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ED Primary Exam > Week 19 Pathology - Liver/Biliary > Flashcards

Week 19 Pathology - Liver/Biliary Flashcards

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1
Q

What percentage loss of liver function before failure occurs?

A

90%

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2
Q

What are the most common causes of liver failure/disease?

A

Acute: viral hepatitis, drugs/toxins –> acute fulminant necrosis

Chronic: most common route to failure, either chronic viral infection, alcoholic or NAFLD steatohepatitis –> cirrhosis

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3
Q

What is the mechanism by which hepatic encephalopathy occurs?

A

Porto-systemic shunt means that ammonia and other toxic metabolites bypass the liver not metabolised to the same extent –> direct toxicity effect on cerebral cortex.

More chronically, derangement of neurotransmitter production causes neuronal dysfunction, fluctuating episodes usually secondary to reversible insults (metabolic, drugs, increased protein load in gut)

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4
Q

What are clinical symptoms/signs of hepatic encephalopathy?

A

Behavioural changes
Confusion/stupor
Flap
Hyper-reflexia
Coma

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5
Q

What is the functional unit of the liver?

A

Lobule

Hexagonal unit, with portal triad on each corner, and central vein in middle. Sinusoids connect the triads to central vein. Bile flows central to peripheral, venous and arterial blood from triads to central vein.

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6
Q

What is cirrhosis?

A

Replacement of normal architecture of liver with fibrous/collagenous tissue

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7
Q

What are the characteristic histological findings of cirrhosis?

A

Bridging Fibrous septa
Parenchymal nodules

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8
Q

What is the ‘Space of Disse’?

A

Space between sinusoidal epithelial cells and hepatocytes

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9
Q

What cell is responsible for the deposition of proteins/collagen in the space of disse?

A

Perisinusoidal stellate cells (usual role is Vit A storage, but become activate into myofibroblast in cirrhosis)

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10
Q

What is the pathophysiology of cirrhosis/liver inflammation?

A

Inflammation/hypoperfusion in liver lobules (from different causes) results in parenchymal atrophy and stellate cell regeneration.

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11
Q

How does cirrhosis lead to ascites?

A

Due to remodelling and destruction of vascular architecture, significantly increased resistance to blood flow through portal system, increased hydrostatic pressure and transudative effect with leakage of fluid into peritoneal cavity

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12
Q

What are kuppfer cells?

A

Resident macrophages of the liver responsible for mopping up GI bacteria/toxins and preventing entry to systemic circulation

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13
Q

List some causes of pre-hepatic, intra-hepatic and post hepatic portal hypertension?

A

Pre = portal vein thrombosis, massive splenomegaly
Intra = cirrhosis
Post = right heart failure, hepatic vein outflow obstruction, constrictive pericarditis

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14
Q

How does the RAAS system exacerbate ascites?

A

Renal retention of sodium and water occurs as under-perfusion of kidneys, despite portal HTN causing leakage of volume into peritoneum –> viscous cycle

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15
Q

What are the sites of collateral circulation in portal HTN?

A

Anterior abdomen - caput medusae
Rectum - haemorrhoids
Lower 1/3 oesophagus - varices

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16
Q

What is hepatorenal syndrome?

A

In setting of severe liver disease, development of renal failure without primary abnormalities of the kidneys (i.e. retina ability to concentrate urine) –> unknown mechanism, but splanchnic vasodilation and systemic vasoconstriction

Clinically presents with reduced urine output, rising urea and creatinine, hyperosmolar urine without protein

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17
Q

What is portopulmonary HTN?

A

Pulmonary arterial hypertension associated with liver disease/portal HTN. Due to pulmonary vasoconstriction and vascular remodelling –> cor pulmonale.

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18
Q

What is hepatopulmonary syndrome?

A

Abnormal intrapulmonary vascular dilation and increased pulmonary blood flow –> increased shunting and V/Q mismatch. Unclear pathophysiology.

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19
Q

What are the common histological feature of alcoholic and NAFL disease?

A
  1. Steatosis –> fatty change/deposition in centrilobular hepatocytes
  2. Hepatitis –> hepatocyte ballooning, swelling and necrosis, neutrophil infiltrations permeate lobule
  3. Fibrosis –> collagen desposition in space of disse
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20
Q

What is the threshold of EtOH consumption for development of ALD?

A

60g/day, 10-15 years

  • 90% develop steatosis
  • 10-35% steatohepatitis
  • 2-20% cirrhosis
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21
Q

What is the rate of HCC in patients with cirrhosis?

