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m2 CA2 > hpb patho (incomplete, summarised version) > Flashcards

hpb patho (incomplete, summarised version) Flashcards

1
Q

Obstructive jaundice is due to obstruction of the bile duct from different aetiologies.

  • _____ conjugated bilirubin
  • conjugated bilirubin found in the ____
A

Obstructive jaundice is due to obstruction of the bile duct from different aetiologies.

  • increased conjugated bilirubin
  • conjugated bilirubin found in the urine
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2
Q

Which of the effects of portal hypertension is a medical emergency?

A

Oesophageal varices
Hepatorenal syndrome

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3
Q

Acute on chronic liver failure is either:
1. An _______________ supervening on a well-compensated late-stage chronic disease
2. Chronic disease has a ___________ that leads directly to liver failure

A

Acute on chronic liver failure is either:
1. An unrelated acute injury supervening on a well-compensated late-stage chronic disease
2. Chronic disease has a flare of activity that leads directly to liver failure

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4
Q

What is chronic liver failure usually associated with?

A

Cirrhosis

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5
Q

What are the causes of chronic liver failure?

A

NAFLD
ALD
Hepatitis B/C
Crytogenic

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6
Q

Gross appearance of cirrhosis?

A

Shrunken, firm, nodular

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7
Q

Histological features of cirrhosis?

A

Loss of normal vascular structure
Fibrosis
Regeneration

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8
Q

How often are liver cirrhosis asymptomatic until most advanced stages?

A

40%

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9
Q

Nonspecific manifestation of liver cirrhosis includes:

A

anorexia, weight loss, weakness

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10
Q

symptoms and signs of liver failure

A

Coagulopathy
Portal Hypertension
Hyperestrogenemia
Dupuytren’s contracture
Cholestasis

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11
Q

What is an additional complication of liver cirrhosis?

A

HCC

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12
Q

What are the most common terminal events in cirrhosis?

A

hepatic encephalopathy
oesophageal varices
bacterial infection

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12
Q

In matrix remodeling in liver cirrhosis

Synthesis (Scarring) is caused by:
Degradation (Regression) is caused by:

A

In matrix remodeling in liver cirrhosis

Synthesis (Scarring) is caused by: hepatic stellate cells
Degradation (Regression) is caused by: matrix metalloproteinases

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13
Q

Whats the concern with splenomegaly that is secondary to portal HTN?

A

increased venous pressure -> congestive splenomegaly -> accumulation of leukocytes, erythrocytes, platelets in spleen -> facilitates capture, phagocytosis, destruction of blood cells by phagocytes -> peripheral cytopenias

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14
Q

Acute liver failure is when there is

A

massive and sudden destruction of hepatocytes

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15
Q

What is acute liver failure associated with?

A

encephalopathy
coagulopathy

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16
Q

What are the causes of acute liver failure?

A

autoimmune hepatitis
acute hepatitis A/B/E
drugs/toxins

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17
Q

Gross appearance of liver in acute liver failure?

A

shrunken liver with wrinkled liver capsule

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18
Q

Histological features of liver in acute liver failure?

A

loss of hepatocytes
RBC extravasation
florid ductular reaction

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19
Q

What are the 5 most common sites for portosystemic shunts? (relate to portal HTN)

A

lower oesophageal
upper anal canal
umbilicus
retroperitoneal
diaphragm surface of liver

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20
Q

The liver has enormous ______________
- so mild liver damage may be clinically masked + liver injury and healing may be asymptomatic
- by the time of clinical presentation, most liver diseases will already be chronic, except acute liver failure

A

functional reserve

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21
Q

What are the parameters for liver function test?

A

Hepatocyte integrity (cytosolic hepatocellular enzymes)
- {{c1::AST}}
- {{c1::ALT}}
- {{c1::LDH}}

Biliary excretory function (increase in normal secretions)
- {{c1::Serum bilirubin (total, unconjugated, conjugated)}}
- {{c1::Urine bilirubin}}
- {{c1::Serum bile acids}}

Bile canaliculus integrity
- {{c1::ALP}}
- {{c1::GGT}}

Hepatocyte synthetic function
- {{c1::Serum albumin}}
- {{c1::Coagulation factors (PT, PTT, Factors 1,2,5,7,9,10)}}

Hepatocyte metabolism
- {{c1::Serum ammonia}}
- {{c1::Aminopyrine breath test (hepatic demethylation)}}

  1. The Child-Pugh liver function test would include (mn “BETA-PTI”)
    - {{c2::Big belly - Ascites}}
    - {{c2::Encephalopathy}}
    - {{c2::Total bilirubin}}
    - {{c2::Serum Albumin}}
    - {{c2::PT Time}}
    - {{c2::INR}}
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22
Q

The Child-Pugh liver function test (in chronic liver cirrhosis) would include:

A

BETA-PTI

Belly - Ascites
Encephalopathy
Total bilirubin
serum Albumin
PT time
INR

23
Q

Hyperbilirubinaemia can be predominantly unconjugated or conjugated.

What is the difference between the 2?

