Hepatobiliary: Part 2 (Paulson) Flashcards
(104 cards)
1
Q
Choledocholithiasis= stones within the ______
A
common bile duct
2
Q
Choledocholithiasis: -many Pts are symptomatic or asymptomatic?
A
**symptomatic: RUQ or epigastric pain, nausea, vomiting. –Pain often more prolonged that that of typical biliary colic –RUQ or epigastric pain on exam, may be jaundiced
3
Q
Choledocholithiasis: -Labs that are elevated early on? -Later on?
A
-AST/ALT elevated early -Later, more typical cholestatic pattern of elevation (bilirubin, ALP, and GGT more pronounced than ALT/AST)
4
Q
What is a cholestatic pattern of elevation?
A
-bilirubin, ALP (alk. phosphatase), and GGT more pronounced than ALT/AST)
5
Q
Choledocholithiasis can result in cholangitis, obstructive jaundice, and ________
A
pancreatitis
6
Q
Choledocholithiasis: -1st imaging study? -if high risk for CBD(common bile duct) stone, ____ should follow
A
-Ultrasound 1st, if high risk for CBD stone–> ERCP with stone removal, followed by cholecystectomy (or cholecystectomy with intraoperative cholangiography, followed by ERCP=endoscopic retrograde cholangiopancreatography)
7
Q
Acute Cholangitis aka ________
A
Ascending Cholangitis
8
Q
Acute Cholangitis= stasis and infection in the biliary tract causes a clinical syndrome with ____ (which Sx?)
A
fever, jaundice, and abdominal pain
9
Q
Acute Cholangitis=Biliary obstruction + _________
A
bacterial infection
10
Q
Acute Cholangitis: -what are the MC causes for biliary obstruction?
A
calculi (kidney stone), stenosis, malignancy
11
Q
Acute Cholangitis: -obstruction causes increased _____
A
Obstruction causes ↑ intrabiliary pressure –> ↑ permeability of bile ductules –> easier for bacteria to be transferred from portal circulation into biliary tract
12
Q
Acute Cholangitis: increased pressure also makes it easier for bacteria to go from bile to _____
A
systemic circulation–> septicemia
13
Q
Acute Cholangitis: -common organisms?
A
E. coli, Klebsiella, Enterobacter. (EEK)
14
Q
Acute Cholangitis clinical manifestations classic presentations: -Charcot Triad?
A
**Fever, abdominal pain, jaundice
15
Q
Acute Cholangitis clinical manifestations classic presentations: -Reynold’s Pentad?
A
-Confusion, hypotension, fever, abdominal pain, jaundice –Associated with suppurative cholangitis
CH + FAJ
16
Q
Acute Cholangitis: -MC presenting symptoms are fever & ______ -____ is a less common at presentation
A
abdominal pain –Pain usually RUQ or diffuse -jaundice less common–> Look in eyes and under tongue 1st
17
Q
Acute Cholangitis: -older Pts and immunosuppressed may have _____
A
atypical presentation —>Perhaps hypotension only
18
Q
Acute Cholangitis: Labs?
A
-Leukocytosis with neutrophil predominance -Cholestatic pattern of LFTs ↑ALP, GGT, and bilirubin (mostly conjugated)
19
Q
Acute Cholangitis: Blood culture?
A
- May have positive blood cultures –All who are suspected of having cholangitis should have blood cultures –If a patient has ERCP, should also culture bile or a stent that is removed
(notes: make sure you get blood cultures on all Pts with whom you suspect Acute Cholangitis aka Ascending Cholangitis)
20
Q
2013 Tokyo Guidelines- Diagnostic Criteria: -diagnosis of acute cholangitis should be suspected if a Pt has:
A
At least 1 from each row:
- Fever and/or shaking chills, lab evidence of inflammatory response (abnormal WBC or ↑ CRP)
- Jaundice, abnormal LFTs
21
Q
2013 Tokyo Guidelines- Diagnostic Criteria: - Diagnosis considered **definite if Pt meets above criteria and also has:
A
- biliary dilatation on imaging
- evidence of an etiology on imaging (**stricture, stone, stent)
22
Q
Acute cholangitis: -Imaging required for Pt’s with Charcot’s triad + abnormal LFTs?
A
ERCP (endoscopic retrograde cholangiopancreatography) –Can confirm the diagnosis and also immediately provide biliary drainage
23
Q
Acute Cholangitis: -imaging required if Charcot’s triad is NOT present?
