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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
What is biliary atresia | Explain how this leads to cirrhosis
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
Three reasons home when you get gallstones | How do these reasons Develop
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
Explain how cholestyramine leads to cholesterol stone
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
What are the two types of gallstones
Cholesterol stones + Bilirubin pigment stones
28
Most common gallstone? Lucent/opaque? Risk factors? Contain what?
Cholesterol stones– 75–80% Radiolucent Clofibrate, Multiparity, Weight Loss Obesity, Crohn's, estrogen therapy, age, native USA Cholesterol + CaCO3 + bilirubin pigment
29
Two types of BilliRubin pigment stones?
Black pigment stone= Radiopaque | Brown pigment stone = radiolucent
30
What are black pigment stones a sign of? | How does XS conjugated bilirubin lead to black pigment stones?
Chronic extravascular haemolytic anaemia = sickle-cell/hereditary spherocytosis XS CB – > UCB – >UCB + Ca2+ -> calcium bilirubinate stones = Black pigment stones
31
What are brown pigment stones a sign of? | How does the infection lead to brown pigment stones?
Sign of common bile duct infection seen in Asians Infection – > (CB – >UCB @ bile)– > Brown pigment stone
32
Explain how oestrogen Increases the risk of cholesterol gallstones
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
Explain how clofibrate, crohns, cirrhosis leads to cholesterol Stones
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
Clinical stuff about cholelithiasis?
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
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
Acute cholecystitis
36
Stage one of acute cholecystitis?
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
Stage two of acute cholecystitis
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
Stage three of acute cholecystitis?
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
Stage four of acute cholecystitis
GB perforated + GB wall distension – > compress lumens of intramural vessels > Gangrenous necrosis + pressure ischaemia
40
Why do we get an increasing alkaline phosphate Due to acute cholecystitis?
Epithelial lining gallbladder + biliary tract = has ALP therefore Damage – >increased serum ALP
41
If no HIDA tracer found @ duodenum where could the Stone be?
Common bile duct stone
42
How does chronically cystitis occur
Long-standing cholelithiasis – >chemical irritation – >chronic inflammation of gallbladder
43
Clinical signs of chronic cholecystitis
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
Explain how cholelithiasis can need to gallstone ileus
Fistula between GB + SI – > air in biliary tree + passage of gallstone into intestine – > obstruct ileocecal valve – > gallstone ileus
45
Histopathologist sees yellow and speckled mucosal surface with cholesterol deposited in macrophages What is this and why
Cholesterolosis due to XS cholesterol @bile
46
Histopathologist sees distended gallbladder and atrophy of mucosa/muscle with clear secretions what is this and why
Hydrops of gallbladder due to chronic obstruction of Cystic duct
47
What is ascending cholangitis due to Symptoms Pathophysiology
bile duct bacterial infection Enteric gram-negative bacteria Walk up ductal system –> jaundice fever RUQ pain and sepsis
48
Why is there an increase in ascending cholangitis + Choledochal lethiasis?
Bile constantly flows – >washes away rising bacteria BUT if have choledochal lethiasis I.e. stone in duct -> have decreased flow – >Bacteria move up
49
Where does gallbladder adenocarcinoma arise from? | Risk factors?
Arise from glandular epithelium @GB wall Risk factor = cholelithiasis – porcelain gallbladder
50
Old woman presents with new onset Coeli cystitis what does she have ?
Cancer poor Prognosis
51
Kid is less than 10 years old presents for jaundice and abdominal pain What does he have Diagnosis? Treatment?
Choledochal cyst Ultrasound/PRCP Surgery
52
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?
Segmental dilation + portal tract fibrosis Liver transplant and resection
53
Explain primary and secondary biliary cirrhosis
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
Explain primary sclerosing cholangitis
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
Causes of cholangiocarcinoma? Location of cholangiocarcinoma? Presentation? Diagnosis?
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
What is jaundice? | What is the earliest sign of jaundice + why here?
Yellow discolouration of skin Scleral icterus = yellow discolouration of ie = Sclera has high affinity for Bilirubin

GI Liver (11 decks)

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