U17 + 18 > HPB Patho > Flashcards

HPB Patho Flashcards

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1
Q

Anatomy of the biliary system

A
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2
Q

What are th eparts of the common bile duct

A
  • Supra duodenal
  • Retroduodenal
  • Pancreatic- retro pancreatic and
  • AMpullary
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3
Q

Patterns on insertion

A

Note - unluje ureter drainage is less strictly gravitational and more difficutl to navigate.

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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
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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
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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
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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
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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
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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%)
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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)
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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
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12
Q

Pancreatitis (Revised atlanta classification)

A
  • Interstitial oedematous pancreatitis ( non-necrotic)
  • Necrotising pancreatitis
  • In addition, traditionally autopsy pathologists recognized acute haemorrhagic pancreatitis
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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%)
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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
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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
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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
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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
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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
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19
Q

BISAP Score for severity in pancreatitis

A
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20
Q

Ransons score on admission in pancreatitis

A

Ranson criteria are used to predict the severity and mortality of acute pancreatitis.

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21
Q

Ransons score at 48horus for pancreatitis

A

Ranson criteria are used to predict the severity and mortality of acute pancreatitis.

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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
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23
Q

Complications of pancreatitis

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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.
25
Prognosis of pancreatitis
* 5% mortality * 35% in severe * 47% in MODS * 3% in oedematous interstitial pancreatitis * 17% in necrotizing pancreatitis * 16-25% recur in first year after first episode, up to 35% in children
26
Function of the liver
* **Synthetic functions-** proteins, enzymes, vitamins * **Metabolic function**s- intermediary and final steps- central role in metabolic homeostasis * Detoxification and excretory functions (endogenous and exogenous) including toxins (xenobiotics)- **FILTRATION** * **Energy release**- glucose and acetoacetate by glycogenolysis, gluconeogenesis, and Beta oxidation of fatty acids * **Storage**- lipoproteins and glycogen, on demand streaming in circulation for peripheral uptake * **Bile production and secretion**- RBC destruction (bilirubin) and cholesterol metabolism (bile salts reabsorbed by enterohepatic circulation) * **Carbohydrate and lipid metabolism** ( as previous) * **Protein metabolism**- Synthesis of albumin (exclusively in liver) and detoxification of protein waste into urea (urea cycle) * Ceruloplasmin (Wilson’s disease) and alpha 1 anti trypsin (Cystic fibrosis) synthesis * **Hepatic acute phase reactant**s- protein synthesis in acute metabolic stress (CRP- C reactive protein, SAA- serum amyloid A protein, alpha 1, 2 and Beta globulin) * **Fat soluble vitamin**s-ADEK- bile dependent absorption due to micellization * Also involved in range of w**ater-soluble vitamins metabolism** for conversion to active product or storage form * Coagulation
27
Coagulation functions of the liver
* Vit K dependent coagulation factors synthesis- II,VII,IX,X * Factor VII has shortest half life * Warfarin blocks synthesis of Vit K dependent factors * Prolonged PT (prothrombin time) and INR (international normalized ratio)
28
Druga nd toxin metabolism function of liver - What are the phases.
* **Phase I-** conversion to a water soluble compound by simple redox reaction or hydrolysis- does not detoxify, may be more toxic (cytochromep450s) * **Phase II-** Detoxification by transferase reaction (conjugation- e.g, conjugated bile by UDP glucoronosyl transferase enzyme- deficient in Crigler Najjar syndrome)- glucoronidation * Liver cell regeneration/plasticity- to adjust liver size on demand (host donor mismatch) * Different zones of liver carry out different functions selectively- hepatocyte heterogeneity- not uniform enzymatic content
29
Structure of ths anatomical liver unit - lpbule
30
Functional/flow unit of th eliver- acinus
31
Whta is the blood uspply to the liver
