Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SBM GI > 02-19 D/O of G.B. and Biliary Tract > Flashcards

02-19 D/O of G.B. and Biliary Tract Flashcards

1
Q

Label Me

A

A = RHD

B = LHD

C = CHD

D = CBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Label Me 2

A

A = RHA

B = LHA

C = HA

D = Celiac a.

E = splenic a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Label me, too

A

A = pancreatic v.

B = sup. mesenteric v.

C = splenic v.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is in bile?

A
  1. bile salts 67%
  2. phospholipids 22%
  3. cholesterol 4%
  4. protein 4%
  5. bilirubin 0.3%
  6. water/ions/solvent drag

**only relevant mechanism for cholesterol secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is bilirubin processed in the liver?

A

conjugated to glucoronic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
  • storage
  • controlled delivery of bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name of communication between common bile duct and duodenum

A

Sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Factors that favor gallstone formation

A
  • high [chol]
  • low [bile acids]
  • low [phospholipids]
  • low gallbladder emptying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When is bile flow the slowest?

A

during fasting, duh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which cells make bile?

A

75% by hepatocytes

25% by cholangiocytes (epithelial cells of the bile duct)

Total: 600mL/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the roles of bile? Mechanism for those roles?

A
  1. 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
  2. elimination of wastes (namely chol)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

  1. Gilbert’s syndrome
    • common
    • benign, presents w/ stress
    • dx of exclusion
    • etio = ‪↓‬ GT
  2. Crigler-Najar
    • rare
    • Type I = no GT
    • Type II = ‪↓‬ ‪↓‬ GT

DIRECT CAUSES

  1. 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
  1. Bili >2mg/dL (not not be jaundiced yet)/gray stool/dark urine
  2. pruritus
  3. Labs:
    • ↑Bili, ↑AlkP, ↑GGT, ↑Chol
  4. Xanthomas
  5. 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

  1. Prevalence?
  2. Types of gallstones?
  3. xray finding?
  4. Presentation and frequency of stones getting stuck at different locations
A

PREV:

  • 10% of adults

TYPES

  1. Cholesterol
    • most common, but radioluscent
  2. 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
Q

Acute Cholecystitis

  • Clinical presentation
  • Exam
  • Labs
  • Imaging
  • Complications
A

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
Q

Choledocholithiasis

  • Clinical Presentation
  • Exam
  • Labs
  • Imaging
  • Complications
A

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
Q

Ascending Cholangitis

  • Etiology
  • Clinical Presentation
    • Two Mnemonics!
  • Exam
  • Labs
  • Imaging
  • Complications
A

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
Q

Risk Factors for Gallstones

A
  • 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
Q

Gallbladder Dz in Pregnancy?

  • Etiology of increased risk
  • Sx/PE
  • Dx
  • Mgmt
A

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
Q

What is most sensitive dx procedure for gallstones and dilated bile ducts

A

abdominal ultrasound

31
Q

ERCP

A

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
Q

MRCP

A

Magnetic resonance cholangiopancreatography

  • Still good: 95% sensitive and specific for CBD stones
  • non-invasive
33
Q

Medical Mgmt for Gallbladder Disease

A

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
Q

Acute Acalculous Cholecystitis

A
  • 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
Q

GB Neoplasms

  • Prevention?
  • Risks?
  • Prognosis
A

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
Q

Sclerosing Cholangitis

A

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
Q

Choledochal Cysts

A

Increases r/o cancer

Five Types: I-V

  • Type I: most common
  • Type V: intrahepatic cysts = Caroli’s dz
38
Q

Cholangiocarcinoma

A
  • 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
Q

Review the cases

A

That the surgeon did

SBM GI (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions