasoconstrict too much )

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70
Q

Hallmark of end-stage cirrhosis, leads to extensive collateral circulation

A 
Portal hypertension (combined c/ hypoalbuminemia and ↑
ADH → ascites)
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71
Q

When anesthetic metabolized

A

TFA–? Go to surface cell of liver and covalently attached to liver cell, body sees as antigen

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72
Q

*****When anesthetic metabolized how they cause TFA?

A

***TFA– Go to surface cell of liver and covalently attached to liver cell, body sees as antigen

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73
Q

Hepatorenal syndrome

A

renal failure associated c/ severe liver disease due to hypovolemia and reduced renal blood flow

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74
Q

Liver can

A

Regenerate

***scar tissue

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75
Q

Complications of Cirrhosis

4. Hyperdynamic circulation:

A

↑ cardiac output (peripheral and splanchnic vasodilation via prostaglandins and interleukins), ↑ intravascular fluid
volume, ↓ blood viscosity, arteriovenous communications

76
Q

Comlications of Hyperdynamic circulation:

A

↑ cardiac output (peripheral and splanchnic vasodilation via prostaglandins and interleukins), ↑ intravascular fluid
volume, ↓ blood viscosity, arteriovenous communications

77
Q

Thrombocytopenia with cirrhosis is because of

A

Spleen –> Eats platelets and store

78
Q

Definitive Dx of cirrhosis

A

Percutaneous liver biopsy

79
Q

Complications of Cirrhosis : Hepatopulmonary syndrome:

A

significant intrapulmonary shunting and V/Q mismatch

80
Q

Cirrhosis Complications Portopulmonary hypertension:

A

co- existing portal vein and pulmonary artery hypertension

81
Q

Complications of Cirrhosis 8-10

A

8.Hypoglycemia (↓ glycogen storage)
9. Impaired immune defense
10. Hepatic encephalopathy
• Made worse by transjugular intrahepatic portosystemic shunt placement (TIPS) 35%
• Restrict protein

82
Q

To decrease portal venous pressure beta blocker

A

Propranolol

83
Q

Complications of Cirrhosis Coagulopathy:

A

hepatocytes produce fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII and protein C and S, and antithrombin
Sinusoidal endothelial cells produce factor VIII and vWF
• The liver clears activated coagulation factors from circulation

84
Q

Complications of Cirrhosis 11. Splenomegaly leading to

A

thrombocytopenia

85
Q

Cirrhosis leads to

A

Hyperdynamic

86
Q

Between arteries and venous

A

Capillaries

87
Q

Cirrhosis ANESTHESIA CONSIDERATIONS: Optimize medically
Evaluate
ADminister
Treat

A
  1. Optimize medically
    • Evaluate and correct coagulation status
    • Administer Vit. K if PT/INR prolonged
    • Treat thrombocytopenia
88
Q

Cirrhosis anesthetic management: Chronic alcohol ingestion

A

↑ anesthetic requirement (MAC) for isoflurane due to

alcohol-induced microsomal enzyme induction

89
Q

Anesthetic considerations for Cirrhosis Acutely intoxicated patients require

A

LESS anesthesia because of the additive depressant effects of alcohol (vulnerable to regurgitating gastric contents; bleeding may be altered due to alcohol-induced platelet aggregation interference)

90
Q

Anesthetic Considerations for cirrhosis ↓ protein binding

A

due to hypoalbuminemia = ↑ pharmacologically active formsmof IV drugs

91
Q

What is protein C

A

Naturally occurring anticoagulants

inactivate factors 5 and 8

92
Q

What is protein S

A

Inactivate factors, naturally occurring anticoagulants

93
Q

Anesthetic Considerations Cirrhosis Administer

  1. Volume distribution is ↑, so the initial dose of nondepolarizing muscle relaxant
    needs to be larger than normal, however subsequent doses should be ↓ due to
    ↓ hepatic clearance
    • The elimination half time of vecuronium is NOT ↑ until the dose exceeds 0.1mg/kg
A

blood slowly

• Clearance of citrate is ↓ in the cirrhotic live

94
Q

In Cirrhosis Avoid instrumentation of

A

the esophagus c/ known esophageal varices (gastric

tubes, esophageal probes, etc.)

