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Pathophysiology Exam 3 > Liver > Flashcards

Liver Flashcards

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1
Q

Explain hepatic portal circulation
A ___ is located b/w two ___ beds. The hepatic portal vein collects __ from ___ in visceral structures located in the ___ and empties into the ___. Hepatic veins __ blood to the __ __ __.

A

A vein is located b/w two capillary beds. The hepatic portal vein collects blood from capillaries in visceral structures located in the abdomen and empties into the liver. Hepatic veins return blood to the inferior vena cava.

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2
Q

What makes up the portal triad?

A

hepatic portal vein (80%)
hepatic artery (20%)
bile duct
lymphatic vessel

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3
Q

Describe the role of hepatocyte function (bile)

A

Liver - hepatocytes synthesize cholesterol to form primary bile acids –> Bile acid pool –> AA (glycine and taurine) conjugate to form bile salts in bile –> Gallbladder: some bile is stored for release during eating and Duodenum and jejunum (bile salts emulsify fats and form micelles to transport fats through the unstirred layer, Micelles release fats at the brush border, Free bile salts proceed through the intestinal lumen –>Rectum: 15%-35% of bile salts are excreted in feces, Ileum and Colon: bile salts are actively transported across the intestinal lumen or are de- conjugated by bacteria into secondary bile acids that diffuse passively across the lumen –> Hepatic portal vein: 65-85% of bile salts and secondary bile acids enter the circulation with protein binding and are transported to the liver

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4
Q

Name 5 hepatic injuries and findings

A 
fibrosis and cirrhosis
lab evaluation of liver disease
jaundice
cholestasis
portal hypertension
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5
Q

Fibrous tissues in formed in response to

A

inflammation

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6
Q

What is bridging fibrosis

A

with time, fibrous stands link regions of the liver

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7
Q

With continuing fibrosis and parenchymal injury, the liver is subdivided into

A

nodules of regenerating hepatocytes surrounded by scar tissue

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8
Q

Fibrosis is considered a _____ consequence of _______ damage and has lasting consequences on patterns of _____ _____ and ______ ___ _______

A

irreversible
hepatic
blood flow and perfusion of hepatocytes

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9
Q

Lab eval of liver disease: hepatocyte integrity

A

serum aspartate aminotransferase (AST, SGOT)

serum alanine aminotransferase (ALT, SGPT)

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10
Q

Lab eval of biliary tract integrity

A

serum alkaline phosphatase (AP, ALP, ALKP, etc)

serum y-glutamyltransferase (GGT)

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11
Q

Lab eval of bilirubin

A

direct (conjugated)

indirect (unconjugated)

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12
Q

Lab eval of hepatocyte function

A

serum albumin
prothrombin time
serum ammonia

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13
Q

Consequences of liver disease

4H, JF, GP, SWM

A

hyPO -albuminemia, ammonemia, glycemia, gonadism
Jaundice and cholestasis
gynecomastia and palmar erythemia
spider angiomas, weight loss, muscle wasting

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14
Q

Consequences of liver disease: Hepatic portal HTN

SEA HC

A 
Splenomegaly
Esophageal varices
Ascites
Hemorrhoids
Caput medusae
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15
Q

Consequences of liver disease: Life Threatening Complications (HHH MEC)

A 
Hepatic encephalopathy
Hepatorenal syndrome
Hepatocellular carcinoma
Multiple organ failure
Esophageal varices rupture
Coagulopathy
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16
Q

Explain bilirubin metabolism and elimination

A
  1. Normal bilirubin production (.2-.3g/day) is derived primarily from the breakdown of senescent circulating erythrocytes, with a minor contribution from degradation of tissue heme containing proteins
  2. Extrahepatic bilirubin is bound to serum albumin and delivered to the liver
  3. Hepatocellular uptake
  4. Glucuronidation by glucuronosyltransferase in the hepatocytes generates bilirubin monoglucuronides and diglucuronides which are water soluble and readily excreted into bile.
  5. Gut bacteria deconjugate the bilirubin and degrade it to colorless urobilinogens. The urobilinogens and the residue of intact pigments are excreted in the feces with some reabsorption and re-excretion into bile
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17
Q

Jaundice: accumulation of excess ___ in ____

A

bilirubin in blood

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18
Q

Jaundice: Causes

A 
excess bilirubin production
reduced hepatic uptake
impaired conjugation
decreased heptocellular excretion
impaired bile flow
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19
Q

Jaudice:
excess bilirubin production, reduced hepatic uptake,
impaired conjugation result in ___ ___ ___

A

increased unconjugated bilirubin

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20
Q

Jaudice:
excess bilirubin production, reduced hepatic uptake,
impaired conjugation result in increased unconjugated bilirubin:
____ to water, tight bound to ___, NOT excreted by ___

A

insoluble in water, tightly bound to albumin, not excreted by kidney

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21
Q

Jaudice:
excess bilirubin production, reduced hepatic uptake,
impaired conjugation result in increased unconjugated bilirubin:
Unbound plasma fraction

A

diffused in tissue
produces toxic injury
increases in hemolytic disease of the newborn
may lead to severe neurological damage

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22
Q

Jaundice: decreased heptocellular excretion, impaired bile flow result in ___ ____ ____

A

increased conjugated bilirubin

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23
Q

Jaundice: decreased heptocellular excretion, impaired bile flow result in increased conjugated bilirubin: ___ in water, ___ bound to albumin, excreted by ____

A

soluble in water, weakly bound to albumin, excreted by kidney

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24
Q

Cholestasis: in the parenchyma, cholestatic heptocytes are ___ with dilated canalicular spaces, ___ cells may be seen, and ___ cells frequently contain regurgitated ___ ___.