* **75% portal vein- nutrient rich O2 poor** * **25% hepatic artery- O2 rich** * Unique admixture in hepatic sinusoids * Drained in hepatic vein and IVC * Unique lining of hepatic sinusoids which changes in hepatocellular carcinoma- diagnostically useful (capillarization of sinusoid) * Portal system- starts and ends in capillaries- hepatic portal system, hypophyseal portal system
32
What is the pringle manouvre
* 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
33
Hepatitides: Causes
* Viral- A,B,C, E etc * Steatohepatitis- fatty liver (alcohol, diabetes, central obesity, metabolic/dysmetabolic/insulin resistance syndrome/ syndrome x- constellation of the other two with hypertension may be in early or preclinical phase with strong family history ) * Autoimmune hepatitis * Biliary hepatitis- due to bile duct pathology * Flow problems * Alpha 1 anti trypsin deficiency * Haemochromatosis * Drug induced liver injury (DILI)
34
Mechanism of viral hepatitis
Cytopathic effect (cell injury) due to encoded viral proteins/antigens
35
Mechanism of steatohepatitis
Cell injury due to abnormally excessive accumulation of normal metabolic products
36
Mechanism of autoimmune hepaittis
Immune mediated injury- non recognition as self antigen
37
Mechanism of biliary hepatitis, haemochromatosis
Excess accumulation of bile due to stasis and iron (HFE gene mutation in hereditary forms)
38
WHy do you get flow problems hepatitis
Ischaemia, congestion
39
Why do you get A1AT deficiency hepatitis
Deficient disorders
40
DILI- durg idnuced lier injury - what is th emechanism that thi leads to hepatitis
Any of the above non infective generic mechanisms (not specific deficiencies) such as immunological, bile stasis, steatosis, flow problems, necrosis
41
WHat drugs can cause durg induced liver injuryies (DILI)
* Most common- herbal medicines over the counter * Aspirin, acetamenophens and NSAIDs (non-steroidal anti-inflammatory drugs) * Anabolic steroids, OCP (oral contraceptive pills)- cholestasis, peliosis (bile and blood flow problem), OCP may cause benign hepatic adenoma * Statins * Antibiotics, sulfa medicines * Antiepileptics (phenytoin, valproate) * Dose dependent (non-recurrent) or immunological susceptibility mediated (recurrent) * Cessation and avoidance is key
42
Complications of hepatitis
* Acute- hepatic failure and encephalopathy * Portal hypertension * Chronic phase- most may pass on to chronic phase (except hepatitis A) * Bridging fibrosis * Partial cirrhosis/Nodular regenerative hyperplasia/NRH (very typical in flow problems) * Cirrhosis * Liver cell dysplasia- small cell dysplasia more significant than large cell dysplasia * Hepatocellular carcinoma (very high in untreated haemochromatosis historically- Moroccan leather cirrhosis- black in colour due to iron)
43
Portal hypertension is \>6MMhG, What are the effects of this and at what pressure does ascites occur
* Fibrosis pressing on portal vein, reduced exchange * Opening up of Portocaval shunts and bleeds * Oesophageal varix, portal hypertensive gastropathy, duodenopathy * Caput medusae- in umbilicus * Ascites- \>8mm Hg
44
What is the mecanism of ascites
* Ascites (Greek askos= wine bag/sac!!) * Overflow and underfill hybrid theory * Portal hypertension- congestion and overflow * Splachnic vasodilation causes * Renal underflow- RAAS activation by juxtaglomerular apparatus * Resulting in salt and water retention
45
What is cirrhosis?
* 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
46
What cells allows the chemical metabolic fnciton of the liver
Hepatocytes
47
What cells and how do these cells allow the scavenging funciton of the liver
* Chemical metabolic function- hepatocytes * Scavenging function- Kupffer cells lining sinusoids for Hb metabolism to produce bilirubin * Secretory function- canaliculi- production of bile
48
What do the canaliculi do?
production of bile - secreotyr function of liver
49
LFTs for hepatocyte injury
Hepatocyte injury- release of aminotransferases-AST (aspartate) and ALT (alanine) and LDH (lactate dehydrogenase) and reduction in albumin and total protein (chronic or fulminant only as 80% hepatocyte loss is required)
50
What LFT are for canalciular obstruction
Canalicular obstruction- Gamma glutamyl transferase (GGT), ALK ( alk phos/alkaline phosphatase) and conjugated bilirubinaemia
51
6 patterns of LFTs
52
What happens to LFTs in Hepatitis
* High AST * High ALT * Hight Lactate dehydrogenase * High Alkaline phosphatase * Normal Total protein * Normal albumin * High bilirubin * Normal ammonia
53
What is th epattern of lFTs on cirrhosis
* AST - Normal * ALT - Normal * Lactate dehydNormalrogenase - * Alkaline phosphatase- N - slightly high- * Total protein - Low * albumin - Low * bilirubin - High * ammonia - High
54
LFT pattern in biliary obstruction
* AST -Normal * ALT - Notmal * Lactate dehydrogenase - Normal * Alkaline phosphatase- High * Total protein - Normal * albumin - Normal * bilirubin - High * ammonia - Normal
55
LFT pattern in space occupying lesion in liver
* AST -Normal or high * ALT - Normal or High * Lactate dehydrogenasHighe - * Alkaline phosphatase- High * Total protein - Normal * albumin - nORMAL * bilirubin - n-h * ammonia - nORMAL
56
LFT pattern in passive ocngestion of liver
* AST -slightly high * ALT - Slightly high * Lactate dehydrogenase - slightly high * Alkaline phosphatase- normal- slightly high * Total protein - Normal * albumin - Normal * bilirubin - N-Slightly high * ammonia - Normal
57
LFT pattern in fulminant failure
* AST - very high * ALT - High * Lactate dehydrogenase - High * Alkaline phosphatase- High * Total protein - Low * albumin - Low * bilirubin - High * ammonia - High
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