A
**Transabdominal ultrasound: –Looking for CBD dilatation or stones: -If seen –> need ERCP within 24 hours for drainage/stone removal -If normal –> MRCP=Magnetic resonance cholangiopancreatography (**might have missed small stones)
24
Q
Acute Cholangitis: tx
A
- Admit to hospital:
- Watch for/manage sepsis
- Abx: Broad spectrum parenteral abx targeted at colonic bacteria –>Modify based upon culture results
- Abx for 7-10 days
Biliary drainage: Should happen ASAP** –ERCP is treatment of choice
–Other options: percutaneous transhepatic cholangiography or open surgical decompression
25
Empiric Abx therapy for gram-negative and anaerobic pathogens for Acute Cholangitis
- Ampicillin-sulbactam
- Pip-taz
- Ticarcillin-clavulanate
- Broad spectrum: Ceftriazone plus metronidazole
26
Acute Cholangitis: -mortality rate %? -who is at risk for recurrence?
-Mortality rates used to be 50—65%, Now 11-20% -Those who develop acute cholangitis from gallstones are at risk for recurrence --Cholecystectomy recommended
27
Acute cholangitis: -if obstruction is from a benign stenosis, may need \_\_\_\_\_
surgical repair or endoscopic therapy
28
Acute cholangitis: -malignant stenosis: recurrent _______ is common
obstruction -Often need stent placement
29
Mirizzi Syndrome is common hepatic duct obstruction from ______ compression -Mirizzi syndrome can result from?
extrinsic -From an impacted stone in the cystic duct
30
Mirizzi Syndrome: -MC Sx?
most Pts present with jaundice, fever, and RUQ pain
31
Mirizzi Syndrome: -Labs?
↑ALP and bilirubin (90% of patients)
32
Mirizzi Syndrome: -Diagnosis? (what is first line)
Ultrasound 1st, usually followed by ERCP
33
Mirizzi Syndrome: -Treatment?
-Surgery, usually cholecystectomy --If poor candidate, lithotripsy option --Associated with high frequency of bladder cancer
34
Cirrhosis is progressive ______ fibrosis
hepatic
35
Cirrhosis: histologically defined by \_\_\_\_\_
-fibrosis & regenerative nodules in the liver
36
Cirrhosis: -How many possible clinical manifestations? -Nonspecific Sx?
-Many possible clinical manifestations -Nonspecific Sx: Fatigue, anorexia, weakness, weight loss/wasting
37
Cirrhosis etiology: -MC causes?
- Alcohol abuse=MC\*\*
- Chronic viral hepatitis (Hep B and Hep C)
- Hemochromatosis
- Nonalcoholic fatty liver disease
38
Cirrhosis etiology -less common causes?
- Autoimmune hepatitis
- Primary and secondary biliary cirrhosis
- Primary sclerosing cholangitis
- Medications (ie: MTX, isoniazid)
- Polycystic liver disease -Right-sided heart failure
- Wilson disease
- Celiac disease
- Alpha-1 antitrypsin deficiency
39
Cirrhosis: -describe the pathophysiology behind this disease process
Regardless of cause, fibrosis develops to the point of architectural distortion--\> Fibrosis disrupts normal portal blood flow --\> raises the blood pressure and impairs the functioning of the liver
40
Cirrhosis Clinical manifestations: Sx of hepatic dysfunction?
-May include: pruritis, jaundice, hematemesis, melena, hematochezia, abdominal distension, confusion, muscle cramps
41
Hematochezia=
passage of fresh blood per anus, usually in or with stools.
42
Melena=
passage of black, tarry stools
43
Cirrhosis: skin findings
- when is Jaundice seen?
- Other skin findings: Where are spider angiomas MC found?
Jaundice= Yellow coloring of skin, eyes, membranes--\> \*\*Usually not seen until bilirubin \>2-3 mg/dL
- Spider angiomata (aka spider telangiectasias)=Vascular lesions --\>Most frequently on trunk, face, & upper limbs
- Palmar erythema--\> Usually peripheral over the palm with central pallor
44
Cirrhosis:
- Chest findings?
- In Men: loss of \_\_\_\_
Gynecomastia: In up to 2/3 of Pts
In men:
- Loss of chest or axillary hair, inversion of normal male pubic hair pattern
- & Testicular atrophy
45
Cirrhosis: Ascites
- How do you test for ascites?
- flank is ____ to percussion
=Abdomen often extremely distended
test for ascites using the \*\*Fluid wave test
-\*Flank is dull to percussion
46
Cirrhosis: abdominal findings
-liver palpation--Cirrhotic Liver may be _____ ?