A

Unconjugated bilirubin is water-insoluble and albumin-bound and cannot be excreted in urine even in high doses but can cross BBB in infants and cause kernicterus

Conjugated bilirubin is water soluble, non-toxic and can be excreted out in the urine

24
Q

Most common cause of post hepatic jaundice is ________

A

large bile duct obstruction

25
Q

Budd-Chiari syndrome is associated with…

They present with a clinical triad of…

A

Budd-Chiari syndrome is associated with hepatic vein thrombosis

They present with a clinical triad of abdominal pain, ascites, liver enlargement

26
Q

In cholangitis (or ascending cholangitis), there is a specific triad and pentad:
Charcot’s Triad
Reynolds’ pentad

A

Charcot’s Triad:
- Fever
- Jaundice
- Right upper quadrant pain

Reynolds’ Pentad:
- Charcot’s Triad
- Hypotension
- Altered mental state

27
Q

Choledochal cyst is {{c1::development malformation of biliary tree, usually CBD}}

What does choledochal cysts predispose the pt to?
{{c1::Stones, stenosis, strictures, pancreatitis, bile duct cancer!!}}

A

Choledochal cyst is {{c1::development malformation of biliary tree, usually CBD}}

What does choledochal cysts predispose the pt to?
{{c1::Stones, stenosis, strictures, pancreatitis, bile duct cancer!!}}

28
Q

Focal Nodular Hyperplasia is due to {{c1::focal alterations in hepatic blood supply}}

A

Focal Nodular Hyperplasia is due to {{c1::focal alterations in hepatic blood supply}}

29
Q

What is Cholangiocarcinoma?

A

Carcinoma with bile duct origin, arising from either inside or outside the liver
2nd most common primary malignancy of the liver, after HCC

30
Q

What are the risk factors of cholangiocarcinoma?

A

Hepatolithiasis
Fibropolycystic liver disease

31
Q

How does the location of the cholangiocarcinoma affect presentation?

A

Intrahepatic: late presentation
Extrahepatic: early presentation and smaller

32
Q

Factors that affect prognosis of hepatocellular carcinoma (HCC)

A

Staging
Grading
Number and size of nodules
Vascular spread
Presence of cirrhosis

33
Q

Islets of Langerhans neoplasms
clinical presentation of insulinoma

A

Whipple Triad:
Hypoglycaemia
CNS manifestations during fasting/exercise
Symptom relief with administration of glucose

34
Q

Most common site of pancreatic carcinoma is…

A

Head of pancreas

35
Q

Gross appearance of pancreatic carcinoma

A

Large pale firm mass with infiltrative borders
Adenocarcinoma with desmoplasia
Perineural and lymphatic involvement

36
Q

Both acute and chronic pancreatitis are initiated by injuries that led to

A

autodigestion of pancreas by its own digestive enzymes

37
Q

What are the normal mechanisms that protects the pancreas from self-digestion?

Pancreatitis occurs when these protective mechanisms are deranged/overwhelmed!!

A
  • digestive enzymes synthesise inactive proenzymes
  • trypsin is activated only in the duodenum
  • inhibitors of trypsin
38
Q

In cases of jaundice, only hepatic and post-hepatic causes will result in ________ being formed. (not pre-hepatic cause)

A

pale stools

39
Q

Acute pancreatitis = {{c1::Reversible pancreatic parenchymal injury associated with inflammation}}

A

Acute pancreatitis = {{c1::Reversible pancreatic parenchymal injury associated with inflammation}}

40
Q

What are the main causes of acute pancreatitis?

A
41
Q

Chronic pancreatitis = {{c1::prolonged inflammation of the pancreas associated with irreversible destruction of exocrine parenchyma and fibrosis}}. In the late stages there is destruction of {{c1::the endocrine parenchyma (Islets of Langerhans)}}

A

Chronic pancreatitis = {{c1::prolonged inflammation of the pancreas associated with irreversible destruction of exocrine parenchyma and fibrosis}}. In the late stages there is destruction of {{c1::the endocrine parenchyma (Islets of Langerhans)}}

42
Q

hepatitis A is associated with the consumption of raw shellfish

A
43
Q

vaccination for hepatitis B prevents hepatitis D infection

A
44
Q

hepatitis E has the highest mortality rate in pregnant women

A
45
Q

between acute viral and chronic viral hepatitis, it is the pattern of injury that is different, not the nature of inflammatory cell infiltrate

acute viral hepatitis: lobular hepatitis
chronic viral hepatitis: portal hepatitis

A
46
Q

both hep B and hep C can progress to chronic hepatitis however patients with hep C infection is more likely to progress to chronic hepatitis while only 20-30% of patients with hep B will progress to chronic hepatitis

A
47
Q

donated blood is usually screened for hep B and hep C

A
48
Q

hep B is the only DNA virus

A
49
Q

hep A is the only one with faecal-oral mode of transmission

A
50
Q

What are the key histologic feature of cirrhosis?

A

loss of normal vascular architecture
fibrosis
regeneration

51
Q

State the common aetiologies for cirrhosis

A

NAFLD
ALD
Chronic hep B/C
a1 anti-trysin deficiency

51
Q

What are the treatment options available for HCC?

A

Surgical resection
Loop Ablation
Immunotherapy
Liver transplantation

52
Q

Congenital abnormalities of the pancreas:

A

Pancreatic division
Annular pancreas
Ectopic pancreas
Agenesis

53
Q

histological features of HCC

A

sinusoidal trabeculae
broad and thick trabeculae
high N:C ratio, nuclear atypia

54
Q

hepatocellular adenoma is a benign lesion that resembles a normal liver and are typically common in women taking oral contraceptives (using oestrogen-containing meds)

A

m2 CA2 (22 decks)

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