A

10-20%

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22
Q

What is the pathogenesis of steatosis in ALD?

A

Shunting of substrates towards lipid biosynthesis, impaired lipoprotein synthesis and secretion, and increased peripheral catabolism of fat –> increased fat deposition in the hepatocytes

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23
Q

What mechanisms perpetuate hepatocyte injury in ALD?

A

1.Metabolism of EtOH to aldehyde uses up a lot of the NAD required for metabolising fats

2.Decreased methionine metabolism = less glutathione, which means more oxidative damage from metabolising EtOH, toxins etc

3.Alcohol metabolism induces production of ROS that can damage cell structures/DNA and cause cell damage

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24
Q

What are the criteria for diagnosis of metabolic disease?

A

HTN
Hyperlipidaemia
Insulin resistance
Obesity

**2 or more

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25
What is the brief outline of bilirubin metabolism?
RBCs --> macrophages, Hb split into heme and globin Haem split into Fe2+ and protoporphyrin --> acted on by enzymes to be converted into biliverdin --> bilirubin. UC bilirubin bound to albumin in plasma, travels to hepatocytes, metabolised there via UGT-1 to conjugated bilirubin --> able to be excreted in bile/urine.
26
What changes occurs to bilirubin in faeces?
Deconjugated via gut bacteria to urobiliniogens, excretion in faeces or reabsorption in ileum/colon and re-excretion in bile.
27
What are causes of unconjugated hyperbilirubinaemia? I.e. too much bilirubin generated, or too little conjugated
Haemolytic anaemia Haemorrhage/GI bleed Haemoglobinopathies Liver disease (hepatitis, cirrhosis, drug induced) Physiological jaundice of the newborn
28
What are the causes of conjugated hyperbilirubinaemia? (Impaired intra-extra hepatic blood flow)
Inflammatory destruction of intrahepatic bile ducts --> Primary biliary cirrhosis, Primary sclerosing cholangitis Gallstones Pancreatic/Gallbladder carcinoma causing obstruction of bile flow
29
What is the mechanism behind Gilbert's syndrome?
Fluctuating unconjugated hyperbilirubinaemia due to decreased levels of hepatic glucuronosyltransferase
30
What are common symptoms/signs of cholestasis?
Jaundice Pruritis (deposition of bile salts) Skin xanthomas
31
What are the differences in patterns of cell injury in acute vs chronic viral hepatitis?
Acute = minimal or absent portal inflammation (i.e. skips the inflammation phase, but cell injury/necrosis occurs Chronic = dense mononuclear portal infiltrates
32
What are the two forms of hepatocyte cell injury/death in viral hepatitis?
1) Ballooning degeneration, emptying pale cytoplasm, swells and ruptures (necrosis) 2) Apoptosis, cell shrinkage, eosinophilic, fragmented nuclei
33
What are the rough time frames for incubation of viral hepatitis(es)?
Oral transmission (A+E) = 2-8 weeks BBV (B,C,D) = 4-26 weeks (2-26 for Hep C)
34
What is the major cause of cellular injury in Hep A virus?
T Cell mediated damage/killing. Virus itself doesn't appear to be toxic to hepatocytes
35
What are the various responses to Hep B infection? (in terms of resolution vs chronic infection?)
1. Acute hepatitis with recovery and clearance 2. Fulminant hepatitis with massive liver necrosis 3. Non progressive chronic hepatitis 4. Progressive chronic hepatitis --> cirrhosis 5. Asymptomatic carrier state
36
What % of Hep B infections progress to chronic infection?
10%
37
What are the different components of the Hep B virus that relate to serology?
Hep B surface antigen Hep B core antigen Hep B DNA
38
Outline the interpretation of serology for Hep B infection vs clearance vs immunity?
HepBsAg = virus present in blood, infection confirmed the supervillain) Hep B cAg = viral particles present in blood, marker of infection HepB eAg = marker of active replication HepB surface IgG Ab/Anti-HBs = immunity (either vaccine or exposure and clearance) HepB core antibodies = infection
39
What is the clinical course with Hep B and associated serological findings?
HepBsAg appears before onset of symptoms , peaks during overt disease, becomes undetectable in 3-6 months HbeAg, HBV-DNA, DNA polymerase in serum soon after HbsAg, signify active replication In chronic infection, HepB C IgM becoming Hep B C IgG = sign of persistent infection/not being cleared
40
What proportion of Hep C progresses to chronic infection?
80%
41
