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NURA 606 Adv Health Assessment > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

Diseases of the GI system frequently result in abnormal gastric function, with potentially increased anesthetic risk caused by? (4)

A
  • increased intragastric pressure
  • delayed gastric emptying,
  • gastric dilation
  • increased gastric secretion.
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2
Q

What are the most common symptoms of GI disease? (6)

A
  • Dysphagia – oral vs esophageal/ mechanical vs motility
  • Heartburn – burning & discomfort (cardiac concerns?)
  • Regurgitation – effortless return of GI content into pharynx
  • Chest discomfort - may be difficult to distinguish from CP
  • Odynophagia – pain with swallowing (ulcers?)
  • Globus sensation – “lump in throat”

Do these symptoms warrant further workup??

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3
Q

What is the triad of symptoms for achalsia and what does this mean your anesthetic?

A
  1. dysphagia
  2. weight loss
  3. regurgitation

High risk of aspiration - full stomach precautions → RSI

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4
Q

What is common complication of achalasia?

A
  • pulmonary aspiration with resultant:
    • PNA
    • lung abscess
    • bronchiectasis
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5
Q

What are 3 common mechanisms of incompetence for GERD?

A
  • (1) transient LES relaxation (elicited by gastric distention)
  • (2) LES hypotension (average resting tone, 13 mm Hg in patients with GERD vs. 29 mm Hg in patients without GERD)
  • (3) anatomic distortion of the GE junction, such as with a hiatal hernia.
  • The reflux contents may include hydrochloric acid, pepsin, pancreatic enzymes, and bile.
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6
Q

What are the 2 most common symtpoms of GERD + additional s/s?

A
  • 2 most common
    • heartburn and regurgitation
  • additional
    • noncardiac chest pain
    • dysphagia
    • pharyngitis
    • cough
    • asthma
    • hoarseness
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7
Q

When a pt has GERD, where can gastric contents reflux and what are some associated complications?

A
  • Gastric contents may reflux into the:
    • pharynx
    • larynx
    • tracheobronchial tree
  • resulting in:
    • chronic cough
    • bronchoconstriction
    • pharyngitis
    • laryngitis
    • bronchitis
    • pneumonia
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8
Q

What is a hiatal hernia and what are the associated symptoms?

A
  • Herniation of part of the stomach into the thoracic cavity through the esophageal hiatus in the diaphragm
  • may be asymptomatic
  • if symptomatic, may have heartburn and abd discomfort
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9
Q

Anesthetic considerations of patients with a hiatal hernia?

A
  • MAY be an apiration risk
  • may be taking PPIs and antacids
    • SE + drug interactions
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10
Q

What is PUD ans what are associated symptoms?

A
  • Ulcers in the mucosal lining of the stomach or duodenum
  • burning epigastric pain exacerbated by fasting and improved with meal consumption is the typical symptom complex
  • Link between H. pylori and PUD - inc. acid secretion
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11
Q

Regarding PUD, what are the risk factors associated with death?

A
  • Bleeding
  • peritonitis
  • dehydration
  • perforation
  • sepsis
  • *****especially in elderly debilitated or malnourished patients*****
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12
Q

What are typical treatments for PUD?

A
  • Antacids
  • PPIs
  • H2 Receptor Antagonists
  • Prostaglandin Analogues
  • Cytoprotective agents
  • surgical repair (if symptoms bad enough)
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13
Q

How does Crohn’s disease typically present?

A
  • Usually presents as:
    • acute or chronic bowel inflammation
    • penetrating-fistulous pattern
    • an obstructing pattern
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14
Q

For crohn’s disease, what is the most common site of inflammation and typical s/s?

A
  • Most common site of inflammation is the terminal ileum
  • s/s
    • recurrent episodes of right lower quadrant pain
    • diarrhea
    • weight loss
    • obstruction, stricture/ fistula formation
    • nutritional deficiencies
      • causing hypoalbuminemia
      • hypocalcemia
      • hypomagnesemia
      • coagulopathy
      • hyperoxaluria with nephrolithiasis
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15
Q

What kinds of surgeries migh we expect for a pt with crohns disease?

A
  • cannot be cured by surgical resection
  • complications of Crohn’s disease may require surgery
  • Most common surgery is resection of an area of small intestine involved in a fistula or obstruction
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16
Q

What are the medical treatments for inflammatory bowel diseases?

