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GI Liver > exocrine Pancreas, Gallbladder > Flashcards

exocrine Pancreas, Gallbladder Flashcards

0
Q

What derives from the dorsal pancreatic bud?

A

Body, tail, accessory pancreatic duct, Isthmus

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1
Q

What’s derives from the ventral pancreatic buds?

A

Uncinate process + Main pancreatic duct

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2
Q

Explain annular pancreas

A

Ventral pancreatic bud abnormally in circles second part of duodenum

Form ring of pancreatic tissue Around 2nd part of duodenum = obstruct/narrow duodenum

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3
Q

Explain pancreas divisum

A

Ventral and dorsal buds failed to fuse @week eight

  1. asymptomatic
  2. Possible chronic pain +/or pancreatitis
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4
Q

How does pancreatitis occur?
What actually happens to the pancreas?
What happens as a result?

A

Premature activation inside pancreas of trypsin – >activate other enzymes

Autodigestion of pancreas by pancreatic enzymes

Inflammation + haemorrhage of pancreas

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5
Q

Causes of acute pancreatitis?

A

Gallstones = obstruct MPDuct/terminal CBDuct

Ethanol = Thicken ductal secretion + Increased Ductal permeability to enzymes + Chemical injury

Trauma (Seatbelt/posterior penetration of duodenal ulcer ) = Mechanical injury of Acinar cells

Steroids

Mumps/CMV/Coxsackie = infect + injure acinar cells

Autoimmune

Scorpion sting

Hypercalcaemia = metabolic activation of enzymes
Hypertriglyceridaemia (>1000/dL) = Chemical injury of acinar cells

E RCP

Drugs – sulphur/NRTIs/protease inhibitors/thiazides

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6
Q

What effect does ethanol have On the sphincter of Oddi

and how does this affect the pancreas

A

Contract sphincter of Oddi @ ampler of vater

Decreased drainage of pancreas – >increased risk of activating premature enzymes

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7
Q

What effect does gallstones have On the pancreas

A

Block ampulla of vater – >Can’t drain pancreas – >decreased pancreas drainage – >increased risk of activating premature enzymes

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8
Q

What proenzyme does trypsin activate

What do these enzymes have an effect on

A

Proteases = damage ACINAR cell structure
Elastased = damage vessel wall + haemorrhage
Lipases + phospholipases = fat necrosis
Activated enzymes circulates blood

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9
Q

Clinical signs of pancreatitis

A

Fever nausea vomiting

Epigastric pain radiating to the back

Flank haemorrhage = Grey Turner Sign
Periumbilical haemorrhage = Cullen sign

Tetany: fat necrosis – >calcium buying to FA’s– >Decreased calcium Hypocalcaemia

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10
Q

What is the third space fluid

How does this relate to pancreatitis

A

It’s sequestered fluid = not available for maintaining the vol @vasc compartment i.e. non-functional ECF

At a P – 3rd space fluid = peripancreatic fluid due to autodigestion

Condition improves –>
3rd SF gets back in vascular compartment – >
fluid overload

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11
Q

Lab results for pancreatitis?

A

FALLSHH

Faecal elastase decreased
Amylase increased
Lipase increased
Leucocytosis neutrophilic
Serum im. reactive trypsin – CF @ babies Increased
HYPOcalcemia
hypoglycaemia – destroyed beta islets
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12
Q

Complications of pancreatitis

A

Trypsin enter Blood – >
(activ8 PT–>DIC)+(Destroy alv-cap interface-> ARDS)

Digest BV’s @Pancreas – >haemorrhage – > SHOCK

Digested pancreas – >
3rd space fluid sequestration – >
accumul8d digested panc. tissue around panc. – >
fibrous tissue surrounds
liquefactive necrosis + pancreatic enzymes – >
Pseudo cyst = Ab mass+ Persistent serum amylase = amylase vol > amylase renal clearance

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13
Q

Pancreatitis treatment

A

Nil by mouth
Meperidine/fentanyl for pain
Oxygen

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14
Q

How does chronic pancreatitis occur

A

Recurrent bouts of AP – >

Fibrosis of panc parenchyma +
duct obstruction = dilated ducts +
Dystrophic calcification concretions @imaging

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15
Q

Causes of chronic pancreatitis

A

CF at children :
Thick secretions – >
decreased pancreatic drainage – >
increased risk of premature enzyme activation

Alcohol addiction

Malnutrition

Auto immune/idiopathic = give octreotide

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16
Q

Clinically what do we see in chronic pancreatitis

A

Epigastric pain radiating to back
+
Pancreatic insufficiency – >

(Malabsorption) + (Steatorrhea-increased fat @ stool)
Fat soluble vitamin deficiency ADEK
Diabetes mellitus – damage islets = late complication

MOTHER
FUCKING
DICKHEAD

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17
Q

why are amylase and lipase not good markers for chronic pancreatitis

A

Because majority of pancreas is destroyed

Therefore not making enough amylase and lipase

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18
Q

Where does pancreatic adenocarcinoma arise from

A

Ducts

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19
Q

Risk factors for pancreatic adenocarcinoma

A

Seven Juicy Cunts And Dicks

Smoking, Jew/Africa, chronic pancreatitis, Age >50, diabetes

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20
Q

Pathogenesis of pancreatic adenocarcinoma

A

KRAS gene mutation
Suppressor gene mutation p16 p53
CA 19–9 tumour marker
– >

Often + pancreatic head (+ @head + tail)– >

Block CBD – >

Jaundice– >Billy Rubin go into blood

Pale stools + palpable gallbladder (backup pressure into GB therefore distended GB)

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21
Q

70 year female = presents for diabetes mellitus type 2 I

Possible DDX?