95
Q

Cirrhosis and BP

A

Maintain normal BP because perfusion to the liver is already compromised

96
Q

Cirrhosis and Muscle relaxants Severe liver disease may

A

Alter plasma cholinesterase activity and prolong

succinylcholine

97
Q

**Cirrhosis and volume of distribution

A

*****Volume distribution is ↑, so the initial dose of nondepolarizing muscle relaxant needs to be larger than normal, however subsequent doses should be ↓ due to
↓ hepatic clearance

98
Q

DO NOT Do this in cirrhosis

A

PUT ANYTHING DOWN THROAT

99
Q

For cirrhosis The elimination half time of vecuronium is NOT

A

↑ until the dose exceeds 0.1mg/kg

100
Q

Cirrhosis and Vecuronim

A

Greater than Intubation dose

101
Q

Acute liver failure =

A

rapid development of severe liver damage c/ impaired function and encephalopathy in someone who
previously had normal liver function.

102
Q

• Fulminant hepatic failure develops

A

8 days of the new onset of symptoms

103
Q

Hepatic Failure Signs and SYmptoms

A 
• Signs and symptoms (rapid progression of symptoms):
malaise, nausea, jaundice,
altered mental status, coma,
respiratory alkalosis, cerebral
edema, hypotension,
hypoglycemia, coagulopathy,
neutropenia, oliguric renal failure •
104
Q

Hepatic Failure Hallmark signs:

A

altered mentation, prolonged prothrombin time

105
Q

Treatment of Hepatic Failure

A

Supportive, cause of failure needs to

be established and treated.

106
Q

Management of Anesthesia of hepatic Failure

A

• End stage liver disease is associated c/ very low SVR
• No elective procedures
• Correct coagulation c/ fresh frozen plasma (has all
clotting factors)
• Critically ill patients should receive low doses of volatiles
or N2O c/ TIVA

107
Q

Hepatic Lactulose therapy preoperative can

A

help decrease ammonia load and prevent hepatic

encephalopathy

108
Q

Hepatic failure metabolic disturbance

A

Respiratory Alkalosis

109
Q

Hepatic Failure correct_____

• Maintain____

A

Correct imbalances and abnormalities

urine output c/ IV fluids

110
Q

Hepatic Failure Invasive monitors may be necessary because

A

patients are at risk for arterial hypoxemia,
metabolic acidosis, hypokalemia, hypocalcemia,
and hypomagnesemia, RESP ALKALOSIS

111
Q

Preservative for liver transplant rich in

A

potassium

112
Q 
Anesthesia for Liver Transplant
• Fluid warmers and rapid infusion should
be considered
• Transplanted liver has impaired
vasoconstrictive response = impaired
protection of hepatic blood flow, no
longer a source for autotransfusion
A

• Anesthesia maintained c/ opioids and inhaled anesthetics combined c/ muscle relaxants that are NOT dependent on hepatic clearance (atracurium, cisatracurium)

113
Q

Anesthesia for Liver Transplant

should be considered

A

Fluid warmers and rapid infusion

114
Q

• Transplanted liver has impaired

A

vasoconstrictive response = impaired protection of hepatic blood flow, no longer a source for autotransfusion

115
Q

Phases of Liver Transplantation I. Dissection

A

– mobilizing vasculature around liver (hepatic artery, portal vein, supra/infrahepatic vena cava), isolating common bile duct, and removing native liver
• CV instability due to hemorrhage, venous pooling, ↓ venous return
III. Reperfusion (neohepatic) phase –

116
Q

Phases of Liver Transplantation II. Anhepatic

A

– blood supply to native liver is clamped (venovenous shunt usually
placed)
• Vigorous retraction may impair ventilation, lack of liver metabolism leads to metabolic
acidosis, ↓ drug metabolism, and citrate toxicity

117
Q

Phases of Liver Transplantation III. Reperfusion (neohepatic) phase

A

reanastomosis of major blood vessels to donor liver
• Most hemodynamically unstable phase:
• Dysrhythmias, severe bradycardia, hypotension, hyperkalemic arrest
• Will normalize soon after graft is rep

118
Q

Most hemodynamically unstable phase

A

Reperfusion

119
Q

• Bound to proteins to form hemoproteins including

hemoglobin and cytochromes P-450

A

• Genetic errors of metabolism characterized by

overproduction of porphyrins and their precursors

120
Q

= most important porphyrin

A

• Heme

121
Q

relevant to anesthesia because they produce life-threatening reactions to certain drug

A

• Only acute porphyrias

122
Q

• Porphyrias are classified by the

A

site of enzyme blockage along the heme production pathway

123
Q

Acute intermittent porphyria is the

A

most common acute form of porphyria, producing
the most serious symptoms such as hypertension, renal dysfunction, and CNS symptoms and can be precipitated by the administration of certain drugs.