A
  • 5-Acetylsalicylic acid (5-ASA) is the mainstay of therapy
  • Oral or parenteral glucocorticoids (Prednisone)
  • Azathioprine and 6-mercaptopurine
  • Methotrexate
  • Cyclosporine
  • Tacrolimus
  • Infliximab- anti–tumor necrosis factor antibodies
  • Natalizumab- immunoglobulin antibody
  • antidiarrheal agents
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17
Q

Ulcerative colitis affects which part of the bowel?

A
  • Mucosal disease involving the rectum and extending proximally to involve part or all of the colon
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18
Q

What are major s/s of ulcerative colitis?

A
  • Major s/s
    • diarrhea
    • rectal bleeding
    • tenesmus
    • passage of mucus
    • crampy abdominal pain
  • severe dx:
    • anorexia
    • nausea, vomiting
    • fever
    • weight loss
  • 1%- severe hemorrhage
  • Perforation of the colon - most dangerous complication
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19
Q

What types of surgeries might we expect to see in someone with ulcerative colitis?

A
  • Nearly 1/2 of patients with extensive chronic UC undergo surgery within the first 10 years of their illness
  • Severe dx: total proctocolectomy and end ileostomy
  • Total proctocolectomy can be a curative procedure in ulcerative colitis
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20
Q

Malnutrition is associated with what complications? (5)

A
  • Prolonged hospital stays
  • Wound infection
  • Abscess
  • Respiratory failure
  • Death
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21
Q

What are 3 values that prompt referral for nutritional assessment?

A
  • BMI value less than 18.5 kg/m 2
  • Serum albumin concentration less than 30 g/L (in the absence of hepatic or renal dysfunction)
  • Weight loss of greater than 10% in last 6 months
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22
Q

What is a carcinoid tumor?

When and where are they found?

A
  • Originate from the GI tract most of the time & can occur in almost any GI tissue
  • Typically secrete GI peptides and/or vasoactive substances
  • Often found incidentally during surgery for suspected appendicitis
  • Symptoms are often vague, so the diagnosis is often delayed
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23
Q

What are symptoms of a carcinioid tumor in the small intestine, rectum, bronchus, thymus, ovaries, and liver?

A
  • Small intestine: abdominal pain, obstruction, tumor, GI bleed
  • Rectum: bleeding, constipation, diarrhea
  • Bronchus: usually asymptomatic
  • Thymus: anterior mediastinal mass
  • Ovaries & testicles: mass
  • Liver: METs, presents as hepatomegaly
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24
Q

What are the most common signs of carcinoid tumors + additional s/s?

A
  • Most common signs:
    • flushing and diarrhea (with the associated dehydration and electrolyte abnormalities)
  • Occasionally associated with pruritus, tearing, diarrhea, or facial edema
  • Hypotension and hypertension
  • bronchoconstriction
  • cardiac manifestations resulting from endocardial fibrosis (right heart, not left heart, because lungs are often able to clear these substances before they get to the left heart)
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25
Q

What is carcinoid crisis and what are the s/s?

A
  • Potentially life-threatening complication of carcinoid syndrome
  • Signs:
    • intense flushing
    • diarrhea
    • abdominal pain
    • and CV signs including tachycardia, hypertension, or hypotension
    • If not adequately treated, it can be fatal
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26
Q

What are anesthetic drugs that can precipitate carcinoid crisis?

A
  • Succinylcholine, mivacurium, atracurium, tubocurarine
  • Epinephrine, norepinephrine, dopamine, isoproterenol, thiopental
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27
Q

The diagnosis of carcinoid syndrome relies on which measurements?

A
  • measurement of urinary or plasma serotonin concentrations or measurement of serotonin metabolites in the urine (5-HIAA)
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28
Q

How do we decide on pre op testing for carcinoid tumors?

A
  • pre op tests are guided by physcial findings
  • Preoperative assessment should include CBC, electrolytes, LFTs, BG, EKG (echo if indicated), and determination of urine 5-HIAA levels.
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29
Q

What are the treatments and management of symptoms for carcinoid tumors?