- Cirrhotic liver may be enlarged, normal sized, or small
- If palpable, generally feels firm and nodular
47
Cirrhosis: abdominal findings
- \_\_\_\_\_\_ is common
- Caput medusa= ?
- Describe the murmur associated with Cirrhosis
- Hernia associated with cirrhosis?
- \*Splenomegaly common
- Caput medusa= dilated veins 2/2 portal HTN
- \*\*Cruveilhier-Baumgarten murmur= Venous hum that may be auscultated in Pts with portal HTN, best heard over epigastrium
- \*Umbilical hernia (2/2 portal HTN)
48
Cirrhosis: Neurologic findings
-Hepatic encephalopathy is associated with the following Sx:
Hepatic encephalopathy:
- Cognitive deficits & impaired neuromuscular function
- Disturbances in sleep pattern often initial changes
- Mood changes, inappropriate behavior, disorientation
- Somnolence, confusion, unconsciousness
- Bradykinesia
- Asterixis= Flapping motion of outstretched, dorsiflexed hands
- Hyperactive or hypoactive reflexes
- Slurred speech
- Nystagmus
- Ataxia
- Focal neurologic deficit (\*\*hemiplegia most common)
- Coma (notes: Liver fx--- gets toxins out of body--- so with cirrhosis the toxins start building up--\> leading to Hepatic encephalopathy
Asterixis= ask Pt to hold their arms out in front of them and their hands start “flapping” (dorsiflexed hands)
49
Hepatic Encephalopathy: ______ is the best known neurotoxin that precipitates encephalopathy
-\*\*Ammonia
50
Hepatic encephalopathy:
-are elevated ammonia levels needed to make the Dx of HE?
NO! Elevated levels are NOT needed to make diagnosis
- Not specific for HE
- Do NOT use to screen asymptomatic patients
51
Cirrhosis: Extremity changes
-change associated w/ nails:
Describe Muehrche nails
Describe Terry nails
Muehrcke nails= Paired white horizontal bands separated by normal color
Terry nails= Proximal 2/3 of the nail plate appears white, distal 1/3 is red
52
Cirrhosis: extremity changes
- Dupuytren’s contracture=
- other extremity changes?
=Thickening & shortening of palmar fascia causes flexion deformities of the fingers
-clubbing
53
Cirrhosis: lab findings
- AST/ALT are \_\_\_\_
- ALP is \_\_\_\_
- GGT levels are \_\_\_\_\_
- Bilirubin levels are _____ as cirrhosis progresses
- AST/ALT usually moderately elevated
- Usually AST more so than ALT
- ALP usually elevated. \<2-3x ULN (upper limits of normal)
- GGT: Levels usually much higher in cirrhosis caused by alcohol than other causes
- Bilirubin levels: ↑ as cirrhosis progresses
(notes: -GGT= much higher in Pts with alcohol abuse problems (GGT= think “gonna get tipsy” (alc causes GGT to leak from liver cells)
54
Cirrhosis: Lab findings
- albumin levels?
- PT?
- Sodium levels?
- Serum Cr?
- Albumin: ↓ as cirrhosis worsens
- PT: ↑ as the ability of a cirrhotic liver to make clotting factors ↓
- Hyponatremia common
- Serum Cr may ↑ as hepatorenal syndrome develops
(liver is the only organ that makes albumin--\> albumin and proteins fx to keep fluid in their cells --- decreased albumin leads to 3rd spacing (ascites and pancreatitis)
55
Cirrhosis: lab findings
-what happens with platelet levels?
Cytopenias: --\>\*\*Thrombocytopenia is MC
-\*\*Leukopenia & anemia develop later
56
Cirrhosis:
-Which diagnostic test is gold standard?
\*\*Liver biopsy is gold standard
-Bx not needed if clinical, lab, and radiologic data strongly support the presence of cirrhosis & won’t change management
57
Cirrhosis: other diagnostic tests
- ultrasound findings?
- noninvasive tests?
Ultrasound:
- Liver may appear small & nodular
- Increased echogenicity with irregular appearing areas
- Noninvasive tests of hepatic fibrosis (ie: FibroScan): Used for staging of fibrosis helps determine treatment
58
Major Complications of Cirrhosis (list 7 ex's)
Variceal hemorrhage
Ascites
Spontaneous bacterial peritonitis
Hepatic Encephalopathy
Hepatocellular carcinoma
Hepatorenal Syndrome
Hepatopulmonary Syndrome
59
Variceal hemorrhage: -varices result from \_\_\_\_\_\_
portal HTN
60
Variceal Hemorrhage:
-Associated with ____ mortality rates
Pts are asymptomatic until they present with:
- Associated with high mortality rates from bleeding episodes
- Asymptomatic until present with: Hematemesis, melena
61
All Pts with cirrhosis should undergo screening for varices with \_\_\_\_\_
EGD
62
If variceal Hemorrhages are found, they typically have \_\_\_\_\_
band ligation
63
Variceal Hemorrhage:
-Pharmacologic prevention?