A

enlarged with dilated canclicular spaces, apoptic cells may be seen and Kupffer cells frequently contain regurgitated bile pigment

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25
Cholestasis: in the portal tract of obstructed livers, there is also bile ___ ____, ___, bile pigment ___, and eventually ____ ____
bile ductular proliferation, edema, bile pigment retention, eventually neutrophilic inflammation
26
____ immediately adjacent to portal trans are ___ and undergoing __ ___
hepatocytes swollen toxic degeneration
27
Hepatic failure is __ and __ hepatic destruction
sudden and massive
28
Hepatic failure is the often end point of
progressive liver damage
29
Hepatic failure means that ___% of liver function must be lost
80-90%
30
Hepatic failure is __ ___
life threatening (multiple organ failure)
31
What are the special problems in hepatic failure?
hepatic encepalopathy | hepatorenal syndrome
32
Cirrhosis impairs __ __ through the liver and causes __ __ __.
blood flow | hepatic portal hypertension
33
Cirrhosis impairs blood flow through the liver and causes hepatic portal hypertension which causes what 3 problems?
``` ascites - edema of the abdomen portosystemic shunts (eso varices, hemorrhoids, caput medusae) splenomegaly ```
34
What are the three different types of portosystemic shunts in cirrhosis?
esophageal varices, hemorrhoids, caput medusae
35
Clinical manifestations of liver inflammation
pain, fever, N/V, anorexia, fatigue
36
Clinical manifestations of Liver necrosis
1.) decreased bilirubin metabolism (hyperbilirubinemia, jaundice) decreased bile in GI tract (light colored stools) Decreased vitamin K absorption (bleeding tendency) Increased urobilinogen (dark urine) 2.) decreased metabolism of proteins, carbs and fats (hypoglycemia) Decreased plasma proteins (ascites and edema) 3.) Decreased hormone metabolism Increased androgens and estrogens (gynecomastia, loss of body hair, menstrual dysfunction, spider angiomas, palmar erythema) Increased ADH and aldosterone (edema) 4.) Biochemical alterations Elevated AST, ALT levels Elevated bilirubin low serum albumin prolonged prothrombin time elevated alkaline phosphatase 5.) liver failure --> hepatorenal failure 6.)hepatic encephalopathy 7.)hepatic coma 8,)Death
37
What are 7 liver and gallbladder diseases?
``` viral hepatitis alcoholic liver disease hemochromatosis obstructive biliary tract disease circulatory disorders primary carcinoma of the liver cholelitiasis and choledocholithiasis ```
38
Viral hepatitis: Causative Agents (6)
hepatitis A,B,C,D,E,G virus
39
Viral Hepatitis: clinical syndromes
carrier state/asymptomatic infection Acute viral hepatitis Chronic viral hepatitis
40
``` Hep A & E both are: self- ___ ___ wk incubation do not cause ___ state do not cause ____ ____ do not cause ____ __ transmission - poor hygiene not usually present in __ ```
``` self-limiting 2-8 week incubaton do not cause carrier state do not cause chronic hepatitis do not cause cancer oral transmission not usually present in USA ```
41
who is winning
I am
42
HAV: common ___ disease in ___ countries adult infection is more ___ ___ infections - associated with ___
common childhood disease in developing countries adult infection is more dangerous sporadic infections - associated with oysters
43
HEV: ___ infections are ___ typically endemic and seen in ____ high (20%) mortality rate in __ ___
sporadic infections are rare typically endemic and seen in travelers high mortality rate in prego women
44
``` HEP B,C,D: cause ___ state cause __ __ cause __ (__ NO increase over __) ___ transmission - close personal contact present in __ ```
``` cause carrier state cause chronic hepatits cause cancer (HDV no increase over HBV) parental transmission - close personal contact present in USA ```
45
Hepatic steatosis aka ____ ____
fatty liver
46
Hepatic steatosis is __ damaged liver cells can take up __ __ normally but cannot incorporate them into ___ for ___
alcohol damaged liver cells can take up fatty acids normally but cant incorporate them into lipoproteins for export.
47
Alcoholic liver disease consists of: (3)
``` hepatic steatosis (fatty liver) (90-100%) alcoholic hepatitis (10-35%) cirrhosis (8-20%) ```
48
Hemochromatosis aka
hereditary iron overload
49
``` Hemochromatosis: uncontrolled uptake of ___ , ~1g/year ___ predominance 5-7:1 (menustration) autosomal ___ ~0.5% ____ carriers ~10% problems appear ___ (__ years old) ```
``` uncontrolled uptake of iron male predominance autosomal recessive heterozygous carriers problems appear late (50+ years old) ```