A
  • Avoiding conditions that precipitate flushing
  • treating heart failure and/or wheezing
  • providing dietary supplementation with nicotinamide, and controlling diarrhea
  • Somatostatin, octreotide, lanreotide
  • Bronchoconstriction: octreotide and histamine blockers combined with ipratropium
  • Surgery is the only potentially curative therapy for nonmetastatic carcinoid tumors
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30
Q

What is pancreatitis?

A
  • Loss of any of protective mechanisms w/in pancreas leads to enzyme activation, autodigestion, and acute pancreatitis
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31
Q

What are causative factors of pancreatitis?

A
  • Gallstones and alcohol abuse (60-80%)
  • AIDS and those with hyperparathyroidism
  • trauma-induced
  • Abdominal and other noncardiac surgery and after cardiac surgery
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32
Q

What are symptoms of pancreatitis?

A
  • Excruciating, unrelenting mid-epigastric pain that radiates to the back - worse when supine
  • N & V
  • Abdominal distention
  • Low-grade fever, hypotension, tachycardia
  • Shock may occur
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33
Q

What are some complications associated with acute pancreatitis?

A
  • 25% of patients who develop acute pancreatitis experience significant complications
  • Shock
  • Hypotension- sequestration of large volumes of fluid in the peripancreatic space, hemorrhage, and systemic vasodilation
  • Arterial hypoxemia - ARDS in 20%
  • Renal failure - poor prognosis
  • GI hemorrhage & coagulation defects - DIC
  • Abscess formation
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34
Q

What is the TX of acute pancreatitis?

A
  • usually based on supportive therapy, potential ICU with invasive monitoring
  • Aggressive intravenous fluid administration
    • may be on pressors - consider if implications if pt comes to OR
  • Opioids are administered to manage the severe pain
  • Nasogastric suction
  • Endoscopic removal of obstructing gallstones
  • Drainage of intraabdominal collections of fluids or necrotic material
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35
Q

What are some important considerations in the GI hx?

A
  • Does the patient have :
    • Nutritional deficiency
    • Weight loss greater than 10% in last 6 months
    • Nausea/Vomiting
    • Occult blood loss
    • Overt GI bleeding
    • Abdominal pain
      • assess current level
      • assess current meds
      • RA great in this population
    • Abdominal distention
      • aspiration risk
    • Abdominal masses
    • Dysphagia
    • Gastric hyperacidity with or without reflux
    • Epigastric pain ​
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36
Q

List current NPO guidelines for “healthy patients.”

A
  • No chewing gum or candy after midnight
  • Clear liquids up to 2 hours before OR
  • Breast milk up to 4 hours before OR
  • Light meal, milk, formula up to 6 hours before OR
  • Fatty foods, fried foods, meats 8 hours or more
  • Sip of water or liquid pre-med up to 1 hour before OR
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37
Q

Which patient populations are considered aspiration risk?

A
  • Extremes of age <1 yr or >70 yr
  • Prematurity
  • Ascites (ESLD)
  • Collagen vascular disease, metabolic disorders (Diabetes, obesity, ESRD, hypothyroid)
  • Hiatal Hernia/GERD/Esophageal disorders
  • Mechanical obstruction (pyloric stenosis, intestinal obstruction)
  • Pregnancy- treated as if they have “full stomach”
  • Neurologic diseases
  • Morbid obesity
  • Severe pain/ anxiety
  • Eaten food
  • Emergency surgery
  • Positioning (lithotomy)
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38
Q

What is Mendelson syndrome?

What are risk factors?

How does It manifest clinically?

A
  • Chemical pneumonitis or aspiration pneumonitis caused by aspiration during anesthesia
  • Characterized according to
    • pH
    • Volume
    • Gastric material aspirated
  • Historically, patient at risk if:
    • pH less than 2.5
    • Gastric volume of > 25 ml (0.4 ml/kg)
  • Clinically manifests as:
    • about 2 - 5 hrs post anesthesia
    • hypoxia
    • Respiratory distress with bronchospasm
    • cyanosis
    • tachycardia with hypotension
    • dyspnea from irritating action of hydrochloric acid and particulate material which are damaging to the lungs
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39
Q

What does the ASA say about routine use of aspiration prophylaxis medications?

A
  • ASA does not promote the routine use of these medications to decrease aspiration in patients with no apparent risk factors
40
Q

What is bicitra?

Use?

Dose?

Common populations administered to?