-Nonselective beta blockers: lower portal pressure and ↓ risk of bleeding I.e.: propranolol, nadolol
64
What is the MC complication of cirrhosis?
\*\*Ascites
65
Ascites is accumulation of fluid in the \_\_\_\_\_
peritoneal cavity
66
Ascites: tx?
- describe diuretic therapy (specific ratio) ?
- describe paracentesis (remove how much fluid?)
For larger fluid overload volumes what can be given?
\*\*diuretics & sodium restriction, alcohol abstinence= 1st line
-Some may need repeated paracentesis
\*\*Diuretic therapy: Spironolactone + furosemide in a ratio of 100:40 mg/day
Paracentesis: For tense ascites, need to rapidly decompress abdomen--\> Remove 4-5L --\>For larger volumes, albumin can be given
67
If SAAG is high, what does this indicate?
SAAG= serum ascites to albumin gradient
if SAAG is high--\> it's prbly due to portal HTN--\> leading to \*\*Ascites
68
Ascites: -describe TIPS?
TIPS= Transjugular intrahepatic portosystemic shunts
\*\*TIPS is used for Pts with refractory ascites
(notes: TIPS procedure decreases portal HTN and helps mediate a lot of these issues (ie ascites-- it's a shunt b/w the portal vein and hepatic vein)
69
Spontaneous Bacterial Peritonitis (SBP) is an infection of the \_\_\_\_\_
ascetic fluid
70
Spontaneous Bacterial Peritonitis: Sx?
Fever, abdominal pain, abdominal tenderness, and AMS (\*\*confusion)
71
Spontaneous Bacterial Peritonitis: diagnosed with positive _____ &/or increased ______ count
-MC cases are due to which 2 organisms?
+ ascetic fluid bacterial culture and/or ↑ polymorphonuclear leukocyte count (≥250 cells/mm3) on eval of ascetic fluid --\>\*\*Most cases due to E. coli & Klebsiella
72
Spontaneous Bacterial Peritonitis:
-mortality rate?
High mortality without early antibiotic treatment
73
Spontaneous Bacterial Peritonitis: -tx?
Start empiric treatment ASAP! Ie: cefotaxime 2 g IV Q8H
-Those who have previously survived an episode should get \*\*daily abx ppx: Norfloxacin or Bactrim
74
Hepatorenal Syndrome= the development of renal failure in a Pt with advanced \_\_\_\_\_\_
-describe what happens to renal perfusion
liver disease
--\>Renal perfusion decreased by hepatic dysfunction (reduced effective blood volume)
75
Hepatorenal Syndrome: -diagnosis?
Diagnosis of exclusion when other causes of renal dysfunction have been excluded
76
Hepatic Hydrothorax= presence of ______ \_\_\_\_\_\_ in a Pt with cirrhosis and no evidence of underlying cardiopulmonary disease
pleural effusion
77
Hepatic Hydrothorax:
- which side is MC and why
- Tx?
- \*\*Usually right sided--\>From movement of ascites into the pleural space through defects in the diaphragm
- Tx: diuretics, & sodium restriction --Thoracentesis if needed
78
Hepatopulmonary Syndrome= abnormal arterial oxygenation caused by \_\_\_\_\_\_
intrapulmonary vascular dilatations (IPVDs) in the setting of liver disease
79
Hepatopulmonary Syndrome: -suspect in Pts with cirrhosis who have \_\_\_\_\_\_\_
dyspnea, Platypnea, impaired oxygenation
80
platypnea=
SOB that is relieved while lying DOWN
81
Hepatopulmonary Syndrome:
- imaging studies?
- what is the ONLY definitive therapy?
- Chest imaging often nonspecific and PFTs often normal
- Progressive
- Only definitive therapy is liver transplantation
- NO effective medical therapies apart from long-term oxygen therapy
82
Hepatic Encephalopathy: address any _________ factors
precipitating (hepatic encephalopathy= a decline in brain function that occurs as a result of severe liver disease. In this condition, your liver can’t adequately remove toxins from your blood. This causes a buildup of toxins in your bloodstream, which can lead to brain damage)
83
Hepatic Encephalopathy: Why should Pts be prescribed lactulose?
