Biliary Flashcards
1
Q
Triangle of Calot is divided by the ____ artery
A
cystic
2
Q
Bile is composed of…
A
bile salts
3
Q
Bile salt functions to
A
aggregate around lipids to form a micelle
4
Q
Bile is important for…
A
fat digestion and absorption
5
Q
Fat soluble vitamins are…
A
A, D, E, K
6
Q
Fat in the duodenum triggers…
A
release of CCK from the duodenum that causes the gallbladder to release bile
7
Q
Gallbladder disease arises from…
A
anything that slows or prevents outflow of bile from the gallbladder.
8
Q
What can slow/prevent outflow of bile from the gallbladder? (five things)
A
- inflammation
- infection
- stones
- stenosis
- obstruction
9
Q
Cholelithiasis & acute cholecystitis occurs most commonly in…
A
“fat, fertile, forty-year old, fai-haired females”
10
Q
Cholethiasis occurs commonly due to
A
gall stones
11
Q
Gall stone composition
A
80% cholesterol
12
Q
Biliary colic etiology
A
spasm of the cystic duct usually from obstruction from a stone
13
Q
What condition are you thinking when you see the following…
- Sudden onset of pain that is constant for 1-5 hours
- RUQ or midepigastric pain, that may radiate to R shoulder blade
- Pain associated with fatty meals
A
Clinical presentation of biliary colic
14
Q
Test of choice for biliary colic
A
ultrasound: see gall stones and no wall thickening or pericholecystic fluid
15
Q
treatment of biliary colic
A
- monitor
- may progress to acute cholecystitis
- elective cholecystectomy
16
Q
Chronic cholecystitis is caused by…
A
repeated bouts of acute inflammation of the gallbladder from biliary colic or mild acute cholecystitis
17
Q
What are the defining characteristics of chronic cholecystitis?
A
chronic inflammation can lead to calcification of the gallbladder known as a “porcelain gallbladder”
18
Q
Etiology of acute cholecystitis
A
blockage of cystic duct, usually cholelithiasis becomes lodged in the duct
19
Q
Acute cholecystitis mimics what other condition
A
Biliary colic, but acute cholecystitis is more severe
20
Q
What condition are you thinking when you see the following…
- RUQ pain radiating to right scapula
- pain worse with movement and lasting >4 hours
- N/V, low grade fever
- +Murphy’s sign
A
acute cholecystitis
21
Q
what is murphy’s sign
A
deep palpation of RUQ - positive when pain occurs with palpation that prevents a deep inspiration
22
Q
Lab studies for acute cholecystitis:
CBC
CMP
A
CBC: leukocytosis with left shift
CMP: increased alkaline phosphate, bilirubin, ALT, AST
23
Q
Imaging for acute cholecystisis
A
RUQ ultrasound is test of choice and see stones
CT: fat stranding (inflammation), stones, dilated duct, r/o abscess
24
Q
Management of acute cholecystitis
Intake?
Pain management?
Surgical?
ABX?
A
- Intake: NPO/IV fluids
- Pain management: demerol to avoid sphincter of oddi contraction
- Surgical: laparoscopic cholecystectomy
- ABX: ceftriaxone and metronidazole
25
Choledocholithiasis is...
- a stone in the common bile duct
| - symptomatic when stone obstructs
26
What condition are you thinking when you see the following...
- anorexia, N/V
- light colored stools, tea-colored urine
- jaundice
- pruritus
Choledocholithiasis
27
Diagnostic gold standard for Choledocholithiasis
ERCP
28
Lab diagnostics of Choledocholithiasis
Elevated GGT
| Elevated ALT, AST, ALP
29
common complication of Choledocholithiasis
acute pancreatitis
30
do you give Choledocholithiasis abx?
yes
31
Cholangitis or Ascending Cholangitis etiology
Infection of the biliary tree caused by stasis of the common bile duct. Stasis is usually due to stone obstructing CBD or inflation post manipulation.
