Hepatobiliary and Pancreatic Pathophysiology Flashcards

1
Q

Gross Anatomy of the Liver

A

Blood rich!
4 lobes- Right, Let, Caudate and Quadrate
Falciform ligament and Round ligament
Hepatic artery, portal vein and hepatic duct at the porta hepatis
Common hepatic duct joins with cystic duct to form common bile duct

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2
Q

The Splanchnic Circulation

A

Abdominal Aorta
-Celiac trunk branches into gastric, hepatic, splenic arteries
Superior mesenteric brings blood to duodenum -> transverse colon
Inferior mesentaric-> transverse colon-> rectum

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3
Q

Hepatic Portal Circulation

A

Vein that drains the spleen, pancreas, stomach, intestines that increases after a meal
Nutrient rich blood delivered to the liver to be processed
After processing in the liver, this blood is sent to the inferior vena cava to be sent to the heart for distribution to the entire body

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4
Q

Microscopic Anatomy of the Liver

A

Liver lobules with liver cells or hepatocytes with sinusoids or fine blood vessels between the hepatocytes
Used for filtration
Filters from outside to central vein
Kupffer cells remove debris and bacteria
Bile canaliculi move the created bile from the inside out to ducts that lead to bigger ducts and then to the hepatic duct

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5
Q

Bile Duct System

A

Hepatic duct drains liver
Cystic duct drains the gall bladder
They join to form the common bile duct
This empties into the duodenum at the hepatopancreatic ampulla. The pancreatic duct also empties into this ampulla. The sphincter of Oddi is a sphincter of bile and digestive enzymes.
When the sphincter is closed, bile backs up into the ducts of the biliary system and then into the gallbladder for storage…What happens when the gallbladder is removed?

Bile made by the liver can no longer be stored between meals. Instead, the bile flows directly into the intestine anytime the liver produces it. Thus, there still is bile in the intestine to mix with food and fat. … The only clear side effect of removal of the gallbladder is diarrhea.

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6
Q

What does the liver do?

A

Produces bile
Stores glucose as glycogen
-Can release glycogen when glucose stores are low
-Can also form new glucose from fats and proteins
Use amino acids to make proteins
Store fat-soluble vitamins
Detoxification
Forms lipoproteins and cholesterol
-Lipoproteins form our HDL, LDL and VLDL
-Cholesterol is the precursor for steroid hormones, bile salts, and also helps by forming part of the cell membrane
Deamination
-This is the removal of the amino group portion of the amino acid
-Converted to ammonia..bad! This is quickly converted into urea or uric acid which is secreted in the urine.. so with high protein diets body may have trouble eliminating all the waste products of protein metabolism

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7
Q

The Gallbladder

A

Green muscular sac under the liver
Stores bile and concentrates it
CCK or cholecystokinin is an intestinal hormone that releases to the blood from the duodenum and stimulates the gallbladder contraction

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8
Q

Bile

A

Yellow-green
Alkaline
Bile salts, pigments, cholesterol, fats, phospholipids
Emulsify fats
Recycled by the enterohepatic circulation
-Bile salts reabsorbed by the ileum (80%), 5-10 times per day
-Returned to liver by hepatic portal blood
-Resecreted

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9
Q

Bilirubin

A

RBCs are broken down in the spleen (and other places like bone marrow and liver)
Form heme and globin (globin is reused as an amino acid)
Heme is converted into bilirubin (yellow brown pigment)
Bilirubin is carried to the liver where it is conjugated (combined with 2 molecules of glucuronic acid) making it conjugated bilirubin (which is less toxic form of bilirubin and also it is water-soluble making it more easily secreted)
Once bilirubin reaches the colon it is converted into urobilinogen and then to urobilin (which is responsible for the color of fees)

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10
Q

Jaundice

A

Hyperbilirubinemia- bilirubin levels in the blood are above the normal range of 0.3-1mg/dl
Jaundice- yellow/brown color in skin and sclera when bilirubin is above 2mg/dl in the blood
May be due to excessive lysis of RBC (hemolytic jaundice) , inability of liver to conjugate or excrete bilirubin (from virus or damage or neontal jaundice with infants in first 1-2 weeks), or obstruction of the bile duct system.