A

carcinoma in the body + tail ->
Pancreatic carcinoma– >
knockout islets – > type2 DM

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22
Q 
Patient presents with 
Pancreatitis
abdominal pain radiating to the back
Weight loss
Trousseau syndrome
Constructive jaundice + Courvoisier sign

What does he have

A

Trousseau syndrome = migratory thrombophlebitis

Palpable non-tender gallbladder = Courvoisier sign.

Pancreatic adenocarcinoma

23
Q

Treatment of pancreatic adenocarcinoma

A

Whipple procedure

Chemo, radiation

24
Q

What is biliary atresia

Explain how this leads to cirrhosis

A

Failure of formation of the lumen/
early destruction of extrahepatic biliary tree ->

Biliary obstruction @ 1st three months of life – >

Presented jaundice = conjugated Billy Rubin – >

Backpressure into liver = cirrhosis

25
Q

Three reasons home when you get gallstones

How do these reasons Develop

A

1.precipitation of Cholesterol or BilliRubin @bile = supersaturation

2.decreased bile salts/acids: help to solubilise cholesterol
Decreased BS/A – >high risk of chol. precipitation

3.gallbladder stasis – >increased risk of bacterial growth – >bacteria deconjugate BilliRubin -> bilirubins gallstones

26
Q

Explain how cholestyramine leads to cholesterol stone

A

Cholestyramine = lipid-lowering agent – >
binds bile acids – >
decrease recycling of bile acids + Ilium – >
decreased by the acids in the bile – >
increased p(cholesterol precipitation) -> chol. Stones

27
Q

What are the two types of gallstones

A

Cholesterol stones + Bilirubin pigment stones

28
Q

Most common gallstone?
Lucent/opaque?
Risk factors?
Contain what?

A

Cholesterol stones– 75–80%

Radiolucent

Clofibrate, Multiparity, Weight Loss
Obesity, Crohn’s, estrogen therapy, age, native USA

Cholesterol + CaCO3 + bilirubin pigment

29
Q

Two types of BilliRubin pigment stones?

A

Black pigment stone= Radiopaque

Brown pigment stone = radiolucent

30
Q

What are black pigment stones a sign of?

How does XS conjugated bilirubin lead to black pigment stones?

A

Chronic extravascular haemolytic anaemia =
sickle-cell/hereditary spherocytosis

XS CB – > UCB – >UCB + Ca2+ ->
calcium bilirubinate stones = Black pigment stones

31
Q

What are brown pigment stones a sign of?

How does the infection lead to brown pigment stones?

A

Sign of common bile duct infection seen in Asians

Infection – > (CB – >UCB @ bile)– >
Brown pigment stone

32
Q

Explain how oestrogen Increases the risk of cholesterol gallstones

A

Oestrogen – >

1.increase HMG CoA reductase –>increase CH synth
2.increased LDL receptor synth @hepatocyte -> increase CH uptake
3.increase HDL synth – >
Increased transport of CH from peripheral tissue to liver – >excrete @bile

33
Q

Explain how clofibrate, crohns, cirrhosis leads to cholesterol Stones

A

Clofibrate (lipid-lowering drug) – >
(Increase HMG-CoA activity – >increase CH synth)
+ (Decrease bile salt/acid – >decrees CH solubility
– >increase CH precipitation

Crohns = Decrease BA/S’s reabsorb @ ileum -> (Decrease bile salt/acid – >decrease CH solubility
– >increase CH precipitation

Cirrhosis = decrease BA/S production @hepatocyte
-> (Decrease bile salt/acid – >decrees CH solubility
– >increase CH precipitation

34
Q

Clinical stuff about cholelithiasis?

A
  1. usually asymptomatic
  2. complications:

a) biliary colic = fatty meal – >
CCK neurohormonal activation – >GB contract – >
force stone into cystic duct = lodged – >
waxing + waning RUQ pain

b) acute/chronic cholecystitis
C) acsending cholangitis
D gallstones ileus
E) gallbladder cancer

35
Q

55 year-old woman >man who happens to be a native American walks in with jaundice midepigastric colickypain that has shifted to RUQ and is Murphy sign positive walks into clinic .
What’s her problem

A

Acute cholecystitis

36
Q

Stage one of acute cholecystitis?