32
Common infecting organisms in Cholangitis or Ascending Cholangitis
E. coli, Klebsiella, Bacteriodes, Enterococcus
33
Cholangitis Clinical Presentation
Charcot’s Triad: fever/chills, RUQ pain, jaundice
Reynold's Pentad: fever, RUQ pain, jaundice, hypotension, mental status change
34
Charcot’s Triad
Cholangitis
Fever/chills
RUQ pain
Jaundice
35
Reynold's Pentad
```
Cholangitis:
Fever
RUQ pain
Jaundice
Hypotension
Mental status change
```
36
Lab diagnostics in ascending cholangitis
CBC
LFT
Blood Cx
CBC: high wbc, >20K
LFT: elevated bilirubin, ALP, ALT/AST (slight)
Blood Cx: + in 50%
37
Imaging diagnostics in ascending cholangitis
ERCP: Visualize stone, maybe able to remove
MRCP (an ERCP with an MRI on the end)
38
How to handle "Pus under pressure" of cholangitis
- Start high dose broad spectrum Abx
- Aggressive IV fluid, thinks SIRS
- Surgery to decompress biliary system
- After “cooling off” patient should undergo cholecystectomy
39
Pancreatic release of enzymes is stimulated by...
gastric acid
CCK from duodenum
Vagal stimulation
40
Insulin is produced in...
beta cells of the islets of langerhans of the pancreas
41
acute pancreatitis
inflammatory disease characterized by autodigestion of the pancreas by proteolytic enzymes, activated and produced from within the pancreases
42
acute pancreatitis etiology
alcohol
biliary tract disease (stones blocking sphincter of Oddi most common)
hypertriglyceridemia (>500)
trauma
drugs (thiazides, estrogen, sulfonamides, slaicylates, HEART)
43
Physical exam of acute pancreatitis shows...
fever
tachycardia
abdominal tenderness, guarding, and distention
44
uncommon signs of severe necortizing pancreatitis
Cullen’s Sign: Periumbilical ecchymosis
Grey-Turner’s Sign: Flank ecchymosis
45
acute pancreatitis laboratory diagnostics
CBC: leukocytosis with left shift
| Elevated lipase
46
why do you not give pain control in mild pancreatitis?
can cause sphincter of oddi contrition which increases pain/severity
47
acute pancreatitis complications to be aware of
pancreatic abscess can lead to a pseudocyts or necrotic area that causes the pancreas to autodigest and leads to clinical deterioration
48
exocrine functions of pancreas
releases lipase, amylase, and proteases
49
endocrine functions of the pancreas
glucagon and insulin
50
chronic pancreatitis
Repeated episodes of acute inflammation leading to chronic damage and ductal obstruction
51
chronic pancreatitis etiologies
alcoholism
cystic fibrosis
idopathic
52
chronic pancreatitis clinical presentation
epigastric pain radiating to back (aggravated by alcohol/fatty meals)
steatorrhea
malabsorption (secondary to loss of exocrine functions)
weight loss
S/Sx of diabetes (3 polys)
53
3 polys of DB s/sx from chronic pancreatitis
polyuria
polydypsia
polyphagia (excessive hunger)
54
What do you start to see on imaging with chronic pancreatitis?
scattered calcifications
55
diagnostics for chronic pancreatitis
ERCP - shows chain of lakes
| MRCP
56
chronic pancreatitis
diabetes: loss of endocrine functions
steatorrhea: loss of exocrine function
pancreatic calcifications
57
pancreatic carcinoma
95% from exocrine portion (adenocarcinoma)
| 75% of cancers occur in head/neck of pancreas
58
Courvoisier's Sign
enlarged palpable non-tender gallbladder in patients with obstructive jaundice caused by tumors of biliary tree or pancreatic head tumors
59
Clinical presentation of pancreatic carcinoma
```
early satiety/anorexia
weight loss
jaundice
abdominal pain
vague/nonspecific
courvoisier's sign
```
60
Diagnostics of pancreatic carcinoma
CT scan
61
Number one cause of liver failure in US
NASH (nonalcoholic steatohepatitis)
62
NASH and alcoholic steatohepatitis
NASH is clinically indistinguishable from alcoholic steatohepatitis
63
definitive diagnosis for NASH
liver biopsy showing steatosis, inflammation, cirrhosis
64
progression of alcoholic liver disease
Alcoholic steatosis →
Steatohepatitis →
Cirrhosis →
Hepatocellular Carcinoma
65
clinical presentation of alcoholic hepatitis
jaundice, fever, anorexia, proximal muscle wasting, hepatomegaly, tenderness to palpation over liver, bruit over liver
66
Diagnostics of alcoholic hepatitis
liver biopsy shows mallory bodies: neutrophil infiltration into the liver & fatty changes
WBC count is normal
67
unique clinical presentations of alcoholic hepatitis
spider angiomata
| palmar erythema
68
inheritance of hereditary hemochromatosis (HH)
autosomal recessive
69
diagnostics of HH
genetic testing
| liver biopsy with iron
70
late clinical findings of HH
DM
71
treatment of HH
Control diet:
Avoid iron rich foods (red meat)
Avoid acidic food (acid make iron more absorable)
Avoid Alcohol
72
Wilson's disease
Rare, hereditary disorder of copper metabolism that results in increased absorption and poor hepatic excretion
Autosomal Recessive
73
Clinical presentation of Wilson's Disease
Kayer-Flesher ring (cooper ring around cornea) and fatty infiltration of the liver leading to cirrhosis
74
Diagnostics & Treatment of Wilson's Disease
low serum ceruloplasmin with liver biopsy
treated with penicillamine
75
Alpha-1 antitrypsin disease
regulates effects o neutrophil elastase produced by neutrophils in the lungs
COPD occurs at a younger age in these populations due to the destruction of the alveoli
76
buildup of α-1 Antitrypsin sequence
Leads to hepatitis leading to cirrhosis leading to HCC
77
Hepatitis A virus transmission & associated with...
