HPB Patho Flashcards
1
Q
Anatomy of the biliary system
A
2
Q
What are th eparts of the common bile duct
A
- Supra duodenal
- Retroduodenal
- Pancreatic- retro pancreatic and
- AMpullary
3
Q
Patterns on insertion
A
Note - unluje ureter drainage is less strictly gravitational and more difficutl to navigate.
4
Q
Why dy do you get Gall stones/Cholelithiasis/Choledocholithiasis
A
- Crystalline precipitation due to increased solute concentration
- Stasis- not a good gravitational drainage unlike ureters
- pH change (less relevant)
- Infection- may act as nidus of solute precipitate
- Chronic haemolysis (pigment stones)
- Prolonged fasting with total parenteral nutrition (TPN)
- Previous ileal disorders
- Bowel resection (short bowel syndrome)- increased enterohepatic recycling
5
Q
Presentation of gallstones
A
- Typical surgical lore- 5F- Fair, fatty, fertile, flatulent, female above 40
- No longer true
- Acute or chronic presentation
- Pain in right hypochondrium
- Acute abdomen- peritonitis
- DD- gastric perforation, acute appendicitis, MI, acute pancreatitis
6
Q
What is this?
A
Chronic calculus cholecystitis =Chronic cholecystitis is swelling and irritation of the gallbladder that continues over time.
- Foamc lls in lamina propria-cholesterolosis
- Transmural chronic inflammation
7
Q
Complications of Chronic claculus cholecystitis
A
- Gangrene, perforation, peritonitis
- Obstructive jaundice – Courvoisier’s sign/law- painless palpable gall bladder is not due to gall stones- may be pancreatic or cholagiocarcinoma
- Mirizzi syndrome types I and II- I (stone in cystic duct or Hartmann’s pouch- at the neck- compresses the CHD) II (stone erodes into CHD forming a cholecystocholedochal fistula)
- Choloduodenal fistula
- Gall stone ileus- typical impacted stone 2ft away from the ICJ (ileocaecal junction)
- Gall stone pancreatitis
8
Q
What are the causes of pancreatitis
A
- Gall stone, alcohol- vast majority
- The following are worth knowing
- Autoimmune (types I and II)- AIP type I- part of IgG4 associated sclerosing disorders- a specific subunit of plasma cells secreting fibrogenic IgG4 and type II AIP- characterized by GEL (granulocytic epithelial lesion)
- Cystic Fibrosis
- Hypertriglyceridemia
- Specific genetic mutations apart from CFTR
- For completion- trauma, drugs, scorpion bite, pancreatic tumour
- Chronic hypercalcaemia usually chronic calcific pancreatitis
9
Q
WHta are the risk factors of pancretitis
A
- Gall stones (2%)
- Alcoholic (2-3%)
- Smokers
- Morbid obesity
- Type II Diabetes in the young (maturity onset diabetes of the young)
- ERCP (5-10%)
10
Q
WHat is the presentation of pancreatitis
A
- Sudden onset constant epigastric or left hypochondrium pain
- Radiating to back, chest or flanks
- Nausea and vomiting
- Fever/Diaphoresis (excessive abnormal sweating in relation to the activity level)
11
Q
Pancreatitis diagnosis
A
- 2 of the following 3 criteria
- Characteristic abdominal pain
- Radiological evidence of pancreatitis on abdominal imaging
- Biochemical evidence of pancreatitis- serum lipase and/or amylase > 3 times the upper limit of reference range for the lab/population
12
Q
Pancreatitis (Revised atlanta classification)
A
- Interstitial oedematous pancreatitis ( non-necrotic)
- Necrotising pancreatitis
- In addition, traditionally autopsy pathologists recognized acute haemorrhagic pancreatitis
13
Q
Pancreatitis grading
A
- Mild- no organ failure, no systemic or local complications (80-85%)
- Moderate- local/systemic complications with/without transient organ failure
- Severe- organ failure > 48 hours (15-20%)
14
Q
2 Phases of pancreatitis
A
- Early- 1-2 weeks characterized by SIRS (systemic inflammatory response syndrome) if persists organ failure may develop
- Late- > 2 weeks, only in patients with severe disease with local complications
15
Q
Clinical findings of pancreatitis
A
