02-19 D/O of G.B. and Biliary Tract Flashcards
(39 cards)
1
Q
Label Me
A
A = RHD
B = LHD
C = CHD
D = CBD
2
Q
Label Me 2
A
A = RHA
B = LHA
C = HA
D = Celiac a.
E = splenic a.
3
Q
Label me, too
A
A = pancreatic v.
B = sup. mesenteric v.
C = splenic v.
4
Q
What is in bile?
A
- bile salts 67%
- phospholipids 22%
- cholesterol 4%
- protein 4%
- bilirubin 0.3%
- water/ions/solvent drag
**only relevant mechanism for cholesterol secretion
5
Q
What is bilirubin and how does it get to the liver?
A
- yellow breakdown product of normal haeme catabolism
- gets to liver via albumin transport
6
Q
How is bilirubin processed in the liver?
A
conjugated to glucoronic acid
7
Q
Fxns of the GB?
A
- concentration
- Na+: 150mM → 280mM
- Na+ pumps
- Acid: <50mM → 300mM
- ph : 7.5 → 6.4
- stops stones
- Micelle formation (bile acid + Phospholipid + chol)
- Na+: 150mM → 280mM
- storage
- controlled delivery of bile
8
Q
Name of communication between common bile duct and duodenum
A
Sphincter of Oddi
9
Q
Factors that favor gallstone formation
A
- high [chol]
- low [bile acids]
- low [phospholipids]
- low gallbladder emptying
10
Q
When is bile flow the slowest?
A
during fasting, duh
11
Q
How is bile secretion controlled?
A
CCK is major mediator, released from duodenum in presence of food
- incr GB contractions
- sphincter relaxation
- release of pancreatic enzymes
- inhibits gastric emptying
12
Q
Secretin?
A
- hormone that both controls the environment in the duodenum by regulating secretions of the stomach and pancreas, and regulates water homeostasis throughout the body.
- produced in the S cells of the duodenum, which are located in the crypts of Lieberkühn.[1]
- Secretin helps in regulating the pH within the duodenum by inhibiting gastric acid secretion by the parietal cells of the stomach, and by stimulating bicarbonate production by the centroacinar cells and intercalated ducts of the pancreas.[4]
13
Q
Which cells make bile?
A
75% by hepatocytes
25% by cholangiocytes (epithelial cells of the bile duct)
Total: 600mL/day
14
Q
What are the roles of bile? Mechanism for those roles?
A
- Fat digestion + fat & Vits ADEK absorption
- Do this via emulsifying micelles that form from amphipathic bile salts
- Micelles needed for emulsion, absorption and transport of fat-solubles
- elimination of wastes (namely chol)
15
Q
Enterohepatic Circulation of Bile Acids
A
- We recycle ~95% of the 3-5g we make qD
- Micelles: absorbed along jejenum & ileum
- Mostly rest absorbed in terminal ileum
16
Q
How is cholesterol processed in bile formation?
A
It is hydroxylated to form bile acids.
500mg converted/day
17
Q
What might interrupt enterohepatic circulation? What s/sx would present?
A
- removal of inflammatory disease of the terminal ileum
- steatorrhea (more fat delivered to colon)
- diarrhea (bile salts act as osmotic laxative)
- nephrolithiasis
- cholelthiasis (b/c less bile salts returned → lithogenic)
18
Q
causes of unconjugated bili jaundice vs. conjugated bili jaundice
A
Unconjugated = indirect
- overproduction of bili (e.g. thalassemia)
- defective uptake from albumin at pancreas
- defective conjugation
Conjugated = direct
- defective excretion (e.g. obstruction)
19
Q
Hereditary Causes of Hyperbilirubinemia?