Does not cause chronic disease or HCC
Spread via fecal-oral route
Epidemic associated with uncooked shellfish, vegetables, and fruit
78
Hepatitis A clinical presentation in children
ASx in >90%
79
Hepatitis B transmission and progression
Transmitted: Blood, Sexual contact, Parenteral contact
HBV is leading cause of cirrhosis and HCC (hepatocellular carcinoma) worldwide
80
HBsAg
Positive= have virus & are chronic carriers
81
HBsAb or Anti-HBs
Positive in vaccinated and people who have cleared the virus.
82
Anti-HBc IgM
Indicates acute or recent infection
83
HBV DNA
Can be quantitatively measured to obtain a viral load
84
Hepatitis C
Most common chronic blood infection
Needles and cocaine (from the shared straw)
Sexually transmitted very rare
85
Leading cause of chronic liver disease
Hepatitis C
86
Most common cause for liver transplant
Hepatitis C
87
Leading cause of HCC (hepatocellular carcinoma)
Hepatitis C
88
Clinical presentation of Acute HCV
HVC is asymptomatic
89
Clinical presentation of ChronicHCV
Majority are asymptomatic
RUQ discomfort
Thrombocytopenia
90
HCV RNA
Detects the presence of virus 1-2 weeks after exposure
Determines genotype
91
Hepatitis D virus
Patients infected with HDV are always infected with HBV
No clinical difference in patients infected with HBV or HBV+HDV.
92
Cirrhosis clinical presentation
Fatigue, Weakness
Fluid Retention, Edema, Ascites
Dupuytren’s Contractures
(Fingers flex in)
Palmar Erythema, Spider Angiomata
Jaundice, ecchymosis
Gynecomastia, Testicular Atrophy
HSM
Abd vein dilation, Caput Medusa
93
Complications of cirrhosis
Hepatic encephalopathy
Esophageal varices
Hepatorenal Syndrome
Spontaneous Bacterial Peritonitis
94
Hepatic Encephalopathy - what is it and what are clinical manifestations
Bacteria in GI track produce ammonia, the liver usually detoxifies, but can’t.
Ammonia builds up and is neurotoxic.
Altered mental status, Personality changes, Obtundent, LOC, “Liver Flap”
95
Esophageal Varices
| - what is it and what are clinical manifestations
Portal vein HTN causes dilatation of veins in esophagus. If ruptures, Pt can bleed out fast and it’s difficult to control the bleeding. Bad
96
Treatment for Hepatic Encephalopathy
Lactulose – binds NH3 and is excreted in feces (need at least three BMs a day).
Rifaximin – Non-absorbed Abx, Kills NH3 producing bacteria in GI tract
97
Treatment for esophageal varices
Reduce portal HTN with nonselective beta-blocker (nadolol)
HR < 50
98
Cirrhosis treatment
5:2 ratio of Spironolactone & Lasix (control ascites and hypoalbuminemia)
Nonselective Beta-blockers (nadolo, propranolol) to control portal HTN
Lactulose to control encephalopathy
ABD US Q6M screen for HCC
99
HCC screening
Screen all cirrhotics Q6M with Abd US
No longer use AFP for screening