124
Q

Porphyrias causing drugs

A 
KEPT MAN
• Ketorolac
• Etomidate
• Pentazocine
• Thiopental &amp; Thiamylal
• Methohexital
•Nifedipine
125
Q

Porphyrias Anesthesia Considerations:

A

• Carbohydrate administration can suppress porphyrin synthesis
(10% glucose in saline recommended)
• NPO time should be minimized
• Thorough neurological exam needed before administering regional anesthesia (document existing muscle weakness)
• Avoid all barbiturates
• Keep the patient warm

126
Q

Treatment of Porphyria

A

Treatment:
• Remove triggering agents
• Adequate hydration and carbohydrate administration
• Treat symptoms as needed
• Hematin (3-4mg/kg IV over 20min) is the only specific therapy for acute porphyric crisis
• Benzodiazepines and propofol can help alleviate symptoms

127
Q

Care for Patients c/ Decreased

Liver Function

A

• Patients c/ liver disease have a diminished physiologic reserve in
response to surgical stress
• ↑ risk for bleeding, infection, hepatic decompensation, and death

128
Q

Significant liver disease NS vs LR

A

NS

129
Q

Care for Patients c/ Decreased

Liver Function• Preoperative care:

A
  • Malnutrition and malabsorption are common = vitamin deficiencies and hypoalbuminemia
  • Monitor blood sugar
  • Hyponatremia results from free water retention
  • Degree of encephalopathy is directly correlated to perioperative mortality
130
Q

Anesthesia for Patients c/ Decreased Liver

Function in a healthy liver

A

• In a healthy liver, lactated ringers is converted to
bicarbonate.
• A diseased liver is unable to do this conversion, so the
kidneys convert that lactate into lactic acid, leading to
hepatic encephalopathy

131
Q

Anesthesia for Patients c/ Decreased Liver
Function
• Preoperative care:
• Patients c/ chronic liver disease (especially c/ ascites)
commonly have

A

↑ gastric volumes and delayed gastric

emptying ➔ Full Stomach

132
Q

• Factors affecting pharmacokinetics: Decreased liver

A

• Impaired hepatic synthetic function, ↑ volume of distribution, ↓ plasma protein binding of medications, and ↓ clearance of drugs

133
Q

Anesthesia for Patients c/ Decreased Liver

Function • Postoperative care •

A

Admit to ICU to maintain hemodynamics, ensure satisfactory oxygenation and ventilation, frequent
assessing of neurologic function, control electrolyte disturbances and coagulopathies

134
Q

improves outcome in decreased liver function

A

• Early enteral feeding

135
Q

Mallor Weiss Syndrome

A

• Mucosal tear - usually caused by vomiting, retching, or vigorous coughing
• May have large blood loss
• Bleeding usually stops c/out treatment in a
few hours- surgery rarely needed

136
Q

• Esophagectomy

A

• Curative or palliative option for malignant esophageal
lesions
• High morbidity & mortality
• Most post op complications-respiratory
• Acute lung injury /(ARDS) may occur (10-20%)
• c/ ARDS- mortality = 50%

137
Q

• Anesthesia considerations: Esophageal Disease

•

A

Malnourished
• Dehydration
• Pancytopenia
• May have had chemo or radiation-> difficult intubation

138
Q

GERD

A

Reflux of gastric contents into esophagus
• Lower Esophageal Sphincter (LES) opens c/ swallowing closes after to prevent gastric acid in the stomach
from refluxing into the esophagus
• At rest, LES exerts pressure high enough to prevent
reflux

139
Q

Inappropriate relaxation/weakness of LES ➔

A

gastric acid reenters the esophagus, causing irritation

140
Q

Reflux into the pharynx, larynx, and tracheobronchial tree results

A

in chronic cough, bronchoconstriction, pharyngitis, laryngitis, morning hoarseness, bronchitis, or pneumonia

141
Q

Recurrent pulmonary aspiration may result in

A

aspiration pneumonia, pulmonary fibrosis, or asthma.