A
  • Non-particulate antacid
  • Customary dose of 30 ml PO to raise gastric pH
  • Disadvantage: increases gastric volume
    • commonly given with reglan
  • Give 15 minutes before surgery (1-3 hrs)
  • generally used in:
    • diabetics
    • morbidly obese
    • pregnant
41
Q

What is omeprazole?

Use?

PK?

Dose?

A
  • Proton pump inhibitor
  • Prevention & treatment of acid-related conditions
  • most potent acid-inhibitory drugs available
    • inhibit all phases of gastric acid secretion
  • 80 mg po the night before and 40 mg repeated after the induction of anesthesia
  • Onset: rapid
  • maximum effect: 2–6 hours
  • DOA: up to 72 hours.
42
Q

What are the available H2 antagonists?

Use?

MOA?

Best time of administration?

PK?

Comparison?

A
  • Cimetidine, Ranitidine and Famotidine (best result)
  • TX: GERD, gastritis active ulcer disease (4–6 weeks of treatment) and as adjuvant therapy (with antibiotics) for the management of H. pylori infection
  • Acts as competitive antagonist of histamine binding to H2 receptors on gastric parietal cells
    • Reduces acid secretion
  • Best if given the night before and repeated 45-60 minutes before surgery
  • Cimetidine and ranitidine decrease gastric acid secretion and increase gastric pH
  • Cimetidine’s effect begins in 1–1.5 hours and lasts for about 3 hours
  • Ranitidine is 4–6 times more potent than cimetidine and has fewer side effects
  • Famotidine can be given intravenously and are similar in effect to ranitidine but have a longer duration of action.
43
Q

What is reglan?

Use?

MOA?

Contraindications?

Antiemetic dose?

A
  • Dopamine receptor antagonist- prokinetic agent
  • Increases the pressure of the lower esophageal sphincter and enhances GI motility which speeds gastric emptying
  • prevents or alleviates nausea and vomiting
  • Contraindicated
    • bowel obstruction
    • Parkinson’s
  • As a perioperative anti-emetic, the effective dosed is usually 25 mg
44
Q

Useful labs for the GI patient.

A
  • hct
  • serum electrolytes
  • BUN
  • serum albumin
45
Q

What are anesthesia considerations for the GI patient?

(long list)

A
  • Vast alterations in fluids/elec, and nutrition, GERD, bowel obstruction, n/v , or hypersecretion of acid
  • Preop NG suctioning, or preop use of histamine receptor blocking drugs (other aspiration prophylaxis)
  • Clotting abnormalities may need to be corrected
  • Closed spaces containing gas expand by absorbing nitrous oxide, as such expansion can lead to ischemic injury, rupture of GI viscera, or both
  • Predisposes the patient to blood stream contamination
  • Respiration may be impaired because of tobacco abuse, peritonitis, abscess, pulmonary obstruction, previous incisions, aspiration
  • Aspiration risk
    • Prophylaxis and airway management considerations; bronchospasm
  • Bleeding causing anemia (T&S or T&C)
  • Nutritional & fluid deficits and/or electrolyte disturbances/ hematologic derangements
  • Preexistent parenteral nutritional
  • Pain control
  • Medications: prophylactic steroid coverage/ vasopressors
  • If carcinoid, cardiac workup needed? Hemodynamically stable? H1 & H2 blockers/ octreotide
  • Invasive monitoring - IABP
  • Post-op course – PACU vs ICU
46
Q

What are the 5 categories of liver function?

A
  • metabolic
  • synthetic
  • immunologic
  • regenerative
  • homeostatic
47
Q

List 7 functions of the liver.

A
  • Reservoir of blood (1L)
  • Carbohydrate, protein, lipid, bile, drug metabolism.
  • Protein synthesis.- albumin is the most abundant plasma protein produced by the liver
  • Detoxification
  • Mediator of endocrine functions
  • Immunologic functions
  • Production of coagulation factors
48
Q

What are the most common causes of chronic liver disease?

A
  • viral hepatitis
  • alcoholic liver disease (ALD)
  • though NASH is becoming a more common indication for LTX
49
Q

List causes of liver disease?

A
  • Developmental or genetic defects
  • Metabolic abnormalities
  • Autoimmune diseases
  • Infectious diseases
  • Neoplasm
  • Alcohol
  • Environmental toxins
  • Drug toxicity
50
Q

What are some major risk factors for liver disease?