A

Food stimulus = GB contract against obstructed duct – >stone forced into CD or/+ CBD (Increase ALP = asc. cholangitis + jaundice/acute pancreatitis) – >
lodge in CD –> Midepigastric pain = colicky because GB contract against obstructed CD – > Nausea + vomit + no pain relief

37
Q

Stage two of acute cholecystitis

A

Stone impact in CD – >mucus accumulates behind obstruction – >
(chemical irritation of mucosa+
Bacterial growth = no invasion)E. coli >enterococcus bacteroides Clostridium
– > Pain shift to RUQ = dull + continuous radiate to right scapula/shoulder

38
Q

Stage three of acute cholecystitis?

A

Bacterial invasion of GB wall – > LLMS

Localised peritonitis & rebound tenderness +
Leukocytosis neutrophilic absolute +

Murphy sign POSITIVE = cos of pain -> inspiratory arrest on RUQ palpation

Subside attack if Stonefalls out of CD = 90% of time or GB perforate

39
Q

Stage four of acute cholecystitis

A

GB perforated + GB wall distension – >
compress lumens of intramural vessels >
Gangrenous necrosis + pressure ischaemia

40
Q

Why do we get an increasing alkaline phosphate Due to acute cholecystitis?

A

Epithelial lining gallbladder + biliary tract = has ALP therefore

Damage – >increased serum ALP

41
Q

If no HIDA tracer found @ duodenum where could the Stone be?

A

Common bile duct stone

42
Q

How does chronically cystitis occur

A

Long-standing cholelithiasis – >chemical irritation – >chronic inflammation of gallbladder

43
Q

Clinical signs of chronic cholecystitis

A

RRP

Rokitansky Aschoff sinus = outpouching of gallbladder mucosa in between smooth-muscle

Vague RUQ pain = radiates to right scapular area after eating

Increase chemical damage to GB wall – >
increase dystrophic calcification –>
porcelain gallbladder – >increased p(GB cancer)

44
Q

Explain how cholelithiasis can need to gallstone ileus

A

Fistula between GB + SI – >

air in biliary tree +
passage of gallstone into intestine – >

obstruct ileocecal valve – > gallstone ileus

45
Q

Histopathologist sees yellow and speckled mucosal surface with cholesterol deposited in macrophages What is this and why

A

Cholesterolosis due to XS cholesterol @bile

46
Q

Histopathologist sees distended gallbladder and atrophy of mucosa/muscle with clear secretions what is this and why

A

Hydrops of gallbladder due to chronic obstruction of Cystic duct

47
Q

What is ascending cholangitis due to
Symptoms
Pathophysiology

A

bile duct bacterial infection

Enteric gram-negative bacteria Walk up ductal system –>
jaundice fever RUQ pain and sepsis

48
Q

Why is there an increase in ascending cholangitis + Choledochal lethiasis?

A

Bile constantly flows – >washes away rising bacteria

BUT if have choledochal lethiasis I.e. stone in duct
->
have decreased flow – >Bacteria move up

49
Q

Where does gallbladder adenocarcinoma arise from?

Risk factors?

A

Arise from glandular epithelium @GB wall

Risk factor = cholelithiasis – porcelain gallbladder

50
Q

Old woman presents with new onset Coeli cystitis what does she have ?

A

Cancer poor Prognosis

51
Q

Kid is less than 10 years old presents for jaundice and abdominal pain
What does he have
Diagnosis? Treatment?

A

Choledochal cyst
Ultrasound/PRCP

Surgery

52
Q

Patient with polycystic kidney disease comes into G I ward. Histopathologist asks you what he sees in the intrahepatic bile ducts + portal tract fibrosis?

Treatment?

A

Segmental dilation + portal tract fibrosis

Liver transplant and resection

53
Q

Explain primary and secondary biliary cirrhosis

A

1.autoimmune reaction = Antimitochondrial AB = IgM – >
(lymphocytic infiltrate + granuloma) – >
destroy intralobular bile ducts (Obstructive jaundice = liver damage = cirrhosis)
– >Conjugated hyperbilirubinaemia

2.
Gallstones + Biliary strictures + Pancreatic cancer
-> extraHEP biliary obstruction ->
increased pressure in intrahepatic ducts – >
fibrosis + bile stasis

54
Q

Explain primary sclerosing cholangitis

A

Unknown cause (Assoc. with ulcerative colitis
p–ANCA positive Hypergammaglobulinaemia)
– >onionskin bile peri ductal duct fibrosis – >

Alternating strictures/dilation/beading of intra + extra hepatic bile ducts on ERCP/MRCP =
Inflammation + fibrosis – >
conjugated hyperbilirubinaemia

(secondary biliary cirrhosis/cholangiocarcinoma )

55
Q

Causes of cholangiocarcinoma?
Location of cholangiocarcinoma?
Presentation?
Diagnosis?

A

Primary school arousing cholangitis, chonorchis, Thorotrast, choledochal cyst, Caroli disease – >

Cancer @:
CBD/ampulla of Vater
L/R hepatic duct junction = Klatskin tumour
Intrahepatic ducts

Jaundice, hepatomegaly, 
palpable GB (Courvoisier sign)

US/ERCP – >surgery

56
Q

What is jaundice?

What is the earliest sign of jaundice + why here?

A

Yellow discolouration of skin

Scleral icterus = yellow discolouration of ie = Sclera has high affinity for Bilirubin

GI Liver (11 decks)

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