Lactulose--\>Leads to decreased ammonia from the GI tract--\>Titrate until patient is having 2-3 loose stools/day -Can be given as an enema if patient can’t take PO (notes: you’re trying to get rid of the ammonia in their system, in order to relieve their confusion -lactulose-- causes increased pooping (2-3 loose stool per day, in order to get rid of that ammonia) this is why Pts aren’t a fan of this med, may be non compliant)
84
Hepatic Encephalopathy:
-other tx options 2nd to lactulose?
- Nonabsorbable antibiotics (ie \*\*rifaximin)
- Generally added to lactulose therapy or used in those who can’t tolerate lactulose
- \*Lactulose & rifaximin often combined
- May have mortality benefit (for Pts taking both meds)
85
Hepatic Encephalopathy:
-those with recurrent HE are given lactulose and Rifaximin as \_\_\_\_\_\_
prophylaxis
86
Pts with cirrhosis have an INCREASED risk of developing ________ carcinoma
hepatocellular carcinoma (HCC)
87
Decompensation in a previously compensated Pt should raise suspicion that ____ may have developed
hepatocellular carcinoma (HCC)
88
Hepatocellular Carcinoma:
sx?
labs?
- Usually asymptomatic except for those related to chronic liver disease
- Some may have upper abdominal pain, weight loss, early satiety, palpable abdominal mass
Labs: usually nonspecific. --May have elevated AFP levels
89
Hepatocellular Carcinoma:
-what is the only effective screening/dx plan?
\*serial ultrasound every 6 months
90
Hepatocellular Carcinoma: tx?
- \*Surgical resection= preferred therapy
- Liver transplant only other possible curative option
91
Portopulmonary Hypertension=
Pulmonary hypertension in patients with portal hypertension
92
Portopulmonary Hypertension: -Sx?
May have fatigue, dyspnea, peripheral edema, chest pain, and syncope
93
Portopulmonary Hypertension:
Dx?
tx?
-mortality?
- Dx suggested on echo--\> Confirmed with Right heart cath
- Very difficult to treat with medical therapy
--High perioperative mortality with liver transplantation
94
Cirrhosis: General Management
- \*\*Abstain from alcohol -Substantially improves survival
- Tx of chronic viral hepatitis
- Vaccinate against Hepatitis for those not already immune
- Medication adjustments if needed for hepatic impairment
95
Prognosis for compensated Cirrhosis
Median survival \>12 years
96
Prognosis for Decompensated Cirrhosis
- Median survival?
- MELD score?
- Median survival ≤ 6 months in patients with decompensated cirrhosis and a Child-Pugh score ≥ 12 or -MELD (Model for End-stage Liver Disease) score ≥ 21
- Those who had been hospitalized with an acute liver-related illness also had a median survival of ≤6 months -
The lower the mean arterial pressure, the worse the survival
97
Child-Pugh Score classification -
Classes: A- score of 5-6, and 7-9= class B, score 10-15= class C
-refer Pt to transplant center if score hits 10
Must order: -LFTs (albumin and bilirubin) & PT & INR
98
MELD Score=
-what labs does it require?
Model for end stage liver disease Labs: Bilirubin, Creatinine, INR, Sodium, (think CISB)
99
MELD:
-Refer Pts with a score of \_\_\_\_
Refer at ≥10
-Usually a candidate for liver transplant at ≥15
100
MELD score also predicts \_\_\_\_\_
outcomes
101
Indications for liver transplantation:
- Acute liver failure (highest priority)
- Cirrhosis with complication
- Some neoplasms
- Liver-based metabolic conditions with systemic manifestations (ie: Wilson disease (systemic dz that effects the liver), CF, hemochromatosis)
102
Contraindications for liver transplantation:
- Uncorrectable cardiopulmonary disease too risky for surgery
- AIDS
- Malignancy outside liver not meeting oncologic criteria for cure
- Uncontrolled sepsis
- Persistent nonadherence with medical care
- Lack of adequate social support
103
Alcoholic liver disease requires a minimum abstinence of at least \_\_\_\_\_\_\_
6 months
104
Decompensated cirrhosis:
- Median survival is \_\_\_\_\_
- Child Pugh score \_\_\_\_\_
- MELD score \_\_\_\_\_\_
- the lower the \_\_\_\_\_, the WORSE the survival
-Median survival ≤ 6 months in patients with decompensated cirrhosis
- Child-Pugh score ≥ 12
- or MELD (Model for End-stage Liver Disease) score ≥ 21
- Those who had been hospitalized with an acute liver-related illness also had a median survival of ≤6 months
- \*\*The lower the mean arterial pressure (MAP), the worse the survival