A
  • History of jaundice
  • Family history of jaundice and liver disease (hemochromatosis, α 1 -antitrypsin deficiency, and Wilson disease)
  • Illicit drugs/Alcohol
  • Current medications including herbals
  • History of blood transfusions
  • Travel history
  • Occupational history
51
Q

How can we categorize liver disease based off of anatomy?

A
  • Divided into two main groups on the basis of the primary anatomy affected:
    • Hepatocellular (parenchymal)- generalized hepatocellular dysfunction
    • Obstructive (biliary)- biliary excretion of substances
  • •May also be described as acute or chronic
52
Q

Describe the pathophysiology of cholestasis.

A
  • Cholestasis is the impairment of bile production or flow
  • impairment of flow leads to an inc in the conc of bile salts in the serum and hepatocytes
  • As the bile salts accumulate in the liver, they dissolve hepatocyte cell membranes
  • As the disease progresses, the serum concentration of conjugated bilirubin increases, giving rise to jaundice
  • The majority of cases of cholestasis are benign; however, severe and prolonged cholestasis can lead to cirrhosis.
53
Q

What are s/s of cholestasis?

A
  • fatigue
  • pruritis
  • dark urine
  • pale stools
  • elevated alk phos
    • **first indication of asymptomatic patients**
    • typically manifests as 2 - 4x the upper limit of normal
54
Q

Why does cholestatic disease predispose a pt to vitamin K deficiency?

Why does this matter and how do we treat It?

A
  • Absorption of Vit K depends on Bile Salt excretion into GI tract
  • Biliary obstruction coagulopathy results from a deficiency of factors dependent on Vit K (II, VII, IX, X)
  • Long term biliary obstruction can cause liver dysfunction interfering with protein synthesis
  • Tx:
    • correct with parental Vitamin K
    • FFP is necessary if emergent surgery or presence of hepatic injury
55
Q

What are expected findings of a pt with cholestatic disease? (4)

A
  • Increased peripheral vasodilation
  • Increased CO
  • Increased portal venous pressure
  • Decreased portal venous blood flow
56
Q

What is hepatitis and how do we categorize It as acute?

A
  • inflammatory disease of hepatocytes that may be either acute or chronic and can progress to cell necrosis and eventual hepatic failure
  • Group of liver disorders of varying etiologies that result in hepatic inflammation and necrosis for
57
Q

List common etiologies of acute hepatitis.

A
  • HBV, HDV, HCV
  • auto-immune
  • drugs, alcohol
58
Q

What are s/s of acute hepatitis?

A
  • Symptoms can be nonspecific
    • fatigue
    • poor appetite
    • n/v
    • abdominal pain
    • many infections are subclinical
  • Signs may include:
    • jaundice
    • serum-sickness-type presentation with fever, arthralgia or arthritis, and rash that results from circulating hepatitis antigen-antibody complexes.
  • Incubation periods can be several weeks to even months and patients may undergo surgery without awareness of illness.
59
Q

What medications are included in TX of acute hepatitis?

A
  • interferon
  • ribarvirin
  • corticosteroids
  • AZT
60
Q

What are surgical recommendations for someone with acute hepatitis?

A

Consensus opinion is that elective surgery should be postponed in patients with acute hepatitis

61
Q

What is the difference between chronic persistent hepatitis and chronic active hepatitis?

A
  • Chronic persistent hepatitis
    • relatively benign
    • confined to portal areas
    • Hepatocellular integrity is preserved, and progression to cirrhosis is rare
  • The most serious form of chronic hepatitis is chronic active hepatitis
    • progressive
    • results in hepatocyte destruction, cirrhosis, and ultimately hepatic failure
62
Q

What are clinical manifestations of chronic hepatits? (aka what should you address in your pre op eval)

A
  • Fatigue
  • Jaundice
  • Neuropathy
  • Coagulopathies
    • thrombocytopenia
    • PT is often prolonged
  • Dehydration
  • Electrolyte abnormalities
  • plasma albumin level decreased
  • presence of glomerulonephritis
63
Q

What is the most common cause of chronic liver disease?

A
  • Nonalcoholic fatty liver disease
64
Q

What is NAFLD?