What serology is important in establishing presence of infection in Hep C?
HCV IgG HCV RNA PCR Viral RNA load marker of ongoing infection if remaining static vs decreasing
42
What are other viruses capable of causing hepatitis?
EBV CMV HSV Yellow fever
43
What is the pathogenesis for cholecystitis?
90% gallstone relating biliary obstruction --> exposure of mucosa to detergent action of bile salts, along with distension and compromised blood flow due to increased intraluminal pressure
44
What is the cause of acalculous cholecystitis?
Sepsis Severe burns Severe trauma Typically occurs in critical illness, hypoperfusion syndrome to gallbladder
45
What are the 2 major types of gallstones?
Cholesterol stones Pigment stones
46
What are risk factors for formation of cholesterol stones?
Dyslipidaemia Female Obesity European/western
47
What is the pathogenesis of cholesterol stone formation?
Concentrations of cholesterol in bile exceed solubilising capacity of bile , precipitates out of solution. Most radiolucent, some have CaCO3- to be radioopaque.
48
What are risk factors for pigmented stones?
Chronic haemolytic (sickle, spherocytosis) -->elevated levels of unconjugated bilirubin in biliary tree
49
What is cholangitis?
Acute inflammation of bile duct wall, usually resulting from bacterial infection
50
What are common causes of cholangitis?
Choledocholithiasis Biliary tree instrumentation Pancreatitis Strictures
51
What does ascending cholangitis refer to?
Bacteria within biliary tree infecting intrahepatic biliary ducts
52
What organisms are commonly responsible for ascending cholangitis?
E. coli Klebsiella Enterococci Clostridium Bacteroides
53
What proportion of acute pancreatitis is causes by alcohol and gallstones?
80%
54
What are the causes of pancreatitis more exhaustively? (IGETSMASHED)
Idiopathic/ischaemia Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion Hypercalcaemia, hypertriglyceridaemia ERCP Drugs (thiazides, chemotherapy, OCP, anticonvulsants)
55
What is the pathogenesis of pancreatitis?
Autodigestion of pancreatic substance by inappropriately activated pancreatic enzymes.
56
What 3 pathways can lead to inappropriate activation of trypsin?`
1. Pancreatic duct obstruction: increased intraductal pressure causes accumulation of enzyme rich interstitial fluid (lipase secreted in active form) 2. Primary acinar cell injury (ischaemic, traumatic, infection) 3. Defective intracellular transport of of proenzymes within acinar cells (i.e. proenzymes and lysosomal hydrolyses packaged together and leading to activation of enzymes) --> EtOH
57
What are morphological changes/features of acute pancreatitis?
- Microvascular leakage causing oedema - Fat necrosis from lipases - Acute inflammatory reaction - Proteolytic destruction of pancreatic parenchyma - Destruction of blood vessels leading to interstitial haemorrhage
58
What are severe complications of pancreatitis?
DIC ARDS Diffuse fat necrosis Shock ATN
59
What are the characteristics of chronic pancreatitis?
Long standing inflammation, fibrosis and destruction of exocrine pancreas --> major difference being irreversible impairment of pancreatic function compared with acute pancreatitis Profibrogenic cytokines lead to remodelling and deposition of collagen --> fibrosis of pancreas
60
What is the clinical presentation of chronic pancreatitis?
Malabsoprtion Diabetes Recurrent abdominal pain
61
How do oesophageal varices form in portal HTN?
Portal HTN makes it harder for returning intestinal venous blood to get back to the IVC, inducing formation of collateral channels via porto-systemic shunts (of which distal oesophagus and stomach are one)
62
What is peptic ulcer disease?
Defect in gastric/duodenal mucosa extending to muscular mucosa
63
What location is most common for the formation of PUD?
Gastric antrum Duodenum
64
What is the underlying pathophysiology of PUD?
Imbalance in mucosal defences between forces causing chronic gastritis
65
What are common causes of gastric hyperacidity?
H. pylori infection Parietal cell hyperplasia
66
What are common cofactors in development of PUD?
NSAID use Smoking Steroids Alcohol
67
What are the major complications of PUD?
Perforation Haemorrhage/GI bleed IDA
68
What cell type is associated with intestinal metaplasia? What complication is associated?
Change from stratified squamous epithelia to pseudo stratified columnar epithelia (Barrett's Oesophagus) Risk of gastric adenocarcinoma
69