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11
Q

Bilirubin Levels

A

Bilirubin levels in adults
Total bilirubin- 0.3mg/dL or 5.0-17.0mmol/L
Direct bilirubin- 0.0-.2mg/dL or 0.0-3.4mmol/L

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12
Q

Kernicterus

A

Hemolytic jaundice in newborns leads to brain damage
Can be dangerous because they cannot keep unconjugated bilirubin out of the blood brain barrier and it can damage the brain
And the kidney can only excrete the conjugated form

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13
Q

Obstructive Jaundice

A

Bile duct gets blocked, and conjugated and unconjugated bilirubin will “back up” into the system
Causes pruitis (intense itching)
Light to gray stools
Can be caused by blocking or scarring of the liver or blocking of the duct system (gallstones tumors etc)

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14
Q

Gallstones

A

AKA biliary calculi
Cholesterol crystalization
Agonizing pain

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15
Q

Hepatitis

A

Hep A- fecal oral route. Shellfish may be contaminated by sewage. Normal immune response clears the virus and creates lifelong immunity.

Hep B virus- more serious. HBC aka Dan particle
Located inside all body fluids, but not in feces. S/S may be more intense than A but usually subside after 4-6 weeks with immunity after that. May progress to a chronic condition. Carriers are those who cannot clear Hep B since they are able to continue to spread the disease (this can happen with a small amount of Hep C patients as well)

Hep D virus- (with another infection) incomplete viral particle that cannot infect unless it is with Hep B infection. When combined can lead to massive liver necrosis. Seen with shared needles and homosexual males.

Hep C virus- Blood bourn and is more difficult to transmit, so usually seen in repeated exposure of drug abusers. 40% idiopathic with the book sighting the example of barbers razors!! No lasting immunity with exposer. Half will have chronic disease with liver dmage due to immune attack on liver cells

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16
Q

Chronic Hepatitis

A

10% of patients have a continued problem beyond 6 months that may last months to years.
Causative agent is usually Hep C.
Damage to the liver may cause necrosis, scarring, and then cirrhosis. Hepatocarcinoma may also be result of this disease.

17
Q

Cirrhosis

A

Long term necrosis caused by damage (10-15%) can lead to this.
Inflammation sets in stimulating fibrosis causing scars with nodules of repairing hepatocytes around the scars
Causes portal HTN and hepatic disfunction
-Portal HTN occurs when blood flow through the liver is obstructed and blood cannot get to the liver
-Blood then backs up into collateral circulation such as hemorrhoids, abdominal surface and esophageal varices may form
-Ascites and splenomegaly

18
Q

Fatty Liver

A

From alcoholism or eating too much
Can also lead to scarring and cirrhosis
Overstress hepatocytes
Severe obesity

19
Q

Pancreas

A

Gland that sits in duodenum
Retroperitoneal
Secretes exocrine and endocrine substances
-Acini are clusters of cells that secrete pancreatic juice
-Islets of Langerhans secrete insulin and glucagon
Main pancreatic duct
-Combines with common bile duct as it enters at the hepatopancreatic ampula

20
Q

Diseases of the Pancreas

A

Pancreatitis

  • May be acute or Chronic
  • The pancreas is damaged by some means. Alcohol drugs, blockage of the ducts that drain it.
  • Can lead to necrosis of the pancreas and damage to the surrounding vasculature causing hemorrhage and hypovolemic shock.
  • This damage is caused by a release of the potent enzymes in the pancreas that attack its own tissues
  • Chronic occurs after repeated acute attacks causing scar tissue of the pancreas. May also lead to DM do to damage of the Islets of Langerhans