142
Q

Succ

A

Increase LES tone,

143
Q

Anesthesia Considerations for GERD

•

A

High aspiration risk-ETT, RSI
• Highest risk of aspiration pneumonitis c/ > 25ml and pH < 2.5 gastric
contents
• Famotidine decrease gastric acid secretion
• Sodium citrate-oral nonparticulate antacid ↑ gastric pH
• Gastrokinetic agent such as metoclopramide should be considered

144
Q

2 drugs that increase LES tone

A

Neostigmine

Succinylcholine

145
Q

Hiatal Hernia

• Adequate LES tone to keep acid out

A

• Herniation of part of the stomach into the thoracic cavity

through the esophageal hiatus in diaphragm

146
Q

• Sliding hiatal hernia =

A

GEJ and fundus slide upward

147
Q

• Paraesophageal hernia =

A

esophagogastric junction remains in normal location and pouch of stomach is herniated next to gastroesophageal junction through the esophageal hiatus

148
Q

• Most patients c/ hiatal hernias

A

do not have symptoms of

reflux esophagitis

149
Q

Carcinoid tumors origination

A
  • 70% originate from one of three sites:
  • Bronchus
  • Jejunoileum
  • Colon-rectum
150
Q

Carcinoid tumors secrete

A
  • Secrete GI peptides and/or vasoactive substances

* Serotonin, ACTH, GHRF

151
Q

Found incidentally during surgery for suspected appendicitis

A

Carcinoid tumors

152
Q

Carcinoid Syndrome

• Occurs in 20% of pts c/ carcinoid tumorsn•

A

Large amounts of serotonin & vasoactive substances enter systemic circulation

153
Q

• Cardiac tumors may have cardiac manifestations resulting from

A

fibrosis involving the endocardium

154
Q

Nicotinamide

A

Vitamin D3

155
Q

Carcinoid tumor typical valvular lesions

A

Pulmonic stenosis and tricuspid regurgitation

156
Q

Carcinoid triad is

A

cardiac involvement, flushing(histamine) & diarrhea

• Serotonin is over produced, histamine is released, & both may cause bronchoconstriction

157
Q

Carcinoid triad Other clinical manifestations:

A

wheezing or asthma-like symptoms and skin

lesions (because of HISTAMINE RELEASE)

158
Q

Carcinoid Tumors

A

• Potentially life -threatening complication of carcinoid syndrome
= carcinoid crisis
• Manifests as intense flushing, diarrhea, abdominal pain, and cardiovascular signs (tachycardia, hypertension or hypotension)
• Can occur spontaneously or provoked by stress, chemotherapy, or biopsy

159
Q

Drugs that may provoke mediator release

A
  • Epinephrine
  • Norepinephrine
  • Succinylcholine
  • Mivacurium
  • Atracurium
  • D-tubocurarine
160
Q

Carcinoid Syndrome Treatment

A
  1. Avoiding conditions that precipitate flushing
  2. Treating heart failure and/or wheezing
  3. Providing dietary supplementation c/ nicotinamide
  4. Controlling diarrhea
  5. If the patient continues to have symptoms, serotonin receptor antagonists
    or somatostatin analogues are useful
  6. Synthetic analogues of somatostatin, (octreotide) control symptoms in>80% of patients
161
Q

Carcinoid syndrome Surgery is the

A

only potentially curative therapy for nonmetastatic carcinoid tumors

162
Q

Carcinoid Syndrome Anesthesia Management

A
  1. A-Line d/t potential for rapid changes in hemodynamic variables
  2. Octreotide preoperatively and before manipulation of the tumor will attenuate most adverse hemodynamic responses
  3. General anesthesia typically used
  4. ↑ levels of serotonin have been associated c/ delayed awakening
  5. Ondansetron, a serotonin antagonist, is a useful and logicalantiemetic choice
  6. Use of epidural analgesia in pts who have been adequately treated c/ octreotide is safe
163
Q

Carcinoid syndrome anesthesia preoperatively and before manipulation of the tumor will
attenuate most adverse hemodynamic responses

A

Octreotide

164
Q

Continous disease

A

Ulcerative Colitis

165
Q

Crohns Disease: WHat is it?

A
  • Acute or chronic bowel inflammation

* Can occur anywhere from mouth to anus

166
Q

Crohns: Most common site of inflammation =

A

terminal ileum

167
Q

• Occurs in patches a.k.a. “Skip Lesions”

A

Crohn’s Disease

168
Q

Crohns Disease

• Symptoms:

A

Diarrhea, anorexia, and fear of eating
• Causes weight loss of 10-20% of ideal body weight
• Over several years, persistent inflammation gradually progresses to fibrostenotic narrowing and stricture
• Diarrhea ↓ and is replaced by chronic bowel obstruction
• Loss of digestive & absorptive surfaces, which results in malabsorption & steatorrhea