A
INDIRECT CAUSES
- Gilbert’s syndrome
- common
- benign, presents w/ stress
- dx of exclusion
- etio = ↓ GT
- Crigler-Najar
- rare
- Type I = no GT
- Type II = ↓ ↓ GT
DIRECT CAUSES
- Dubin-Johnson and Rotor Syndrome
- Problem w/ excretion after conjugation
20
Q
Define cholestasis
types?
A
blockage of post-conjugation bile flow
- Intrahepatic
- intrinsic liver dz
- defect in secretion across canalicular membrane
- Extrahepatic
- bile duct obstructed
21
Q
CLin criteria to dx cholestasis
A
- Bili >2mg/dL (not not be jaundiced yet)/gray stool/dark urine
- pruritus
- Labs:
- ↑Bili, ↑AlkP, ↑GGT, ↑Chol
- Xanthomas
- Malabsorption of fats and fat-soluble vitamins
- Vit K deficiency presents first b/c it has shortest T1/2
22
Q
Causes of extrahepatic (i.e. obstructive) cholestasis?
A
- gallstones
- strictures (inflamm or malig)
- neoplasm
- parasites
23
Q
Cholelithiasis
- Prevalence?
- Types of gallstones?
- xray finding?
- Presentation and frequency of stones getting stuck at different locations
A
PREV:
- 10% of adults
TYPES
- Cholesterol
- most common, but radioluscent
- Pigment/Calcium
- caused by: hemolysis, cirrhosis, biliary infx
- radiopaque)
PRESENTATION
- 75% asx
- symptomatic: 1-2% r/o complications/yr
- sx:
- 30 min crescendo-plateau-decrescendo pain in RUQ w/ n/v
- often at night
- atypical in: oldies, immunodefic, bad DM, RF pts
COMPLICATIONS
- cholecystitis
- 20%: intermittent cystic duct → intermit colic
- 10%: impacted cystic duct → acute cholecystitis
- 0.1%: impacted distal cystic duct, compresses CHD
- 0.1%: long-standing cholelithasis → GB Ca
- choledocholithiasis = 5%
- (see separate card)
- pancreatitis
- biliary enteric fistula
- gallstone ileus (passed stone → ileus)
- porcelain gallbladder
- Mirizzi Syndrome
24
Q
Mirizzi Syndrome
A
stone lodged in the cystic duct or neck of gallbladder causing CBD compression
25
Acute Cholecystitis
* Clinical presentation
* Exam
* Labs
* Imaging
* Complications
Clinical presentation
* ongoing (building; vs. lithiasis) RUQ pain w/o resoultion
Exam
* Murphy's sign
Labs
* Elevation in Bili, AST, ALT, Alk P
* (vs. nl bili in lithiasis, methinks)
Imaging
* US w/ typical findings
Complications
* empyema, gangrenous Gb, perf, peritonitis, fistula
26
Choledocholithiasis
* Clinical Presentation
* Exam
* Labs
* Imaging
* Complications
jaundice, biiary colic-type pain w/ r/o ascending cholangitis or acute biliary pancreatic
**Clinic**: Recurrent RUQ/epigastric pain
May resolve
Preceding episodes
**Exam**: nonspecific
**Labs**: Bili, ALP, GGT (AST, ALT)
May be transient
**Imaging**: US with typical findings
**Complications**: Cholangitis, pancreatitis, cirrhosis
27
Ascending Cholangitis
* Etiology
* Clinical Presentation
* Two Mnemonics!
* Exam
* Labs
* Imaging
* Complications
**Etio**: Obstruct → Stasis → Bact. overgrowth → Infx
**Clinic**: acute, life threatening
preceding pain episodes
**Charcot’s triad**: RUQ pain, jaundice, fever
**Reynold’s pentad**: Charcot + MS changes + shock
**Exam**: toxic-appearing, jaundice, tender
**Labs**: Elevation in Bili, ALP, GGT, AST, ALT
**Imaging**: US (dilated CBD)
\*\*Don't let the sun set on cholangitis." -R.R.