What are the 4 categories of diarrhoea?
1) Secretory (isotonic stool, persists during fasting) 2) Osmotic (occurring i.e. due to lactase deficiency, unabsorbed luminal solutes ,improves with fasting) 3) Malabsorptive (inadequate nutrient absorption, i.e. steatorrhoea) 4) Exudative (inflammatory disease, purulent, bloody stools, persist during fasting)
70
What is the causative organism for cholera, and how does it cause diarrhoea?
Vibrio cholera, gram -ve flagellated bacterium Preformed enterotoxin activates adenylyl cyclase which leads to increased intracellular cAMP and opening of CFTR chloride channels --> releasing chloride ions into bowel lumen, and impairing sodium and bicarbonate absorption --> SECRETORY DIARRHOEA
71
What are the 4 virulence factors associated with C. jejuni?
1. Motility 2. Adherence 3. Toxin production 4. Invasion
72
What is shigella classified as?
Gram -ve, non motile, facoltative anaerobe
73
What diarrhoea syndrome does shigella cause? What is the pathophysiology?
Dysentery - resistent to acid of stomach, divides intracellularly, and escapes to invade colonic epithelia via lamina propria
74
What classification exists for different types of E. coli?
Enterotoxigenic: - traveller's diarrhoea, heat labile and heat stable toxin, increases intracellular cGMP, watery diarrhoea Enterohaemorrhagic: - gives rise to HUS, produces Shiga toxin, causes bloody stool Enteroinvasive: - resembles shigella, doesn't produce toxin, causes bloody diarrhoea Enteroaggregative: - Produce labile toxin, can cause less severe but more protracted diarrhoea
75
What is the cause of pseudomembranous colitis?
C. difficile - Gram +ve bacillus
76
What is the pathophysiology of pseudomembranous colitis?
Toxins release by c. difficile cause disruption of epithelia, loss of tight junctions, apoptosis. Pseudomembrane composed of layer of inflammatory cells + debris at site of mucosal injury
77
What are features of rotavirus?
Encapsulated virus, infects mature enterocytes in small intestine - causing repopulation with immature secretory cells --> net loss of absorptive capacity and and osmotic diarrhoea from incompletely absorbed nutrients
78
What are the defining patterns of mucosal injury that differentiate ulcerative colitis and Crohn's disease?
UC = limited to colon and rectum, extending only to mucosa and submucosa Crohn's = any area of GIT, frequently transmural
79
What are the macroscopic differences between Crohn's and UC?
Ulcers: deep and narrow for Crohn's, broad and shallow for UC Inflammation: transmural Crohn's, mucosa/submucosa UC Skip lesions, Crohn's Fistulas Crohn's, not UC
80
What are the microscopic differences in Crohn's vs UC?
Marked lymphoid reaction in Crohn's, less so UC Granulomas Crohn's, not in UC
81
What effect does Crohn's have on fat/vitamin absorption?
Can be impaired, Fe2+ absorption too in terminal ileal disease
82
Which form of IBD does toxic megacolon occur in?
Ulcerative colitis
83
What are complications of Crohn's disease?
IDA Short gut syndrome Malabsorption/malnutrition Strictures Fistulas Perforation
84
What are extra-intestinal features of Crohn's disease?
Uveitis Migratory polyarthritis Erythema nodosum Clubbing of fingers Primary sclerosing cholangitis
85
What part of the bowel is always involved in UC?
Rectum, then extends proximally
86
Why is screening colonoscopies important for UC/Crohn's?
Risk of colonic epithelial dysplasia and adenocarcinoma
87
What are some causes of acute Ischaemic bowel?
Severe atherosclerosis and plaque rupture Aortic aneurysm Septic or arterial emboli
88
What are some subacute causes of watershed/not territorial bowel ischaemia?
Cardiac failure/shock Vasoconstrictive drugs Vasculitides
89
What can cause gut ischaemia involving increased venous pressure?
Cirrhosis/portal HTN Mesenteric vein thrombosis
90
What are the two distinct phases involved in bowel ischaemic injury?
1) initial hypoxic insult, where epithelial cells remain pretty resistant to transient hypoxia 2) Reperfusion injury: restoration of blood supply, and associated free radical production and neutrophil infiltration and inflammatory cytokine release
91
What are the watershed zones of intestinal anatomy?
Splenic flexure (where superior and inferior mestenteric circulation terminate) Rectosigmoid colon (termination of inferior mesenteric pudendal and iliac arterial supply)
92

ED Primary Exam (46 decks)

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