169
Q

Granulomas common

A

Crohn’s Disease

170
Q

Granulomas uncommon

A

UC

171
Q

Inflammatory Bowel Disease

Treatment

A
  1. Sulfasalazine is the mainstay of therapy
    • Anti-inflammatory therapy
    • 30% of pts experience allergic reactions or significant side effects such as headache, anorexia, nausea, and vomiting
  2. Oral or parenteral glucocorticoids
  3. Methotrexate
    • Impairs DNA synthesis
  4. Cyclosporine: Alters the immune response by acting as a potent inhibitor of T cell–mediated
    responses
172
Q

Acute Pancreatitis

A
  • Acute inflammatory disorder of pancreas
  • Incidence: ↑ 10-fold since 1960s (alcohol abuse and/or improved diagnostic techniques and gallstones)
  • Common in patients c/ AIDS,hyperparathyroidism (associated hypercalcemia)
  • Trauma-induced acute pancreatitis associated c/ blunt trauma rather than penetrating injury
173
Q

• Postoperative pancreatitis o

A

ccurs after
abdominal and non-cardiac or cardiac
thoracic surgery, especially procedures that
require CPB

174
Q

• Clinical pancreatitis

A 
develops in 1% to 2% of
patients following (ERCP)
• Indomethacin suppository
175
Q

Signs & Symptoms of Pancreatitis

A
  1. Excruciating, unrelenting mid-epigastric abdominal pain that radiates to back ➔ Nausea and vomiting can occur at peak of pain
  2. Ileus ➔ abdominal distention
  3. Pleural effusions or ascites ➔ dyspnea (ARDS c/ 20% of pts.)
  4. Low-grade fever, tachycardia, and hypotension
  5. Obtundation and psychosis = alcohol withdrawal
  6. Hypocalcemia ➔ Tetany
  7. Hallmark- ↑ in serum amylase concentration
  8. Renal failure (25%)
176
Q

Acute Pancreatitis Treatment

A 
1. Hypovolemia, Bleeding, or Albumin Loss
• Aggressive intravenous fluid
• Colloid replacement
2. NPO to rest pancreas
3. Opioids for severe pain
4. NGT for persistent vomiting or ileus
177
Q

Chronic Pancreatitis

A

May be asymptomatic or abdominal pain may be
attributed to other causes
• There is loss of both exocrine and endocrine
function

178
Q

Signs & symptoms of chronic Pancreatitis

A

• Epigastric pain that radiates to the back
frequently postprandial
• Steatorrhea (fat in stool; foul smelling)
• At least 90% of pancreatic exocrine function is lost
• Diabetes mellitus is the end result of loss of
endocrine function

179
Q

Pathogenesis Chronic pancreatitis

A

Chronic alcohol abuse

180
Q

Treatment of chronic pancreatitis

A

Management of pain, malabsorption, and

diabetes mellitus

181
Q

Appendicitis peak incidence

A

Peak incidence of acute appendicitis in 2 nd & 3rd decades of life

182
Q

Appendicitis

A

Perforation & ↑ mortality are more common in infants and the elderly

183
Q

Appencitis, In elderly,

A

pain & tenderness are often blunted, & diagnosis is frequently delayed, so there is a 30% incidence of
perforation in patients older than 70 years

184
Q

Signs/Symptoms Initial:

A

mild crampy abdominal pain resulting from appendiceal contractions or distention of the appendiceal lumen
• Poorly localized pain c/ urge to defecate or pass flatus

185
Q

• Appendectomy should be

A

performed as soon as the patient can be prepared

186
Q 
Anesthesia Considerations
Anesthesia Considerations
• Usually appear \_\_\_\_\_\_
• These patients are \_\_\_\_\_\_\_\_\_
• \_\_\_\_\_\_\_\_ induction
• \_\_\_\_\_\_\_ tube
• Either \_\_\_\_\_or \_\_\_\_\_\_\_\_procedure.
• If Laparoscopic: \_\_\_\_\_\_\_\_\_\_
• Keep patient relaxed, but can be short procedure.
• Low dose \_\_\_\_\_\_\_
A

• Usually appear after-hours (Add-On/Emergent
Cases)
• These patients are considered a full stomach
• Rapid sequence induction
• Oral gastric tube
• Either open or laparoscopic procedure.
• If Laparoscopic: Trendelenburg intraop c/ slight
left tilt position.
• Keep patient relaxed, but can be short procedure.
• Low dose NMBDs

SRNA3CoExisting (16 decks)

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