50
Hemochromatosis: Problems with fully developed disease:
cirrhosis (~100%) DM (80%) Skin pigmentation (80%)
51
Another primary iron overload disease is
bantu siderosis
52
Secondary iron overload diseases:
Transfusion : 1 transfusion=0.25g of iron | Ineffective erythripoiesis: B-Thakassemia, Sideroblastic anemia
53
Obstructive biliary tract disease: secondary biliary cirrhosis is the
obstruction of extra hepatic biliary tract
54
Obstructive biliary tract disease: secondary biliary cirrhosis : common causes
gallstones, biliary atresia, malignancies of biliary tree or pancreas, strictures resulting from surgery
55
``` Obstructive biliary tract disease: primary biliary cirrhosis: destruction of ___ ___ ___ elevated ___ and ___ ____ late in disease _____ antibodies often ___ ```
``` destruction of intrahepatic bile ducts elevated alkaline phosphatase and cholesterol hyperbilirubinemia late in disease antimitochondrial antibodies often fatal ```
56
``` Obstructive biliary tract disease: primary sclerosing cholangitis: ____ + ____ bile ducts associated with ___ ___ (70%) develops after __ ___ elevated __ ___ generally without __ ___ ```
``` intrahepatic and extrahepatic bile ducts associated with ulcerative colitis develops after UC elevated alkaline phosphatase generally without antimicrobial antibodies ```
57
What are the 4 circulatory disorders of the liver?
hepatic vein outflow obstructon impaired intrahepatic blood flow impaired portal vein inflow impaired hepatic artery inflow
58
Circulatory disorders of the liver: Hepatic vein outflow obstruction causes
hepatic vein thrombosis (Budd-Chiari syndrome) | veno-occlusive disease
59
Circulatory disorders of the liver: Hepatic vein outflow obstruction manifestations (HAA EJ)
hepatomegaly, ascites, abdominal pain | Elevated transaminases, jaundice
60
Circulatory disorders of the liver: Impaired intrahepatic blood flow causes
Cirrhosis, sinusoid occlusion, systemic circulatory compromise
61
Circulatory disorders of the liver: Impaired intrahepatic blood flow manifestations (AEE)
Ascites (cirrhosis) esophageal varices (cirrhosis) elevated transaminases
62
Circulatory disorders of the liver: Impaired portal vein inflow causes
portal vein obstruction by thrombosis or tumor
63
Circulatory disorders of the liver: Impaired portal vein inflow manifestations (I SEA)
Intestional congestion splenomegaly esophageal varices ascites
64
Circulatory disorders of the liver: Impaired hepatic artery inflow causes
complications of liver transplantation
65
Circulatory disorders of the liver: Impaired hepatic artery inflow manifestations
ischemia to bile ducts and parenchyma | potential loss of graft
66
Primary carcinoma of the liver aka
hepatocellular carcinoma (HCC)
67
Hepatocellular carcinoma: | arise from ___
hepatocytes
68
Hepatocellular carcinoma: caused by
``` HBV Chronic liver disease (HCV and alcohol) aflatoxin tyrosinemia (40%) cirrhosis (90%) ```
69
Hepatocellular carcinoma: early ___ gives great __ rate rate of ___ varies with __ rate worldwide mean survival ~ ___ ___
early HBC gives great rate to HCC rate of HCC varies with HBV rate worldwide mean survival ~7 months
70
Cholelithiasis aka
gallstones
71
``` Cholelithiasis: ___ million Americans (~10% adults) ___ variability (4% Asia, 40% South America) ____ new cases/year (___ surgery) ___ deaths/year usually ___ (70-80%) ```
``` >20 million americans worldwide variability ~1 million new cases/year (~2/3 surgery) ~1000 deaths/year usually asymptomatic ```
72
Risk factors for cholesterol stones (80%) (5F GH)
``` Fair Fat Fertile Forty Female Gallbladder stasis Hyperlipidemia ```
73
Risk factors for pigment stones (20%)
Chronic hemolytic syndromes Biliary infection GI disorder (Crohn disorder) Asian>Western
74
What is Choledocholithiasis?
presence of stones in the biliary tree
75
Choledocholithiasis: problems
``` biliary obstruction pancreatitis cholangitis hepatic abscess chronic liver disease with biliary cirrhosis acute calculous cholecystitis ```
76
Acute pancreatiitis: causes "I GET SMASHED"
Idiopathic Gallstone Ethanol Trauma Steriods Mumps (Paramyxovirus, E-Barr, Cytomegalovirus) Autoimmune disease (Lupus, polyarteritis nodosa) Scorpion sting (Tityus Trinitatis, snake bites) Hyper-calcemia, lipidemia, triglyceridemia HYPOthermia ERCP (Endoscopic retrograde cholangio pancreatography Drugs
77
Who knows this material?
I DO :)
78
Who is going to get an A+?
I AM :)

Pathophysiology Exam 3 (2 decks)

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