—If you wait to long: rupture → sepsis
28
Risk Factors for Gallstones
* Increasing age
* Female sex (2-3X ♂!! cholesterol stones)
* Pregnancy (2nd most common indication for surg while preg!)
* Exogenes estrogens
* Genetics, FHx
* Lifestyle factors
* Obesity
* Abstinence of ETOH
* Low physical activity
* Diet: high caloric, high carbohydrate, low fiber
* Rapid weight loss
* Diseases
* DM, high insulin, high Tgl
* Crohns disease
29
Gallbladder Dz in Pregnancy?
* Etiology of increased risk
* Sx/PE
* Dx
* Mgmt
Pathophysiology:
↑ Gb residual and fasting volume
↓ Gb contractility and rate of emptying
Symptoms / Physical exam:
—absent Murphhy’s sign
—AP less helpful (elevated in pregnancy)
Diagnosis: US (EUS)
Management: conservative in 1st and 3rd trimesters; ERCP for choledocholithiasis; safest time to undergo cholecystectomy 2nd trimester
30
What is most sensitive dx procedure for gallstones and dilated bile ducts
abdominal ultrasound
31
ERCP
Endoscopic Retrograde Cholangiopancreatography
* gold std for dx of choledocholithiasis
* for tx
* pull stone out with grabber or insert balloon proximal to ballon, blow up and pull out
* risk of pancreatitis (5%!!)
32
MRCP
Magnetic resonance cholangiopancreatography
* Still good: 95% sensitive and specific for CBD stones
* non-invasive
33
Medical Mgmt for Gallbladder Disease
Still hasn't really panned out.
Options include: Oral dissolution therapy w/ ursodeoxycholic acid (ursodiol)
* Successful in small (\< 1 cm) non-calcified stones
* Success rate 60% - 80%; stones recur in 30-50%
34
Acute Acalculous Cholecystitis
* Typically in patients with severe and acute systemic illnesses (e.g. sepsis, burns, trauma, ICU patients on parenteral feeding)
* Most likely due to ischemia, gallbladder stasis, biliary sludge formation, and secondary bacterial contamination
1. Dehyd from multiple transfusions → pigment load
2. GB stasis w/ hyperalimentation & assisted ventil
3. Accum of biliary sludge, viscous bile, and GB mucus
4. Cystic duct obstruction in absence of frank stone formation
5. Inflamm & edema of wall, compromising blood flow
6. Bact contamination & generation of lysolecithins
35
GB Neoplasms
* Prevention?
* Risks?
* Prognosis
**Polyps**
* bigger = bigger r/o transforming to ca
* prevent by resect when \>1cm
**Gallbladder Carcinoma**
Prevalence
* Less than 1% of US Ca
Risks
* Gallstones (present in ≥60%)
* Chronic cholecystitis & porcelain GB
* Chroning infection (Clonorchis sinensis, Ascaris lumbricoides)
* Primary sclerosing cholangitis
* Congenital anomalies (Choledochal cysts)
Prognosis
* Poor prognosis b/c late dx
36
Sclerosing Cholangitis
**Common cause of liver transplants!**
**Primary sclerosing cholangitis (PSC)**
chronic, fibrosing, inflammatory process of the bile ducts
→ obliteration of biliary tree
→ biliary cirrhosis
**Secondary sclerosing cholangitis**
Chronic biliary obstruction with secondary fibrosing process
→ biliary cirrhosis
37
Choledochal Cysts
Increases r/o cancer
Five Types: I-V
* Type I: most common
* Type V: intrahepatic cysts = Caroli's dz
38
Cholangiocarcinoma
* Tumor of cholangiocytes
* Rare, but rising incidence
* 10-15% of all hepatic malignancies
* Poor survival (\<5% within 5 years)
* Risks: PSC, Clonorchis sinensis, congenital cysts
\*\*“Klatskin tumor” = carcinoma of the bifurcation\*\*
39
Review the cases
That the surgeon did