- Restless patient, may flex knees compressed against the abdomen to alleviate pain
- Hypertension due to pain or hypotension due to shock
- Basal crepts and rales due to pleural effusion (milky lipaemic quality)
- Abdomen rigid with guarding, distended, rebound tenderness
- Core temperature- may be high or low
- Raised respiratory and heart rate
- Altered mentation, peri umbilical ecchymoses due to haemorrhage and jaundice in severe cases
16
Q
Treatment of pancreatitis
A
- Common supportive treatment- fluid and electrolyte balance, pain control, nutritional support
- Further management based on cause and complications
- Biliary pancreatitis- ERCP (endoscopic retrograde cholangiopancreatography, biliary sphinctreotomy +/- cholecystectomy
- Antibiotics for infected necrosis
- May require ICU escalation
17
Q
Ix in pancreatitis
A
- USG- for stones, if negative- CT/MRI/EUS (endoscopic ultrasound when stable)
- Blood- serum lipase, amylase, C reactive protein, blood urea, creatinine, haematocrit, Alkaline phosphatase, ALT, bilirubin, Gamma Glutamyl transferase- for diagnosis, cause and treatment monitoring
- Serum triglycerides and calcium if no stones
18
Q
WHat is the modified marshall score for pancreatitis
A
- To assess organ failure in acute pancreatitis
- Assess 3 organs
- Lung (PaO2:FiO2- arterial partial pressure of O2 to fraction of inspired O2)
- Kidney - serum creatinine
- Heart- systolic blood pressure
19
Q
BISAP Score for severity in pancreatitis
A
20
Q
Ransons score on admission in pancreatitis
A
Ranson criteria are used to predict the severity and mortality of acute pancreatitis.
21
Q
Ransons score at 48horus for pancreatitis
A
Ranson criteria are used to predict the severity and mortality of acute pancreatitis.
22
Q
What is the criteria for pancreatitis escalation to ICU
A
- SIRS
- Organ failure
- BISAP score > 2 within 24 hours of admission
- APACHE II score >8 within 24 hours of admission
- Acute physiology and chronic health evaluation score- out of scope of this lecture
23
Q
Complications of pancreatitis
A
- Exocrine insufficiency
- Endocrine dysfunction
- Bowel infarction, perforation, septic shock, MOD/ARDS
- Duct disruption- stenting/resection
- Bowel compartmental syndrome- new onset organ failure due to high intra abdominal pressure
- Peripancreatic vascular complications- splenic vein thrombosis, pseudoaneurysm (latter with high mortality if cannot be embolized or resected)
- Exacerbation of pre-existing comorbidities
- 5% mortality due to MODS rather than necrosis
- Recurrence unless modifiable causative factor
- Pancreatic pseudocyst - Retropancreatic lfuid collection. No true epithelial lining. High cyst fluid amylase. Cholesterol crystals, haemosiderin laden macrophages, giant cells, bile pigment, but no true peithleial cells on cytology.
- Pancreatic fat necrosis: “bright side of the moon”: Saponification, due to lipase, distincitive histological diagnosis. Often firts manifestation of pancreatic cancer (acinic cell carcinoma). Another distinctive manifestationis necrolytic migratory erythema. Can also get the image due to pancreatic glucagonoma.
29
Q
Structure of ths anatomical liver unit - lpbule
A
30
Q
Functional/flow unit of th eliver- acinus
A
32
Q
What is the pringle manouvre
A
- First described by James Hogarth Pringle
- Hepatoduodenal ligament compression reduces bleeding from liver
- As it limits the dual supply through portal vein and hepatic artery
45
Q
What is cirrhosis?
A
- Advanced bringing fibrosis (centro-portal, porto-portal, porto-central) with altered architecture resulting in nodularity
- Biopsy diagnosis- challenging
- Needs complex staging and grading system for degree of activity/inflammation and stage of fibrosis
- Different grading for steatohepatitis, and haemochromatosis
- Assessment of abstinent changes in alcoholic liver disease
51
Q
6 patterns of LFTs
A