A
  • accumulation of hepatic fat that is not due to heavy alcohol use
  • two main types of NAFLD:
    • nonalcoholic fatty liver (NAFL)
    • NASH
  • NAFLD ranges in severity from simple fat deposition (steatosis) to fat deposition together with inflammation and hepatocellular necrosis (steatohepatitis or NASH)
65
Q

What are risk factors for NAFLD?

A
  • NIDDM
  • obesity
  • TPN
  • patients who have had jejunal-ileal bypass weight loss surgery
  • certain medications (amiodarone, calcium channel blockers, glucocorticoids)
66
Q

What are the s/s of NAFLD?

A
  • Asymptomatic but elevated liver enzymes (AST & ALT) found on physical exam
  • Produces some degree of hepatocyte necrosis which promotes the accumulation of inflammatory cells in liver
  • NASH- leads to cirrhosis
  • Wt loss (even 5 lbs) can reverse the elevated liver enzymes
67
Q

How do we diagnose the 3 types of alcoholic liver disease?

A
  • clinical features do not distinguish from the 3 types
  • Liver biopsy is necessary to give definitive diagnosis
    • Steatosis (fatty liver)
    • Alcoholic hepatitis (precursor cirrhosis)
    • Cirrhosis
68
Q

Patients with alcoholic steatosis or steatohepatitis may be clinically __________, but on physical exam demonstrate ____________.

A

asymptomatic; hepatomegaly

69
Q

ALD: Patients who progress to cirrhosis may pressent wtht eh class stigmata of chronic liver disease including what s/s?

A
  • spider angiomata
  • jaundice
  • icterus
  • palmar erythema
  • gynecomastia
  • multiorgan failure marked by
    • worsening ascites
    • peripheral edema
    • neuropathy
    • pancreatic dysfunction
    • platypnea/orthodeoxia
    • renal failure
    • hepatic encephalopathy with or without asterixis
70
Q

What are s/s of alcoholic liver disease?

A
  • malaise
  • nausea
  • anorexia
  • weakness
  • abdominal discomfort
  • hepatomegaly
  • jaundice
71
Q

What are the s/s of early alcohol withdrawal?

When will symptoms manifest?

Treatment?

A
  • alcohol withdrawal (early)—most pronounced 3-6 hours post withdrawal
  • S/S-tremors, hallucinations, tachycardia (ANS hyperactivity), N/V
  • TX: Benzodiazepines and beta antagonists
  • 6-8 hours may become tremulous
  • 6-24 hours hallucinations and seizures
72
Q

What are delirium tremens and when do they manifest? S/S? TX?

A
  • Alcohol withdrawal/delirium tremens—most common 2-4 days post withdrawal
  • S/S: hallucinations, combativeness, hyperthermia, tachycardia, hypertension, hypotension, and grand mal seizures
  • TX: Diazepam 5-10 mg IV, beta antagonists, correct e’lyte abn (Mg, K), thiamine, lidocaine for dysrhythmias
73
Q

How do we define cirrhosis and what are the most common causes in the US?

A
  • Steady or recurrent episodes of parenchymal inflammation and necrosis with resultant disruption of normal hepatic architecture
    • Blood flow through the liver is disrupted
  • Commonly due to hep C, ALD, NASH
74
Q

What are s/s of cirrhosis?

A
  • Esophageal varices
  • Ascites and edema
  • Coagulation disorders w/ bleeding
  • Encephalopathy
  • Portal hypertension
  • Cardiac manifestations- high cardiac output, low arterial blood pressure, and low systemic vascular resistance/ “cirrhotic cardiomyopathy”/ autonomic dysfunction
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
75
Q

What is the purpose of the Child Pugh score?

Factors assessed?

How is It categorized?

A
  • important prognostic factors for perioperative mortality
    • originally used to predict mortality during surgery, it is now used to determine the prognosis, as well as the required strength of treatment and the necessity of liver transplantation.
  • Five factors
    • ​albumin
    • bilirubin
    • ascites
    • encephalopathy
    • PT
  • Three classes of severity (class A, B, or C, with C representing the most severe hepatic dysfunction)
76
Q

What is the purpose of the MELD?

Factors assessed?

How is It categorized?

A
  • scoring system for assessing the severity of chronic liver disease
  • predict mortality within 3 months of surgery
  • subsequently found to be useful in determining prognosis and prioritizing for receipt of a LTX
  • Factors
    • bilirubuin
    • creatinine
    • INR
77
Q

What are important questions to consider in liver evaluation?

A
  • Alcohol consumption, use of recreational or illicit drugs, medications (including herbal products)
  • sexual promiscuity
  • blood transfusions
  • exposure to hepatotoxins
  • prior bouts of jaundice
  • family hx of genetic diseases such as hemochromatosis, α 1 -antitrypsin deficiency, and Wilson disease
  • Presence of tattoos
  • Consumption of raw seafood
  • History of travel to areas in which hepatitis is endemic
  • Symptoms of fatigue, anorexia, weight loss, nausea, vomiting, easy bruising, pruritus, dark-colored urine, biliary colic, abdominal distention, and gastrointestinal bleeding warrant further investigation for the presence of liver disease
78
Q

What are some mild or nonspecific symptoms of liver disease?

A
  • ***Often no signs or symptoms of liver disease until it is quite advanced***
  • Loss of appetite
  • Fatigability
  • Malaise
  • Disrupted sleep patterns
  • Subtle cognitive changes
  • Pruritus
  • Easy bruising and changes in urine or stool color
79
Q

What are some s/s of advanced liver disease?

A
  • ***Often no signs or symptoms of liver disease until it is quite advanced***
  • Jaundice
  • Scleral icterus
  • Ascites
  • Spider angiomas
  • Xanthoma
  • Asterixis
  • Palmar erythema
  • **symptoms may also include mild or nonspecific symptoms!**
80
Q

List hepatotoxic medications.

A
  • Acetaminophen
    • Accidental or intentional overdose of is the most common drug-induced liver disease that causes fulminant hepatic failure
  • PCN, Bactrim, tetracyclines, erythromycins
  • Anticancer drugs
  • Antiepileptic drugs-Dilantin
  • Nonsteroidal anti-inflammatory drugs-ASA, ibuprofen
  • Methotrexate
  • Sulfonylureas
  • Amiodarone
  • Herbals
  • Cocaine, ecstasy, angel dust, glues/solvents
81
Q

What should be included in the physical exam of a patient with liver disease?

A
  • General inspection (wt., vital signs, mental status)
  • Exam patient’s hands, looking for:
    • Palmar erythema
    • Asterixis
    • Dupuytren’s contracture
  • Check sclera for jaundice or pallor
  • Exam chest for gynecomastia or spider nevi- signs liver disease
  • Skin color (jaundice), scratches (itching)
  • Skin turgor
  • Dependent edema
  • Auscultate breath sounds
    • Pleural effusions
  • Abdominal examination
    • Auscultate bowel sounds
    • Palpate abdomen
    • Note guarding and pain
    • Note hepatosplenomegaly, ascites
  • •Percuss
82
Q

What are some common mechanisms underlying pulmonary abnormalities in patients with liver disease?

A
  • ventilation-perfusion abnormalities associated with:
    • underlying obstructive airways disease
    • fluid retention
    • pleural effusion
    • decreased lung capacities secondary to large volume ascites.
83
Q

How is portopulmonary hypertension defined?

A
  • mean PAP > 25 mm Hg (i.e., pulmonary arterial HTN) in a patient with known liver disease and portal HTN
84
Q

What is hepatopulmonary syndrome?

What are the clinical manifestations?

A
  • triad consisting of liver disease, hypoxemia, and intrapulmonary vascular shunting
  • intrapulmonary shunting causes VQ mismatch and an increased alveolar-arterial oxygen gradient
  • Classically these patients may have platypnea and orthodeoxia.
    • Platypnea: SOB relieved by lying down and worsens when sitting or standing up.
    • Orthodeoxia: hypoxemia worse in an upright position and gets better when lying down
85
Q

Which labs can we use to asses the liver?

A
  • Albumin (normal 3.5-5.0 g/dl)
  • Complete CBC
  • Coagulation studies (especially PT/INR)
  • Serum electrolytes and glucose levels
  • Serum BUN/ Cr
  • Serum transaminases (LFTs)
  • Serum ammonia levels
  • Platelet count >100,000
  • Bilirubin
  • ABG
86
Q

What are AST and ALT? Compare and contrast AST and ALT as LFTs.

A
  • Both are aminotransferases, enzymes involved in gluconeogenesis
  • AST is also found in non-hepatic tissues (including the heart, skeletal muscle, kidney, and brain), elevations are not specific for hepatic disease
  • ALT is primarily localized to the liver
    • mainly a cytoplasmic liver enzyme
  • LFTs (AST/ ALT): assess cellular injury
  • Concomitant elevations in AST and ALT usually represent liver injury
87
Q

How is the AST/ALT ratio helpful in differentiating Wilson diseae and ALD from viral hepatitis?

A
  • Wilson disease and ALD are classically associated with an AST-ALT ratio > 2
  • ratio of is more common in NASH and viral hepatitis
88
Q

What kind of elevation of AST/ALT might we expect to see with chronic viral hepatitis, acute viral hepatitis, and shock liver?

A
  • Chronic viral hepatitis
    • often presents with mildly elevated AST and ALT
  • acute viral hepatitis
    • often associated with levels > 25x normal
  • Shock liver
    • can be associated with the highest levels of liver enzymes (i.e., levels > 50 times normal)
89
Q

What are expected findings related to coagulation labs in the pt with liver disease?

A
  • Disorders of coagulation rapidly develop in patients with severe liver failure
  • Factors II, V, VII, IX, X all reduced in liver failure
  • PT and INR elevated
  • Thrombocytopenia
    • a function of platelets is to promote thrombin generation
    • Platelet counts below a threshold of 100,000/mm3 negatively correlate with thrombin production. Platelet transfusions are not indicated in the absence of bleeding.
  • Abnormal fibrinogen
90
Q

The liver is the site of synthesis for all procoagulant and anticoagulant factors, with the exception of?

A
  • tissue thromboplastin (III)
  • calcium (IV)
  • von Willebrand factor (VIII)
  • also the site for clearance of activated factors
91
Q

What is vitamin K?

Who can develop vitamin K deficiency?

What are expected lab findings?

A
  • fat soluble and requires bile salts for the absorption into the jejunum
  • necessary for the hepatic synthesis of Factors II, VII, IX, X, and Protein S and Protein C
  • deficiency develops in:
    • patients on parenteral nutrition
    • biliary obstruction
    • pancreatic insuff
    • malabsorption
    • GI obstruction
    • rapid GI transit
  • prolonged PT, PTT
92
Q

What are some causes of coagulopathy and what is the therapy?

A
  • vitamin K deficiency (from cholestasis)
  • factor deficiency (from loss of synthetic function)
  • thrombocytopenia (from splenomegaly and portal hypertension)
  • Therapy:
    • directed at the cause
    • Vitamin K, fresh frozen plasma, or platelets may correct deficiencies
93
Q

Table of common LFTs

A
94
Q

What are anesthetic considerations (regarding pre op and assessment) for the patient with liver disease?

A
  • Careful assessment of a patient’s level of hepatic dysfunction must be performed
  • Patients with known or suspected liver disease should have appropriate lab testing
  • Anesthetic management of these cases should be tailored to the comorbidities of the patients, the surgical approach (open, laparoscopic), the anticipated extent of resection, and the need for vascular occlusive maneuvers
  • Clotting abnormalities may need to be corrected
  • Addressing nutritional deficiencies
  • Adequate large- bore venous access should be obtained
  • Potential for significant blood loss – blood salvage techniques
  • IABP - cases during which significant hemorrhage/ need for vascular occlusion maneuvers is anticipated
  • CVP monitoring
  • TEG-guided transfusion – coagulation management
  • TEE - caution with esophageal varicies
95
Q

What are anesthesia considerations regarding induction and maintenance of anesthesia?

A
  • RSI should be considered in patients with significant ascites – aspiration risk
  • Maintenance of general anesthesia- both VA and IV
  • Anesthetic dosing should be titrated - PK/PD of common anesthetic agents in patients with liver disease
  • Vascular occlusion strategies - hemodynamic effects
  • Diminished physiologic reserves
    • increased perioperative risk of bleeding, infection, deterioration in liver function, and death compared to those w/o liver disease
96
Q

flow chart: evaluation of patients presenting with some degree of chronic liver disease

A

NURA 606 Adv Health Assessment (9 decks)

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